General Flashcards

Question

Jugular bulb venous oxygen saturation monitoring (SjVO2) measures...

Answer 1

Jugular bulb venous oxygen saturation monitoring (SjVO2) measures the mixed venous oxygen saturation in the jugular venous bulb. Represents balance between global cerebral oxygen supply and demand.

Answer 2

At a PaCO2 level below 25 mmHg, the vasoconstriction response to PaCO2 is blunted. At PaCO2 levels of 20 mmHg, cerebral ischemia occurs due to a leftward shift in the oxyhemoglobin dissociation curve, with a subsequent decrease in CBF. Anaerobic metabolism and decreased oxygen consumption occur at PaCO2 levels below 20 mmHg.

Answer 3

Temperature changes CBF by 6% for every 1 degree Celsius, due to corresponding changes in CMRO2 (metabolism). CBF decreases in hypothermia and increases in hyperthermia. This has led to extensive use of hypothermia for multiple types of surgeries including cardiac, thoracic aneurysm repair, and cerebral aneurysm repair. NOTE: Cerebral blood flow is also directly affected by a number of other factors that DO NOT AFFECT *metabolism* including arterial partial pressures of carbon dioxide (PaCO2) and oxygen (PaO2) and mean arterial blood pressure (MAP).

Answer 4

32-36 celsius

Answer 5

All volatile anestetics (including NO) cause cerebral vasodilation and increase CBF. ALWAYS KEEP MAC <1.0 IN NEURO CASES WHERE ICP IS A CONCERN!!!

Answer 6

Sevoflurane All volatile anesthetics cause reduction in myocardial contractility. However, Isoflurane and Desflurane compensate with an increase in heart rate due to preserved carotid baroreceptor reflex and thus little/no change in overall CO. Sevoflurane blunts carotid baroreceptor reflex. NO, on the other hand, tends to increase sympathetic output increasing HR and CO.

Answer 7

The Meyer-Overton correlation states that lipid solubility is directly correlated with anesthetic potency. Related potency of volatile anesthetics in olive oil.

Answer 8

NMDA antagonist (noncompetitive) - primary anesthetic effect GABA-A agonist - anxiolysis Opioid receptor agonist (indirect, induces release of endogenous opioids) - analgesic Nitrous oxide’s primary anesthetic effect is through its inhibition of NMDA receptors.

Answer 9

Nitrous oxide does not signficantly increase PONV when used under 1 hour. NOTE: Using nitrous oxide in laparoscopic surgery can lead to difficult surgical visualization in prolonged surgeries (>1 hr)

Answer 10

PVR- increases (esp in pts with pulmonary HTN and mitral stenosis) SVR- increases Nitrous oxide is commonly combined with potent volatile anesthetics to maintain general anesthesia. Nitrous oxide increases sympathetic activity and vascular resistance when given in a 40% concentration. When N2O is combined with volatile anesthetics, systemic vascular resistance and BP are greater than when equipotent concentrations of the volatile anesthetics are evaluated without N2O. These effects might not be due soley sympathetic activation from N2O per se, but may be partially attributed to a decreases in concentration of the coadministered potent volatile anesthetic required to achieve a MAC equivalent when using N2O.

Answer 11

The relatively higher concentrations of nitrous oxide (up to 70%) required to maintain general anensthesia compared to other potent inhaled anesthetics and its low solubility result in the rapid alveolar elimination of large amounts of nitrous oxide following cessation of the anesthetic. The flooding of nitrous oxide results in the displacement of oxygen and CO2 in the alveoli, leading to a temporary hypoxia. Diffusion hypoxia can last for 5-10 minutes. Treat with supplemental oxygen.

Answer 12

**Nitrous oxide has decreased fat solubility relative to volatile anesthetics.** Thus, leading to lower accumulation of nitrous oxide in fat tissue and faster removal from the body after discontinuation. In fact, Nitrous oxide's solubility is relatively similar in the fat, muscle, and vessel-rich groups. In contrast, the volatile anesthetics have much higher fat solubility than the muscle and vessel rich groups.

Answer 13

SVR- vasodilation PVR- vasoconstriction (HPV) Hypoxia produces vasodilation in systemic circulation due to local nitric oxide production. In the acute phase nitric oxide induced vasodilation tends to dominate over chemoreceptor induced sympathetic discharge and circulating catecholamines. Hypoxia produces vasoconstriction in pulmonary circulation due to increased intracellular calcium within endothelial cells in setting of low oxygen (mechanism of HPV).

Answer 14

a2 agonist At the brainstem, Dexmedetomidine acts within the pons at the locus cereleus (responsible for arousal, primary source of adrenergic neurotransmitters in the brain) inhibiting the presynaptic release of norepinephrine to produce sedation (sedation resembles natural sleep pattterns, w/ delta waves on EEG) At the spinal cord, Dexmedetomidine acts on interneurons in the doral horn causing hyperpolarization and decreasing substance P and glutamate transmission to produce analgesia. NOTE: Dexmedetomidine is more selective for a2 than clonidine. (a2:a1 receptor ratio 1600:1 vs a2:a1 receptor ratio 220:1) Dexmedetomide commonly causes bradycardia and hypertension after an initial bolus dose (brady from the baroreceptor reflex). If followed by an infusion, bradycardia and hypotension can be seen. The reported overall frequency of side effects are hypotension > hypertension > bradycardia.

Answer 15

Obstructive Sleep Apnea >10 sec with >90% airflow reduction WITH respiratory effort Central Sleep Apnea >10 sec with >90% airflow reduction WITHOUT respiratory effort

Answer 16

CMRO2- decreases CBF- decreases Dexmedetomidine demonstrates a dose-dependent reduction in CBF which is correlated to a decrease in CBV. This action is primarily mediated by its ability to reduce CMRO2 through its alpha-2 receptor agonism. By decreasing CMRO2, cerebral autoregulation will concomitantly decrease CBF and therefore CBV despite the vasodilating effect on Dexmedetomidine.

Answer 17

Dose reduction of Dexmedetomidine is recommended in patients with severe hepatic dysfunction. Dexmedetomidine is metabolized and cleared by the liver. Dose reduction is not required with renal insufficiency. NOTE: Dexmedetomidine has no CYP450 drug interactions.

Answer 18

NO, Dexmedetomidine does not affect the ventilatory response to hypercarbia. Ventilatory response to hypercarbia is present even at doses associated with unresponsiveness. Dexmedetomidine does, however, decrease minute ventilation. NOTE: Elimination half life is 2-3 hrs. Context sensitive half life is 4 min after a 10 minute infusion and 250 min after an 8 hr infusion.

Answer 19

Increase in V/Q mismatch due to dysregulated hypoxic pulmonary vasoconstriction.

Answer 20

1) Direct sympathetic stimulation 2) Inhibits catecholamine reuptake 3) Vagal nerve inhibitor NOTE: In catecholamine depleted states (critical illness, shock), ketamine can cause a paradoxical decrease in HR and/or BP.

Answer 21

See attached picture NOTE: Ketamine should be avoided in patients with increased ICP, increased IOP, severe or uncontrolled CAD, severe liver disease (metabolized in liver), severe renal dysfunction (exreted by kidneys), pregnancy, and underlying psychiatric disease associated with psychosis. Ketamine produces dissociative anesthesia that can be described as a trance-like cataleptic unconcious state (eyes open, spontaneous respiration, unconcious, nonresponsive to painful stimuli). The dissociative state seems to result from a functional dissociation: inhibition of thalamocortical pathways and stimulation of the limbic regions of the brain. Psychomimemtic effects of ketamine (vivid dreams, hallucinations) can be minimized with concomitant use of benzodiazepines. The risk of laryngospasm due to secretions is higher with IM administration than with IV adminstration.

Answer 22

Easy way to remember is: 0.3mg/kg bolus prior to incision 0.2mg/kg/hr infusion "The ideal dose of sub-anesthetic ketamine is 0.1-0.3 mg/kg as a bolus and 0.1-0.3 mg/kg/h as an infusion." Ketamine has been shown to be an effect adjunct in the management of post-operative pain. Antagonism of the NMDA receptor by ketamine is thought to decrease 1) central sensitization 2) opioid tolerance and 3) pain intensity. Thus reducing postoperative opioid requirements as well as nausea and vomiting. NOTE: Ketamine should be avoided in patients with increased ICP, increased IOP, severe or uncontrolled CAD, severe liver disease (metabolized in liver), severe renal dysfunction (exreted by kidneys), pregnancy, and underlying psychiatric disease associated with psychosis. Ketamine produces dissociative anesthesia that can be described as a trance-like cataleptic unconcious state (eyes open, spontaneous respiration, unconcious, nonresponsive to painful stimuli). The dissociative state seems to result from a functional dissociation: inhibition of thalamocortical pathways and stimulation of the limbic regions of the brain. Psychomimemtic effects of ketamine (vivid dreams, hallucinations) can be minimized with concomitant use of benzodiazepines. The risk of laryngospasm due to secretions is higher with IM administration than with IV adminstration.

Answer 23

Ketamine has a context-sensitive half life similar to Propofol.

Answer 24

Context sensitive half time describes the time required for the plasma concentration of a drug to decrease by 50% after stopping an infusion of the drug. It reflects primarily two opposing processes: drug plasma clearance and drug redistribution. Drugs with a slow plasma clearance and a high rate of tissue to plasma redistribution will have a high CSHT. Drugs with rapid plasma clearance and a low rate of tissue to plasma redistribution will have a low CSHT. Keep in mind that CSHT's are different from elimination half-lives since the latter are the result of metabolism and excretion from the whole body, not just the plasma. EXAMPLES: Fentanyl (green), like propofol, is highly lipophilic and has a large volume of distribution. However, fentanyl has a longer CSHT than propofol due to its rapid redistribution. The rapid redistribution back to plasma prevents the plasma concentration from quickly falling after the infusion is stopped, even though fentanyl is rapidly cleared. Alfentanil (purple0 has a small volume of distribution due to its lower lipid solubility and high degree of protein binding (90%). SInce much less of the drug redistributes into the peripheral tissues, redistribution back to the plasma does not significantly affect plasma concentration. This explains why the CSHT of alfentanil does not increase after about two hours of infusion. Note, however, for short infusions of alfentanil the CSHT is higher than fentanyl. This occurs since the plasma clearance of alfentanil is significantly lower than fentanyl . Remifentanil (red) has a flat and low CSHT curve. Remifentanil is hydrolyzed by plasma esterases. It has a very high plasma clearance.

Answer 25

The blood supply to the brain comes from two sources: 70% from the internal carotid arteries. 30% from the basilar artery (formed by the two vertebral arteries). The internal carotid arteries and basilar artery form the circle of Willis, which supply the brain via the anterior, middle, and posterior cerebral arteries.

Answer 26

see picture

Answer 27

see picture

Answer 28

NOTE: Water moves across the BBB specifically by chanel-mediated transport by aquaporin-4.

Answer 29

The venous drainage of the brain consists of deep and superficial veins that drain into dural venous sinuses, which are valveless vessels between the dura mater and the skull periosteum. All dural venous sinuses eventually drain into the sigmoid sinuses, which empty into the internal jugular vein.

Answer 30

The artery of Adamkiewicz (also referred to as the great anterior radiculomedullary artery or arteria radicularis magna) can be found spanning across several vertebral levels most commonly between T9 and L2 (left side) supplying the watershed zone of the lumbar and sacral spinal cord. The spinal cord receives its blood supply from three major vascular structures - one anterior spinal artery and two posterior spinal arteries. The anterior spinal artery provides vascular supply to the anterior portion of the spinal cord. In particular, the anterior two-thirds of the spinal cord is dependent vascularly from the anterior spinal artery. The two posterior spinal arteries provide vascular supply to the posterior of the spinal cord. However, only the posterior one-third of the spinal cord is dependent vascularly from the posterior spinal arteries. Anterior spinal artery is fed by radicular arteries with the largest radicular artery being the artery of Adamkiewicz. Posterior spinal arteries are fed by the vertebral arteries. The artery of Adamkiewicz provides blood supply to the thoracolumbar anterior spinal cord and may be ligated during a thoracoabdominal aortic aneurysm (TAAA) repair or damaged during surgical manipulation of the axial skeleton. The use of MEPs provides the perioperative team with a modality to detect relative decreases in spinal cord perfusion pressure (SCPP). Such decreases in SCPP may be treated intraoperatively in order to reduce the risk of postoperative paraplegia.

Answer 31

The artery of Adamkiewicz (also referred to as the great anterior radiculomedullary artery or arteria radicularis magna) can be found spanning across several vertebral levels most commonly between T9 and L2 (left side) supplying the watershed zone of the lumbar and sacral spinal cord.

Answer 32

Pleural adhesions Large tumor (> 5cm) Central tumors (eg. hilar tumors) The probablity of conversion when these factors are present may exceed 20% NOTE: VATS (Video-Assisted Thorascopic Surgery) is associated with decreased perioperative inflammation, pain, respiratory dysfunction, and bleeding compared to open thoracotomy.

Answer 33

The most important predictor of hypoxemia on OLV is hypoxemia on two-lung ventilation. Predictors: Hypoxemia on two-lung ventilation Righ sided thoracotomy Supine positioning during OLV High FEV1 on PFTs (unclear why) HIgh perfusion of operative lung on preop V/Q scan

Answer 34

In patients with a large bronchopleural fistula, PPV delivered through a single lumen ETT placed in the trachea will be ineffective and potentially fatal because PPV will preferentially be lost through the fistula. Maintenance of spontaneous ventilation is important, but, if PPV is required the appropriate lung must be isolated.

Answer 35

Driving pressure Inspiratory time Respiratory rate FiO2 Humidity NOTE: No control over TVs. No ETCO2 monitoring (need frequent ABGs). Incompatibile with volatile anesthetics (need TIVA). Exhalation is PASSIVE.

Answer 36

Hypoxia Hypercarbia (esp with transtracheal and subglottic) PTX Pneumomediastinum Subcutaneous emphysema Loss of airway Necrotizing tracheobronchitis (esp prolonged use) Impaired ciliary function

Answer 37

Supraglottic Subglottic Transtracheal

Answer 38

Aortic arch rupture Aortic annulus rupture Perivalvular regurgitation Coronary ostium obstruction leading to myocardial ischemia Cardiac tamponade 2/2 ventricular wall perforation Arrhythmia (commonly AV block as aortic valve close to pacemaker cells) Perforation of ilio-femoral axis leading to retroperitoneal hemorrhage.

Answer 39

DECREASE Inhalational agents including nitrous oxide (All of the volatile anesthetics produce dose-dependent effects) Anemia (hgb <10, reducing O2 carrying capacity) MINIMAL/NO EFFECT Propofol Dexmedetomidine Opiates INCREASE Ketamine Etomidate OTHER: Somatosensory evoked potentials (SSEP) are used intraoperatively to assess lateral and posterior spinal cord perfusion. Detection of the SSEP signal takes place in the patient's brain. Motor evoked potentials (MEP) are used to evaluate anterior spinal cord perfusion. Detection of MEP signaling occurs distally in the peripheral musculature.

Answer 40

(MOST SENSITIVE) Visual Motor Sensory Brainstem auditory (LEAST SENSITIVE) NOTE: Visual = Very Motor = Mostly Sensory = Somewhat Brainstem auditory = Barely

Answer 41

Alpha and slow-delta oscillations

Answer 42

Isoflurane, sevoflurane, desflurane, propofol, etomidate, barbiturates, as well as hypothermia are capable of causing burst suppression and eventually an isoelectric EEG pattern. In contrast opioids, midazolam, ketamine, precedex, and nitrous oxide do not cause burst suppression or an isoelectric EEG even at high doses. Burst suppression represents a near-maximally reduced CMRO2 while still providing predictability of recovery and awakening once the infusion of the IV anesthetic is turned off. Isoelectric EEG is not desirable. NOTE: In general opioids cause a decrease frequency and increase amplitude on EEG.

Answer 43

The lateral spinothalamic tract carries signals of pain and temperature from the periphery to the somatosensory cortex.

Answer 44

Type A, delta fibers

Answer 45

The dorsal column tract carries signals of fine touch, pressure, vibration, proprioception from the periphery to the somatosensory cortex.

Answer 46

The spinocerebellar tract carries signals of proprioception from the periphery to the cerebellum.

Answer 47

An isoelectric EEG indicates cerebral silence and the maximal decrease in **CMRO2** Burst suppression, however, is the desired EEG pattern when using an infusion of pentobarbital (also applies to infusions of propofol or etomidate). It allows a maximal reduction in CMRO2 while indicating that regular EEG activity will return predictably following cessation of the infusion..

Answer 48

The importance of ICP was recognized more than 200 years ago and is referred to as the Monro-Kellie Doctrine (or hypothesis), which states that 1) The brain is enclosed in a nonexpandable case of bone 2) The brain parenchyma is nearly incompressible 3) The volume of blood in the cranial cavity is therefore nearly constant 4) A continuous outflow of venous blood from the cranial cavity is required to make room for incoming arterial blood. The intracranial vault is composed of 3 compartments: 1) Brain parenchyma 2) Blood volume (arterial & venous) 3) Cerebral spinal fluid (CSF) Intracranial hypertension and elevated ICP occur when the volume of one of the compartments increases, and further compensation by a decrease in another compartment is no longer possible.

Answer 49

Ventriculostomy catheter

Answer 50

Normal ICP in healthy adult is between 7-15 mmHg.

Answer 51

TBW is made up of 1/3 extracellular fluid and 2/3 intracellular fluid. Extracellular fluid volume is further subdivided into 3/4 interstitial fluid and 1/4 plasma fluid. TBW 60% in men TBW 50% in women Neonates have the highest TBW (most extracellular, hence why they need high doses per kilo because of the greater volume of distribution) Elderly have the lowest TBW (decrease in TBW with age) NOTE: When different fluids are given, they distribute differently in the different compartments. Dextrose 5% distributes across the extracellular and intracellular compartments. Normal saline and balanced crystalloids remain in the extracellular compartment and distribute in the interstitial and intravascular compartment. Colloids, in theory, remain entirely in the intravascular compartment when the glycocalyx is intact but become less efficacious when the glycocalyx is disrupted. The luminal side of the capillary endothelium is lined by the glycocalyx, a network of proteoglycans and glycoproteins. The glycocalyx plays a pivotal role in fluid physiology. The capillary lumen and the interstitial space are separated by the glycocalyx, which creates a protected region called the subglycocalyx space without protein, which augments intravascular hydrostatic pressure. The glycocalyx retains plasma constituents and prevents their extravasation to the interstitial space. However, the glycocalyx can be disrupted by inflammatory states (for example, during sepsis and surgery) and excessive fluid administration.

Answer 52

The volume of distribution (Vd) is a pharmacokinetic parameter representing an individual drug’s propensity to either remain in the plasma or redistribute to other tissue compartments. By definition, Vd is a proportionality constant that relates the total amount of drug in the body to the plasma concentration of the drug at a given time. The following equation can represent VD: Volume of Distribution (L) = Amount of drug in the body (mg) / Plasma concentration of drug (mg/L) Based on the above equation: A drug with a high VD has a propensity to leave the plasma and enter the extravascular compartments of the body, meaning that a higher dose of a drug is required to achieve a given plasma concentration. (High VD -> More distribution to other tissue) Conversely, a drug with a low VD has a propensity to remain in the plasma meaning a lower dose of a drug is required to achieve a given plasma concentration (Low VD -> Less distribution to other tissue). Drugs with a high degree of plasma protein binding, lower degree of tissue protein binding, and hypdrophilic nature have a small VD.

Answer 53

ZERO ORDER: For some drugs, elimination may depend on the action of a specific enzyme or transporters. These enzymes or transporters can reach their maximum capacity and become saturated. When saturation is reached at a given plamsa concentration, the amount of drug removed is a **constant amount per unit time** regardless of the plasma concentration. In zero-order kinetics, drug elimination occurs in a **linear declining** manner. Examples- Phenytoin, Ethanol, Aspirin (PEA) A simple analogy would be an athlete signing an autograph on a picture. Regardless of the total amount of photographs that must be signed, the athlete can only sign one autograph every 15 seconds. The rate-limiting factor of this analogy and zero-order kinetics is time. FIRST ORDER: Approximately 95% of drugs used in clinical practice are eliminated by first-order kinetics. Drugs are eliminated primarily the liver or kidneys. In first-order kinetics, drug elimination occurs in an **exponentially declining** manner with the rate of elimination being proportional to the plasma concentration. The amount of drug removed is a **constant fraction per unit time** rather than a constant amount. To utilize the same analogy, now the entire team can sign the photographs. The more photographs there are to sign, the more athletes can sign. The rate-limiting factor of this analogy and in first-order kinetics is the initial concentration. SUMMARY:: Zero = constant amount, linear First = constant fraction, exponential

Answer 54

Left-sided Coronary perfusion pressure (CPP) is represented as the difference between the aortic diastolic pressure (AoDP) and the left ventricular end-diastolic pressure (LVEDP). CPP = AoDP - LVEDP Left coronary perfusion predominately occurs in diastole. Right coronary perfusion, however, occurs throughout the cardiac cycle (systole & diastole). Right-sided CPP during systole = AoSP-RVEDP Right-sided CPP during diastole = AoDP-RVEDP Diastolic predominance in right coronary flow can occur with chronic pulmonary artery hypertension due to RV hypertrophy.

Answer 55

Isoflurane, Desflurane, and Sevoflurane Isoflurane is the most potent. NOTE: Volatile anesthetics administered before or immediately after some time of ischemic event can reduce the size of any myocardial infarct that may have occurred. This is thought to be due to reduced loading of calcium into myocardial cells.

Answer 56

There are not clearly defined cut-off values that mandate platelet transfusion. It is largely accepted that severe thrombocytopenia with platelet levels of less than 10,000/µL should receive transfusion for increased risk of spontaneous bleeding. For minor surgeries, the platelet levels should be greater than 30,000/µL. For major surgery, levels greater than 50,000/µL are appropriate. For neurosurgical operations the level should be greater than 100,000/µL.

Answer 57

Nasotracheal Intubation (NTI) Indications: - Impending airway compromise (Nasotracheal intubation is typically performed on the awake patient in this case to avoid loss of airway protection reflexes during the process of intubation. NTI causes less gagging and is better tolerated in awake patients than oral intubation) - Intraoral/oropharyngeal surgery - Rigid laryngoscopy - Maxillofacial or orthognathic surgery - Complex intraoral procedures involving mandibular reconstruction - Dental surgery Absolute contraindications: - Previous history of old or recent skull base fractures (basilar fracture) - Anterior skull base fractures (may result in passage of the tube intracranially) - Midface instability - Coagulopathy (that can predispose patient to epistaxsis) Relative contraindications: - Recurrent epistaxis - Large nasal polyps - Known/suspected nasal foreign body - Recent nasal surgery

Answer 58

Aspirin - irreversible COX-1 and COX-2 inhibitor Clopidogrel (Plavix)- P2Y12 receptor inhibitor Ticagrelor (Brilinta)- P2Y12 receptor inhibitor Prasugrel (Effient)- P2Y12 receptor inhibitor Dipyridamole- PDE3 inhibitor Antiplatelet drugs are commonly prescribed in patients with compromised arterial blood flow to prevent platelet aggregation in syndromes such as coronary artery disease, peripheral artery disease, or ischemic strokes. Because anticoagulants tend to prevent clot formation in the venous system, antiplatelet drugs will tend to be used in patients with occlusive arterial disease. The antiplatelet drugs that are used in clinical practice tend to work through one of three mechanisms, though there are other novel anti-platelet medications outside of these. These mechanisms include cyclooxygenase (COX) inhibition, P2Y12 receptor inhibition, and glycoprotein IIB/IIIA inhibition. Of these, the glycoprotein IIB/IIIA inhibitors can only be given via an intravenous route. Inhibition of any of these pathways will lead to a decrease in ultimate thromboxane production and decreased platelet aggregation.

Answer 59

Aspirin irreversibly inhibits COX-1 and COX-2 in the arachandonic pathway preventing the production of: * Thromboxane- platelet aggregation, vasoconstrictor * Prostacyclin- platelet activation, vasodilator * Prostaglandin- vascular tone NOTE: With low dose ASA therapy, prostacylcin production is selectively spared decreasing clot formation and vasoconstriction seen with thromboxane production while still allowing vasodilation from prostacyclin.

Answer 60

Clopidogrel (Plavix) **irreversibly** inhibits P2Y12 receptor on platelets, thus preventing ADP-mediated platelet activation and aggregation. Ticagrelor (Brilinta) **reversibly** inhibits P2Y12 receptor on platelets, thus preventing ADP-mediated platelet activation and aggregation. NOTE: Though Brilinta prevents blood from clotting more effectively, it also tends to have an increased risk of side effects compared to Plavix, such as a higher chance of bleeding.

Answer 61

Aspirin = 7-10 days Plavix and Brilinta = 5 days Prasugrel- 7 days NOTE: Aspirin can be safely continued in patients undergoing minor surgery. Patients on Aspirin for primary or secondary prevention should discuss whether the risks outweights the benefits with surgeon. Patients on Aspirin for a prior hx of PCI should continue unless the risk of bleeding outweights the benefits of preventing MI. Aspirin should be continued until the day of surgery for patients with a hx of CAD scheduled for an elective CABG but P2Y12 inhibitors should be stopped 5 days before elective CABG. Aspirin should be continued until the day of surgery for patients scheduled for elective carotid endarterectomy.

Answer 62

5 days (check INR) The chart below outlines risk of thromboembolism after stopping Warfarin for surgery. High risk patients include mitral valve prosthesis, caged-ball or tilting aortic valve prosthesis, recent CVA (< 6 months), CHADS 5-6, rheumatic valvular heart disease (unrepaired), recent CTE (< 3months) and severe thrombophilia.

Answer 63

Perioperative steroid supplementation with hydrocortisone should be administered to patients taking >20mg/day of prednisone (or equivalent) for at least 3 weeks in the previous year and may be considered in patients taking 10-20mg/day. Chronic corticosteroid use can lead to suppression of HPA axis and places patients at risk for developing secondary adrenal insufficiency in the setting of abrupt cessation of their glucocorticoids or in the setting of high physiologic stress (eg. surgery). This occurs since the adrenal gland is unable to secrete cortisol in response to stress and a patient's chronic steroid dose is adequate only for daily activity and minor stress. The most dangeous manifestation is hemodynamic instability that is not responsive to fluids or pressors. There is no proven optimal regimen for perioperative steroid replacement. Based on the data, patients who take 5-10mg/day of prednisone (or equivalent) do not usually have clinically significant HPA axis suppression and therefore do not need perioperative corticosteroid supplementation. Patients who take > 20mg day of prednisone (for longer than 3 weeks within the last year) are at risk for AI and should be supplemented based on the amount of anticipated surgical stress. Patients on steroid doses between these two levels may benefits from supplementation. Patients using > 2g/day of topical steroids or > 800 mcg/day of inhaled steroids on a long-term basis should probably also receive supplementation. NOTE: Primary adrenal insufficiency: low glucocorticoid + low mineralocorticoid Secondary adrenal insufficiency: low glucocorticoid (no electrolyte abnormalities)

Answer 64

Clopidogrel (Plavix) Prasugrel (Effient) Clopidogrel (Plavix) is a prodrug that requires activation by hepatic cytochromes, most specifically CYP 2C19 in order to exert its clinical effect. This active metabolite will then bind to the platelet adenosine diphosphate (ADP) receptor and prevent platelet aggregation. This characteristic of Clopidogrel caused the US Food and Drug Administration to release a black box warning regarding its use. Because around 2 to 14% of the population has a mutant phenotype of CYP 2C19, these patients are at an increased risk of thrombotic death due to the failure of clopidogrel therapy due to decreased conversion of clopidogrel into its active metabolite. Ticagrelor (Brilinta) is NOT a prodrug. NOTE: Clopidogrel (Plavix) is associated with Thrombotic Thrombocytopenic Purpura (TTP).

Answer 65

Polymorphisms of which cytochrome enzyme leads to altered drug metabolism of Warfarin (Coumadin)? CYP2C9 NOTE: Polymorphisms are variants in DNA sequence that occurs in at least 1% of the population and can lead to altered patient response to medications.

Answer 66

St Johns Wart is a CYP inducer and can reduce the effectiveness of both Digoxin and Warfarin.

Answer 67

Two supplements that can reduce the effectiveness of Warfarin by inducing CYP450 (2C9) are... St Johns Wart Ginseng

Answer 68

Polymorphisms of which cytochrome enzyme leads to altered drug metabolism of BB's, CCBs, antiarrthymics, Tramadol, Codeine, Oxycodone, Hydrocodone, Hydromorphone? CYP2D6 NOTE: Polymorphisms are variants in DNA sequence that occurs in at least 1% of the population and can lead to altered patient response to medications.

Answer 69

Codeine Tramadol Oxycodone Hydrocodone Hydromorphone NOTE: All metabolized by CYP 2D6

Answer 70

Hydromorphone (Dilaudid) is metabolized by the liver into hydromorphone-3-glucuronide which can accumulate in patients with renal dysfunction and result in agitation, tremor, myoclonus (neuroexcitatory). NOTE: Transdermal buprenorphine, transdermal fentanyl, and oral hydromorphone are the most tolerable opioids in these patients; hydrocodone, oxycodone, and methadone are useful but require careful monitoring; and tramadol, codeine, morphine, and meperidine should be avoided due to risk of accumulation and adverse events.

Answer 71

Polymorphisms of which cytochrome enzyme leads to altered drug metabolism of fentanyl, alfentanil, sufentanil, midazolam, digoxin, amide local anesthetics, methadone, dexamethasone? CYP3A4 NOTE: Polymorphisms are variants in DNA sequence that occurs in at least 1% of the population and can lead to altered patient respone to medications. Midazolam inhibits CYP3A4 which can prolong the effects of Fentanyl. BaD^2 FAM Benzos (midazolam, diazepam) Decadron, Digoxin Fentanyls Amide local anesthetics Methadone

Answer 72

Fentanyl Alfentanil Sufentanil Midazolam Diazepam Amide local anesthetics Dxamethasone Methadone BaD^2 FAM Benzos Decadron, Digoxin Fentanyls (except Remi obviously) Amide locals Methadone

Answer 73

Polymorphisms of what receptor is associated with red hair and may affect sensitivity to general anaesthetics and pain response? MC1R Red hair results from distinct mutations of the melanocortin-1 receptor (MC1R). There is some evidence suggesting that redheads are less sensitive to general anaesthetics and this has been linked to variants MC1R gene. Red hair females are reported to have an increase in MAC of 19% compared to dark hair counterparts.

Answer 74

Inducers = STARBS Inhibitors= GQC MAPS

Answer 75

Muscle rigidity (pharyngeal = glottic closure, thoracic aka "wooden chest syndrome", abdominal muscles); usually with high dose fentanyl >4mcg/mg treat with roc, naloxone, benzos Increased CBD tone and sphyincter of oddi tone (treatment: glucagon, naloxone); can lead to misinterpretation of perioperative cholangiograms Paralytic ileus Immunosuppression

Answer 76

LAD - anterior wall (including anteroseptal and anteroapical) and left atrium LCX - lateral wall (including anterolateral and inferolateral) RCA - most of the right atrium, lateral right ventricle, and basal and mid inferior left ventricular wall

Answer 77

The anterolateral papillary muscle is supplied by the LAD and LCx. The posteromedial papillary muscle is supplied by either the RCA or LCx. Most patient are right dominant so more likely RCA.

Answer 78

There is some variability in the extent of additional coverage by the RCA. In most “right dominant” individuals (85%), there is additional coverage through a posterior descending artery (PDA) branch from the RCA that provides perfusion to the apical inferior wall and superior-posterior interventricular septum. Approximately 5% of individuals have what is referred to as left dominant circulation, in which the PDA is a branch of the LCX. Approximately 10% of individuals are co-dominant, in which the PDA receives blood supply from both the RCA and the LCX. In 60% of individuals, the sinoatrial (SA) node is also supplied by the RCA. The LAD provides perfusion to the SA node in the other 40% of individuals.

Answer 79

The "upper airway" consists of the Pharynx (naso-, oro-, hypo-) and the Larynx. The pharynx is divided into the naso-, oro-, and hypopharynx. The nasopharynx begins at the nasal cavity and ends at the soft palate The oropharynx begins at the soft palate and continues to the hyoid bone. The hypopharynx begins at the epiglottis and ends at the cricoid cartilage. The hypopharynx connects the oropharynx to the esophagus and larynx. The larynx contains the epiglottis and vocal cords and extends from the superior border of the epiglottis to the cricoid cartilage. NOTE: Notice that the hypopharynx and larynx both end at the cricoid cartilage. Soft palate, epiglottis, and cricoid cartilage are good landmarks to separate divisions in your head.

Answer 80

Tranexamic acid (TXA) is a anti-fibrinolytic and will help decrease hemorrhage.

Answer 81

The primary management technique of resuscitation is transfusion of blood products in a 1:1:1 ratio and this is often started with packed red blood cells and fresh frozen plasma, followed by platelet therapy when available. 1PRBC: 1FFP: 1plts

Answer 82

Type O, Rh negative As type O blood lacks the A and B antigens it will not be hemolyzed by the presence of anti-A and anti-B antibodies in the recipient's blood. This is why type O blood is considered the universal RBC donor and why it is preferentially administered in situations where emergency transfusion is necessary. That said, some donors of type O blood produce high titers of anti-A and anti-B antibodies which could potentially cause hemolysis of recipient RBCs if they express the A or B antigen. It is for this reason that type O Rh-negative packed RBCs are preferred to whole blood as packed RBCs contain a lower volume of donor plasma and therefore decreased amount of potential anti-A and anti-B antibodies. If a sufficient volume of uncrossmatched type O Rh-negative whole blood is administered it is considered unsafe for a patient with either an A, B, or AB blood type to receive type-specific RBC transfusions until it is confirmed that the serum titers of anti-A and anti-B antibodies have decreased to a safe level.

Answer 83

ALL blood products are SAFE to transfuse through a fluid warmer including PRBCs, platelets, FFP, and cryopercipitate. NOTE: It was previously thought that warming platelets would result in damage to platelets but no evidence supporting this. Using a fluid warmer is advised when giving >2 units of blood products or 3L of fluid to prevent reduction of core temperature and hypothermia.

Answer 84

Vitamin-K antagonist Warfarin is a vitamin-K antagonist that inhibits the enzyme vitamin K epoxide reductase, decreasing the synthesis of active forms of Vitamin K. As a result there is a decrease in the gamma carboxylation of the glutamate residues on factor II, VII, IX, X, Protein C, Protein S. Warfarin is used in the management of atrial fibrillation, mechanical assist devices, and artificial heart valves.

Answer 85

PCC or FFP IV Vitamin K

Answer 86

PCC FFP requires time for type and screen, time for thawing, large volumes (10-30cc/kg), is less reliable than PCC. IV Vitamin K should still be given with PCC to generate new clotting factors. IV Vitamin K takes 6-8 hours to correct INR.

Answer 87

Prothrombin Complex Concentrate (PCC): Vitamin K–dependent clotting factors (II, VII, IX, X, Protein C, Protein S) NOTE: Brand Name: Kcentra PCC reverses the effect of warfarin (a coumarin anti-coagulant) and is used in cases of significant bleeding in patients with a coagulopathy (INR > 8.0, prolonged prothrombin time, raised d-dimer). Examples include gastrointestinal haemorrhage or intracranial haemorrhage.

Answer 88

Parkland formula: 4 mL/kg x weight (kg) x %TBSA over 24 hours Half the volume is given over the first 8 hours. After 24 hours, colloids are preferred to continue resuscitating. "Wallace Rules of 9" to calculate %TBSA (see picture) NOTE: Fluid boluses and the use of glucose-containing crystalloids should generally be avoided (can cause peripheral edema and hyperglycemia). Albumin should generally be avoided specifically in the first 24 hours as it may worsen edema. Fluid choise: LR

Answer 89

Medications to prevent emergence delirium include... Propofol Fentanyl Ketamine Dexmedetomidine Midazolam

Answer 90

Tearing Salivation Grimacing Gagging/coughing/swallowing Increased HR Increased BP NOTE: Signs correspond to return of cranial nerve function (VII, IX, and X) in the pons and upper medulla. Reaching for ETT can occur in phase II of emergence and does not provide evidence that the patient is ready for extubation.

Answer 91

Response to oral commands Spontaneous eye opening NOTE: Spontaneous eye opening is the last sign seen. Occurs well after an appropriate return of motor function and responsiveness to commands. Generally, patients tend to keep their eyes closed even after conciousness has returned. They may respond reliably to verbal commands but do not yet open their eyes spontaneously despite a substantial return of motor functions. Reaching for ETT can occur in phase II of emergence and does not provide evidence that the patient is ready for extubation.

Answer 92

Emergence delirium is terminated either spontaneously or after the administration of midazolam, propofol, dexmedetomidine, fentanyl, or ketamine.

Answer 93

The two main risk factors for developing emergence delirium are patient age (2-6 years) and type of anesthetic. Emergence delirium occurs most commonly with *less-soluble* volatile anesthetics (sevoflurane and desflurane).

Answer 94

Emergence delirium occurs during or immediately after emergence from general anesthesia POD is usually notable from postoperative day 1 and up to 1 week after surgery.

Answer 95

Predisposing factors for Post-Operative Delirium (POD) are: * Age > 65 years * Male sex * Preexisting cognitive impairment or depression * Pre-existing functional impairment * Sensory impairment (e.g. visual and hearing deficiencies) * Medication (opioids, benzodiazepines, anticholinergics) * High-risk surgical procedures (cardiac, thoracic, orthopedic operations esp hips)

Answer 96

POCD is characterized by new cognitive deficits including impaired memory, inability to combine tasks, and impaired psychomotor dexterity that can be seen immediately postoperative and can last for up to six months. POCD typically resolves in days to months, but it may persist in 1% of patients. Risk factors for developing postoperative cognitive dysfunction (POCD)- **increasing age, low educational level, history of CVA without deficits. ** Procedural risk factors include major surgeries (especially cardiac and major orthopedic surgeries) and long surgeries, and intraoperative complications (such as extensive blood loss) are independent risk factors for POCD. In contrast to delirium, fluctuating state of conciousness and hallucinations are not seen with POCD, and POCD typically resolves within days to months but may persist in 1% of patients. Chronic POCD is important to identify because it is associated with an increased incidence of 1-year mortality.

Answer 97

YES. The use of propofol total intravenous anesthesia is associated with a significant reduction in risk.

Answer 98

Ketamine reduces the incidence of emergence delirium in patients who have undergone general anesthesia with volatile anesthetics. It can be given as a bolus of 1 mg/kg IV followed by an infusion of 1 mg/kg/hr or as a single dose of 0.25 mg/kg IV at the end of surgery.

Answer 99

Maintaining end-tidal volatile concentrations of **0.7 **MAC or above can significantly reduce the risk of awareness.

Answer 100

MAC-awake = ~0.4-0.5 MAC-awake is the MAC value at which voluntary reflexes (no longer opens eyes to command, shouting, shaking) and perceptive awareness are lost. NOTE: Interestingly, the MAC-awake is generally higher at induction (0.4-0.5 MAC in order for loss of conciousness) than at emergence (as low as 0.15 MAC to regain conciousness). Mechanism is unclear. ASA recommends maintaining at least 0.7 MAC during general anesthesia to significantly reduce the risk of awareness.

Answer 101

MAC-movement= 1.0

Answer 102

MAC-EI= ~1.3 MAC necessary to prevent laryngeal response to endotracheal intubation.

Answer 103

MAC-BAR= 1.7-2.0 MAC-BAR is the MAC at which the adrenergic response to noxious stimuli is blunted. BAR (blunt adrenergic response)

Answer 104

PROVIDER Use of paralytics (#1) TIVA PATIENT Obesity Difficult intubation Chronic alcohol, benzo, opioid use SURGERY C-sections (highest rate) Cardiac surgery w/ bypass Emergency/trauma surgery NOTE: Incidence of intraoperative awareness in 1:14,000-19,000. Paralytics- physiological response of purposeful movement to surgical stimulus is absent TIVA- unable to monitor depth of anesthesia compared to anesthetic end-titdal CO2 (use BIS monitor) Difficult intubation/obesity- wearing off of induction dose, higher doses of anesthetic required for obese patients Chronic alcohol use induces CYP450 2E1 which metabolizes inhalation agents, opioids, and benzos. Cardiac surgery w/ bypass- use of lower dose of anesthesia due to poor cardiac reserve. C-section- due to difficult intubation, short duration between induction and surgical incision, use of lower doses of anesthetic agents due to concerns for fetal or maternal wellbeing (incidence 1:256-1,600) Emergency/trauma- use of lower anesthetic doses due to hemodynamic instability.

Answer 105

NO Opioids do not affect BIS values (eg. Propofol gtt with Remi gtt)

Answer 106

Hyponatremia

Answer 107

Hypernatremia Diabetes insipidus (DI) leads to low urine osmolality (<300 mOsm/kg) and high plasma osmolality (>305 mOsm/kg) due to the loss of antidiuretic hormone (ADH), resulting in an inability to concentrate urine and massive diuresis. Hypernatremia (>145 mEq/L) occurs from excessive water loss.

Answer 108

Diabetes insipidus is often caused by damage to the pituitary or hypothalamus, as in severe head injury or near brain death (central DI) or in reduced renal sensitivity to ADH (nephrogenic DI), which can occur from certain renal diseases (eg, chronic renal failure, pyelonephritis, polycystic kidney disease), electrolyte disturbances (eg, chronic hypokalemia or hypercalcemia), or certain drugs (eg, amophotericin B, demeclocycline, lithium). While patients with DI are generally euvolemic, they make become hypovolemic if they do not consume enough water. The treatment for central DI is ADH replacement with vasopressin or desmopressin. The treatment for nephrogenic DI is salt restriction, thiazide diuretics, and correcting any electrolyte disturbances along with discontinuation of drugs that may be contributing to the pathologic state.

Answer 109

Causes: CNS distrubance (stroke, infection,hemorrhage, trauma) Malignancy (small cell lung cancer, head/neck) Hormone deficiency (hypopituitarism and hypothyroidism) Drugs (carbamazepine, oxcarbazepine, chlorpropamide, cyclophosphamide, SSRIs) Infection (PNAs, HIV) Hereditary SIADH Treatment: Salt tablets Water restriction Furosemide (to increase plasma osmalility) Hypertonic saline Vasopressin antagonists (conivaptan, tolvaptan) The rate of correction is an important factor. It should not exceed more than 8 mEq/L per 24 hours or 0.5 to 1 mEq/L per hour. More rapid correction can result in osmotic demyelination of the CNS, leading to severe lethal complications such as osmotic demyelination syndrome ("locked-in" syndrome), causing quadriplegia.

Answer 110

Serum osmolality= 2[Na] + BUN/2.8 + glucose/18 Sodium is the largest contributor to plasma osmolality and is the most abundant positive ion of the extracellular fluid compartment. Osmolality is defined as the number of osmotically active particles per kilogram and can be estimated by the equation 2 x [Na+] + [Glucose]/18 + [BUN]/2.8. Normal plasma osmolality ranges from 275-290 mOsm/kg. The serum Na+ is multiplied by 2 to account for the sodium salts such as sodium chloride and sodium bicarbonate. The 18 and 2.8 are used to convert the units for glucose and BUN in mg/dL to mOsm/kg. Thus, in normal healthy patients, the determinants of plasma osmolality are Na+, glucose, and urea with Na+ being the primary determinant. NOTE: Uosm: Posm ratio of > 1.5 indicates pre-renal pathology (dehydration, hypovolemia).

Answer 111

Hyponatremia Hypokalemia Hypomagnesemia Respiratory alkalosis Hyperuricemia

Answer 112

D1-agonist Fenoldopam is a dopamine agonist that acts on the dopamine-1 receptor, causing vasodilation, especially of the splanchnic, mesenteric, and renal arterioles, which can increase renal blood flow. This promotes diuresis and natriuresis. Fenoldopam does appear to have some potential as an antihypertensive (second-line) because it does not have the same tachyphylaxis or rebound hypertensive properties as other nitrovasodilators. It has a rapid onset (10min) and short duration (10min) For severe hypertension, initiate treatment at 0.2 mcg/kg/minute then increases by 0.3 to 0.5 mcg/kg/minute at 20 to 30 minute intervals until target blood pressure is reached or until reaching a max of 0.8 mcg/kg/minute.

Answer 113

AKI occurs in up to 30% of patients following cardiac surgery. Mortality increases by 60-80% in post-cardiopulmonary bypass patients who go on to require renal replacement therapy. Preoperative creatinine greater than 1.2mg/dL, combined valve and bypass procedures, emergency surgery, and preoperative intraaortic balloon pump are risk factors most strongly correlated with post-CABG AKI. Other well-known minor risk factors include: female gender, CHF, depressed LVEF, COPD, insulin-requiring DM. SIDE NOTE: Dopaminergic agents (Dopamine, Fendoldapam) agonize D1 and D2 receptors and induce vasodilation in the renal, mesenteric, peripheral, and coronary arteries. Specifically, within the kidney, the D1 receptor seems to be concentrated in the medulla, while the D2 receptor tends to be more prevalent in the renal cortex. By stimulating either of these receptors but especially the D1 receptor, blood flow will theoretically increase in the renal medulla and help to prevent the ischemic injury that is implicated in perioperative AKI. Despite this theoretical benefit, no decrease in the incidence of acute kidney injury has been seen with the perioperative administration of these drugs. Fenoldopam = D1 agonist Dopamine= D1 and D2 agonist (also beta and alpha agonist)

Answer 114

NSAIDs are COX-II inhibitors and lead to a decrease in the production of prostaglandins. Prostaglandin E2 is the key mediator of both central and peripheral pain sensitization. Centrally, prostaglandins enhance pain transmission at the level of the dorsal horn by increasing the release of substance P and glutamate from first-order pain neurons, increasing the sensitivity of second-order pain neurons, and inhibiting the release of neurotransmitters from the descending pain-modulating pathways. Peripherally, prostaglandins do not directly mediate pain; rather, they contribute to hyperalgesia by sensitizing nociceptors to other mediators of pain sensation such as histamine and bradykinin.

Answer 115

1-3 months

Answer 116

In healthy patients, succinylcholine will cause an increase of plasma potassium levels by approximately 0.5 mEq/L.

Answer 117

NSAIDS (#1) Lidocaine (#2) Defasisculating dose of Rocuronium (#3)

Answer 118

Bradycardia occurs most often in children because children have a high vagal tone. Children have a high vagal tone because they have more acetylcholine receptors in the SA node. Succinylcholine is metabolized by pseudocholinesterase to succinylmonocholine which has cholinergic activity. Bradycardia can be prevented by predaministration of atropine. Bradycardia can also occur in adults when a second dose is given.

Answer 119

NO. Succinylcholine has been used in children with CP for more than 50 yr without a single report of a hyperkalaemic response. Keep in mind however that cerebral palsy patients have an increased incidence of gastroesophageal reflux and aspiration.

Answer 120

Lambert-Eaton Syndrome DMR: Increased sensitivity NDMR: Increased sensitivity Neostigmine is ineffective for reversal of NDMR

Answer 121

Myasthenia Gravis DMR: Resistant NDMR: Increased sensitivity

Answer 122

Weakness in Myasthenia Gravis WORSENS with activity whereas weakness in Lambert Eaton IMPROVES with activity.

Answer 123

Several risk factors have been identified that predict the requirement for postoperative ventilation in patients with MG who are undergoing anesthesia including: * Evidence of bulbar symptoms preoperatively * History of myasthenic crises * Disease duration of > 6 years * Pyridostigmine dose of >750 mg daily * History of COPD * Vital capacity of less than 2.9 L (in some sources, ~2 L) * Serum acetylcholine receptor antibody level >100 nM/mL * Intraoperative blood loss of >1 L Myasthenia gravis is an autoimmune disorder in which a patient develops antibodies against nicotinic acetylcholine receptors at the neuromuscular junction, resulting in activity-exacerbated weakness. Most patients have anti–acetylcholine receptor antibodies, although some patients have antibodies against muscle-specific tyrosine kinase or lipoprotein-related protein 4. The primary symptom of MG is weakness of skeletal muscles that is exacerbated by repetitive use. Although any muscle group can be affected, muscles controlled by cranial nerves tend to be most affected, predisposing patients to bulbar symptoms that can cause aspiration. A myasthenic crisis can be caused by poor disease control, stress, hyperthermia, or infection and is characterized by respiratory failure with muscle weakness, often requiring intubation and mechanical ventilation. Diagnosis of MG is primarily based on clinical history, serodiagnostic testing, and electrodiagnostic testing. Treatment most commonly consists of cholinesterase inhibitors (eg, pyridostigmine), steroids, intravenous immunoglobulin, and/or immunosuppression. Plasmapheresis is sometimes used in patients who are in crisis or who have refractory symptomatology. There is an association of thymoma with MG, and many patients undergo thymectomy.

Answer 124

Prothrombin time (PT) is a measure of the synthetic function of the liver as the liver synthesizes the coagulation factors that affect the PT. The liver produces all vitamin K dependent factors including factors II, VII, IX, and X along with protein C and protein S. PT is used to assess procoagulant capabilities of these Vit K dependent factors. These clotting factors are not synthetized in the case of severe hepatic dysfunction leading to prolonged PT. Among these factors, factor VII has the shortest half life (4 hours) and can therefore serve as an early and reliable measure of possible liver dysfunction. PT measures the activity of factors I, II, V, VII, and X which are components of the extrinsic clotting pathway. PT is the most sensitive standard laboratory test for acute changes in or the current status of the synthetic function of the liver. Other measures of hepatic synthetic function include fibrinogen (half-life of four days) and albumin (half-life of 20 days). NOTE: Albumin accounts for 15% of proteins synthesized by the liver.

Answer 125

I, II, V, VII, IX, X, XI, XII, XIII NOTE: VIII and vWF are increased in liver disease as they are produced by endothelial cells (extrahepatic) “348 produced outside the livers gate”

Answer 126

III, IV, VIII "348 produced outside the liver's gate"

Answer 127

The recommended duration of DAPT in a patient with a drug-eluting stent is at least 6 months before holding for an elective surgery. The guidelines now state that noncardiac elective surgery should be delayed optimally for at least 6 months, but, at 3 months, interruption of DAPT for surgery may be considered for time-sensitive surgeries (eg oncological).

Answer 128

After an MI, patients should wait 14 days after balloon angioplasty, 30 days after BMS, 60 days if no coronary intervention, and 180 days after DES for *elective noncardiac surgery.*

Answer 129

The liver recieves 25% of cardiac output. The hepatic artery delivers 25% of the blood volume and the portal vein delivers the other 75%. Despite the disproportionate blood flow, both vessels each supply 50% of the liver's oxygen due to the hepatic artery carrying more oxygenated blood. The portal blood flow is regulated by the hepatic arterial buffer response system which can increase blood flow via the hepatic artery by as much as 100%. This system is driven by the local concentration of adenosine, a metabolic byproduct of the liver. When portal venous blood flow is reduced, adenosine accumulates resulting in vasodilation of the hepatic artery and increasing blood flow via the hepatic artery (Adenosine DOES NOT cause dilation of portal vein, just the hepatic artery).

Answer 130

Loop diuretics Thiazide diuretics

Answer 131

1. Osmotic (Mannitol, a sugar alcohol) 2. CA inhibitors (ACTZ, Brinzolamide) 3. Loop (Furosemide, Torsemide, Bumetanide, Ethacrynic Acid) 4. Thiazides (HCTZ, chlorthalidone) 5. K sparing (Spironolactone [Aldactone], Eplerenone, Amiloride, Triamterene) Pneumonic: SEAT BELT Spironolactone, Eplerenone, Amiloride, Triamterene Bumetanide, Ethacrynic Acid, Lasix (Furosemide), Torsemide

Answer 132

Increased plasma volume Increased CO Increased BP Decreased ICP Increased PCWP (caution w/ HF patients as can cause pulmonary edema) Increased RBF and UOP (increases osmotic pressure in PCT and loop of henle, decreasing passive reabsoprtion of water) Hyponatremia (diultional)-> Hypernatremia (hemoconcentrated) Hypokalemia vs. hyperkalemia Metabolic acidosis (dilution of bicarb) NOTE: Rapid bolus of mannitol can acutally cause a transient increase in ICP. Appropriate bolus dose is 0.25-1g/kg over at least 10-15min.

Answer 133

Hypokalemic metabolic acidosis NOTE: CA in the PCT works to increase Na, Cl, and HCO3 reabsorption. Inhibition of CA by acetazolamide causes Na, Cl, and HCO3 excretion.

Answer 134

Hypokalemic hypochloremic metabolic alkalosis

Answer 135

Hyperchloremic metabolic acidosis

Answer 136

Loop inhibits NaKCl(2) Thiazide inhibits NaCl

Answer 137

Spironolactone & Eplerenone are competitive antagonists of mineralocorticoid receptor sites. Amiloride and Triamterene directly block sodium channels. Overall, K+ sparing diuretics prevent K+ secretion by antagonizing the effects of aldosterone in the collecting tubules.

Answer 138

Sodium deficit= 140-plasma Na x TBW TBW (Total Body Water)= weight (kg) x 0.6 Symptomatic patients with serum Na+ < 120 mEq/L should have their serum osmolality corrected by 3% hypertonic saline (HS). Serum electrolytes should be assessed regularly and HS should be discontinued once symptoms resolve and/or Na+ rises above 120 mEq/L. Central pontine myelinolysis (CPM), a demyelinating CNS lesion, may result from rapid increase in serum osmolality during HS therapy. Typically, 50% of the Na+ deficit is corrected during the first 24 hours, and the rate of hypertonic saline administration should never be higher than 100 mL/hr. EX: Serium sodium= 110mEq/L Sodium deficit = (140 mEq/L – 110 mEq/L) x (100 kg x 0.6) = 1800 mEq

Answer 139

Describe the effects of PPV on the following: VR/preload- decreases RV afterload- increases RV SV- decreases Pulmonary vascular resistance- increases LV afterload- decreases LV stroke volume- decreases CO- decreases Although PPV can decrease the work of breathing, it can have significant hemodynamic effects. Positive pressure ventilation results in an increase in intrathoracic pressure that compresses the inferior vena cava and right atrium, decreasing venous return to the heart. In addition, the increased intrathoracic pressure increases the afterload on the right ventricle. The increase in alveolar pressures compresses the pulmonary valsculature leading to an increase in pulmonary vascular resistance, increasing the right ventricular afterload. Combining the decreased preload and increased afterload leads to a decreased right ventricular stroke volume. Effects seen on the left side of the heart include a decreased preload (due to decreased right-sided stroke volume). A decreased afterload also occurs due to a reduction in the left ventricular end-systolic transmural pressure and an increased gradient between the intrathoracic aorta and extrathoracic systemic circuit; however, this is minor compared to the reduced preload. The decreased preload results in a decrease in left ventricular stroke volume and in overall cardiac output.

Answer 140

CVP is normal in TRALI. CVP is elevated in TACO. Normal CVP = 8-12mmHg TRALI occurs most often after the administration of fresh frozen plasma (FFP) and platelets and carries a mortality of up to 5%. Anti-HLA antibodies have been implicated, though an immune response is not always evident. A “two-hit” theory has thus been proposed that includes an initial priming insult followed by transfusion as the “second hit.” TRALI typically develops rapidly after transfusion, usually within six hours. It presents as chills, fever, respiratory distress or increased inspiratory pressures in the mechanically ventilated patient, and noncardiogenic pulmonary edema. Bilateral patchy infiltrates are commonly seen with TRALI as inflammatory mediators lead to fluid extrusion in the lungs. No signs of heart failure. Transfusion-associated circulatory overload (TACO) results from the rapid administration of more blood products than the patient’s cardiovascular status can support. Hypertension and elevated central venous pressure (CVP) are more common in the initial phases of TACO due to volume overload. Progression to cardiovascular collapse can result in hypotension in TACO as well, though signs of heart failure are typically seen.

Answer 141

FFP (#1) Platelets

Answer 142

Increased CO Decreased SVR (decreased viscocity)

Answer 143

Commonly used guidelines for the application of HBO therapy in CO poisoning include: 1. HbCO level >25% 2. Neurologic impairment (including dizziness and loss of consciousness) 3. Evidence of acute cardiac abnormalities (ischemia, arrhythmias, ventricular failure) Carbon monoxide is an odorless, nonirritating gas that binds to hemoglobin with an affinity 200 times greater than that of oxygen. When a patient is exposed to smoke from a fire or combustion of any kind, carbon monoxide toxicity should be assumed until proven otherwise. Clinical effects of HbCO include headache, nausea, vomiting, dizziness, myocardial ischemia, loss or altered consciousness, and fetal distress during pregnancy. Carboxyhemoglobin and HbO2 absorb light at the same wavelength; thus, a standard pulse oximeter will not detect carbon monoxide levels. Increasing PaO2 will hasten the removal of CO from the blood. The half-life of HbCO is 200 to 300 minutes when patient is breathing room air, and it is about 40 to 80 minutes when 100% O2 at 1 atm is administered. With HBO therapy, the half-life of HbCO becomes 15 to 30 min at 2.5 atm. Hyperbaric oxygen therapy increases oxygen delivery to the tissues by increasing the amount of oxygen dissolved in the plasma PaO2. It has been hypothesized that the increased PaO2 "pushes" the CO molecules off hemoglobin. Hyperbaric oxygen therapy will reduce the half-life of HbCO even further. NOTE: Dissolved oxygen within the blood is independent of circulating carbon monoxide. The PaO2 should therefore be increased during CO poisoning in order to increase arterial oxygen content. This may be achieved through 100% face mask oxygen, endotracheal intubation with 100% FiO2, or hyperbaric oxygen (HBO) treatment. This latter form of treatment subjects the patient to 2-3 atmospheres of oxygen. This allows PaO2 to reach approximately 1500-2500 mm Hg.

Answer 144

New generation carbon dioxide absorbents (calcium hydroxide, calcium chloride) **do not contain strong bases (such as sodium hydroxide or potassium hydroxide).** Old generation carbon dioxide absorbents include soda lime and barium hydroxide. Volatile anesthetic degradation can produce carbon monoxide (Desflurane > Isoflurane > Sevoflurane). Dessicated (dried out) absorbents generate significantly more carbon monoxide and may lead to carbon monoxide poisoning.

Answer 145

ALL volatile anesthetics blunt hypoxic pulmonary vasocontriction, but at HIGH DOSES. Though earlier animal studies indicated that volatile anesthetics (especially halothane) potently inhibited HPV, this effect was most profound at high doses—such as those required to produce 1.5-2.0 MAC. Such inhibition may be related to the direct vasodilatory properties of volatile agents. Newer volatile anesthetics like isoflurane, sevoflurane, and desflurane do not appear to inhibit HPV as profoundly, and their clinical effects on HPV are virtually negligible at doses around 1.0 MAC.

Answer 146

Volatile anesthetics (>1.0 MAC) Nitric oxide ACE-i/ARBs PDE-i Prostacyclins NOTE: Hypoxia, hypercarbia, and acidosis CAUSE pulmonary vasoconstriction. alpha-1 agonists (phenylephrine, norepinephrine) CAUSE pulmonary vasoconstriction

Answer 147

1) Blunting of HPV Patients with advanced COPD who otherwise exhibit substantially elevated shunt fractions due to the presence of under-ventilated and hypoxic alveoli, are therefore highly dependent on HPV to maintain adequate gas exchange. Unfortunately this tenuous balance is easily disrupted. When supplemental O2 is applied, PAO2 increases in under-ventilated alveoli, decreasing the degree of HPV and increasing blood flow to those alveolar units. However, these under-ventilated alveoli continue to maintain a high CO2 tension (PACO2) which disfavors the release of CO2 from the pulmonary capillary blood. The result is a significant increase in systemic CO2 retention with the rapid development of hypercapnia. 2) Haldane Effect (minor contributor) Increase in arterial O2 tension will result in more CO2 offloading from hemoglobin.

Answer 148

Hypokalemia Hypophosphatemia Hypomagnesemia "Leave Me a Plate Please"= Low Mag, Phosp, Potassium Total parenteral nutrition is an intravenous infusion of nutrients used to support patients who cannot receive enteral feeding. It typically contains dextrose, amino acids, and lipids to support the patient’s metabolism as well as the electrolytes sodium, chloride, potassium, magnesium, phosphate, and, sometimes, calcium. Total parenteral nutrition also contains the vitamins and trace minerals required to support metabolism; however, TPN is associated with several notable derangements in electrolyte levels if it is not properly managed. Hypophosphatemia (phosphate level below 2.5mg/dL) is common in patients receiving TPN. The glucose loading in TPN causes an intracellular shift of phosphate, causing a precipitous drop in phosphate with the initiation of TPN. Phosphate levels below 1 mg/dL may cause seizures, heart failure, tachypnea, hemolytic anemia, and death. A slowly advanced TPN regimen and frequent phosphate monitoring and repletion can mitigate this complication. Hypomagnesemia and hypokalemia are also frequently seen in patients receiving TPN. When a patient develops hypomagnesemia, hypokalemia, and hypophosphatemia after initiating TPN, this is termed refeeding syndrome. Calcium is the electrolyte that is often elevated in patients receiving TPN, which is why calcium is sometimes omitted from TPN solutions. Before TPN is initiated, assessing and correcting for any electrolyte abnormalities is essential.

Answer 149

Some common causes of hypophosphatemia are * Catecholamine therapy (intracellular redistribution of phosphate) * Refeeding syndrome (insulin-induced cellular phosphate uptake) * Alcoholism or malnutrition (inadequate intake or absorption) * Acute alkalemia (hyperventilation causing respiratory alkalosis and intracellular redistribution of phosphate) * Renal impairment (diuretic therapy, renal tubular defects) * Gastrointestinal losses (malabsorption syndrome or use of phosphate-binding antacids) Hypophosphatemia = phosphate <2.5 mg/dL Phosphate is an electrolyte that plays an important role in cellular energy, and hypophosphatemia can lead to respiratory, neurologic, and hematologic manifestations. This occurs especially when levels drop below 1 mg/dL, which can result in significant organ dysfunction.

Answer 150

Hypocalcemia Thus, loop diuretics (eg. Lasix) is often used to treat hypercalcemia.

Answer 151

Hypercalemica Thiazide-induced blockade of Na+ entry enchances the Na+/Ca2+ antiporter activity and increases overall reabsorption of Ca2+ NOTE: Thiazides are useful in the prevention of calcium-containing kidney stones caused by hypercalciuria.

Answer 152

Diuretics, such as Lasix, will decrease preload or LVEDV and therefore cause a left-shift along the curve. It will NOT shift the curve up as it does not affect contractility. The Frank-Starling curve is shifted down and to the right with increased afterload or decreased inotropy (eg. systolic heart failure) Decreased afterload and increased inotropy will shift the curve up and to the left. Increased LVEDV for a given state of inotropy and afterload will shift the curve up and to the left. Decreases in LVEDV (eg diuretics) will cause a left shift along the curve.

Answer 153

First line treatment: Rehydration (isotonic saline) Patients with hypercalcemia are often significantly dehydrated. Rehydration lowers calcium levels slightly via a dilutional effect. Additionally, rehydration prevents sodium and calcium reabsorption from the thick ascending limb of the loop of Henle. Second line treatment: Loop diuretics, calcitonin, bisphosphonates NOTE: Metabolic acidosis causes hypercalcemia (increased ionization of calcium and thus less protein binding). Metabolic alkalosis causes hypocalcemia (decreased ionization of calcium and thus more protein binding).

Answer 154

Normal serum magnesium levels are between 1.5 and 2.5 mg/dL. Hypermagnesemia is > 2.5 mg/dL and can result from kidney impairment, overuse of magnesium-based laxatives or enemas, over-infusion of magnesium in preeclampsia treatment, and disorders such as milk-alkali syndrome. Hypermagnesemia results in neurotoxicity by decreasing transmission of the impulse across the neuromuscular junction, resulting initially in diminished deep tendon reflexes. As the magnesium levels rise (table), the reflexes disappear. Cardiotoxicity results from magnesium acting as a calcium and potassium channel blocker, disrupting cardiac function and leading to complete heart block and cardiac arrest (> 12 mg/dL). Due to its calcium channel blocker effects, magnesium can lead to hypotension, bradycardia, and changes seen on electrocardiogram (ECG), including prolonged PR interval and widened QRS. Stopping the source of magnesium is the first step in the treatment of hypermagnesemia. If the patient is symptomatic, calcium gluconate can be administered. The elimination of magnesium can be further increased by adding a loop diuretic and increasing diuresis with normal saline. If the patient has renal failure, dialysis is indicated.

Answer 155

The Haldane effect is a physicochemical phenomenon which describes the increased capacity of blood to carry CO2 under conditions of decreased haemoglobin oxygen saturation (ie hypoxia). More CO2 binds to haemoglobin at lower oxygen saturation. This effect facilitates the removal of CO2 from the tissues

Answer 156

The Bohr effect describes hemoglobin’s lower affinity for oxygen secondary to increases in the partial pressure of carbon dioxide and/or decreased blood pH (ie. hypercapnia, acidosis). This lower affinity, in turn, enhances the unloading of oxygen into tissues to meet the oxygen demand of the tissue.

Answer 157

First line treatment is Atropine Atropine is indicated for symptomatic bradycardia regardless of the conduction cause. However, it may be ineffective for second-degree Type II and third-degree blocks.

Answer 158

Cisatracurium Atracurium NOTE: Cisatracurium is a nondepolarizing neuromuscular blocking agent that is of intermediate duration (20-50 min) ,with an onset of 4 to 6 minutes. It was created to reduce the histamine release associated with atracurium. Because of its potency, 5 times less cisatracurium is used compared to atracurium, resulting in a minimal histamine release. Cisatracurium is not reliant on liver or kidney function because it spontaneously degrades in the plasma via Hofmann elimination and ester hydrolysis into inactive metabolites. As a result, it is used clinically in patients with severe renal dysfunction. The Hofmann elimination is pH- and temperature-dependent, with an increase in pH increasing degradation and hypothermia slowing down the degradation.

Answer 159

Increased pH Increased temperature

Answer 160

Succinylcholine Mivacurium NOTE: Patients with pseudocholinesterase deficiency will have prolonged neuromuscular blockade. Also note ester local anesthetics are metabolized by pseudocholinesterases as well. Somethings "SMeLs" fishy

Answer 161

Atracurium Mivacurium "My allergies are worse in the AM"

Answer 162

Pancuronium Likely due to a vagolytic effect secondary to inhibition of M2 receptors plus direct and indirect sympathetic stimulation.

Answer 163

Vecuronium Pancuronium

Answer 164

A Dibucaine Number (DN) under 30% suggests pseudocholinesterase deficiency. Dibucaine is a local anesthetic that was found to inhibit normal pseudocholinesterase activity by 80%. A normal patients Dibucaine number is thus 80. This number is proportional to the amount of normal pseudocholinesterase. Normal = DN 80 Heterozygous pseudocholinesterase deficiency = DN 50-60 Homozygous pseudocholinesterase deficiency = DN 20-30

Answer 165

Clevidipine Esmolol Remifentanil NOTE: Hence fast onset/offset of each.

Answer 166

Rocuronium Vecuronium "Sugammadex RV"

Answer 167

Diaphragm (first to recover) Laryngeal muscles Corrugator supercilli Abdominal muscles Orbicularis occuli Adductor pollicis Upper airway NOTE: Stimulation of corrugator supercilli draws the two eyebrows together medially and inferiorly. Stimulation of the orbicularis occuli closes the eyelid.

Answer 168

modified y-cyclodextrin (lipophilic core, hydrophilic periphery)

Answer 169

Duration of action: Atropine 15-30min Glycopyrrolate 2-4hrs

Answer 170

Mydriasis Photophobia Dry mouth Tachycardia Constipation Urinary retention

Answer 171

YES Rocuronium is metabolized by the liver and eliminated primarily by the hepatobiliary system (70%) and to a lesser degree renally eliminated. Because of this the elimination of rocuronium is slightly extended in renal failure but has not been shown to be significant clinically.

Answer 172

PANCURONIUM Pancuronium is the most dependent on renal metabolism, and its pharmacokinetics would be most significantly impacted in the setting of renal disease (neuromuscular blockade is prolonged). The metabolite of pancuronium, 3-desacetylpancuronium, is half as potent as its parent compound and can accumulate in renal failure due to its significant (85%) renal elimination, leading to prolongation of the neuromuscular blockade. VECURONIUM Vecuronium is primary eliminated through the biliary system. However, there is a small amount of vecuronium that is eliminated by the kidneys. Additionally, vecuronium has an active metabolite, 3-desacetylvecuronium, which has about 80% the potency of vecuronium and is primarily eliminated through the kidneys. The duration of action of vecuronium is also increased with age, which means that the same dose of vecuronium will have longer lasting effects. One study showed the duration increases from 44 minutes to 73 minutes; dosing could therefore be decreased by 36% per this study. "Very Prolonged in renal failure"

Answer 173

ED95 is the median dose required to achieve 95% block of a single twitch in 50% of individuals. For effective relaxation during intubation, one to two times the ED95 is administered.

Answer 174

During TURP, the wide plexus of venous sinuses is often opened and the absorption of the irrigation fluid causes a group of symptoms and findings that is called TURP syndrome. Absorption of the irrigation fluid (2000 ml or more) may lead to TURP syndrome which causes headaches, anxiety, confusion, dyspnoea, arrhythmia, hypotension and seizures and can be fatal if not treated. The symptoms of TURP are generally caused by an excessive fluid load in circulation. Different symptoms may occur depending on the solute used in the irrigation fluid. Excessive absorption of the irrigation solutions used during TURP, which are highly hypotonic can cause dilutional hyponatremia and hypo-osmolality resulting in severe neurological symptoms.

Answer 175

Untreated bleeding disorder/blood thinners UTI Pregnancy (can cause miscarriage, placenta displacement, low birth weight) Large aortic aneurysms

Answer 176

The hepatic arterial buffer response (HABR) is the system within the liver responsible for maintaining constant hepatic blood flow and is *unaffected by intravenous or volatile anesthetics. * The system functions in a manner such that when portal venous blood flow decreases, the hepatic artery vasodilates to maintain perfusion. The main determinant controlling this hepatic blood flow is adenosine. It is produced in the space of Mall which surrounds the hepatic vasculature and diffuses into the portal vein. When the portal venous blood flow decreases, the adenosine accumulates resulting in vasodilation of the hepatic artery increasing blood flow to the liver by the hepatic artery.

Answer 177

Propofol is the only anesthetic that increases blood flow to the liver. The effects of anesthetics on hepatic blood flow stem from their ability to alter perfusion to the liver. Total hepatic blood flow is the sum of portal venous blood flow plus the hepatic artery blood flow. When there is a reduction in portal venous blood flow, the hepatic artery increases blood flow via the hepatic arterial buffer response. Volatile anesthetics reduce portal venous blood flow by decreasing mean arterial pressure and cardiac output. Despite this, isoflurane, desflurane, and sevoflurane mostly preserve total hepatic blood flow at 1 minimum alveolar concentration (MAC) by leaving the hepatic arterial buffer response intact. At concentrations higher that 1 MAC, isoflurane will reduce total hepatic blood flow in a dose-dependent manner. Intravenous and neuraxial anesthetics also alter blood flow. Propofol increases hepatic blood flow, while barbiturates, benzodiazepines, dexmedetomidine, and etomidate have little effect on hepatic blood flow but may decrease somewhat. Ketamine does not alter hepatic blood flow. Use of propofol, an intravenous anesthetic, results in an increase in blood flow to the liver, and it is the only anesthetic to increase blood flow. NOTE: Glucagon, D1 agonism, B2 agonsim, Adenosine (A2 agonism) all increase HBF.

Answer 178

Hepatic metabolism Propofol has a very high hepatic extraction ratio (near 1)

Answer 179

ETOMIDATE Thrombophelbitis is a condition where a vein becomes inflamed related to a thrombus that has formed in the vein (thrombo-phleblitis). Risks include small vein, slow injection, and high doses. Etomidate is poorly water-soluble and therefore formulated as a solution in PEG. This preparation of PEG is analogous to an extremely hyperosomolar solution compared to normal serum osmolality. Hyperosmolality is thought to be the major contributing factor in pain on injection and venous irritation. There are reports of phlebitis and thrombophlebitis after injection with PEG preparations of Etomidate up to 7 days after surgery.

Answer 180

Binds to GABA-A receptor and enhances affinity of GABA-A receptor for GABA.

Answer 181

Glucagon is a catabolic peptide secreted by the pancreatic α-cells located in the islets of Langerhans in response to hypoglycemia, B2 stimulation (eg. epinephrine, NE), and cortisol.

Answer 182

1mg IM Glucagon

Answer 183

Glucagon activates G-protein coupled recepotors activating adenyl-cyclase to increase cAMP levels. Results: - Increased gylcogenolysis - Increased gluconeogenesis - Inhibition of glycogenesis - Increased lipolysis - GI muscle relaxation - Decreases biliary and LES tone - Increases hepatic and splanchnic blood flow - Positive chronotrope (increases HR) - Positive inotrope (increases contractility) NOTE: Glucagon enhances activation of adenyl cyclase in the myocardium but its effects are not blocked by beta blockers. Glucagon may be useful in treatment of beta blocker overdose by increasing cAMP in the myocardium while bypassing the second messenger system. Glucagon is contraindicated in pheochromocytoma due to the risk of hyperglycemia and severe hypertension.

Answer 184

Activation of guanylate cyclase and increase in cGMP. Another medication that is commonly used to increase intracellular cGMP is nitroglycerin. This medication is rapidly converted to NO in the body and this vasodilatory effect is leveraged to provide systemic vasodilation, either when a patient is having anginal symptoms or in more controlled circumstances in the operating room or ICU. The medication sildenafil, originally created to treat pulmonary hypertension, has the same clinical effect as iNO. Sildenafil is a phosphodiesterase V inhibitor (which breaks down cGMP) and causes its clinical effect through the relaxation of smooth muscle in the pulmonary vasculature identically to iNO.

Answer 185

Mean Pulmonary Artery Pressure (MPAP) > 25

Answer 186

Nitric Oxide Nitroglycerin Nitroprusside Nesiritide Milrinone Dobutamine PDE-3 inihbitors NOTE: Avoid hypoxia, hypercarbia, acidosis as these increase PVR.

Answer 187

If arterial air embolism is suspected while on cardiopulmonary bypass it is reasonable to... Initiate steep Trendelenburg positioning Deep hypothermia (decrease CRMO2) Retrograde cerebral perfusion Mantain arterial oxygenation Permissive hypercapnia (cerebral vasodilation) Maintain/elevate CPP

Answer 188

FFP contains all coagulation factors, including normal levels of factors V and VIII.3 NOTE: Used to treat dilutional coagulopathy during massive transfusion, coagulopathy related to hepatic deficiency, TTP, specific factor deficiencies, Warfarin reversal, anti-thrombin III deficiency.

Answer 189

Factor V Factor VIII NOTE: Factor V and VIII are the least stable in blood products and can degrade above 4 degrees celcius. This is mainly why FFP is frozen for storage. FFP can be transfused up to 5 days after thawing, at which significant reductions occur in factor V and factor VIII.

Answer 190

Factors II, VII, IX, X, Protein C, Protein S

Answer 191

Factors VIII, XIII, fibrinogen, vWF

Answer 192

10 units of cryopercipitate will typically raise a 70kg patient's fibrinogen by 70mg/dL. NOTE: Cryopercipitate contains approximately 200mg/unit of fibrinogen. Cryopercipitate is often given during massive transfusion after several units of other blood products have been given. The normal range for fibrinogen levels is typically between 200 and 400 milligrams per deciliter (mg/dL). Checking fibrinogen levels during massive transfusion can assist with management of cryopercipitate. Cryopercipitate is also used to treat vWF disease and hemophilia A.

Answer 193

Use of factor VIII during massive transfusion is theoretical and not proven. Factor VIII levels have to decrease to below 30% to alter hemostasis. Because PRBCs contain very little coagulation factors, it is theoretical that levels could decrease during massive transfusions. However, both fresh frozen plasma and cryoprecipitate contain factor VIII; these products are typically transfused during a massive transfusion protocol thus administration of factor VIII concentrate is not necessary.

Answer 194

Amount FFP Needed (mL) = (Target Level - Present Level) * kg For example, let's say we have a 70kg patient who is bleeding with an INR of 7.5 and our goal INR is 1.4. We would need (40% - 5%) * 70 kg, which is 2450 mL of FFP to make this correction. A single unit of FFP typically is 200-250 mL.

Answer 195

Hemophilia A is an X-linked recessive disorder caused by deficiency of factor VIII (treatment: desmopressin, factor VIII concentrate) Hemophilia B is an X-linked recessive disorder caused by deficiency of factor IX (treatment: recombinant factor IX)

Answer 196

Ideal body weight (IBW) is the optimal weight associated with maximum life expectancy for a given height. Ideal body weight (male) = 50 + (0.91 × [height in centimeters − 152.4]) Ideal body weight (female) = 45.5 + (0.91 × [height in centimeters − 152.4]).

Answer 197

Lean body weight (male) = 1.1 (weight [kg]) – 128 (weight / height) ^ 2 Lean body weight (female) = 1.07 (weight [kg]) – 148 (weight / height) ^ 2

Answer 198

Propofol should be dosed based on lean body weight.

Answer 199

Rocuronium should be dosed base on ideal body weight.

Answer 200

Specific medications in anesthesia and how dosage should be calculated: Total body weight: succinylcholine, maintenance infusion dose of propofol, dexmedetomidine, opioids, midazolam Lean body weight: induction dose of propofol, etomidate, opioids (morbidly obese) Ideal body weight: rocuronium, vecuronium, remifentanil NOTE; That obese patients have increased butrylcholinesterase activity and increased ECF hence sucinnylcholine should be based on total body weight. Totally Sux (total) Propofol Lean'n {lean) Rocky Deal (ideal)

Answer 201

The following changes occur in the elderly (≥65 years) affecting the function, duration, and elimination of NMBAs: * Increased total body fat * Decreased total body water * Decreased lean body mass * Decreased renal and hepatic blood flow * Decreased hepatic function * Decreased glomerular filtration rate * Decreased cardiac output As a result of a decrease in cardiac output, the circulatory time is increased, leading to a slower onset for NMBAs. Prolongation of the duration of action is also seen due to decreased metabolism and clearance for NMBAs that rely on hepatic and renal excretion and metabolism as well as distribution due to changes in blood flow and body mass. In addition, there is a decrease in the dosing requirements for maintenance of the neuromuscular blockade, which is evident clinically by an increased duration between dosing intervals required to maintain the same depth of neuromuscular blockade compared to that in younger patients.

Answer 202

IHD CHF CVA DM requiring insulin Cr >2 High risk procedure Using a risk stratification scoring system such as the Revised Cardiac Risk Index (RCRI) is helpful in determining patients at risk of postoperative mortality from MI on the basis of their risk factors. The risk of an adverse cardiac event increases with the number of risk factors present. The RCRI establishes a 30-day mortality risk for patients, depending on the risk inherent to the surgery itself (according to the RCRI scoring system, "high risk" surgeries include intraperitoneal, intrathoracic, or suprainguinal vascular surgery), history of ischemic heart disease, history of congestive heart failure, history of stroke, poor kidney function, or insulin-dependent diabetes. On the basis of the original data used to create the RCRI, the risk of a major cardiac event is 0.4% with zero points, 1% with one point, 2.4% with two points, and 5.4% with three or more points. Other factors to consider prior to surgery involve preoperative functional capacity evaluation, cardiac markers, and using pharmacologic or treadmill stress testing to establish a functional cardiac baseline. The American College of Cardiologists and the American Heart Association recommendations require that all patients must be able to achieve an activity level equal to 4 or more metabolic equivalents (MET) prior to undergoing surgery as studies have shown that patients who cannot achieve 4 METs are at increased risk of adverse perioperative cardiac events.

Answer 203

An emergency exists when life or limb is threatened if the patient is not in the operating room within six hours. An urgent procedure is required when life or limb is threatened if the patient is not in the operating room within 24 hours. A time sensitive procedure can be delayed 1-6 weeks for evaluation if it will change management. An elective procedure can be delayed up until one year.

Answer 204

(Base Unit (BU) + Time Unit (TU) + Modifying factors) x Conversion Factor Modifying factors include physical status, specialized monitoring, and qualifying circumstances (QCU). QCU includes extremes of age, emergency conidtions, controlled hypotension, hypothermia.

Answer 205

Aphase II block is characterized by fade of TOF, tetanic fade, and post-tetanic potentiation. A phase II block is seen with the following: 1) Non-depolarizing NMBAs 2) Prolonged exposure to succinylcholine (repeated doses > 4mg/kg, infusions) 3) Single dose of succinylcholine in a patient with pseudocholinesterase deficiency NOTE: A single, normal dose of succinylcholine should only produce a phase I block often preceeded by muscle fasiculation. A phase I block is characterized by a diminished but equal height in the TOF.

Answer 206

1) Increased occupancy of AcH-R by the NDNMBA. 2) Diminishing release of AcH into the NMJ with each successive twitch

Answer 207

Non-depolarizing NMBAs also block presynaptic acetylcholine receptors. Succinylcholine does not block presynaptic acetylcholine receptors.

Answer 208

A single dose of Succinylcholine will produce a phase 1 block.

Answer 209

Repeated dose of Succinylcholine or infusion of Succinylcholine will produce a phase II block.

Answer 210

Succinylcholine administered to a patient with pseudocholinesterase deficiency will produce a phase II block.

Answer 211

Phenomenom where tetanic stimulation increases the effect of a single twitch applied immediately after. Occurs due to increased Ca2+ in presynaptic neurons and thus increase in acetylcholine at the motor endplate. It is most useful when deep levels (TOFC = 0) are present.

Answer 212

TOF count and corresponding % nACR blockade: 0: 100% 1: 90% 2: 80% 3: 70-80% 4: < 70%

Answer 213

The recommended target for intraoperative blood glucose levels is <180 mg/dL.

Answer 214

The classic teaching is that Metformin must be stopped the day before surgery for fear of lactic acidosis forming in the perioperative period. Miller Clinical Anesthesia states that "Metformin does not have to be routinely discontinued the day before surgery." The problem with routine discontinuation of Metformin is the possibility of worsening glycemic contnrol, something we know is problematicand causes poor outcomes. The risk of lactic acidosis is very low and exists in patients who then go on to develop renal and hepatic failure while taking Metformin. In specific patients with renal or hepatic failure who are being exposed to IV contrast or having procedures with significant blood loss or hemodynamic instability, it may be reasonable to hold Metformin.

Answer 215

The issue of perioperative continuation of angiotensin converting enzyme inhibitors and angiotensin receptor blockers is not entirely settled. The 2014 ACC/AHA guidelines state is it "reasonable" to continue them perioperatively, but anesthesia textbooks urge caution as they **may cause refractory hypotension. ** In a more recent large prospective observational study, continuation of angiotensin-converting enzyme inhibitors/angiotensin II receptor blockers was associated with a higher risk of death and postoperative vascular events.

Answer 216

Whether or not to stop a diuretic is controversial and depends on the patient's history and the surgery planned. Most experts would recommend holding the diuretic especially for a surgery that has the potential for volume shifts (eg open abdominal) and significant blood loss. The concern with continuation includes volume management, potential hemodynamic derrangements, and electrolytes abnormalities. Potassium derrangements can lead to arrhythmias, altered response to muscle relaxants, and potentiation of ileus. Studies have NOT shown an increased risk of intraoperative hypotension when the patient is on chronic therapy.

Answer 217

Carbohydrate-rich drinks given 2h before surgery INCREASES insulin sensitivity. A systematic review of 17 studies (1445 patients) showed carbohydrate loading reduced postoperative insulin resistance. In patients undergoing major abdominal surgery, carbohydrate loading has also been associated with a reduced hospital length of stay.

Answer 218

YES. According to the American College of Cardiologists/American Heart Association 2014 guidelines, patients taking long-term or chronic beta-blockers should continue these medications through the perioperative period including the day of surgery. Results of several well-powered studies have provided evidence that individuals who stop taking their long-term beta-blockers within 48 hours of surgery have an elevated mortality risk of cardiac ischemia after noncardiac surgery. OTHER: Beta-blocker therapy is an important treatment consideration for high-risk patients undergoing non-cardiac surgery. Identifying patients at high risk for ischemia, either from their risk factors or their planned surgery, and considering beta-blocker therapy preoperative is potentially beneficial to alter their risk of major adverse cardiac events. Patients with known inducible ischemia may receive even more benefit from preoperative beta-blocker therapy and thus it should be highly considered in that patient population. It is known that beta-blocker therapy should not be started within 1 day of surgery as that significantly increases the risk of stroke and death. Thus the recommendation from most experts/guidelines is to initiate therapy at least 2 days, but preferably 7-45 days prior to surgery. Additionally, anyone who is currently on a beta-blocker should have that medication continued in the perioperative period.

Answer 219

Beta Blockers Clonidine NOTE: Holding Clonidine > 24hrs can lead to marked hypertension, tachycardia, and even severe delirium.

Answer 220

Hypoglycemia Shown to decrease postprandial blood glucose in patients with and without diabetes. In the setting of perioperative fasting prior to surgery this can result in hypoglycemia. Animal studies demonstrate direct stimulation of insulin release. Bleeding Potentially irreversible platelet inhibition- inhibition of platelet aggregation that may be permanent and may increase bleeding. May also interefere with Warfarin anticoagulation. NOTE: Patients should hold Ginseng 7-14 days prior to surgery. Herbal supplements starting with the letter "G" inhibit platelet aggregation and can increase risk of bleeding (Garlic, Ginger, Ginseng, Ginko)

Answer 221

Delayed emergence Altered drug metabolism (CYP450 inducer can affect benzos, lidocaine, alfentanil, warfarin, digoxin) Risk of serotonin syndrome (SNRI-inhibitor risk of serotonin syndrome with other meds)

Answer 222

Bleeding It inhibits platelet aggregation and increases fibrinolysis. Can increase risk of bleeding especially when patients are on other antiplatlet agents. NOTE: Garlic should be held 7 days prior to surgery. Herbal supplements starting with the letter "G" inhibit platelet aggregation and can increase risk of bleeding (Garlic, Ginger, Ginseng, Ginko)

Answer 223

The cardioselective (β1) blockers may be remembered by using the mnemonic “BEAM” (Bisoprolol, Esmolol, Atenolol, and Metoprolol).

Answer 224

Vecuronium, Pancuronium "Very Prolonged" in renal failure Pancuronium is the most dependent on renal clearance and prolongation has been reported in patients with significant renal impairment.

Answer 225

Sugammadex is a reversal agent for the *steroidal* neuromuscular blocking medications rocuronium and vecuronium. Sugammadex is a*modified y-cyclodextrin* with an 8-member ring with a central core that encapsulates the steroid nucleus of rocuronium and vecuronium (intermediate-acting neuromuscular blocking agents). Sugammadex is relatively selective for *steroidal* neuromuscular blocking drugs but does additionally bind to the steroidal portions of toremifene, flucloxacillin, progesterone, and fusidic acid. Oral contraception has been known to be affected by sugammadex, with the administration of sugammadex being equivalent to missing 1 daily oral dose; thus, it is recommended to use alternative means of birth control for 1 week after sugammadex administration.

Answer 226

Incidence of anaphylaxis is estimated to be anywhere between 1:5000 to 1:20,000 (< 1%). Incidence of hypersensitivity reaction (nausea, pruritis, urticaria) is much higher (7-9%). Sugammadex is a synthetic, modified γ-cyclodextrin. Therefore, a patient with hypersensitivity to cyclodextrins is at significantly increased risk for an anaphylactic reaction to sugammadex, and its use is contraindicated. Adverse effects: Anaphylaxis or hypersensitivity reactions Bradycardia (1% with 2mg/kg & 4mg/kg, 5% with 16mg/kg) Tachycardia Hypotension Prolongation of PT/INR and PTT (incidence of 25%, 1 hour after administration, no studies showing increased risk of bleeding) Risk of unintentional pregnancy

Answer 227

The CCP is determined by the difference between aortic diastolic pressure (AoDP) and left ventricular end-diastolic pressure (LVEDP) by the equation CPP = AoDP − LVEDP.

Answer 228

Larynx is innervated by two nerves branching from VAGUS NERVE (CN X) SUPERIOR LARYNGEAL NERVE: Sensory: internal branch supplies sensation to mucosa from epiglottis to vocal cords Motor: external branch supplies CRICOTHYROID MUSCLE (lengthens vocal cords). RECURRENT LARYNGEAL NERVE: Sensory: mucosa below vocal cords Motor: ALL OTHER INTRINSIC MUSCLES of larynx except cricothyroid muscle The left recurrent laryngeal nerve branches off the left vagus nerve, loops under the aorta, and travels superiorly between the esophagus and trachea. The right recurrent laryngeal nerve branches off the right vagus, loops under the right subclavian artery, and travels superiorly between the esophagus and trachea on the right.

Answer 229

If there is a unilateral recurrent laryngeal nerve injury, there will be ipsilateral paralysis of all intrinsic laryngeal muscles except for the cricothyroid muscle. Thus, on inspiration, the paralyzed vocal cord will not abduct properly. The patient may be asymptomatic or present with hoarseness. With phonation, the paralyzed vocal cord will have assumed a paramedian position due to the unopposed action of the cricothyroid muscle. With time, the unparalyzed vocal cord will move toward the paralyzed vocal cord, and phonation will improve. In bilateral recurrent laryngeal nerve injury, the vocal cords will not abduct properly and may present as fixed airway obstruction. In unilateral superior laryngeal nerve injury, there will be decreased pitched and weakened voice. Bilateral superior laryngeal nerve injury is rare and will present with coughing; choking episodes; and a weak, husky voice.

Answer 230

Two other nerves that should be anesthetized for an awake nasal FOB intubation include: Glossopharyngeal Nerve (CN IX) (Sensory innervation to posterior 1/3 of tongue, pharynx, and areas above epiglottis0 Trigeminal Nerve (CN V)- Ophthalmic Branch (V1): sensory innervation to anterior portion of nasopharynx Maxillary Branch (V2): Sensory innervation to posterior portion of nasopharynx

Answer 231

Glossopharyngeal Nerve (IX) (Afferent limb) Vagus Nerve (X) (Efferent limb) The gag reflex (or pharyngeal reflex) is triggered by afferent signaling via the glossopharyngeal nerve (CN IX) and produces pharyngeal muscle contraction mediated primarily by the bilateral vagus nerves (CN X). This reflex prevents entry of debris into the hypopharynx and thus protects against aspiration and asphyxiation. However, the gag reflex may also complicate airway management and provoke emesis in an awake or lightly anesthetized patient.

Answer 232

Oculocardiac reflex Afferent Limb: Trigeminal nerve, ophthalmic division (V1) Efferent Limb: Vagus (X) Triggered by 1) Direct pressure on the eye 2) Traction on EOM 3) Retrobulbar block

Answer 233

The Bainbridge reflex is mediated by type-B stretch sensitive mechanoreceptors in the right atrium and cavoatrial junction. When cardiac preload is increases, stretch receptors send signals via the vagus nerve (CN X) to the medulla. Medulla sends efferent response to inhibit parasympathetic activity which increases heart rate.

Answer 234

Isovolumetric relaxation Rapid filling Slow filling ("diastasis) Atrial kick NOTE: Patients with diastolic dysfunction in times of stress will be less able to increase filling pressures any further which leads to a decreased ability to improve cardiac output. Patients with diastolic dysfunction are also unable to tolerate atrial fibrillation well because a greater fraction of LV filling depends on atrial kick.

Answer 235

Head/neck flexion Trendelenburg Pneumoperiotneum/insufflation NOTE: Trendelenburg and pneumoperitoneum/insufflation doesnt actually move the tip of the ETT but pushes the lung up and trachea cephaled relative to the tip of the ETT. Conversely, head/neck extension and reverse RT will cause cephalad movement of the ETT. With respect to head/neck flexion and extension just remember that the "hose follows the nose"

Answer 236

Major contraindications for LMA use include, but are not limited to: * Patients with a high risk for aspiration of gastric contents (full stomach, hiatal hernia, gastroesophageal reflux disease, intestinal obstruction, and delayed gastric emptying) * Lung disease (low compliance, high airway resistance) * Airway obstructions (glottic, subglottic) * Lmited mouth opening (generally less than 1.5 cm) OTHER: Most (2 in 3) patients that have aspirated are asymptomatic by two hours and require no additional intervention. Of those who develop respiratory symptoms (1 in 3), non-invasive or invasive ventilation may be temporarily required, and there is a mortality of approximately 10%. Patients who are ventilated > 48 hours have a nearly 50% mortality rate.

Answer 237

See picture NOTE: Although routinely used to decrease risk of aspiration, recent evidence suggests cricoid pressure may actually increase for reflux in anesthetized patients. Cricoid pressure decreases LES tone without influencing gastric pressure. This leads to a decreased barrier pressure (difference between LES pressure and gastric pressure) and therefore potentially increases the risk of aspiration. The clinical signficance of this however has not been determined. Opponents of cricoid pressure affirm that succinylcholine increases LES tone making the need for cricoid pressure during RSI questionable. Succinylcholine increases LES tone and intragrastric pressure, but LES > intragastric pressure. Unless the patient has an incompetent LES, there is no increased risk of aspiration.

Answer 238

Lower esophageal sphincter (LES) pressure is approximately 25 mmHg ("barrier pressure").

Answer 239

Volume > 25cc pH < 2.5

Answer 240

Position (trendelenberg) -> suction -> intubation -> PPV NOTE: Bronchoalveolar lavage is not indicated after aspiration as it may force aspirate further into distal airways. If possible, avoid PPV before suctioning and intubation for the same reason.

Answer 241

Inappropriate fasting status Morbid obesity (BMI >40, class III obesity) Diabetic gastroparesis Hiatal hernia Pregnancy Symptomatic gastroesophageal reflux disease Nasogastric tube in place

Answer 242

Although it is uncommon, laryngeal mask airway (LMA) use has been associated with **lingual, hypoglossal, and recurrent laryngeal nerve injuries.** These complications have been associated with overinflation of a small-fitting cuff (>40mmHg), prolonged operative time (>2-4 hours), lidocaine lubrication, difficult insertion, use of nitrous oxide, and cervical joint disease. Pressure neuropraxia from the LMA tube and/or cuff is the most common cause of these nerve injuries. The increased oropharyngeal soft tissue pressure leads to injury of the lingual nerve, hypoglossal nerve (CN XII), and recurrent laryngeal nerve, which may cause tongue numbness, oropharyngeal swelling, and transient vocal cord palsy leading to difficulty with phonation. The use of nitrous oxide(NO2) can cause an increase of up to 30 mmHg in LMA cuff pressure on the soft tissue because NO2 can displace air within the cuff. Adjusting LMA placement and/or changing to a larger size LMA is appropriate when more than the recommended air insufflation is required to maintain a mask seal (typically, 60 cm H2O or 44 mmHg). Correct positioning may be best verified by generating an airway pressure of 20 cm H2O and the ability to ventilate manually using the reservoir bag.

Answer 243

Water based lubricant

Answer 244

Sodium Citrate (non-particulate acid) NOTE: According to the ASA guidelines, medications should not be routinely administered preoperatively solely to reduce pulmonary aspiration risk in patients who have no apparent increased risk of pulmonary aspiration. The ASA guidelines state that medications can be given to high-risk patients. High-risk patients typically include those with multiple aspiration risk factors, such as diabetic gastroparesis, hiatal hernia, inappropriate fasting status, morbid obesity (body mass index >40 kg/m2, now known as class III obesity), nasogastric tube in place, pregnancy, and symptomatic gastroesophageal reflux disease. The overall goal of using these medications is to decrease gastric volume and increase pH. Particulate acids are not used because if they aspirate it then it can cause pulmonary shunting and hypoxemia.

Answer 245

Female sex Age <50 years Nonsmoker History of PONV or motion sickness Use of post-operative opioids Specific surgeries (laparoscopic esp chole, gynecologic) Use of volatile anesthetics or NO Long duration of anesthesia Medications for PONV target the chemoreceptor trigger zone (CTZ) in the area postrema of the brainstem. The CTZ contains dopamine (D2), histamine (H1), muscarinic acetylcholine (M1), neurokinin (NK1), opioid, and serotonin (5HT3) receptors. Multimodal use of dopamine antagonists (e.g. IV droperidol 0.625 mg, haldol), histamine antagonists (diphenhydramine, promethazine), neurokinin antagonists (aprepitant), muscarinic antagonists (scopolamine), serotonin antagonists (IV ondansetron 4 mg, palonosetron), and steroids (dexamethasone 4mg) may be used for PONV.

Answer 246

Reduction in PONV Reduction in airway irritation and post-extubation cough Rapid and predictable emergence with minimal lingering effects Reduction in risk of laryngospasm and bronchospasm by up to 50% in pediatric patients Decreased risk of emergence delirium Reduction in post-operative cognitive impairment in elderly patients.

Answer 247

Famotidine (Pepcid) MOA: H2-antagonist; Increases gastric pH and deceases gastric volume Onset (IV): 30min

Answer 248

Metoclopramide (Reglan) MOA: Dopamine (D2) antagonist; Decreases gastric volume, no effect on gastric pH, relaxation of pyloric sphincter and duodenal bulb, increases lower esophageal sphincter tone Onset (IV): 3 min Metoclopramide is a weak antiemetic, and, at a dose of 10 mg IV, it is not thought to be effective when used in combination with other antiemetics for prophylaxis. Metoclopramide is a more effective antiemetic at 25 to 50 mg, but, at these higher doses, the risk of adverse effects such as tachycardia, hypotension, and extrapyramidal symptoms is also higher. The current SAMBA guidelines suggest using metoclopramide only when other dopamine antagonists (such as droperidol) are not available. NOTE: Metoclopramide has NO EFFECT ON GASTRIC PH.

Answer 249

1) NR3C1 agonist (anti-inflammatory effect) Glucocorticoids such as dexamethasone agonize nuclear receptor subfamily 3, group C, member 1 (NR3C1), also known as the glucocorticoid receptor (GCR). Agonism of NR3C1 aka GCR treats inflammation. GCR regulates metabolism and immunity in most cells. In macrophages, upregulation of GCR leads to increased expression of anti-inflammatory proteins and inhibition of the expression of pro-inflammatory proteins. 2) Phospholipase A2 inhibitor (analgesic effect) Corticosteroids also inhibit prostaglandin synthesis at phospholipase A2 at the beginning of the arachidonic acid pathway; thus, they have similar analgesic effects to NSAIDs, which block COX at the next step in the pathway.

Answer 250

NK1 antangonist Aprepitant antagonizes the NK1 receptors in the CTZ. It blocks the actions of dopamine, NK1, and NK2. Early trials have shown equal efficacy between aprepitant and ondansetron for their effects on nausea; however, aprepitant has been shown to be more efficacious against vomiting. IV Aprepitant has good efficacy for the prevention of vomiting for up to 48 hours postoperatively. Aprepitant has not been shown to cause any changes in ECG, whereas several other antinausea medications such as droperidol, haloperidol, and ondansetron can cause QT prolongation. Many of the antinausea, antiemetic medications target receptors in the chemoreceptor trigger zone (CTZ) (also known as the area postrema) along with the nearby nucleus tractus solitarius (both located in the medulla oblongata of the brainstem) are felt to contain dense quantities of emetogenic chemoreceptors. Receptors identified in this area so far include dopamine, NK1, acetylcholine, serotonin, histamine (D-NASH).

Answer 251

Droperidol (Inapsine) MOA: Dopamine (D2) antagonist Dose: 0.625-1.25mg

Answer 252

Dexamethasone Scopalamine patch (anti-cholinergic) Benadryl (anti-histamine, anti-cholinergic) Succinylcholine Ketamine Glaucoma is a group of eye disorders in which the optic nerve is damaged and leads to visual loss. Most commonly this is caused by elevated intraocular pressure (IOP) which then impairs capillary blood flow to the optic nerve. Open-angle glaucoma: IOP elevated due to impaired aqueous humor drainage in the setting of an antomically open anterior chanmber angle (angle between iris and cornea). Closed-angle glaucoma: acute, sudden onset of eye pain and blurred vision. Result of closure of the angle between iris and cornea. Considered an emergency requiring immediate IOP reduction (via medication or surgery). Several classes of perioperative medications should be used cautiously or avoided in patients with glaucoma. Medications that cause mydriasis (eg. anticholinergics, antihistamines) can impair aqueous humor drainage and acutely increase intraocular pressure (IOP). Their use is contraindicated in patients with or at risk for closed angle glaucoma and should be used cautiously in patients with open angle glaucoma. Corticosteroids can increase IOP and even cause steroid-induced glaucoma and they should be used cautiously in patients with glaucoma. Succinylcholine and ketamine generally avoided as they both can increase IOP Zofran does not cause or worsen glaucoma and is safe to use. Atropine and glycopyrrolate (although anti-cholinergics, antimuscarinics) are generally considered safe to use in either population.

Answer 253

Conciousness Activity Oxygenation Respiration Circulation NOTE: Patients can be discharged from Phase 1 PACU with a score of 9 or 10 (max score is 10). They must have a score of 9 or 10 to go from OR directly to phase 2 PACU.

Answer 254

Conciousness Activity Oxygenation Respiration Circulation Pain Emetic symtoms NOTE: Shares 5 components of the Modified Aldrete scoring system but includes pain and emetic symptoms. Patients can be discharged from Phase 1 PACU with a score of at least 12 (max score 14) and no score <1 in a single category.

Answer 255

Administration of an anticholinergic medication such as **benztropine or diphenhydramine** quickly and reliably treats extrapyramidal symptoms caused by antidopaminergic medication administration. Second-line therapies include benzodiazepines, beta blockers, and atropine. Thinks B's for EPS - Benztropine, Benadryl, Benzos, BBs. Although often effective for the treatment of postoperative nausea and vomiting (PONV), antidopaminergic drugs (e.g. droperidol, metoclopramide, prochlorperazine) can cause extrapyramidal symptoms (EPS) by altering the cholinergic-dopaminergic balance in the central nervous system, notably in the basal ganglia. They work by restoring the CNS cholinergic-dopaminergic balance. Extrapyramidal side effects include acute dystonias (abnormal movement or posturing due to involuntary/sustained muscle contractions), akathisia (restlessness and the need to be in constant motion), and tardive dyskinesia (involuntary repetitive or purposeless movements)

Answer 256

A transdermal scopolamine patch must be applied ≥2 hours prior to the patient's entering the operating room

Answer 257

M1 anatgonist H1 antagonist NOTE: Scopolamine is able to cross the blood-brain barrier

Answer 258

Sedation Agitation Dizziness Blurred vision (20%) Mydriasis (pupil dilation) Cycloplegia (paralysis of accomadation) Dry mouth (xerostomia) NOTE: Elderly patients are particularly more sensitive to scopolamine because 1) increased blood:brain permeability and 2) decrease ACH neurotransmission. Due to its mydriatic and cycloplegic effects, scopolamine is contraindicated in patients with glaucoma. Scopolamine should be avoided in patients with preclampsia as it can cause seizures (eclampsia).

Answer 259

Vagus Nerve- SLN (Afferent limb) Vagus Nerve (X)- RLN (Efferent limb) A critical physiologic function of the glottis is to prevent the entry of solids or liquids into the trachea and, thus, guard against pulmonary aspiration. The glottic closure reflex is an important contributor to this function in awake patients, allowing the vocal cords to rapidly and involuntarily adduct in response to stimulation of the supraglottic airway, at which point the entry of debris into the tracheobronchial tree may be imminent. However, this key mechanism is often undesirable when the airway is instrumented perioperatively because glottic closure may produce acute airway obstruction and render ventilation impossible. Inappropriate activation of the glottic closure reflex produces laryngospasm, which may evolve into an airway emergency. The internal branch of the superior laryngeal nerve (a branch of the vagus nerve), which supplies sensory innervation to the portion of the hypopharynx above the glottis and the superior aspects of the vocal cords, is the main afferent mediator of the glottic closure reflex arc. This nerve registers stimulation at the hypopharynx as a result of direct instrumentation, pooled secretions, or other irritants. Activation of the reflex arc then leads to the abrupt closure of the glottis—that is, laryngospasm—via the motor functions of the bilateral recurrent laryngeal nerves at the vocal cord adductors (especially the lateral cricoarytenoid and transverse arytenoid muscles). Severe complications of laryngospasm may include hypoxia, hypercapnia, negative-pressure pulmonary edema, and death due to asphyxiation. Additional Information: The efferent branch of the laryngospasm reflex is mediated by the recurrent laryngeal nerve. The recurrent laryngeal nerve innervates all the intrinsic muscles of the larynx, with the exception of the cricothyroid muscle which is innervated by the external branch of the superior laryngeal nerve. The lateral cricoarytenoid and transverse arytenoid muscles are major adductors of the vocal cords. Additionally, the cricothyroid muscle tenses the vocal cords. These muscles are responsible for laryngospasm. The larynx is a hollow structure composed of muscles and cartilage that extends from the epiglottis to the inferior aspect of the cricoid cartilage. The nerves that supply innervation to sensory and motor aspects of the larynx are the superior laryngeal and recurrent laryngeal nerves. The superior laryngeal nerve is divided into the external and internal branches. The internal branch supplies all sensation to the mucosa above the vocal folds. The external branch supplies the motor innervation to the cricothyroid muscle. The recurrent laryngeal nerve supplies sensory innervation below the vocal cords as well as all motor innervation to the laryngeal muscles except the cricothyroid muscle.

Answer 260

1) Deep suction (remove offending agent) 2) Positive pressure w/ 100% FiO2 3) Larson maneuver 4) Deepen anesthetic (Propofol), Succinylcholine (0.1-0.5mg/kg IV) 5) Reintubation w/ full dose induction agent and NMB Laryngospasm refers to the sudden and forceful spasm of the true vocal cords that results in complete occlusion of the tracheal opening. This condition arises as an exaggerated laryngeal closure reflex that is triggered by either a mechanical or chemical stimuli of the pharynx or larynx. These stimuli tend to be more potent in the setting of pre-existing local inflammation as is present in patients with severe gastroesophageal reflux disease or in patients with a recent upper respiratory tract infection. Of the upper airway reflexes, the laryngeal closure reflex is the most resistant to the deepening of anesthesia, while the coughing reflex is the most sensitive. Laryngospasm may be clinically diagnosed based upon the clinical judgment of the anesthesiologist. In general, apparent and increasing abdominal and chest wall efforts to breathe without evidence of air movement, such lack of ETCO2, lack of mask fogging, or worsening desaturation. These inspiratory efforts may manifest as suprasternal retractions, paradoxical chest and abdominal movements, and supraclavicular retractions. These signs will typically arise during the patient's clinical course as they are proceeding through stage 2 of anesthesia during either induction or emergence. **Treatment of laryngospasm varies according to the source or guidelines but generally follows the following algorithm. First, the irritant stimulus is removed if apparently present. This may include suctioning of the airway to remove excess secretions. Second, airway manipulation is attempted using a chin-lift and jaw-thrust maneuver in combination with continuous positive airway pressure (CPAP) administered with 100% oxygen through a tight-fitting mask. Up to 86% of patients who develop laryngospasm and are treated with CPAP and positive pressure ventilation will develop clinically significant abdominal distension which may require decompression via an orogastric or nasogastric tube in order to prevent regurgitation and subsequent aspiration of gastric contents. ** Pressure in the "laryngospasm notch" just anterior to the pinna of the ear and under the angle of the mandible may be attempted at this time in order to stimulate and awaken the patient in an effort to proceed through stage 2 of anesthesia faster. This is referred to as the Larson maneuver. Should air movement not be apparent with this maneuver, either deepening of the anesthetic back into phase 3 of anesthesia or the administration of a muscle relaxant may be considered. The choice between these courses of action will depend on the availability of intravenous access. If IV access is available, propofol administration may be sufficient to reverse the laryngeal muscle spasm, though the patient will often become apneic following this course of action. In a case such as this question where IV access is not obtained, intramuscular succinylcholine may be administered to relax the laryngeal musculature. Intramuscular atropine should be considered if succinylcholine is administered given the risk of profound bradycardia and cardiac arrest following its administration. It must be noted that hypoxemia will eventually cause the laryngeal musculature to relax and permit positive pressure ventilation. Waiting until this occurs, however, is not recommended, as this degree of hypoxia will raise the risk of severe bradycardia and cardiac arrest. The longer that the patient experiences laryngospasm, the greater their risk is for post-obstruction pulmonary edema, though this risk is relatively low in younger patients and increases to adult levels as they approach puberty. The cause for this protection against post-obstructive pulmonary edema is simply that younger patients are unable to generate sufficiently negative intrathoracic pressures to cause injury during upper airway obstruction. NOTE: If IV access unavailable Succinylcholine can be given IM (4mg/kg)

Answer 261

Laryngospasm Afferent Limb: Superior laryngeal nerve (*internal* branch) Efferent Limb: Recurrent laryngeal nerve

Answer 262

The Posterior Cricoarytenoid Muscle is supplied by RLN and is the only muscle that causes ABDUCTION of the vocal cords. Therefore, RLN damage leads to unopposed tensing and adduction of the cords.

Answer 263

The carotid bodies have chemoreceptors sensitive to changes in PaO2. PaO2 values of around 60mmHg generate nerve impulses that are transmitted to the central respiratory centers in the medulla via the sinus nerve of Hering, an afferent branch of **CN IX**, which increases ventilatory drive (increased RR, TV, & MV). Central chemoreceptors in the medulla are affected by increased PaCO2 and decreased CSF pH. The peripheral chemoreceptors, such as the carotid and aortic bodies, are affected by a decrease in PaO2 (< 60 mmHg), an increase in PaCO2, and a decrease in arterial pH. The main peripheral chemoreceptor is the carotid body located at the bifurcation of the common carotid artery. It detects changes in the PaO2, PaCO2, and pH, with PaO2 being the most significant driver. When PaO2 is < 60 mmHg, signals are sent via the glossopharyngeal nerve to the medulla to increase respiration by tidal volume and respiratory rate, increasing minute ventilation. The response to a decreased arterial pH and increased PaCO2 is minor. Damage to the carotid body, such as in carotid endarterectomy, can lead to altered responses to hypoxemia, especially when there is denervation of the carotid bodies. When only one side is affected, it may result in a decreased ventilatory response to mild hypoxemia. When both sides are affected, such as in bilateral carotid endarterectomy, there is a complete loss of ventilatory response to acute hypoxia, leading to a higher than normal resting PaCO2. When both carotid bodies are affected, the central chemoreceptors are the drivers for changes in ventilation. Opioid administration may cause the impaired ventilatory response to be exacerbated.

Answer 264

CN IX (glossopharyngeal) Unilateral- moderate attenuationn Bilateral- obliteration Below PaO2 of 100mmHg, increased neuronal activity along IX. Below PaO2 of 60mmHg, increased neuronal activity along IX and these signals results increased ventilatory drive.

Answer 265

A 10 cm change in the height of the level of the transducer will change the reading by 7.5 mmHg in the opposite direction.

Answer 266

Carotid sinus hypersensitivity Hypersensitivity or reactivation of the carotid sinus can result after CEA, leading to decreased in systemic BP. NOTE: Increased systemic BP results in activation of carotid and aortic arch baroreceptors,* increasing signaling* via cranial nerves IX and X to the medulla, resulting in reflex vasodilation. The converse is true, with decreased signaling along the cranial nerves.

Answer 267

Cortisol Growth hormone Glucagon Catecholamines NOTE: Hyperglycemia in patients with diabetes who undergo surgery is associated with increased rates of surgical site infection, MI, stroke, and death.

Answer 268

Cerebral salt wasting is another cause of hyponatremia in patients with CNS disturbances. The mechanism is not well understood, but generally leads to inappropriate renal salt wasting, which leads to hyponatremia and low plasma osmolarity along with high urine sodium and urine osmolarity. These are the same electrolyte disturbances seen in SIADH, so the main distinguishing factor is that patients with cerebral salt wasting are hypovolemic. SIADH: Euvolemic, hypervolemic CSW: Hypovolemic

Answer 269

Side effects of thiazide diuretics include - Hyponatremia - Hypokalemia - Hypochloremia - Metabolic alkalosis - Hypercalcemia - Hyperuricemia - Hyperlipidemia

Answer 270

1) RLN damage (unilateral= stridor, hoarseness, bilateral= aphonia, airway obstruction) 2) Malpositioning of NIM tube (use glidescope) 3) Paralytic (thus, use succinylcholine and remi gtt) 4) Secretion accumulation (suction, glyco)

Answer 271

The ventilatory drive is dependent on both peripheral and central chemoreceptors. Central chemoreceptors originate in the central medullary centers and are responsive to ACID-BASE changes in the cerebrospinal fluid (CSF). Peripheral chemoreceptors are located in the aortic body and carotid bodies are primarily responsive to changes in PaO2 (the carotid bodies are most responsible for changes in ventilation and the aortic bodies are most responsible for hemodynamic changes).

Answer 272

Obstruction is seen as a result of the FEV1/FVC ratio being <70% of predicted. Both FEV1 and FVC are reduced as is the ratio of FEV1 to FVC. Restrictive type lung conditions demonstrate decreases in the FEV1 and FVC. However, the FEV1/FVC proportions remain normal.

Answer 273

(see photo) G protein-coupled receptors are composed of three elements: receptor with seven transmembrane helices, G-protein (Gs, stimulates adenylyl cyclase; Gi, inhibits adenylyl cyclase; and Gq, stimulates phospholipase C), and a second messenger (eg, cAMP).

Answer 274

G protein-coupled receptors are composed of three elements: receptor with seven transmembrane helices, G-protein (Gs, stimulates adenylyl cyclase; Gi, inhibits adenylyl cyclase; and Gq, stimulates phospholipase C), and a second messenger (eg, cAMP).

Answer 275

Oliguria is defined as urine output less than 0.5 mL/kg/hr. Positive pressure ventilation increases intrathoracic pressure which can decrease urine output through four main effects: 1) Impaired renal perfusion and renal venous drainage 2) Decreased preload and increased right ventricular afterload 3) Stimulation of the sympathetic nervous system 4) Release of inflammatory cytokines Increased intrathoracic pressure increases IVC pressure. This directly decreases renal perfusion (by impairing venous drainage) which decreases urine production. Increased intrathoracic pressure also increases right ventricle afterload and reduces venous return, thereby decreasing preload. These two effects can decrease cardiac output which further decreases renal perfusion and urine production. Additionally, they can reduce left atrial volume which decreases atrial natriuretic peptide (ANP) release. Since ANP promotes sodium and water excretion, a decrease can contribute to oliguria. Finally, decreased preload signals the posterior pituitary to release antidiuretic hormone (ADH) which increases renal water reabsorption and decreases urine output. Through the changes above, PPV decreases cardiac output and systemic blood pressure. This causes carotid and aortic baroreceptor-mediated increases in sympathetic nervous system (SNS) activity. This leads to stimulation of the renin-angiotensin-aldosterone system (RAAS), renal vasoconstriction, antidiuresis, and antinatriuresis, all of which can contribute to oliguria. Finally, positive pressure ventilation, particularly with high tidal volume and low PEEP, can stimulate the release of pro-inflammatory cytokines and other inflammatory mediators. These are thought to be responsible for acute lung injury seen with positive pressure ventilation. However, the inflammatory mediators can also cause acute inflammation in the kidneys leading to acute kidney injury from renal epithelial cell dysfunction and apoptosis. This is less likely to be seen intraoperatively but may be a contributor to postoperative oliguria. Lung-protective ventilation strategies significantly decrease this risk.

Answer 276

The most sensitive and specific test for the detection of an acute hemolytic transfusion reaction is the direct antiglobulin test (DAT) which is also known as a direct Coombs test. In this test, red blood cells (RBCs) are drawn from the patient that is suspected of having immune-mediated hemolytic anemia (e.g. acute hemolytic transfusion reaction). If these donor RBCs are coated in antibodies that are bound to antigens on the RBC surface, then when they are exposed to anti-human antibodies (Coombs reagent), the anti-human antibodies will bind to all of the antibodies on the RBCs and cause agglutination.

Answer 277

Renin is created and stored by the cells in the afferent arterioles of the kidney. Renin secretion can be caused by 3 different mechanisms: 1) Hyponatremia (chemoreceptors in macula densa) 2) Hypotension (baroreceptors within JGA) 3) B1 activity Decreases in blood pressure, such as that displayed by the patient above, would cause a release of renin into the serum by at least one of these mechanisms. Renin then acts by cleaving the peptide angiotensinogen to create angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II (Ang II) has several effects, which combine to increase systemic perfusion in patients. The most immediate response to Ang II is an increase in blood pressure caused by an increase in systemic vascular resistance. Ang II activates the angiotensin1 (AT1) receptors on vascular smooth muscle cells, causing constriction of the arterioles. Ang II also augments the sympathetic nervous system by inhibiting norepinephrine reuptake into nerve terminals. It also stimulates the release of catecholamines from the adrenal medulla. In addition, Ang II causes a centrally mediated increased thirst and enhances the release of vasopressin. These effects are almost immediate, but are not long-lasting. Ang II also has longer lasting effects in the body. In addition to its effects on blood pressure, it stimulates remodeling of the cardiovascular system, causing hypertrophy of cardiac cells and increased collagen deposition. It also has profound effects on the kidney, causing a decrease in the urinary excretion of both sodium and water. Lastly, Ang II stimulates the adrenal cortex to synthesize and release aldosterone. Aldosterone also acts on the kidneys to decrease the urinary excretion of sodium and water. This ultimately leads to an increase in blood volume and therefore blood pressure.

Answer 278

Contraindications to BiPAP: Cardiac or respiratory arrest Severe agitation Voluminous secretions/vomiting/GI bleeding Inability to protect airway (GCS < 8) Facial trauma Hemodynamic instability

Answer 279

A common complication (25-45%) of sitting craniotomies is Venous Air Embolism (VAEs). It occurs because non-collapsible venous channels such as venous sinuses can be violated during surgery and air is entrapped in them due to the negative pressure gradient between the surgical site and the heart. VAEs generally travel to the heart and, if small, can be absorbed in the pulmonary vasculature. However, if large, they can cause pulmonary occlusion, increased pulmonary pressures, and even right heart failure with decreased cardiac output. The most sensitive method of detecting VAEs is via TEE with precordial doppler being second. In some instances or at some institutions, it is commonplace to have a right atrial catheter in place for these surgeries in order to aspirate air if a VAE is detected.

Answer 280

1) Flood field with normal saline (or pack with wet gauze) 2) Administer 100% FiO2 & discontinue NO if using 3) Head down, left lateral positioning (if feasible) 4) Vasopressors & inotropes 5) Aspiration via RA catheter (if present) 6) TEE (highest sensitivity for diagnosing VAE) - OTHER: Hyperbaric oxygen has some demonstrated efficacy if there is cardiac, pulmonary, or neurological defects, however, it is not typically available in a rapid time frame.

Answer 281

Endobrochial intubation Subcutaneous emphysema Venous air embolsim Capnothorax Pneumothorax

Answer 282

Ability to ventilate through catheter (connection for jet ventilation and manual ventilation). Possible to connect the catheter to a capnograph to monitor respiration (ETCO2). NOTE: Both have depth markings to ensure proper depth. Both have potential to cause airway trauma.

Answer 283

Intubation Catheter (IC) NOTE: Both an intubation catheter and airway exchange catheter can be used to ventilate a patient and monitor ETCO2. Only an intubation catheter, however, can be loaded onto a flexible bronchoscope. Airway exchange catheters have a small diameter and cannot be loaded onto a flexible bronchoscope.

Answer 284

**TEE** Methods for detecting VAE from most to least sensitive are as follows: TEE Precordial Doppler PAC EtCo2 EKG (lowest!) NOTE: Highly tested

Answer 285

Notice that a history of esophageal varicies is not a contrainidication. However, a recent varicieal bleed or active GIB is an absolute contraindication.

Answer 286

Postoperative visual loss is most commonly associated with surgeries in the prone position. A small percentage of these cases (~10%) are a consequence of central retinal artery occlusion, which is directly correlated to poor positioning and increased pressure on the eyes. Periorbital and scleral edema can be found on exam of these patients. However, most cases (~90%) of postoperative visual loss are secondary to ischemic optic neuropathy, which to date is still considered an idiopathic process. It is not thought to be the result of optic globe compression or faulty positioning. It is however associated with prone position, Mayfield pin use, anesthetic duration >6 hours, blood loss greater than 1000 mL, preexisting retinal disease, diabetes, hypertension, atherosclerosis, and anemia

Answer 287

A CAT MUDPILE

Answer 288

Metabolic acidosis Excessive diarrhea leads to GI losses of bicarb. "Bicarbarrhea"

Answer 289

The major hemoglobin in adults is hemoglobin A (HbA), which consists of four globin polypeptide chains; two α chains and two β chains.

Answer 290

The major hemoglobin in utero and the first 6 months of lfie is fetal hemoglobin (HbF), which is composed of two α globin chains and two γ globin chains. Hence, Infants with beta-thalassemia minor or major, however, are asymptomatic at birth. Beta-thalassemia minor- patients are heterozygotes, inheriting only one defective Beta globulin allele. Beta-thalassemia major-patients are homozygotes, inheriting two defective beta alleles. Severe symptoms after 6 months- anemia 2/2 hemolysis w/ hepatosplenomegaly.

Answer 291

Initial treatment for patients with suspected sepsis or septic shock includes initiation of fluid administration (30 mL/kg recommended) within the first hour and completion within three hours of initial presentation. Fluid boluses are preferred to treat hypotension before initiating vasopressors and should be continued until blood pressure and tissue perfusion is adequate or if patients are nonresponsive to fluid resuscitation. Multiple randomized trials and meta-analyses has provided no evidence of significant difference in mortality between albumin and crystalloid solutions in managing sepsis or septic shock (SAFE trial).

Answer 292

Norepinepherine

Answer 293

Administration of norepinephrine (α1 > α2 > β1 >β2) leads to intense vasoconstriction, causing slight reflex bradycardia. Despite the bradycardia, cardiac output is maintained via a decrease in venous capacitance, resulting in an increase in preload and stroke volume. The β1 increase in myocardial contractility further increases the stroke volume, and, despite a decrease in heart rate, cardiac output is maintained or slightly increased. NOTE: Remember that norepinephrine gets both alphas and both beta receptors with preferentially activity from left to right (α1 > α2 > β1 >β2)

Answer 294

Increases EDV (preload) with subsequent increase in SV. Moves from point X to point A (see picture on front of card).

Answer 295

B1 > B2 Increased inotropy, chronotropy, dromotropy, lusitropy Vasodilation and bronchodilation (minimal) NOTE: DoButamine = Double B (B1 > B2)

Answer 296

Patients who have had a heart transplant in the past will having resting heart rates between 90-110 bpm. Due to loss of cardiac autonomic plexus. Parasympathetic nervous system no longer innervates the heart.

Answer 297

The qSOFA criteria are scored from 0-3 with one point for each of the following: altered mental status (GCS < 15), respiratory rate ≥ 22, and systolic blood pressure ≤ 100 mm Hg. The quick sequential organ failure assessment (qSOFA) is a screening tool developed from the SOFA (see below) that can be used to identify adult ICU patients with a suspected infection that are likely to have a prolonged ICU stay or poor outcome. Additionally, the qSOFA score can be used in adult out-of-hospital, emergency room, and general ward patients with suspected infection to identify those that are more likely to have poor outcomes typical of sepsis. In either case, a score of ≥ 2 indicates a worse prognosis. A significant benefit of the qSOFA compared to the full SOFA is its ability to be a quick, repeatable bedside assessment tool that does not require calculated or laboratory values. It is important to recognize that although SOFA and qSOFA are discussed in detail within the 2016 third international consensus definitions for sepsis and septic shock (“Sepsis-3”), neither tool is used to diagnose sepsis or functions as a stand-alone definition for sepsis. Rather, the assessments should be used to identify patients with a potentially worse prognosis and perhaps prompt an escalation of care. Additionally, a positive qSOFA score can be used to prompt consideration of possible infection in patients not otherwise recognized as having an infection. Failure to meet ≥ 2 qSOFA/SOFA criteria should not cause a delay in care otherwise deemed necessary. The SOFA includes assessments of respiration (PaO2/FiO2), coagulation (platelet count), liver function (bilirubin), cardiovascular function (MAP and pressor dose), mental status (GCS), and renal function (creatinine and urine output) with each category scored from 0-4. The full details of the system can be found in the Sepsis-3 reference and are beyond the scope of this question.

Answer 298

The primary indication for initiating nutritional support is preventing or treating malnutrition among patients unable or unwilling to sustain sufficient oral intake. Enteral nutrition should be initiated within 48 hours of a critically ill patient’s admission without contraindications to enteral feeding. Enteral nutritional support should not be initiated in patients with** intractable vomiting and diarrhea, bowel obstruction, gastrointestinal ischemia or bleeding, hemodynamic instability, severe and protracted ileus, or high-output fistulas. ** Patients who are initiated on early enteral nutritional support have a lower incidence of infection and mortality.

Answer 299

Femoral (highest) Internal Jugular Subclavian (lowest)

Answer 300

A rapid shallow breathing index (RSBI) of < 105 is a sufficiently low respiratory rate to tidal volume ratio and is consistent with readiness for extubation. Criteria for extubation include * Resolution of the process that initially necessitated mechanical ventilation * Hemodynamic stability * Adequate oxygenation on minimal fractured of inspired oxygen (< 40%-50%) * The ability to protect the airway and clear secretions * Favorable respiratory mechanics. Favorable respiratory mechanics values include a negative inspiratory force (NIF) of more than −20 cm H2O, an RSBI of < 105, and a vital capacity of > 10 mL/kg * The RSBI, also known as the Yang Tobin index, reflects the breathing pattern that predicts postextubation respiratory distress: RSBI = respiratory rate / tidal volume (L). A result > 105 indicates a rapid shallow breathing pattern, while a result < 105 is consistent with readiness for extubation.

Answer 301

An airleak leak pressure of less than 12-15 cmH20 is reassuring that a patient airway exists.

Answer 302

Abdominal compartment syndrome is defined as new organ dysfunction with significant intra-abdominal hypertension (increase in intra-abdominal pressures >20 mmHg with or without intra-abdominal perfusion pressure <50 mmHg). This syndrome can be caused by multiple clinical conditions, including liver transplants, major abdominal/trauma surgery, burn injuries (requiring large amounts of fluids), severe bowel obstruction, massive fluid resuscitation, pancreatitis, peritonitis, ascites, and intraperitoneal hemorrhage. The intra-abdominal pressure can be measured with an indwelling Foley catheter and by using the same pressure tubing apparatus used for arterial line blood pressure monitoring. The Foley catheter is then clamped distal to the instillation port, and 50 mL of normal saline is instilled within the bladder, measuring intravesicular pressure. Immediate management for this syndrome after it has been recognized includes immediate paracentesis and opening the abdomen for urgent decompression. Intra-abdominal pressure may be chronically elevated (up to 12 mmHg) in obese adults. However, this has not been shown to be associated with end-organ dysfunction.

Answer 303

Manometry tubing in CVC kits can be attached to the catheter to confirm placement by connecting the catheter to the tubing and raising the tubing vertically to measure the pressure. The blood in the column of blood should be < ____ cm and will vary with respiration (expiration: goes up, inspiration goes down). NOTE: Tip of catheter should be at inferior aspect of SVC for internal jugular CVCs.

Answer 304

Linear- high frequency Curvilinear- low frequency Phased array- low frequency High frequency probes (linear) provide improved resolution of superficial structures. Low frequency probes (curvilinear) provides deeper penetration (good for deep structures or on obese patients). Phased array probe (low frequency) is used for cardiac examination.

Answer 305

Acoustic Impedance (Z1) is the product of the density of a medium and the propagation speed of sound through that medium. Ultrasound reflection that occur at the interface of different mediums are due to the changes in acoustic impedance. Since propagation speed changes only slightly between biological mediums, **acoustic impedance is primarily dependent upon density.** Z1 = p1 x c1

Answer 306

PCO2 (Expected) = (1.5 * [HCO3]) + 8 +/- 2 Winters' formula gives an expected value for the patient's PCO2; the patient's actual (measured) PCO2 is then compared to this. If the two values correspond, respiratory compensation is considered to be adequate. If the measured PCO2 is higher than the calculated value, there is also a primary respiratory acidosis. If the measured PCO2 is lower than the calculated value, there is also a primary respiratory alkalosis.

Answer 307

HARDASS Hyperchloremia/Hyperailmentation Addision's Disease Renal tubular acidosis Diarrhea (loss of bicarb in stool) Acetazolamide Spironolactone Saline infusion

Answer 308

Hyperchloremic non-anion gap metabolic acidosis NOTE: Excessive chloride impairs bicarb reabsorption in the PCT of the nephrons. The decrease in bicarb compensates for the increase in chloride thus maintaining electroneutrality.

Answer 309

Hyponatremia Hypokalemia Hypochloremia Metabolic alkalosis (elevated bicarb)

Answer 310

Hyperchloremic metabolic acidosis In primary hyperparathyroidism, parathyroid hormone (PTH) levels are elevated. Parathyroid hormone has been shown to be an important inhibitor of renal bicarbonate reabsorption. Increased renal bicarbonate loss leads to a metabolic acidosis. Furthermore, PTH has been shown to inhibit the sodium chloride cotransporter in the distal convoluted tubule of the nephron leading to hyperchloremia. Although not particularly common, patients with hyperparathyroidism may have a lower than normal pH, slightly decreased PaCO2 due to respiratory compensation, a decreased bicarbonate level, and a normal anion gap.

Answer 311

A normal alveolar-arterial (A-a) oxygen gradient is in the range of 5 to 10 mm Hg. An increased A-a gradient indicates a barrier to oxygen transfer. Elevations in the A-a gradient would be seen as a result of a ventilation-perfusion mismatch in the lungs. Examples would include pneumonia, acute respiratory distress syndrome, obstructive lung disease, atelectasis, and pulmonary embolism. In conditions of high altitude or alveolar hypoventilation (eg, opioid-induced respiratory depression, obesity-hypoventilation syndrome, peripheral neuropathy, myasthenia gravis), the A-a gradient will remain within normal limits.

Answer 312

Respiratory splinting is defined as reduced inspiratory effort due to sharp pain during inspiration. As a result, patients hypoventilate with decreased chest wall movement and decreased functional residual capacity, leading to atelectasis and hypoxemia, the potential requirement for intubation and mechanical respiratory support, and an increased risk of pneumonia. Patients with splinting may have rapid shallow breathing, a weak cough, and decreased mucociliary clearance. Thoracic epidurals have been shown to be effective in reducing the morbidity of splinting.

Answer 313

In an otherwise healthy individual without parenchymal lung disease, the peripheral chemoreceptors will begin to stimulate the respiratory centers in the brainstem when the arterial oxygen tension drops below 50 mmHg. As can be seen in the Figure below, by the position of the star on the below curve this arterial oxygen partial pressure occurs right before a precipitous drop in arterial hemoglobin oxygen saturation. Because of this relationship between arterial oxygen tension and hemoglobin saturation, a PaO2 of around 50 mmHg is roughly the lowest physiologically sustainable arterial oxygen tension before oxygen delivery to the tissues begins to become extremely inefficient. Thus, the body will generate a robust hypoxic ventilatory drive should arterial oxygen tension drop below this point in order to ensure adequate oxygen delivery to the tissues. In situations where hypoxic drive is blunted, such as during anesthesia, it is even more important to ensure SpO2 remains > 85% as oxygen delivery is not fully effective below this level.

Answer 314

The **adductor pollicis muscle** is supplied by the ulnar nerve and responsible for **adduction of the thumb.** This muscle can be stimulated by placing two electrodes over the course of the **ulnar nerve **at the wrist or placement of electrodes over the dorsal and palmar sides of the hand between the first and second digits. This muscle is relatively sensitive to neuromuscular blockade. *Recovery at this location lags behind the diaphragm* ensuring adequate respiratory function if adequate response is obtained.

Answer 315

The **corrugator supercilii muscle** is responsible for movement of the eyebrow and is innervated by the **facial nerve.** This muscle *most resembles* blockade effects upon the **laryngeal adductors** and can be useful to determine favorable intubating conditions.

Answer 316

An obstructive apnea is one that lasts longer then 10 seconds with an > 90% air flow reduction despite respiratory effort. A central apnea is one that lasts longer then 10 seconds with > 90% air flow reduction without respiratory effort.

Answer 317

FAST, FULL, FORWARD! The hemodynamic goals for patients with AI who require anesthesia include avoidance of bradycardia, avoidance of increases in systemic vascular resistance, and minimizing myocardial depression. A mnemonic for both aortic insufficiency and mitral insufficiency is: fast, full, forward which means fast heart rate (or avoiding bradycardia), full preload, and forward flow (avoiding afterload).

Answer 318

Same as aortic regurgitation! FAST, FULL, FORWARD! The hemodynamic goals for patients with mitral reguritation who require anesthesia include avoidance of bradycardia, avoidance of increases in systemic vascular resistance, and minimizing myocardial depression. A mnemonic for both aortic insufficiency and mitral insufficiency is: fast, full, forward which means fast heart rate (or avoiding bradycardia), full preload, and forward flow (avoiding afterload). NOTE: Phenylephrine should be avoided as it increases afterload but also decreases HR causing more time spent in diastole and increased filling.

Answer 319

SLOW, STRONG, SINUS! Patients with AS tend to hemodynamically prefer a slower heart rate (50-60 bpm) and an increased SVR. The slow heart rate, in this case, allows for longer diastolic filling times, which are often required to allow adequate filling in a thickened and stiff LV and provide an adequate period of diastole to perfuse the thickened LV itself. Maintaining a higher SVR will encourage a higher coronary perfusion pressure (diastolic blood pressure - left ventricular end-diastolic pressure) to ensure that the thick LV is adequately perfused. An elevated SVR in the setting of AS may seem counterintuitive, as there is an obstructive lesion in the LV outflow tract. However, in severe or critical AS, this stenotic aortic valve provides much greater resistance to LV outflow than any physiologic SVR that can be generated. Thus, increases in SVR serve only to increase coronary perfusion in these cases. In patients with chronic aortic stenosis (AS), the atrial kick can contribute up to 40% of the left ventricular end-diastolic volume and is crucial to maintaining an adequate cardiac output. When inducing and maintaining anesthesia in these patients, one must make every effort to ensure continued sinus rhythm to benefit from this atrial kick.

Answer 320

Severe Aortic Stenosis (AS) is defined as: Aortic Valve Jet Velocity: > 4 m/s Mean Gradient (mmHg): > 40mmHg Aortic Valve Area (cm^2): < 1.0

Answer 321

MABL = EBV x (HCT-i x HCT-f/HCT-i) EBV = Estimated blood volume EBV (Male) = 75mL/kg EBV (Female)= 65mL/kg HCTi = initial preoperative hematocrit (in %) HCTf = final hematocrit after blood loss (in %) The concent of MABL allows us to calculate the amount of blood that must be lost to reach a selected transfusion threshold. Typically, for an adult the lowest accetable HCT is 25% (HCT-f) The ratio of hematocrit to hemoglobin in healthy people is typically three to one. On this assumption, if you've only had your hemoglobin measured, you can estimate the hematocrit by multiplying it by 3. You can also convert the value of hematocrit to hemoglobin by dividing it by 3.

Answer 322

**CStat=TV/(Pplateau − PEEP) ** NOTE: Lung compliance measures the extent to which both lungs will change the volume for a given change in pressure. Lung compliance is typically calculated as the change in volume / change in pressure. Lung compliance can be divided into static and dynamic compliance. Static compliance (Cstat) represents the compliance at a given volume in the absence of airflow and **measures elastic resistance.** It is determined at the end of inspiration when there is no airflow (hence "static") which can be done during an inspiratory pause in a mechanically ventilated paralyzed patient. Here, the transpulmonary pressure (gradient between the inside of the alveoli and outside pleural pressure) is equal to the elastic recoil pressure of the lungs. Static compliance is best measured in the paralyzed patient during an inspiratory hold, and it is used to select the ideal level of PEEP. Cstat = TV/(Pplateau − PEEP) Dynamic compliance is the continuous measurement of compliance as the patient breathes, **monitoring both elastic and airway resistance.** Cdyn= TV/(Ppeak-PEEP) When both static compliance and dynamic compliance are increased, both peak pressures and plateau pressure are increased, there is overall decreased pulmonary compliance. The pathologies lies within pulmonary parechyma or there is external compression of the thorax. Differential includes pulmonary edema, fluid over load, ARDS, TRALI, PTX, pleural effusion, chest wall rigidity, obesity, abdominal insufflation, abdominal compartment syndrome. If only the dynamic compliance is worsened, by only the peak inspiratory pressure being increased, it is generally due to worsened airway resistance. This resistance can be anywhere from ventilator circuit to the ETT to the trachobronchial tree. This increased PIP but unchanged Pplat is generally not due to pathology of lung parenchyma. Differential includes kinked circuit, ETT obstruction, acute asthma attack, bronchospasm.

Answer 323

**Cdyn= TV/(Ppeak-PEEP) ** NOTE: Lung compliance measures the extent to which both lungs will change the volume for a given change in pressure. Lung compliance is typically calculated as the change in volume / change in pressure. Lung compliance can be divided into static and dynamic compliance. Static compliance (Cstat) represents the compliance at a given volume in the absence of airflow and **measures elastic resistance.** It is determined at the end of inspiration when tehre is no airflow (hence "static") which can be done during an inspiratory pause in a mechanically ventilated patient. Here, the transpulmonary pressure (gradient between the inside of the alveoli and outside pleural pressure) is equal to the elastic recoil pressure of the lungs. Static compliance is best measured in the paralyzed patient during an inspiratory hold, and it is used to select the ideal level of PEEP. Cstat = TV/(Pplateau − PEEP) Dynamic compliance is the continuous measurement of compliance as the patient breathes, **monitoring both elastic and airway resistance.** Cdyn= TV/(Ppeak-PEEP) When both static compliance and dynamic compliance are increased, both peak pressures and plateau pressure are increased, there is overall decreased pulmonary compliance. The pathologies lies within pulmonary parechyma or there is external compression of the thorax. Differential includes pulmonary edema, fluid over load, ARDS, TRALI, PTX, pleural effusion, chest wall rigidity, obesity, abdominal insufflation, abdominal compartment syndrome. If only the dynamic compliance is worsened, by only the peak inspiratory pressure being increased, it is generally due to worsened airway resistance. This resistance can be anywhere from ventilator circuit to the ETT to the trachobronchial tree. This increased PIP but unchanged Pplat is generally not due to pathology of lung parenchyma. Differential includes kinked circuit, ETT obstruction, acute asthma attack, bronchospasm.

Answer 324

Control breathing system pressure during manual ventilation or spontaneous breathing. Releases excess circuit gas to scavenger system.

Answer 325

Because of citrate, a calcium-binding anticoagulant in PRBCs, FFP, and platelets.

Answer 326

Ioninized calcium levels begin to decrease when blood is transfused at 6 units/hr. Rule of thumb is you want to give calcium at or before 6 units of products.

Answer 327

In the first hour of anesthesia, redistribution of cool blood from the skin to the core is responsible for the initial drop in core temperature. Prewarming the skin with warmed blankets or, more effectively, a forced-air warmer can prevent this initial drop in temperature. Forced-air warmers are the most effective way to raise a patient's temperature in the preoperative, intraoperative, or postoperative setting.

Answer 328

The four sites at which core temperature can be measured are the pulmonary artery, distal aspect of the esophagus, tympanic membrane, and nasopharynx. The tympanic membrane is the MOST ACCURATE site for core body temperature measurement in adults.

Answer 329

By inhibiting COX-mediated prostaglandin production, NSAIDs inhibit renal afferent arteriolar vasodilation and promote afferent arteriolar vasoconstriction. This is the most prominent mechanism of renal injury or impairment associated with NSAID use.

Answer 330

Decreased hemostasis Impaired bone healing Renal dysfunction Gastrointestinal hemorrhage Note: Decreased hemostasis via inhibition of thromboxane A2 and platelet dysfunction

Answer 331

Hemodynamic goals in a patient with hypertrophic obstructive cardiomyopathy (HOCM) include: - Adequate full preload - Increased afterload (phenylephrine preferred, avoid vasodilators) - Depressed myocardial contractility (AVOID INOTROPES) - Normal to low heart rate (BBs) - Sinus rhythm

Answer 332

What steps should be taken if IV infiltration occurs with a vasopressor? * Keep IV catheter in place initially * Aspirate about 5cc of blood to remove as much of drug as possible * Elevate the effect limb to decrease swelling and promote venous drainage * Apply warm compresses * Phentolamine (alpha blocker, causes smooth musce relaxation and vasodilation, recommended dose is 5-10mg within 12 hours, dilute to 0.5mg/mL and inject 1mL increments around the border of extravasation site) NOTE: Extravasated vasoconstrictors usually have 4-6 hr window before onset of tissue necrosis.

Answer 333

Transfusion of an ABO-incompatible unit of packed red blood cells (PRBCs) results in an Acute Hemolytic Transfusion Reaction (AHTR), in which recipient IgM-mediated antibodies attack donor cell ABO blood group antigens. Laboratory testing will result in a positive direct Coombs test.

Answer 334

IgG NOTE: Delayed Hemolytic Transfusion Reactions are typically less fulminant compared with acute hemolytic transfusion reactions and are due to "minor," non-ABO blood group antigens.

Answer 335

Delayed hemolytic transfusion reaction is a result of recipient antibodies (IgG) targeting donor minor red blood cell antigens to which the recipient has previously been exposed, leading to hemolysis of the donated red blood cells. Delayed hemolytic transfusion reactions are typically secondary to antibodies associated with the Rhesus (Rh), Kidd, or Kell systems (or other “minor” antigens). Delayed hemolytic transfusion reaction occurs *days to weeks* after a transfusion. It occurs in patients who have been previously sensitized to red blood cell antigens during a previous transfusion, transplant, or pregnancy. The alloantibodies that form are usually toward minor blood antigens. When the patient is re-exposed, the antibody response leads to an increase in alloantibodies within days to weeks following the transfusion, causing extravascular hemolysis. Most patients are asymptomatic but can present with mild fever; anemia; jaundice; or chest, abdomen, or back pain. Laboratory testing will result in a positive direct Coombs test.

Answer 336

During acidosis, excess H+ enter cells, resulting in the extracellular movement of potassium to maintain electrical balance, thus increasing the measured serum [K+]. During alkalosis, extracellular potassium ions move into cells to balance the extracellular movement of hydrogen ions, resulting in decreased plasma [K+]. This is the mechanism underlying bicarbonate administration in the setting of severe hyperkalemia.

Answer 337

Acidosis causes hypercalcemia Alkalosis causes hypocalcemia.

Answer 338

Calcium carbonate + sodium bicarbonate Calcium Carbonate or Calcium Chloride Excess serum potassium has the effect of lowering the resting membrane potential of myocardial cells as well as shortening the overall duration of myocardial action potential. Calcium carbonate will counter these effects by increasing the resting membrane potential ("myocardial protection"). Of note, calicum administration will have no effect on potassium levels. Sodium Bicarbonate Works by alkalinizing the blood causing an intracellular shift of potassium via the H/K exhange. **Sodium bicarbonate is the fastest treatement of hyperkalemia.** OTHER: Insulin (15 min) Albuterol (30min) Furosemide (hours to days) Patiromer (7 hours)- oral potassium binder Hemodialysis (slow to initiate)

Answer 339

10 units Regular insulin 10 units IV should be administered with 25 grams of IV dextrose followed by a 5% dextrose infusion. Blood glucose should be monitored. A dose of 10 units will lower serum potassium by approximately 1mEq/L. If a patient has a blood glucose of > 250mg/dL, then the dextrose can be withheld.

Answer 340

A dose of 10 units of IV regular insulin will lower serum potassium by approximately 1 mEq/L in 10 minutes.

Answer 341

Aldosterone Insulin Cortisol

Answer 342

Hypokalemia Hyocalcemia Increased PaCo2, EtCO2 In the setting of acidosis, excess hydrogen ions enter cells, resulting in the extracellular movement of potassium to maintain electrical balance, thus increasing the measured serum [K+]. Conversely, during alkalosis, extracellular potassium ions move into cells to balance the extracellular movement of hydrogen ions, resulting in decreased plasma [K+]. This is the mechanism underlying bicarbonate administration in the setting of severe hyperkalemia. Sodium bicarbonate can transiently lower blood calcium levels. Calcium binding to albumin is dependent on serum pH. In states of acidosis, the excess hydrogen ions displace calcium bound by albumin and thus ionized levels of calcium increase. This process is reversed in the setting of alkalosis and should be considered before administering sodium bicarbonate to a patient with preexisting hypocalcemia. Intravenous sodium bicarbonate combines with a hydrogen ion to produce carbonic acid that dissociates into CO2 and water (50 mEq of bicarbonate produces approximately 1,250 mL of CO2). The partial pressure of CO2 in the blood is temporarily elevated until it is eliminated via the lungs. Theoretically, this increase in CO2 would cause cerebral vasodilation and increase intracranial pressure, although direct clinical evidence for this has not been found. Sodium bicarbonate is converted by carbonic anhydrase to water and CO2. After sodium bicarbonate administration, it is common to see an increase in end-tidal CO2.

Answer 343

Strong Ion Difference (SID) is difference between the sum of the strong cations minus the sum of strong anions. SID = (strong cations) − (strong anions) = (Na + K + Ca2 + Mg2) − (Cl + lactate) SID is normally ~40 mEq/L due to unmeasured anions (such as lactic acid and keto acids). When the SID is > 0, the unmeasured ions result in alkalosis. When the SID is < 0, the results is acidosis. The following strong ion changes result in the following SID changes: ↓ [Na+] → ↓ SID and acidosis ↑ [Na+] → ↑ SID and alkalosis ↑ [Cl−] → ↓ SID and acidosis ↑ organic acids → ↓ SID and acidosis

Answer 344

Anion Gap (AG) = (Na + K) - (Cl + HCO3)

Answer 345

NOTE: Beta 2 agonism causes activation of Na/K ATPase shifting K intracellulary and can cause hypokalemia (Terbutaline also works in this way). So Beta 2 antagonist will have the opposite effect causing hyperkalemia. Mannitol is hypertonic will draw water intravascularly and K will follow. ACE-i and ARBs prevent aldosterone release from the adrenal cortex.

Answer 346

Leakage of interleukin (IL)-1 by donor white blood cells (WBC) is the cause of febrile nonhemolytic transfusion reaction. Febrile nonhemolytic transfusion reaction is caused by a release of cytokines, mainly IL-1, in blood products due to WBC breakdown and leakage. The IL-1 then stimulates the production of prostaglandin E2, which causes a fever. Patients will present within six hours of transfusion with fever and/or chills but will not have any other systemic symptoms such as scleral icterus, jaundice, back pain, hemoglobinuria, or hypotension. A nonhemolytic febrile reaction occurs in about 2%-4% of transfusions. In general, a positive direct antiglobulin test (Coombs test) is diagnostic for a *hemolytic* reaction.

Answer 347

A transfusion reaction in which donor T lymphocytes attack recipient cells expressing human leukocyte antigen (HLA) as foreign. GVHD most commonly presents in patients who are immunocompromised (eg. B-cell mediated malignancies, ALL, HL, immunosuppressive drugs, congenital immunodeficiency syndromes). Transfusion-associated GVHD is rarer than GVHD caused by allogeneic hematopoietic cell "stem cell" transplantation, but the two entities share similar pathophysiology. Donor lymphocytes are able to proliferate and attack the host because of severe compromise of host lymphocyte function (immunocompromised) or the inability to detect the donor lymphocytes as foreign (partial HLA matching). Patients will present 4 to 21 days after transfusion with fever, diarrhea, maculopapular rash, and bone marrow failure. Graft versus host disease is, unfortunately, difficult to treat because it often becomes fatal (>90%) before a suitable hematopoietic stem cell donor can be identified for the patient. Some researchers have examined the use of T-cell immunosuppression with some success. The risk of GVHD is greatly reduced by the use of irradiated blood products in patients at risk (those with lymphocyte immunodeficiencies).

Answer 348

Preoperative self donation (ie autologous blood transfusion) Intraoperative cell salvaging (ie cell saver) NOTE: Autotransfusion describes a procedure in which a patient receives there own blood for transfusion. Advantages over allogenic- decreased infectious risk, elimination rejection risk (uses their own blood), preserved erythrocyte functionality (minimizes storage time)

Answer 349

The most common complication of an autologous blood transfusion is **infection** caused by improperly stored blood. Autologous transfusion DOES NOT place the recipient at risk of immune-mediated reactions. Autologous transfusions reduce the incidence of complications associated with allogenic donor blood, such as hemolytic and non-hemolytic (febrile, urticarial, and post-transfusion purpura) reactions resulting from donor proteins triggering an immune-mediated reaction in the recipient. Autologous blood does not contain non-self antigens and does not trigger these reactions. Transfusion-related immunomodulation (TRIM) results from the downregulation of several immune functions following allogenic, but not autologous, transfusion.

Answer 350

Platelet depletion Coagulation factor depletion NOTE: Process filters out platelets and coagulation factors.

Answer 351

In susceptible individuals who receive blood, antibodies in the donor blood bind to the recipient’s leukocytes, which then adhere to the vascular capillary bed in the pulmonary circulation. This causes damage and extravasation of intravascular fluid. TRALI results in a non-cardiogenic pulmonary edema that usually occurs within 6 hours of transfusion. TRALI is characterized by respiratory distress/failure with bilateral infiltrates seen on chest X-ray. The incidence of TRALI is 1:5000 transfusions and it occurs more often in blood donated by multiparous females.

Answer 352

Predictors of poor perioperative outcome following pneumonectomy include: PaCO2 >45 mm Hg PaO2 < 50 mm Hg on room air FVC < 50% FEV1 < 2 L FEV1/FVC < 50% MVV < 50% DLCO < 50% Maximum voluntary ventilation (MVV) breathe deeply and quickly for 10 seconds

Answer 353

Hypocalcemia cause QT prolongation Hypercalcemia cause QT shortening NOTE: QTc prolongation (>440ms in men, > 460ms in women) QT interval varies with HR. QT is shorter at fast heart rates, QT is longer at slow heart rates. QT interval can be corrected for heart rate: QTc = QT/cardiac cycle (seconds)

Answer 354

Autonomic dysreflexia (AD) (also known as autonomic hyperreflexia) occurs most often in patients with spinal lesions above the midthoracic (T5-7) level. These levels correspond with the splanchnic outflow distribution within the sympathetic nervous system. Autonomic dysreflexia has been known to occur in patients with a lesion as low as T10, although lesions at or above T6 involve the highest risk. Autonomic dysreflexia occurs when a noxious cutaneous or visceral stimulus below the SCI causes a signal to be transmitted to the dorsal root of the spinal cord. An increase in sympathetic outflow and vasoconstriction occurs below the level of the lesion. Examples of triggering events include bladder or bowel distension, cystoscopy and other urinary tract procedures, surgical stimulation of the pelvic region, uterine contraction and manipulation during childbirth, and lower extremity burns and surgery. When there is no spinal cord injury, inhibitory impulses from the brain modulate the sympathetic outflow. When there is a lesion at the midthoracic level (T5-7) or above, this inhibition is blocked so the sympathetic outflow goes unchecked. Spinal cord reflexes from the above stimuli trigger sympathetic activity (preganglionic sympathetic nerves) along the splanchnic outflow tract, but because of the SCI, inhibitory impulses from higher CNS centers (e.g., cerebral cortex, cerebellum, and brain stem) cannot reach below the level of the SCI. Accordingly, intense generalized vasoconstriction occurs below the level of the SCI while reflex cutaneous vasodilation occurs above the level of SCI (usually in proportion to the magnitude of the inciting stimulation). Signs and symptoms of AH reflect the imbalance outlined above. The intense sympathetic response below the level of injury can cause acute hypertension (at least 20-40 mm Hg above baseline), reflex bradycardia, cardiac arrhythmias (e.g., premature ventricular contractions or atrial-ventricular conduction abnormalities), and myocardial infarction. Hypertension can further lead to headaches, blurred vision, retinal hemorrhage, intracranial hemorrhage, stroke, seizure, and/or cerebral edema. Additionally, the intense vasoconstriction leads to cool, dry, pale skin below the level of the SCI. The reflex cutaneous vasodilation above the level of the SCI leads to nasal congestion, sweating, and warm, flushed skin on the upper extremities, shoulders, neck, and face. Prevention of AH during surgery is best done with spinal or epidural anesthesia with a local anesthetic and/or deep general anesthesia. Narcotic-only regional anesthesia and sedation techniques do not reliably prevent AH. Treatment includes cessation of the triggering event and administration of direct vasodilators, such as sodium nitroprusside, nitroglycerin, or nicardipine. Beta-blockers should be used cautiously as they can worsen reflexive bradycardia and, if given in the setting of unopposed α-stimulation, may lead to severe vasoconstriction, hypertensive crisis, and congestive heart failure.

Answer 355

C3 Significant cervical spinal cord injury (SCI) at or above C3 (aside from producing quadriplegia and quadriparesis) frequently causes weakness/failure of diaphragm and accessory muscle of respiration.

Answer 356

Sweat glands Post-ganglionic neurons secrete acetylcholine Adrenal glands (medulla) Single preganglionic sympathetic neuron secretes norepinephrine, epinephrine, and small amounts of dopamine. NOTE: Sympathetic neurons preganglionic neurons originate between T1-L2. Ganglia are closer to the spinal cord. Parasympathetic neurons originate from cranial nerves III, VII, IX, X, and S2-S4. Ganglia are closer to the organ (think "para" like next to organ)

Answer 357

Acetylcholine

Answer 358

PTT, ACT, or anti-Xa levels Activated clotting time (ACT) is used to monitor the effect of high-dose UFH therapy in situations where aPTT is not clinically useful or takes too long (e.g. cardiopulmonary bypass).

Answer 359

300-400U/kg >400 ACT

Answer 360

Severe obstructive CAD Aortic insufficiency Manipulation of aortic vavle or coronary ostia NOTE: Retrograde means it is shot in the coronary sinus not the aortic arch.

Answer 361

**Platlet factor 4 antibody ** Platelet factor 4 is exposed when heparin binds to platelets. Unfractionated heparin causes HIT 10x more often than LMWH. HIT typically develops 4-10 days following the initiation of heparin therapy. Platelet count of a patient with HIT often drops by more than 50% of pre-heparin values.

Answer 362

Low dose SQH should be held 4-6 hrs before neuraxial anesthesia. LMWH (eg. Lovenox) should be held 12 hrs before neuraxial anesthesia.

Answer 363

The anticoagulant response to enoxaparin (Lovenox) can be monitored by measuring factor Xa activity. Enoxaparin binds and enhances the effects of AT3. However, the enoxaparin-induced conformational change of AT3 makes enoxaparin preferentially inhibit factor Xa. Monitoring may be recommended in patients with extreme BMIs (high or low), renal impairment, or in pregnant patients.

Answer 364

Prevent binding of plasmin to fibrin. Plaminogen --tPA-->Plasmin Plasmin binds to fibrin and causes clot breakdown (fibrinolysis) Antifibrinolytics (TXA, aminocaproic acid) prevent bleeding by preventing clot breakdown.

Answer 365

The caliber of the small airways of the lung is the primary determinant of dynamic airway resistance. Cholinergic stimulation via the Vagus Nerve (X) of M3 receptors on the bronchiolar smooth muscle results in an influx of ionized calcium, smooth muscle contraction, and bronchoconstriction. In contrast, the beta-2 adrenergic receptor plays a very important role in bronchiolar smooth muscle relaxation. By stimulating this receptor, there is an efflux of ionized calcium from the cell and into the sarcoplasmic reticulum causing rapid muscle relaxation. Interestingly, when bronchospasm is mediated by a pure reflexive vagal stimulus, the bronchoconstriction tends to be in the larger airways and more central. When this same activity is stimulated by an antigen mediated histamine response the bronchoconstriction tends to be in the more distal bronchioles in the periphery of the lung.

Answer 366

Ipratropium MOA: M3 antagonist Effect: Bronchodilation NOTE: Activation of the B2 receptor causing bronchodilation (Albuterol is a B2 agonist) while activation of the M3 receptor causes bronchoconstriction (countered by Ipratroium, a M3 antagonist).

Answer 367

Activation of the B2 receptor causing bronchodilation while activation of the M3 receptor causes bronchoconstriction.

Answer 368

Signs: * Oxygen desaturation * ETCO2 (Upsloping, decreasing, or absent) * High PIP with minimal to no change in plateau pressures * Decreasing tidal volumes * Wheezing on chest auscultation Treatment: * FiO2 100% * Deep anesthesia (IV propofol or ketamine bolus) * Hand ventilate (to assess pulmonary compliance and to assess any other possible reasons for high circuit pressure) * Albuterol * IV epinephrine (severe) (5-10mcg/kg) * IV steroids (severe) (125mg methylpred, takes 6 hours to have effect) * IV magnesium sulfate (severe) (refractory bronchospasm) (2g infusion over 20min) * Anticholinergics- atropine, glycopyrrolate (severe)

Answer 369

Inhaled nebulized racemic epi Inspird cooled saline Systemic steroids Consider reintubation (with smaller tube) NOTE: Often due to difficult intubation, prolonged intubation, surgery itself (eg. rigid bronchoscopy). Presents with respiratory distress and inspiratory wheeze.

Answer 370

Heliox is a mixture of helium and oxygen (typically 70% helium, 30% oxygen) can be used in the treatment of severe bronchospasm. This gas mixture has a lower density compared to air or supplemental oxygen, thus, promoting laminar flow. In bronchospasms, flow becomes turbulent due to increased velocity of flow through constricted airways.

Answer 371

NOTE: Only applies to laminar flow

Answer 372

If Re is < 2000, flow is most likely laminar If Re is >4000, flow is most likely turbulent Thus, increasing gas density, mean velocity, and length or decreasing gas viscocity will increase turbulent flow. Low fresh gas flows in the anesthesia circuit will exhibit more laminar flow and less turbulent flow. This can help is situations in the OR such as increased airway resistance.

Answer 373

Increase fresh gas flows Replace valve

Answer 374

A full cylinder of oxygen contains 660L and has a psig of 2200.

Answer 375

A full cylinder of nitrous oxide contains 1590 L and has a psig of 745. NOTE: NO is a liquefied gas at ambient temperature, is stored in E cyclinders in the liquefied form under high pressures. Therefore, the pressure of NO above its liquefied form remains constant at 745psig regardless of how much liquid remains. Once all the liquefied gas has evaporated the pressure will start to fall as the gaseous NO form is used which is when ~250L (16%) of NO remains in the tank. This is due to NO having a critical temperature of above room temperature (20 celcius) allowing it to exist as a liquid and a gas under pressurized conditions at room temperature. As gas is removed from the NO cyclinder, the liquid portion will evaporate maintaining a consistent pressure of 745mmHg until all the liquid NO is evaporated into gas form. The point when all the liquid NO is evaporated is when 16-25% of the total NO is remaining. After this point, the pressure guage will decrease proportionally to zero as the gas form is used.

Answer 376

NO oxidizes the cobalt in Vitamin B12 (cyanocobalamine) *irreversibly* inactivating Vitamin B12. Vitamin B12 is normally used as a cofactor for methionine synthase. Methionine synthase is unable to methylate homocysteine to methionine which is important in DNA synthesis and myelin formation and can lead to pernicious anemia and CNS/PNS demyelination. Elevated homocysteine levels can also lead to vascular inflammation and risk of thrombosis. NOTE: Reasonable to avoid NO in pediatric patients with methionine synthetase deficiency.

Answer 377

NO > Desflurane > Isoflurane > Sevoflurane "N****, smoke DIS gas" A high vapor pressure indicates the substance is more likely to evaporate at a given temperature than a susbstance with a lower vapor pressure.

Answer 378

Increase RR Decrease TV Decreased ventilatory resposne to hypercarbia Bronchodilation Decreased FRC

Answer 379

Converts upstream pressure of 2,200 psi to a downstream pressure of 45 psi

Answer 380

This fail-safe device prevents hypoxic mixtures if there is a decreased oxygen supply at the flowmeters’ level. It does this by interrupting the supply of the other gases (eg. NO) if the oxygen supply is reduced to a certain level, **usually below 30 psi. **That level is the opening threshold pressure for use of the other gases.

Answer 381

Hospital pipeline pressure (O2, NO, air) is regulated at 50-55 psig.

Answer 382

Time left = (Current PSI/3)/ flow rate

Answer 383

Pair the following gas type and cylinder color: Oxygen- green Carbon dioxide- gray Air- yellow Nitrous oxide- blue Nitrogen- black Helium- brown

Answer 384

End-titdal CO2, volatile agents, and NO are measured by the anesthesia machine using infrared absorption spectrophotometry (IRAS).

Answer 385

There are three main types of oxygen analyzers seen in clinical practice: Paramagnetic Galvanic/Clark cell Polarographic

Answer 386

The purpose of the isolated (ungrounded) power system is to prevent macroshocks.

Answer 387

The purpose of the line isolation monitor is to monitor the integrity of the isolated (ungrounded) power system.

Answer 388

The first stage regulator allows preferential use of the pipeline oxygen when the higher pressure in this system is sensed. The oxygen cylinder tanks enter at a lower pressure. When the first stage regulator is functioning properly it closes off the oxygen tank (if it has been left in the on position). If this is faulty, depletion of oxygen in the back up tank can occur. The pipeline system delivers oxygen at a pressure of 50-55 psig. Another source of oxygen is the oxygen cylinder which is regulated to enter at 40-45psig. This supply pressure difference is deliberate because it allows the anesthesia machine to preferentially obtain oxygen from the constant pipeline source that is much less likely to run out. The preferential use of oxygen is the job of the first stage oxygen regulator, which closes off the valve to the oxygen tank if the higher pipepline pressure is sensed. In other words, the higher pressure (50-55psig) closes off the lower pressure tank valve (40-45psig). This closure of the valve prevents the tank oxygen from being used when the pipeline is operational.

Answer 389

1) Disconnect the pipeline connection at the wall 2) Open the oxygen cyclinder fully 3) Ventilate by hand with the anesthesia breathing circuit

Answer 390

Aspirin and other NSAIDs can increase airway reactivity and lead to bronchospasm through the inhibition of cyclooxygenase enzymes in patients with asthma. Histamine-releasing drugs, such as morphine and atracurium, can also increase the risk of bronchospasm in patients with reactive airway disease. Avoided nonselective β-blockers (BEAM), NSAIDs, morphine, and atracurium.

Answer 391

Tricuspid Regurgitation

Answer 392

Tricuspid Stenosis

Answer 393

Constrictive Pericarditis

Answer 394

Atrial Fibrillation

Answer 395

Cardiac Tamponade

Answer 396

Complete AV block

Answer 397

The primary cause of hepatic encephalopathy is cerebral edema resulting from the ammonia combining with glutamate to form the osmotically active compound glutamine within cerebral astrocytes. Glutamine acts as an osmotic agent, causing the swelling of astrocytes and, ultimately, cerebral edema. Ammonia + Glutamate = Glutamine Remember that ammonia is supposed to be coverted to urea by the liver via the urea cycle for excretion. With decreased hepatic function you get more ammonia and less urea (BUN). Lactulose works by acidifying the lumen of the intestines trapping ammonia produced by colonic bacteria as ammonia ions.

Answer 398

Decreased arterial pH may cause vasodilation. This is because protons themselves may act as vasodilatory metabolites in the systemic arteriolar tree and capillary networks. This phenomenon is perhaps best illustrated by the finding that severe acidemia (ie, pH <7.2) may be associated with catecholamine-refractory vasoplegia.

Answer 399

Systemic = vasodilation Pulmonary= vasoconstriction Diffuse systemic vasodilation—accompanied by a net reduction in systemic vascular resistance (SVR)—is common in the first few hours after the onset of acute hypoxia. However, compensatory sympathetic activation may ultimately produce an increase in the blood pressure, resulting from an increased heart rate and cardiac output after the initial acute period. The vasodilatory response is also present with localized oxygen deficiency (such as ischemia) in an attempt to restore adequate oxygen delivery. Rapid-onset hemodynamic changes in the setting of decreased systemic oxygen availability include a peripheral chemoreceptor-mediated increase in sympathetic tone—with a resulting increase in heart rate and cardiac output—as well as global systemic vasodilation as a direct response to hypoxia. While a rise in circulating catecholamine levels may partially offset the initial vasodilatory response, a net decrease in SVR is often observed in the acute of hypoxia while it may start to increase in the subacute phase. The responses of the pulmonary and systemic vascular networks to hypoxia are generally opposed. When the peripheral arterial oxygen tension is low, the vascular tone in the systemic circulation decreases due to increased local nitric oxide production, while pulmonary vascular tone tends to increase in the setting of hypoxia. The latter phenomenon, termed hypoxic pulmonary vasoconstriction (HPV), may arise from an increase in intracellular calcium in the absence of oxygen and is a largely beneficial response in various states of focal lung disease because HPV may shunt blood away from hypoxic to well-oxygenated alveoli. Diffuse alveolar hypoxia, however, may cause global pulmonary vasoconstriction and pulmonary hypertension.

Answer 400

Sodium nitroprusside, nitroglycerin, and hydralazine release **nitric oxide **as they are metabolized. Nitric oxide is a naturally occurring vasodilator that is released by endothelial cells to produce arteriolar AND venous smooth muscle dilatation. **Nitric oxide activates guanylyl cyclase, which synthesizes cGMP, producing vasodilatation. ** Nitric oxide can be administered via inhalation to cause pulmonary vasodilation in patients with pulmonary hypertension. NOTE: Nitric oxide is NOT nitrOUS oxide. Nitric oxide decreases PVR. Nitrous oxide increases PVR. Nitroglycerin and nitroprussive cause arterial AND venodilation. Nitroglycerin causes more venodilation (decreasing preload, useful in patients with decompensated HF from ischemia because it reduces myocardial oxygen demand; patients with hypovolemia or inferior MI should not be treated with NTG as it may cause dramatic hypotension). Nitroprusside in more balanced in terms of arterial and venous vasodilation (decreases preload and afterload). Hydralazine causing arterial vasodilation only.

Answer 401

Decreases LV preload = less wall stress

Answer 402

Dihydropyridine ("-dipine" suffix) (nifedipine, nicardipine, nimodipine, clevedipine) Non-dihydropyridine (diltiazem, verapamil) NOTE: All CCBs inhibit L-type volatage gated Ca2+ channels on smooth muscle causing vasodilation.

Answer 403

Arterial vasodilation only (including coronaries) NOTE: CCBs are particularly useful for post-operative CABG patients because they cause coronary arterial vasodilation and inhibit coronary artery vasospasm (Cardene gtt). Nimodipine, particularly, has enchanced activity within cerebral vascular beds which is why it is used in patients with SAHs to prevent cerebral vasospasm.

Answer 404

Dihydropyridines (nifedipine, nicardipine, nimodipine, clevedipine)

Answer 405

Dihydropyridines (nifedipine, nicardipine, nimodipine, clevedipine) NOTE: Dihydropyridines can potentially increase myocardial oxygen demand due to reflex tachycardia. Non-diihydropyridines (esp diltiazem) are used to treat angina as the supply of oxygen is increased without a subsequent increae in demand (negative chronotrope, inotrope, and dromotrope).

Answer 406

Arterial vasodilator (verapamil < diltiazem) **Negative chronotropy Negative inotropy (verapamil > diltiazem) Negative dromotropy ** NOTE: Non-dihyropyridine CCBs not only act on L-type Ca2+ in smooth muscle **but also L-type Ca2+ in cardiac tissue** which explains why this group of CCBs have the above cardiodepressant effects. Dihydropyridines DO NOT have any chronotropic, inotropic, dromotropic effects. Negative chronotropic effect explains why reflex tachycardia is not seen with non-dihyropyridine CCBs while they are seen with dihydropyridine CCBs.

Answer 407

Due to the negative chronotropic, dromotropic, and inotropic effects of non-dihydropyridine CCBs they should be avoided in patients with: * Acute MI * Decompensated heart failure * Cardiogenic shock * Sick sinus sydrome * Concurrent administration of intravenous beta-blockers * AV block (2nd or 3rd degree) * AF/A Flutter with associated accessory bypass tract (i.e., Wolff-Parkinson-White syndrome) * Wide-complex V-tach FDA Approvals: Verapamil * Angina (chronic stable, vasospastic, unstable angina) * Hypertension (as add on therapy) * Paroxysmal supraventricular tachycardia (PSVT) prophylaxis * Supraventricular tachycardia (SVT) Diltiazem * Angina (chronic stable) * Hypertension (as add on therapy) * Atrial arrhythmia (AF w RVR) * Paroxysmal supraventricular tachycardia (PSVT)

Answer 408

BB or CCB NOTE: CCBs, however, should be avoided in patients with cardiogenic shock, decompensated HF, WPW. Because of its potential toxicities, amiodarone should only be used after consideration of risks and when other agents have failed or are contraindicated.

Answer 409

Stable- antiarrhythmic (Adenosine, Amiodarone) Unstable- synchronized cardioversion NOTE: AV blocking agents (BB, CCB) should be avoided until WPW can be ruled out because giving AV blocking agent will encourage conduction through accessory pathway.

Answer 410

Class III antiarrhythmic * K+ channel blocker (prolongs duration of action potential and increases the refractory period of atrial, nodal and ventricular tissues. * Also blocks Na+, Ca2+, b-adrenergic receptors (decreasing conduction via SA and AV node) NOTE: Amiodarone is the only antiarrhytmic with little to no negative inotropic effects, making it a good option for patients with reduced ejection fraction. Amiodarone is commonly used to treat ventricular tachycardia, persistent ventricular fibrillation after defibrillation, refractory atrial fibrillation.

Answer 411

Bradycardia Bradycardia as a result of calcium channel blocking properties of Amiodarone. Bradycardia is more common than QTc prolongation (>440ms in men, > 460ms in women). MOA: * K+ channel blocker (prolongs duration of action potential and increases the refractory period of atrial, nodal and ventricular tissues. * Also blocks Na+, Ca2+, b-adrenergic receptors (decreasing conduction via SA and AV node)

Answer 412

a1- antagonist (arteriolar vasodilation) b1- antagonist (reduction in HR & contractility) b2- antagonist AND partial agonist (overall, arteriolar vasodilation) NOTE: SV and CO are typically unchanged because the arteriolar vasodilation properties of labetalol offset the decrease in HR and decrease in contractility. Ratio of alpha:beta blockade is 1:7 when administered via IV. One key feature of labetalol is its blockade of reflex tachycardia, seen with other vasodilators. Duration of action: 6 hours (but can have an effect on BP for 16-18hrs). Metabolized by liver.

Answer 413

a1 >> a2 antagonist (irreversible) Used as preoperative antihypertensive treatment in phenochromocytoma patients

Answer 414

a1 > a2 antagonist (reversible) Used to diagnose phenochromocytoma. Used as antidote of choice for the extravasation of vasoactive medications that work on alpha receptors: phenylephrine, norepinephrine, epinephrine, dopamine, and dobutamine.

Answer 415

a1 antagonist (reversible) Used to manage and treat hypertension, benign prostatic hyperplasia, PTSD-associated nightmares, and the Raynaud phenomenon.

Answer 416

Hydralazine has a duration of action of 2-6 hours.

Answer 417

Fast acting anti-hypertensives including esmolol, nitroglycerin, nitroprusside have an onset of action of < 1min and have a duration of action of approximately 5-10 minutes.

Answer 418

Systemic: increases SVR Pulmonary: decreases PVR (via inhibition of hypoxic pulm vasoconstrication) Cerebral: vasoconstriction There is evidence that hyperoxia may lead to neurotoxicity, retinopathy, tracheobronchitis, lung injury, and even myocardial ischemia due to paradoxical coronary vasoconstriction. Insufficient experimental data exist to definitively determine the effects of perioperative hyperoxia on all-cause mortality, surgical site infection, or postoperative nausea and vomiting when compared to normoxic anesthetic conditions. Oxygen toxicity secondary to hyperbaric oxygen therapy (treatment for CO poisoning) can result in pulmonary and central nervous system manifestation. Central nervous system manifestations of oxygen toxicity include nausea, vomiting, numbness, and dizziness and, possibly, abnormal acoustic, olfactory, and gustatory sensations. In severe cases, nonfocal tonic-clonic seizures can occur.

Answer 419

Associated airway abnormalities seen in acromegaly include hypertrophy of the posterior pharyngeal structures such as the epiglottis and the aryepiglottic folds. Acromegaly leads to the expansion of cartilaginous structures in the neck, which can cause recurrent laryngeal nerve paralysis and abnormal movement of the vocal cords. Associated chondrocalcinosis of the larynx also leads to vocal cord thickening and stricture formation. Because of these anatomical challenges to intubation, the patient should be considered for awake fiberoptic intubation, and a smaller endotracheal tube should be considered because of possible narrowing of the cricothyroid ring and glottic opening.

Answer 420

Proper volume management is crucial to help decrease the development of AF. Both hypovolemia and hypervolemia can increase the risk. Hypovolemia causes a decreased venous return to the right atrium which reduces stroke volume and cardiac output. Both of these cause decreased tissue oxygen delivery, which induces catecholamine release – both can increase the risk of AF development. Hypervolemia leads to mechanical stimulation of the right atrium, leading to myocardial stretch and an increase in atrial cell triggering. Perioperative atrial fibrillation (AF) risk factors include atrial injury, ischemia, inflammation, increased catecholamines, hypervolemia or hypovolemia, and electrolyte disturbances. The exact mechanism causing atrial fibrillation is not completely understood, but there are also likely patient factors that influence the risk along with surgical risk factors. Some of the patient factors shown to increase the risk include advancing age, male sex, the presence of hypertension, prior history of AF, obesity, chronic obstructive pulmonary disease, asthma, valvular disease, left atrial size, and left ventricular ejection fraction.

Answer 421

FENa = (uNa × pCr) / (pNa × uCr) × 100% The FENa is used to compare the value of sodium in the urine to sodium in the plasma. If there is relatively little sodium in the urine, this provides evidence that the kidneys are trying to maintain intravascular volume by reabsorbing sodium in the nephron. Higher sodium in the urine is reflected by a FENa of 3%, which generally reflects an intrarenal cause of oliguria. A FENa between 1% and 3% is indeterminate. Patients who are taking diuretics will have a relatively high amount of sodium in the urine regardless of oliguria etiology because diuretic medications frequently inhibit sodium reabsorption in the nephron. For patients who are taking these diuretics (commonly hydrochlorothiazide and furosemide), the FEUrea can be used instead. Fractional excretion of urea is calculated in the same way as FENa but with the substitution of urea for sodium. The equation for FEUrea is FEUrea = (uUrea x pCr) / (pUrea x uCr) × 100%

Answer 422

Morphine has the potential for significant accumulation of metabolites in the setting of renal dysfunction. Morphine is broken down into: - Morphine-3-glucuronide, which can cause neuroexcitation (eg, seizures) when it has accumulated - Morphine-6-glucuronide, a more potent (100x) analgesic and respiratory sedative compared with morphine alone. "Three you seize, Six you're fixed"

Answer 423

Morphine Morphine has a duration of action of approximately 4 hrs. Dilaudid has a duration of action of approximately 2 hrs. NOTE: 1-2-4 rule (Fentanyl 1hr, Dilaudid 2 hrs, Morphine 4hrs)

Answer 424

MORPHINE Morphine causes dose-dependent histamine release. Results in tachycardia, hypotension (preload AND afterload), bronchospasm, increase in PVR.

Answer 425

Alfentanil This is due to Alfentanil's low pKA (high unionized fraction at physiologic pH) and moderate lipid solubility. Recall that: 1) Opioid *onset* of action is related to unionized fraction (pKA) and lipid solubility (lower pKA = faster onset). 2) Opioid *duration* of action is related to lipid solubility (low lipid solubility = longer duation). 3) Opioid *analgesic potency* is related to the drug's affinity and efficacy at the mu opioid receptor.

Answer 426

Mu agonist Kappa agonist Meperidine also has some local anesthetic effects because of interactions with sodium ion channels. Also, meperidine has stimulant effects by inhibition of the dopamine transporter (DAT) and norepinephrine transporter (NET). NOTE: Meperidine is structurally similar to Atropine may see increase in HR and other anticholinergic effects.

Answer 427

The accumulation of the active metabolite of meperidine, normeperidine, is neurotoxic and can cause seizures. It is renally excreted thus can accumulate in renal dysfunction. NOTE: Morphine should also be avoided in renal dysfunction. Morphine is metabolized to morphine-3-glucuronide and morphine-6-glucuronide. Morphine-6-glucuronide can also increase risk of seizures in patients with renal dysfunction. BOTH meperidine and morphine should be avoided in patients with renal dysfunction. Meperidine is an opioid that also inhibits serotonin reuptake and should be avoided in patients on MAO-i due to risk of serotonin syndrome. This exact scenario resulted in the death of an 18 yr old which is why we have an 80hr work week restriction.

Answer 428

Morphine Hydromorphone (Dilaudid) Meperidine Tramadol

Answer 429

Midazolam is highly lipid soluble and accumulates in the tissues with infusion, providing prolonged sedation due to a significant context-sensitive half-life. This prolonged sedation can be even greater in the setting of renal dysfunction due to its active, renally-excreted metabolite, 1-hydroxymidazolam (also known as alpha- hydroxymidazolam). NOTE: Midazolam should also be used with caution in patients with liver disease and avoided in the third trimester. Midazolam is highly protein bound so in hypoalbuminemia should be used with caution (increased free fraction). Bioavailability of oral Midazolam in 40% (fun fact)

Answer 430

The SIADH is typically associated with the following electrolyte abnormalities: 1) Urine osmolality > 100 mOsm (often > 200-300 mOsm) 2) FENa > 1% 3) Urine Na+ >20 mEq/L 4) Low serum uric acid and BUN 5) Dilutional, euvolemic hyponatremia (serum Na+ < 135 mEq/L)

Answer 431

Physiologic changes that take place during insufflation include: - Decreased lung compliance and increased inspiratory pressure, due to an increase in intra-abdominal pressure and Trendelenburg position. - Increased ventilation-perfusion (V/Q) mismatch, due to atelectasis and decreased functional residual capacity (FRC). - Elevated CO2, due to CO2 insufflation and decreased lung perfusion and ventilation. Most patients require an increase of 30% in minute ventilation to counter the increase in CO2 from insufflation. A modest increase in inspiratory pressures is needed to counter the reduced lung compliance and FRC associated with pneumoperitoneum. During laparoscopic procedures, it is best to use either volume-control or pressure-control volume-guaranteed modes of ventilation. Pressure control alone can assist with achieving appropriate tidal volumes, but at the risk of over-ventilation with position changes and desufflation. The most significant decrease in FRC occurs with > -30 degrees trendelenburg.

Answer 432

Displacement of cephalad pressure from the diaphragm by allowing the abdomen and its contents to freely hang (increases ERV thus FRC)- primary mechanism Displacement of the heart away from the left lung (allows left lung to be maximally expanded). Overall, more optimized V/Q matching and shunt fraction is decreased.

Answer 433

Functional residual capacity is the amount of air remaining in the lungs at end-exhalation of a normal, tidal breath. It represents the point at which the lung's tendency to recoil is equal to the chest's tendency for expansion and is made up of the expiratory reserve volume + residual volume. NOTE: FRC of an adult is about 30mL/kg.

Answer 434

Male (large lung volumes) Advanced age (loss of elastic tissue) Tall (large lung volumes) COPD (loss of elastic tissue)

Answer 435

"PANGOS" Pregnancy Ascites Neonates General anesthesia Obesity Supine positioning OTHER: Females, short, s/p lung resection, pulmonary fibrosis

Answer 436

FRC (cc)/O2 consumption (cc/min) x FiO2 For adults, FRC is approximately 30cc/kg For adults, average O2 consumption is approximately 3cc/kg/min FiO2 = 1.0 (or 100%) For an 70kg adullt: 2100/210 x 1.0 = 10 minutes NOTE: FRC is becomes the sole source of oxygenation during apnea. Equation above may overestimate time because: * FRC is reduced 10% in supine position (compared to upright) * FRC is reduced another 10% with induction of general anesthesia * Obese patients and neonates and increased O2 consumption

Answer 437

Closing Capacity (CC) is the sum of the closing volume (volume at which small airways begin to collapse/close) and residual volume. CC = CV + RV Decreasing FRC relative to closing capacity will lead to increased atelectasis. Factors that INCREASE Closing Capacity include "ACLS-S" Age COPD LV failure Smoking Surgery (esp long surgery) NOTE: In patients with decreased FRC (PANGOS- Prengancy, Ascites , Neonates, General anesthesia, Obesity, Supine), Closing Capacity can exceed FRC resulting in atelectasis and hypoxemia.

Answer 438

Head up positioning (>30 degrees) with CPAP Will extend time to desaturation by improving FRC, decreases atelectasis, and improves V/Q mismatch.

Answer 439

Risk factors for placental abruption include: Advanced maternal age (age > 35 years) Maternal hypertension Preeclampsia History of prior abruption Increasing parity Tobacco use (maternal and paternal) Cocaine use Trauma Premature rupture of membranes Chorioamnionitis Bleeding in early pregnancy

Answer 440

Disseminated intravascular coagulation is often described as a thrombo-hemorrhagic disorder. Patients can present with thrombosis or bleeding at different times or simultaneously. Disseminated intravascular coagulopathy (DIC) is a disorder characterized by systemic activation of coagulation that results in an imbalance of hemostasis. It is associated with a comorbid condition such as infection, inflammation, or malignancy which causes widespread activation of the coagulation cascade. Clinically, DIC involves diffuse thrombosis that may lead to multi-organ system failure or consumptive coagulopathy and bleeding.

Answer 441

Mature postjunctional nAChRs have five subunits: (α2βδε) 2 α (alpha) 1 β (beta) 1 δ (delta) 1 ε (epsillon) Immature extrajunctional nAChRs (aka fetal nAChRs) also have five subunits, but have a γ subunit (α2βδγ) in place of an ε subunit. ("epsillon at the endplate, gamma goes out") 2 α (alpha) 1 β (beta) 1 δ (delta) 1 γ (gamma) Postjunctional nicotinic acetylcholine receptors are ligand-gated ion channels located at the motor endplate responsible for muscle end plate depolarization. When two acetylcholine molecules bind the α subunits, the channel opens, allowing an influx of sodium and efflux of potassium to create a motor end plate potential sufficient for depolarization of the cell, which leads to muscular contraction (excitation-contraction coupling). Immature extrajunctional receptors have **long open times and low-amplitude channel currents**, in contrast to mature junctional receptors that have shorter open times and high-amplitude channel currents. **The immature receptors have opening times up to 10x longer compared with mature receptors, allowing for efflux of significant amounts of potassium resulting in hyperkalemia. ** The immature extrajunctional form is present in states of decreased muscle activity such as the fetal state prior to muscle innervation as well as immobilization, burns, upper motor neuron injury, lower motor neuron injury, or sepsis. **Immature receptors are sensitive to succinylcholine while having relative resistance to nondepolarizing NMBAs.**

Answer 442

Succinylcholine should be avoided **> 24 hours** after an initial burn injury and for at least **2 years **after the burn skin has healed. NOTE: In other words, its safe to use succinylcholine within 24 hours from an initial burn and the hyperkalemic risk with succinylcholine due to extrajunctional ACH-R can last a long time. These patients are sensitive to succinylcholine and resistance to NDMAs.

Answer 443

Non-depolarizing NMBA > Resistance Depolarizing NMBA (aka Sux) > Prolonged relaxation

Answer 444

Depolarizing- decreased sensitivity (resistance) Non-depolarizing- increased sensitivity Exercise conditioning (eg. preparing for a marathon) results in increased stimulation of the nAChRs due to repetitive use leading to downregulation of mature nAChRs and increased sensitivity to nondepolarizing NMBAs

Answer 445

Depolarizing- decreased sensitivity (resistance) Non-depolarizing- increased sensitivity Chronic acetylcholinesterase use (eg. pyridostigmine in patients with myasthenia gravis) results in increased stimulation of the nAChRs due to repetitive use leading to downregulation of mature nAChRs and increased sensitivity to nondepolarizing NMBAs. NOTE: For the same reason, organophosphate poisoning also leads to the same effect.

Answer 446

Depolarizing- increased sensitivity Non-depolarizing- decreased sensitivity (resistance) When patients have decreased stimulation at the NMJ, such as when they are immoblized for extended periods of time after a CVA, there is an upregulation of immature (fetal) nAChRs. This upregulation of immature nAChRs results in an increased sensitivity to acetylcholine and succinylcholine but a decreased sensitivity to non-depolarizing NMBAs.

Answer 447

α (alpha) subunit TWO acetylcholine molecules bind to the α (alpha) subunit to activate the receptor. Each bind acetylcholine molecule binds to an α (alpha) subunit.

Answer 448

Physostigmine

Answer 449

Physostigmine

Answer 450

Atropine Pralidoxime Atropine counters the cholinergic crisis at muscarinic receptors (given first) Pralidoxime counters the cholinergic crisis at nicotinic receptors (given second). Pralidoxime, specifically, is an *acetylcholinesterase enzyme re-activator.* Because organophosphate poisoning results from the inhibition of acetylcholinesterase, patients are treated with atropine to counteract the cholinergic crisis at muscarinic receptors. Because atropine does not bind to nicotinic receptors, the neuromuscular symptoms will still be present, so an oxime (pralidoxime or obidoxime) should be administered to regenerate acetylcholinesterase but only after administration of atropine to avoid the transient worsening of oxime-induced acetylcholinesterase inhibition.

Answer 451

The mnemonic SLUDGE-Mi can be used remember cholinergic symptoms, such as those seen with acetylcholinesterase inhibitors, organophosphate poisoning, and nerve agents. SLUDGE-Mi: Salivation, Lacrimation, Urination, Defecation, Gastrointestinal upset, Emesis, Miosis. Saying the mnemonic as "Sludge Me" helps differentiate miosis and mydriasis. The opposite symptoms are therefore seen with the use of anticholinergic medications.

Answer 452

Clinical pharmacologic effects of anti-cholinergic drugs include: Tachycardia Decreased respiratory tract secretions Relaxation of bronchial smooth muscle Mydriasis

Answer 453

Age > 70 yrs old Morbid Obesity BMI >40 ASA III or IV CAD Pulmonary HTN OSA Chronic liver failure (MELD > 10) Chronic renal failure According to the American Society of Anesthesiologists (ASA) Closed Claims Project Database, the most common characteristics for monitored anesthesia care claims associated with oversedation leading to adverse outcomes include ASA physical status of III or IV (45% of cases), age > 70 (42%), and the use of propofol combined with other sedatives (50%). Nearly 50% of the closed medical malpractice claims could have been prevented with better monitoring. According to the American Society of Anesthesiologists Closed Claims Project Database for monitored anesthesia care claims associated with oversedation, 12% of claims involved pulse oximetry, 20% of claims involved capnography, and 1% of claims involved both pulse oximetry and capnography, providing evidence that increased monitoring may lead to better outcomes. NOTE: Greatest risk of MAC is respiratory depression due to oversedation and airway fire.

Answer 454

The most common type of medication error is improper labeling. The most common cause of medication errors include: Confusing drug names, Illegible hand writing, Labeling errors, Excessive provider workload NOTE: Most medications errors occurs and adverse drug events occur within 20 minutes of induction.

Answer 455

NONE There are no absolute contraindications for MAC. Relative contraindications include inability to lie still enough for the procedure, inability to cooperate, and inability to cooperate with the care team.

Answer 456

To establish a medical malpractice lawsuit, 4 elements must be proven: 1) Causation 2) Duty to the patient 3) Negligence or breach of duty 4) Damages Causation asks whether the act of care or omission of care caused the poor outcome. Duty to the patient refers to the provider's responsibility to the patient to provide care. Negligence or breach of duty means that the standard of care in the community was not met. Standard of care is defined as what a reasonable physician with similar education, training, and experience would have provided for a patient in this situation, so, when this does not occur, the practicing physician is deemed to be negligent or in breach of duty. The alleged damages, which can be physical, psychological, or financial, must be foreseeable by the average and reasonably minded practitioner. Damages also refer to the compensation for loss or injury, bills, punitive damages, or medical malpractice.

Answer 457

Aldosterone, insulin, and cortisol are the primary modulators of potassium homeostasis. Aldosterone is a mineralocorticoid released following activation of the renin-angiotensin-aldosterone pathway in response to hypovolemia and renal hypoperfusion. Aldosterone acts primarily (but not exclusively) in the distal renal tubules and collecting ducts to upregulate the Na+/K+ pumps, leading to increased reabsorption of sodium (and water) and potassium secretion into the urine. Cortisol (hydrocortisone) is a glucocorticoid with numerous effects, including electrolyte homeostasis. Cortisol facilitates sodium transport and inhibits gastrointestinal sodium loss, promoting sodium retention. Cortisol also enhances cellular sodium and potassium exchange and renal potassium secretion, similar to mineralocorticoids. Insulin also has numerous physiologic effects, including potassium homeostasis. Insulin enhances cellular potassium uptake (particularly by skeletal muscle), lowering serum potassium concentration.

Answer 458

There are four MRI safety zones. Zone IV is the MR scanner room. Zone III is the area surrounding the MR scanner room that requires screening and may be subject to magnetic forces (control room). Zone II is the interface between the general public and the restricted zone III (the dressing/holding room). Zone I is all areas freely accessible to the general public. NOTE: Patients must be screened to enter zone III. Zone III is the last place that a non-MRI compatabile device can be in. If an emergency occurs in zone IV (eg. cardiac arrest), the patient should be first removed from zone IV before life-saving measures (eg. CPR).

Answer 459

Testes, ovaries, small intestine, bone marrow, lymphoid tissue "LOST Marrow"

Answer 460

Evaporation Heat loss through the breathing circuit can be explained by evaporation; for this reason, inspired gases, particularly in vulnerable pediatric patients, are humidified to minimize this loss. For anesthesia machines, a heat-moisture exchanger (HME) is commonly used. Evaporation refers to heat loss via the conversion of water to gas. For example, perspiration uses evaporation to cool the body. In the case of the anesthesia breathing circuit, moisture from the airway that is expired evaporates and leads to cooling.

Answer 461

Increase ETCO2 by increasing dead space

Answer 462

During mechanical ventilation the bellows rise during exhalation and fall inspiration.

Answer 463

Radiation Radiation describes heat loss via photons, given off to the surrounding atmosphere. This type of heat transfer accounts for up to 60% of heat lost in the operating room setting, representing the most significant source of heat loss. Hypothermia in the operating room occurs secondary to a cooler environment compared to the patient's temperature, their inability to initiate behavioral responses, and anesthetic drugs. Volatile anesthetics, propofol, morphine, and meperidine promote heat loss through vasodilation and, in addition, they alter thermoregulation in the hypothalamus in a dose-dependent manner. Opioids also decrease sympathetic outflow. The effect causes a higher threshold for heat response and a lower threshold for cold response. Along with environmental exposure, this helps explain why hypothermia is seen with recreational opioid overdose (illicit street use). Nitrous oxide depresses thermoregulation less than other inhalational anesthetics, and midazolam (along with the other benzodiazepines) has almost no effect on temperature. OTHER: After induction of general anesthesia, the initial 1-2° C drop in body temperature is due to the redistribution of heat from the core to the periphery by means of peripheral vasodilation. After equilibrium, the majority of continuous heat loss occurs by mechanism of radiation in addition to the evaporative heat loss through the surgical wound. Redistribution (1st) -> Radiation (2nd, most significant approximately 67%) The first phase (redistribution) can be prevented by prewarming the patient with warm blankets (preferablly forced air) which increases the temperature in the periphery thus decreasing the core-peripheral temperature gradient decreasing redistribution. The core temperature is tightly regulated and does not chagne much with ambient warming. Hypothermia can lead to several deleterious effects. These include coagulopathy, decreased drug metabolism, delayed awakening, decreased MAC, altered mental status, arrhythmia, decreased oxygen availability (left-shift on hemoglobin-oxygen saturation curve), delayed wound healing, and increased infection risk.

Answer 464

Impairs peripheral vasoconstrictive response to hypothermia Impairs shivering NOTE: In contrast, warm thermoregulatory mechanisms such as sweating are not impaired by volatile anesthetics. Peripheral vasodilation in response to hyperthermia is actually enchaced by volatile anesthetics.

Answer 465

When clinically significant changes in temperature are intended, anticipated, or suspected. General consensus is that when general anesthesia exceeds > 30 minutes core temperature monitoring should be performed. Additionally, when neuraxial anesthesia exceeds > 30 minutes core temperature monitoring should be performed.

Answer 466

Hypothermia has several pathological effects: 1) COAGULOPATHY/PLT DYSFUNCTION- impairment of platelet function, thromboxane generation, and local hemostatic vasoconstriction. This leads to bleeding that may be irreversible. The degree of coagulopathy may not be adequately captured by laboratory tests since they are rewarmed to 37 degrees Celsius 2) INFECTION- Even mild hypothermia can increase the risk of postoperative wound infection, leading to sepsis in these already critically ill patients. Hypothermia leads to local vasoconstriction, low oxygen tension, impaired chemotaxis, and increased bacterial growth 3) Impaired anesthetic medication clearance via hepatic due to reduced portal vein flow and hepatic metabolism (especially true of propofol and etomidate) 4) Impaired central nervous system, with obtundation, excess sedation, poor response to hypoxemia and hypercarbia (can manifest as delayed emergence) 5) Cold-induced vasoconstriction leads to high catecholamine concentration with increased myocardial ischemia 6) Severe hypothermia (under 33 degrees Celsius) leads to multiple organ damage and failure 7) Prolonged duration of NMBAs

Answer 467

32-36 C x 24hrs NOTE: 32-36 = minimal shifts in EEG frequencies < 25 = burst suppression < 18 = isoelectric (complete suppression)

Answer 468

Meperidine (Demerol)- most effective a2 agonists (Precedex, Clonidine) Ketamine Zofran Tramadol NOTE: Complications of shivering include tachycardia, hypertension, and increased oxygen consumption.

Answer 469

PROLONG/POTENTIATE: Acute use of anticonvuslants (phenytoin, carbamazepines) Antibiotics (eg. CLAP iT) Antiarrhythmics (CCBs) Dantrolene Ketamine Local anesthetics (high doses) Lithium Hypocalcemia Hypermagnesemia Volatile anesthetics (esp Desflurane) SHORTER/ATTENUATE: Chronic use of anticonvulsants (phenytoin, carbamazepines) Cholinesterase inhibitors (eg. neostigmine) Hypercalcemia Hypomagnesemia NOTE: Calcium mediates fusion of acetylcholine containing vesicles with the presynaptic membrane with SNaRE proteins. Thus stimulation of nerve leads to accumulation of calcium within the presynaptic neuron and greater release of acetylcholine. Thus, hypcalcemia potentiates and hypercalcemia attenuates. Magnesium inpairs the influx of calcium into the presynaptic membrane, resulting in a decrease in acetylcholine release into the synaptic cleft. Thus, hyermagnesemia potentiates and hypomagnesemia attenuates. CLAP iT (clindamycin, lincomycin, aminoglycosides [esp gent], polymyxins, tetracyclines). These antibiotics either reduce presynaptic ACH release of decrease postsynaptic aCh-R sensitivity to ACH. Thus, these antibiotics potentiate. Notice that there are NO antibiotics that attenuate NMBAs. Lithium inhibits presynaptic neuromuscular transmission and postsynaptic muscle contraction. Thus, lithium potentiates. Inhalational anesthetics potentiate the blockade by directly acting on the nicotinic acetylcholine receptors, with the potentiation affected by the type of inhalational anesthetics and duration. The potentiation order is desflurane > sevoflurane > isoflurane > nitrous oxide.

Answer 470

Adductor policis is the last muscle to recover from NMBA. Order of recovery from first to last: Diaphragm -> laryngeal muscles-> corugator supercilli (eyebrow contraction)-> abdominal muscles -->orbicularis oculi (closes eyelid)-> adductor policis NOTE: Despite being the first muscle to be paralyzed, the diaphragm is relatively resistant to NMBAs (due to high concentrations of ACH-R) and recovers much more quickly than any other muscle.

Answer 471

Desflurane Desflurane can augment neuromuscular blockade by as much as 60% in healthy patients. Inhalational anesthetics augment neuromuscular blockade via direct and indirect mechanisms. The direct mechanism includes relaxation of the skeletal muscle, particularly when >1 minimum alveolar concentration (MAC) is administered. This effect is especially pronounced in the setting of preexisting musculoskeletal diseases that produce skeletal muscle weakness, such as myasthenia gravis. Nitrous oxide does not directly relax skeletal muscle. The indirect mechanism includes the synergistic action of inhalational anesthetics at the neuromuscular junction with neuromuscular blocking drugs (NMBDs), though the details of this mechanism are not fully understood. Volatile anesthetics may have a central alpha-adrenergic effect on motor neurons and interneurons and/or a direct inhibition of the postsynaptic nicotinic acetylcholine receptors. These effects are more pronounced with the aminosteroid nondepolarizing NMBDs (e.g. rocuronium, vecuronium, pancuronium) than the benzylisoquinoline nondepolarizing NMBDs (e.g. cisatracurium, mivacurium, atracurium). These effects are dependent on the volatile anesthetic levels present within the blood. Although the combination of rocuronium and inhalation anesthetics augments the intensity of neuromuscular blockade, it does not significantly increase the duration of or slow the recovery from the blockade. Overall, it has been estimated that desflurane most significantly augments neuromuscular blockade (by as much as 60%), followed by isoflurane and sevoflurane (as much as 40%), then nitrous oxide (20%).

Answer 472

Volatile anesthetics (isoflurane, sevoflurane, desflurane) are purported to disrupt a variety of chemical mediators in the brain and spinal cord. Volatile anesthetics likely potentiate the inhibitory effects of γ-aminobutyric acid (GABA) via enhanced presynaptic GABA release as well as postsynaptic GABA and glycine effects in the central nervous system. Despite the many years of safe and effective use, the mechanism of action of volatile anesthetics remains largely theoretical, with incomplete evidence to support one clear mechanism of action. However, it has been suggested that volatile anesthetics act at several sites in the brain and in the spinal cord, resulting in anesthesia, amnesia, and immobility. The immobilizing effect of inhaled anesthetics is due, in large part, to effects in the spinal cord. One animal study demonstrated that, to produce immobility in test subjects, the required dose of volatile anesthetic in the brain was four times higher than when the spinal cord and brain received the same volatile agent. Results of a study involving knockout mice without typical GABA-A receptors provided evidence that GABA is not responsible for immobility. Anesthesia and amnesia, however, are due to the enhancement of GABA and glycine and the inhibition of glutamate and, possibly, potassium. Volatile anesthetics enhance inhibitory effects presynaptically by increasing GABA release and elevating the basal levels of GABA. In addition, volatile agents increase postsynaptic sensitivity to GABA and glycine at their ligand-gated channels as well as increasing extrasynaptic sensitivity by enhancing the effects of GABA at those receptors. Excitatory transmission of glutamate is reduced presynaptically, while postsynaptic glutamate receptors are inhibited. In addition, presynaptic and postsynaptic potassium channels are altered, resulting in altered transmission states in the nervous system. There is some evidence that central nicotinic receptors may be inhibited as well, contributing to amnestic effects.

Answer 473

Acute = Potentiation Chronic = Attenuates

Answer 474

PR interval prolongation QRS interval prolongation QT interval prolongation (potenially Torsades) NOTE: QTc prolongation (>440ms in men, > 460ms in women) QT interval varies with HR. QT is shorter at fast heart rates, QT is longer at slow heart rates. QT interval can be corrected for heart rate: QTc = QT/cardiac cycle (seconds)

Answer 475

Nervous System - Decreased gray/white matter - Decreased neurotransmitters (acetylcholine, dopamine) - Decreased epidural space - Decreased CSF volume - Increased permeability of dura mater Cardiovascular System - Decreased alpha & beta-receptor responsiveness (due to downregulation of intracellular signal coupling NOT a decrease in number of receptors) - Increased sympathetic activity - Decreased parasympathetic activity - Decreased baroreceptor reflex (due to decrease in HR response rather than vascular tone) - Decreased ventricular compliance (due to stiffening of myocardium) - Negative lusitropy - Decreased vascular compliance (due to stiffening of arteries and veins) - Increased afterload - Conduction changes (due to myocardial fibrosis and loss of SA nodal cells) Respiratory System - Decreased vital capacity - Increased residual volume - Increased closing capacity - Increased anatomic dead space - Increased lung compliance - Increased pulmonary vascular resistance Hepatic System - Decreased hepatic blood flow

Answer 476

The current KDIGO1 guidelines define AKI as: Increase in serum creatinine by 0.3 mg/dL over 48 hours Increase in serum creatinine to ≥1.5x baseline within 7 days Urine volume of < 0.5 ml/kg/hr for ≥6 hours Renal ischemia is the most common cause of AKI and occurs when the mean arterial pressure (MAP) falls below the particular threshold for filtration in a particular patient. In general, during elective non-cardiac surgery, a MAP < 60 mm Hg is associated with increased risk of AKI. Even more critically, the risk of AKI goes up with as little as one minute spent with a MAP of ≤55 mm Hg and increases linearly with additional time.

Answer 477

NOTE: GFR is a better indication of renal function in patients > 40 years old. As we get older we have fewer functioning nephrons and less renal blood flow resulting in a progressive decline in GFR. Creatinine, however, is unlikely to significantly change after the age of 40 (due to decreased muscle mass).

Answer 478

Afferent arteriole vasoconstriction

Answer 479

Efferent arteriole vasodilation

Answer 480

Recurarization, or reparalyzing, occurs when neostigmine's duration of action is shorter than that of the NMBA used. Recurarization can be prevented by ensuring that the patient has an appropriate train-of-four (TOF) count prior to administration of neostigmine and by avoiding the use of a long-acting NMBA such as pancuronium. Neostigmine is metabolized by the liver and excreted by the kidneys; thus, decreased renal function will prolong the effects of neostigmine, which helps outlast the effect of NMBAs that are excreted renally, such as rocuronium and vecuronium.

Answer 481

Bradycardia Block (Complete heart block / asystole) Bronchoconstriction Increased salivation Nausea Diarrhea NOTE: Neostigmine competitively inhibits acetylcholinesterase at muscarinic and nicotinic sites.

Answer 482

In 1984, a scoring system was developed by Cormack and Lehane describing the different laryngoscopic views ranging from I to IV. Grade I view is given when the epiglottis and vocal cords are in complete view (entire glottic aperture). Grade II-a is when the posterior cords + arytenoids are visible Grade II-b is when only the arytenoids are visible (no cords seen). Grade III is when the epiglottis is only visible. Grade IV view is the visualization of only the soft palate as the epiglottis or the larynx cannot be visualized.

Answer 483

Plamsa and platelets TRALI is immunologically mediated by the passive transfusion of donor antibodies that target host leukocytes and result in an inflammatory cascade and leukoagglutination that causes an acute lung injury. Because of this pathogenesis, the transfusion of blood products that contain higher concentrations of donor plasma, such as thawed plasma or platelets, is associated with a higher incidence of TRALI. It is for this reason as well that plasma is not generally accepted from female donors as women who are multiparous will tend to generate the relevant antibodies following exposure to fetal blood. Thus, plasma tends to be collected only from male donors in the USA. This policy is thought to be largely responsible for the decreased incidence of TRALI seen over the past decade.

Answer 484

Primary hyperthyroidism is characterized by elevated T3, T4 (free and total), elevated thyroid hormone binding ratio, and a low/ normal TSH.

Answer 485

Factors II, VII, IX, X, and protein C and S

Answer 486

**Ketamine and Nitrous Oxide ** Propofol, barbiturates, and dexmedetomidine are associated with a reduction in cerebral blood flow (CBF) and cerebral metabolic consumption of oxygen (CMRO2). Ketamine and nitrous oxide increase both CBF and CMRO2. Volatile anesthetics uncouple CBF and CMRO2 (cerebral flow-metabolism uncoupling), causing a reduction in CMRO2 with a simultaneous dose-dependent increase in CBF with high concentrations (> 1 minimum alveolar concentration). Benzodiazepines may decrease CMRO2 without a significant effect on CBF. Opiates do not typically change CBF or CMRO2.

Answer 487

The superior laryngeal nerve is the most commonly injured nerve during thyroid and parathyroid surgery. The superior laryngeal nerve provides innervation to the cricothyroid muscle. This muscle is the only tensor of the vocal cords and is associated with a voice that tires more easily. The symptoms are often subtle when the superior laryngeal nerve is injured, so the diagnosis may be missed. The voice may become slightly weak, hoarse, or change in pitch. The most prevalent symptom is that the patient's voice often tires easily. The superior laryngeal nerve is more likely to be injured when the superior thyroid or parathyroid is operated on.

Answer 488

Voltage-gated sodium channel blockers Local anesthetics target the *intracellular domain* of voltage-gated sodium channels *along the axons* preventing action potential propogation with the effects of analgesia and anesthesia.

Answer 489

Concentration (higher is faster) Lipid solubility (higher is faster) pKA (lower is faster) Enviromental pH (higher is faster) NOTE: Local anesthetics are weak bases that bind to the *intracellular* portion of voltage gated sodium channels and prevent nerve conduction. Although the active form of local anesthetics is the ionized form [charged cation (BH+)] the speed of onset of efffect is determined by the portion of local anesthetic in the unionized form [basic, uncharged (B)]. Essentially, anything that increases the cocentration or proportion of local anesthetic in its **unionized** form will speed the onset of analgesia. pKA of a drug refers to the pH at which the drugs exists in equal parts of ionized and unionized forms. Local anesthetics with a lower pKa will have a greater unionized fraction (and faster onset) at physiological pH (7.4). The more lipid soluble the more quickly the molecule can pass through the lipid membrane and reach its site of action.

Answer 490

Most regional anesthesia blocks are performed by placing and injecting local anesthetic outside the EPINEURIUM.

Answer 491

What methods exist to prevent peripheral nerve injury during regional anesthesia? **1) Ultrasound** **2) Injection pressure monitoring** (>20 PSI is sensitive for intrafasicular needle tip placement = bad) **3) Electrical nerve stimulation** (motor response < 0.2mA occurs with intraneural needle tip placement = bad) 4) Low pressure injection (high pressure injection = bad) NOTE: For electical nerve stimulation, the negative node is attached to the stimulator needle and the positve node is attached to the patient (negative on the needle, positive on the patient).

Answer 492

Ropivacaine and Bupivacaine Addition of epinephrine has not been shown to prolonged duration of Ropivacaine and Bupivacaine based blocks and epidurals.

Answer 493

Epinephrine (exception of Ropi and Bupi) Dexamethasone Clonidine NOTE: Addition of bicarb speeds onset of block by causing LAs to convert to nonionized form. Bicarb does NOT, however, affect duration of action.

Answer 494

A peripheral nerve comprises three main connective tissue sheaths: - Endoneurium - Perineurium - Epineurium. The endoneurium wraps individual axons, the perineurium covers nerve fascicles, and the epineurium surrounds the entire peripheral nerve. Most regional anesthesia blocks are performed by placing and injecting local anesthetic outside the epineurium. TrueLearn Insight: There are generally two types of intraneural injections: Extrafasicular blocks: Needle placement within the epineurium but outside of the perineurium avoids puncture of the fascicle. It has been referred to as an extrafascicular block or an epineural intraneural injection. On ultrasound, it may be seen as nerve swelling and separation of the fascicles. Extrafascicular injections within the epineurium may or may not cause nerve damage. Intentional injection within the epineurium is controversial and is currently being studied. Infrafasicular blocks: Puncture of the epineurium and the perineurium places the needle within the fascicle and is called an intrafascicular block or subepineural intraneural injection. It is well accepted that intrafascicular injection can lead to permanent nerve damage and should be avoided.

Answer 495

The RAAS is involved in the maintenance of blood pressure and water-electrolyte homeostasis. The first enzyme involved in the system is the proteolytic enzyme renin, which is released by the juxtaglomerular apparatus of the renal cortex in response to: 1. Decreased renal perfusion pressure (glomerulus) 2. Hyponatremia (NaCl sensed my macula densa in DCT) 3. B1 stimulation Renin then cleaves angiotensinogen, synthesized in the liver, into angiotensin I (ATI) which is then converted in the lungs by angiotensin-converting enzyme (ACE) to angiotensin II (ATII). Angiotensin II causes: 1) Renal efferent arteriolar vasoconstriction 2) Release of aldosterone by the adrenal cortex 3) ADH release from the posterior pituitary 4) Sodium reabsorption by the proximal tubule. Aldosterone, in turn, further stimulates sodium and water reabsorption in the distal tubules and collecting ducts leading to intravascular volume expansion.

Answer 496

TrueLearn Insight: Atrial natriuretic peptide (ANP) is a peptide secreted by the atrial myocytes in response to increased stretch caused by volume expansion. Atrial natriuretic peptide blocks the reabsorption of sodium in the distal tubules and collecting ducts, leading to natriuresis. Additionally, ANP secretion causes systemic vasodilation, increases the glomerular filtration rate, inhibits the release of renin, antagonizes ATII, and decreases aldosterone secretion.

Answer 497

Severe hypernatremia is defined as serium sodium 120 < mEq/L and is an indication for hypertonic 3% saline. NOTE: Goal to increase serum sodium levels 1-2 mEq/L per hour. Should not exceed 12mEq/L over 24hrs as risk of pontine demyelination.

Answer 498

TV: 4-6 mL/kg predicted body weight Plateau pressure: < 30cm H20 Low tidal volumes are believed to decrease alveolar overdistension caused by mechanical ventilation, which can worsen lung injury and increase mortality. Although PEEP is used to maximize and maintain alveolar recruitment, there is no optimal setting for PEEP; however, a minimum of 5 cm H2O is recommended Note that similar TV and plateau pressures (lung protective ventilation) use for one lung ventilation.

Answer 499

Acute respiratory distress syndrome (ARDS) is an acute, hypoxemic respiratory failure that is often due to direct injury to the lung injury (aspiration, pneumonia, or chemical) or systemic inflammation caused by extrapulmonary infection or trauma. Acute respiratory distress syndrome leads to increased lung permeability and diffuse alveolar edema and is characterized by noncardiogenic pulmonary edema, severe hypoxemia, and heterogeneous consolidation. According to the 2012 Berlin definition for ARDS, the following must be present to formulate a diagnosis: 1) The onset of respiratory symptoms within one week of clinical insult 2) Respiratory failure cannot be explained by cardiac failure or fluid overload 3) Presence of bilateral opacities on chest radiograph or computed tomography that is not explained by another mechanism 4) Impairment of oxygenation must be present as defined by the PaO2/FiO2 ratio, with the severity of hypoxemia defined as follows (ventilator settings must have positive end-expiratory pressure (PEEP) or continuous positive airway pressure ≥5 mm Hg): Mild: 200-300mm Hg Moderate: 100-200 mm Hg Severe: ≤100 mm Hg

Answer 500

Assist-control ventilation (AC) is the most commonly used ventilation mode in most intensive care units. Tidal volume and a minimum respiratory rate are set. It is time or pressure initiated, volume limited, and time or volume cycled. If a patient is not spontaneously breathing, AC is essentially identical to VCV. If a patient does take spontaneous breaths, the ventilator synchronizes with each spontaneous inspiration and delivers a positive pressure breath of the set tidal volume. Spontaneous breathing independent of the ventilator is not allowed. Use of AC decreases work of breathing in spontaneously ventilating patients and allows the patient to essentially set his/her own minute ventilation above the programmed minimum. Use of AC in patients with high respiratory rates may lead to breath stacking (initiation of a breath before exhalation is fully complete) resulting in increasing auto-PEEP and baro- or volutrauma. The attached figure illustrates AC with two synchronized breaths and one ventilator-driven breath.

Answer 501

Synchronized intermittent mandatory ventilation is often used in the operating room to transition a patient from controlled to spontaneous breathing. Tidal volume and a minimum respiratory rate for the mandatory breaths are set, yielding the minimum minute ventilation. It is time or pressure initiated, volume limited, and cycled by time or volume. The SIMV mode attempts to synchronize the mandatory breaths with a patient’s spontaneous inspiratory effort. Accordingly, the interval between mandatory breaths may be irregular. If a patient does not initiate enough spontaneous breaths to meet the minimum set respiratory rate, SIMV then closely resembles VCV. If the patient breathes above the mandatory (minimum) rate, the breaths do not receive any ventilator support. Use of SIMV improves patient tolerance of mechanical ventilation, decreases ventilator dyssynchrony, and ensures a minimum minute ventilation. It is preferred over AC in patients with a high respiratory rate as it reduces the risk for hyperinflation, auto-PEEP, and volutrauma. A major disadvantage is increased work of breathing during non-mandatory breaths (due to breathing through the high-resistance circuit). Accordingly, it should be avoided in patients with respiratory muscle weakness.

Answer 502

In PCV, the airway pressure for the breath is set, and the breath size or volume is variable. This means that the volume of each breath changes depending on **chest wall compliance, lung compliance, and airway resistance.** NOTE: VCV delivers a breath at a set frequency under a constant flow rate until the set volume of air is delivered. In VCV, airway pressure is a dependent variable of the breath. The volume of the breath being delivered *will not change based on intrinsic factors of the lungs. *

Answer 503

"A PALM Seed Makes Another Little Palm' The right main bronchus should give rise to a very close right take-off, which is the right upper lobe that will have three take-offs, which are the anterior, posterior, and superior lung segments of the right upper lobe. The left main bronchus has two take-offs, which are the upper and lower lobes of the left lung. The distance between the left upper lobe bronchus and the carina is roughly double the length as the distance between the right upper lobe and carina. Therefore, it is less likely that a provider will accidentally obstruct the left upper lobe with the bronchial cuff of a left-sided tube than a provider will inadvertently obstruct the right upper lobe with the bronchial cuff of a right-sided tube.

Answer 504

ASIA ALPS *Apico-posterior Superior lingua Inferior lingula Anterior *Antero-medial Lateral Posterior Superior

Answer 505

Bronchial blockers are indicated for the following exceptions: * Anticipated difficult airway, especially if awake fiberoptic bronchoscopy is anticipated * Requirement for nasal intubation (a DLT cannot be advanced through the nares) * Presence of tracheostomy (a DLT cannot be placed through the stoma) * Distortion of tracheobronchial anatomy (eg, by vascularity, tumor) * Requirement for selective lobar blockade * Bronchial blockers be preferred for patients who require prolonged intubation because their use avoids the requirement for an endotracheal tube exchange

Answer 506

Bronchial blockers have high pressure, low volume cuffs (potential for mucuosal damage) Single and double lumen tubes have low pressure, high volume cuffs

Answer 507

Stainless steel ETT (metal Norton ETT)

Answer 508

Armored reinforced ETT NOTE: Not compressible but flammable and should not be used in laser procedures.

Answer 509

Dislodgement of bronchial blocker into tracheal.

Answer 510

Endotracheal tubes, depending on size, add 5-10 cm H20 of airway resistance.

Answer 511

Phenylephrine (Afrin) Oxymetazoline Cocaine (avoid in CAD) NOTE: Minimizes mucosal bleeding AND increases diameter of nasal passages by shrinking of the nasal mucosa.

Answer 512

Basilar skull fracture Midface instability Coagulopathy Relative includes nasal foreign body, nasal polyps, recurrent epistaxis, recent nasal surgery.

Answer 513

POI: Autosomal Dominant Pathophysiology: Point mutation in Factor V, prevents activated protein C from inactivating Factor V, results in increased thrombin (II) and thus hypercoaguable state. Presentation: VTE (DVT, PE, cerebral, mesenteric, portal). Arterial thrombus is rare. Treatment: Wafarin (INR goal 2-3) or Xa inhibitor Several situations exist where long-term therapy should be given to prevent recurrences. In patients with factor V Leiden, the situations where lifelong therapy is recommended are: - Two or more spontaneous thromboses - One spontaneous thrombosis if the patient has factor V Leiden plus another prothrombotic mutation - One spontaneous life-threatening thrombosis (e.g. near-fatal PE) - One spontaneous thrombosis at an unusual site (e.g. cerebral or mesenteric vein)

Answer 514

Direct Xa inhibitors "FEAR” Fondaparinux (Arixta) Edoxaban (Lixiana) Apixaban (Eliquis) Rivaroxaban (Xarelto)

Answer 515

Direct IIa (thrombin) inhibitors "DAB" Dabigatran (Pradaxa) - oral Argatroban (Acova) - IV Bivalirudin (Angiomax)- IV

Answer 516

Indirect inhibtion of factor Xa Binds to antithrombin III (ATIII) enhancing degradation of factor Xa. NOTE: Lovenox does not require monitoring, but can be monitored by anti-Xa levels (in patients with obesity or renal insufficiency). Lovenox needs to be renally dosed (relies on renal clearance for up to 40% of its elimination).

Answer 517

LMWH has a half life of 6 hrs. UFH has a half life of 2 hrs.

Answer 518

Indirect inhibtion of factor Xa and IIa (thrombin) Binds to antithrombin III (ATIII) enhancing degradation of factor Xa and IIa. NOTE: UFH is monitored with PTT, ACT, or anti-Xa levels. UFH does not need to be renally dosed. Used for emergent anticoagulation in ACS, PE, cardiopulmonary bypass, vascular surgery. Reverse w/ Protamine. Common complication is thrombocytopenia.

Answer 519

Direct oral anticoagulants (DOACs) are oral medications that specifically inhibit factors Xa or IIa. They are also known as new oral anticoagulants (NOACs) and include: F**EAR D**ABs Edoxaban, Rivaroxaban, Apixaban are Xa inhibitors Dabigatran is a IIa inhibitor (direct thrombin inhibitor)

Answer 520

Ester local anesthetics are metabolized by plasmacholinesterase. Amide local anesthetics are metabolized by hepatic metabolism. NOTE: If it contains only 1 letter “i” then it is an ester. If it contains 2 of the letter “i” then it is an amide. ESTER local anesthetics undergo metabolism by pseudocholinESTERase. Ester local anesthetics are more commonly implicated in hypersensitivity reactions compared to amide local anesthetics. This is because ester local anesthetics are metabolized to para-aminobenzoic acid (PABA) which is found in many other substances and is a known allergen. Despite this, Ig-E mediated type I hypersensitivity reactions (anaphylaxis) is extremely rare.

Answer 521

Bupivacaine Some of the features of Bupivacaine thought to account for Bupivicaine's cardiotoxicity include tighter binding from cardiac sodium channels, slower dissociation from cardiac sodium channels, and *direct* myocardial depression. Increased serum levels of local anesthetics decrease cardiac contractility, delay depolarization/conduction, and delay repolarization.

Answer 522

Bupivicaine Local anesthetics with higher degree of protein binding will have a longer duration of action. Bupivicaine is the local anesthetic with the highest degree of protein binding (95%) and elimination half life (210 min).

Answer 523

Benzocaine Prilocaine

Answer 524

20% Intravenous Lipid Emulsion (ILE) Initial bolus 1.5cc/kg (over several minutes) Followed by an infusion at 0.25cc/kg/min (over 30-60 min or until hemodynamic stability is achieved) The hypothesis for ILE's efficacy in treating cardiotoxicity is the formation of an intravascular lipid phase that absorbs the lipophillic drug. This redues the amount of free drug available to bind to the myocardium and exert negative effects. LAST manifests as CNS excitation to CNS depression followed by CV excitation to CV depression: CNS Agitation, auditory change, metallic taste Seizures, CNS depression CV Dysrhythmias Bradycardia, AV block, asystole, diminished contractility

Answer 525

20% Intravenous Lipid Emulsion (ILE) Initial bolus 1.5cc/kg (over several minutes) Followed by an infusion at 0.25cc/kg/min (over 30-60 min or until hemodynamic stability is achieved)

Answer 526

Max dose of local anesthetics Bupi- 2.5mg/kg Ropi- 3mg/kg Lido- 4.5mg/kg Lido w/ epi- 7mg/kg

Answer 527

Max dose of local anesthetics Bupi- 2.5mg/kg Ropi- 3mg/kg Lido- 4.5mg/kg Lido w/ epi- 7mg/kg

Answer 528

Lip & tongue numbness NOTE: Local anesthetic toxicity tends to present in a very specific pattern of CNS findings. Numbness around the lips and tongue are the first signs/symptoms. VIsual and auditory disturbances (tinnus) then follow. Followed by dizziness, muscular twitching, unconciousness, and seizure activity. Then cerebral edema, increased ICP, coma, respiratory arrest, and ultimately cardiovascular depress and death.

Answer 529

Lidocaine TNS is defined as paradoxical back pain with radiation down extremities (w/o any other neurological features). Occurs 2-24 hours after the resolution of spinal anesthesia. Incidence 4-40%. Risk factors are use of lidocaine based spinal, lithotomy position, ambulatory anesthesia. Treatment with NSAIDs.

Answer 530

Synthetic colloids: Hydroxyethyl starch (>20mL/kg/day) Dextran

Answer 531

1 Intravascular : 3 interstitial

Answer 532

Crystalloids- 20-30min Colloids- 3-6hrs

Answer 533

Coagulopathy Renal injury Anaphylactic/anaphylactoid reactions Mortality

Answer 534

Dextrans have an antithrombotic effect and can increase blood loss by : 1) Decreasing factor VIII levels 2) Decreasing vWF levels 3) Inhibits platelet aggregation Also, RBC coating by dextrans has the potential to interfere with blood type cross-matching.

Answer 535

1) Diminished alveolar membrane surface area (pulmonary fibrosis, emphysematous tissue destruction, small lungs, hx of lung resection) 2) Increased thickness of the alveolar membrane (chronic pulmonary hypertension d/t remodeling, chronic inflammatory states) 3) Small pressure gradient between the alveolar gas partial pressure and the capillary gas tension

Answer 536

Most pulmonary pathology results in a decreased DLCO, but there are also causes of an increased DLCO. The DLCO is increased in patients with * Asthma * Obesity * High altitudes * Factors that increase the amount of blood exposed to the ventilated air (eg. polycythemia, left to right shunt, heart failure)

Answer 537

Hyponatremia (poor intake, vomiting, diarrhea, impairs free water excretion) Hypokalemia (poor intake, vomiting, diarrhea) Hypomagnesemia (poor intake, diarrhea) Respiratory alkalosis (sympathetic activation during withdrawal leads to hyperventilation, lactic acidosis leads to compenstory hyperventilation) Hyperuricemia (beer contains purines which are metabolized to uric acid. Ethanol also increases adenine degradation which produces xanthine and hypoxanthine which are subsequently metabolized to uric acid. Ethanol metabolism raises lactate levels which in turn inhibits the renal excretion of uric acid.)

Answer 538

Leukoreduction refers to the process of removing *leukocytes* from blood components PRIOR to transfusion. This process can involve several different methods including buffy coat removal, freezing and declycerolizing, microaggregate and leukocyte reduction filters, and saline washing. BENEFITS: - Decreases incidence of febrile non-hemolytic transfusion reaction - Prevents HLA alloimmunization - Reduce the risk for transmitting CMV, EBV, Human T-lymphotropic virus Leukoreduction has NOT been found to reduce the risk of bacterial infection, death, TRALI, hemolytic transfusion reaction, or transfusion-associated graft-versus-host disease.

Answer 539

Leukoreduction prevents: HLA Alloimmunization Febrile non-hemolytic transfusion reactions Transfusion-transmitted CMV infections

Answer 540

ABO Typing (mixing recipient **RBCs** with anti-A, anti- B, anti-AB antibodies) Rh Typing (mixing recipient **RBCS** with anti-D antibodies) Antibody Screen (mixing recipient **serum** with known surface antigens on commercially supplied type O RBCs)

Answer 541

Mixes the recipients serum with donor RBCs to examine for any incompatibilities that were not screened out, as well as setting aside the desired number of blood products for potential transfusion.

Answer 542

Fetal hemoglobin shifts the oxygen hemoglobin dissociation curve to the LEFT.

Answer 543

NOTE: 2,3-diphosphoglycerate (2,3-DPG) is an intermediate step in the glycolytic pathway and this product of cellular metabolism is a factor in the shifting of the oxyhemoglobin dissociation curve. Given that it is indicative of cellular metabolism occurring, increases in its production shifts the curve to the right, favoring oxygen unloading at the level of the tissues. Conditions where 2,3-DPG is decreased, such as in the storage of red blood cells or in the formation of glucose and glycogen, cause the curve to shift to the left. Despite preservatives, such as citrate-phosphate-dextrose solution with adenine (CPDA), being used for red blood cell preservation, metabolic changes continue to occur. Hypophosphatemia also causes a left shift. Hypophosphatemia commonly occurs secondary to sepsis, malnutrition, refeeding syndrome, acute liver injury, and DKA. Inorganic phosphate is a susbtrate for 2,3 DPG production and if hypophosphatemia is not corrected, the decrease in 2,3 DPG results in an increased affinity of oxygen for hemoglobin. "CADET face right!" is a mnemonic that can help you remember some causes of rightward shift of the oxyhemoglobin dissociation: Carbon dioxide, Acidosis, 2,3-Diphosphoglyceric acid, Exercise, and Temperature. Cadets like to unload (fire) their guns, and a rightward shift increases oxygen unloading.

Answer 544

The term P50 is designated as the partial pressure of oxygen (in mm Hg) when oxygen saturation (SaO2) is 50%. P50 can be used to relate the oxygen affinity for hemoglobin. When the oxyhemoglobin dissociation curve shifts to the left or to the right, P50 will decrease or increase respectively. In newborns, oxygen affinity is very high and P50 is very low (approximately 18 mm Hg). This is due to hemoglobin F, which is produced in-utero, and is useful for oxygen transfer from the maternal blood to the fetus. The presence of hemoglobin F and low 2,3-diphosphoglycerate (2,3-DPG) levels in newborns result in a very low P50. In fact, P50 is lowest in newborns. After birth, levels of hemoglobin F begin to decline resulting in a decrease in the total hemoglobin concentration. This results in a physiological anemia of infancy. During this same period of time, 2,3-DPG levels begin to increase causing the oxyhemoglobin dissociation curve to shift to the right (P50 increases). The P50 will surpass that of an adult (27 mm Hg) and will reach a maximum of 30 mm Hg by about 12 months of age. Children will continue to have a higher P50 for the first decade of life. In a normal adult, P50 is 27 mm Hg.

Answer 545

X-linked recessive Common among African Americans, Asians, Middle-Easterns. Triggers cause hemolysis (Sulfa, Cipro, NItrates) Drug triggers are due to the fact that inadequate levels of G6PD enzyme needed to break them down which results in reactive oxygen species that damage RBCs. NOTE: Other triggers includee hypoxia, hypothermia, and stress.

Answer 546

At sea level (barometric pressure 760 mm Hg), oxygen has a partial pressure (PO2) of approximately 150-160 mm Hg (21% of 760, with the variation due to water vapor pressure). As altitude increases, the concentration of oxygen in air stays the same, but the PO2 decreases since barometric pressure decreases (Dalton law of partial pressures). At an altitude of 5,300 ft (Denver, Colorado or a typical cabin altitude in a commercial airliner), barometric pressure is approximately 630 mm Hg with a PO2 of 120-130 mm Hg (21% of 630, with variation again due to water vapor pressure). More dramatically, barometric pressure at the top of Denali (20,300 ft) in Alaska is 345 mm Hg leading to a PO2 of ~70 mm Hg. The human body is able to adapt to altitude-related decreases in PO2 through a variety of acute and chronic physiologic changes. Initially, peripheral chemoreceptors sense a relative hypoxemia and trigger hyperventilation to increase minute ventilation. Although this improves oxygen uptake, it also causes a respiratory alkalosis (from decreased PaCO2 and CSF alkalization) which would ordinarily decrease respiratory rate and minute ventilation. In order to permit continued hyperventilation, bicarbonate loss in the CSF occurs over the next 48-96 hours. This normalizes CSF pH which causes central chemoreceptors to become less sensitive to a drop in PaCO2, more sensitive to increases in PaCO2, and allows hyperventilation to continue. The kidneys increase bicarbonate excretion (decreased bicarbonate reabsorption) over the following week in order to restore normal blood pH (compensatory metabolic acidosis). Oxygen delivery to tissues is enhanced by several mechanisms. The immediate response to acute altitude-related hypoxemia is an increase in cardiac output, primarily via increased heart rate. Over the next 12-48 hours, the oxygen-hemoglobin dissociation curve shifts to the right to promote oxygen unloading to tissue. This shift is caused by an increase in 2,3-DPG in response to respiratory alkalosis. However, further decreases in PaO2 and PaCO2 will eventually lead to a leftward shift of the oxygen-hemoglobin dissociation curve to enhance oxygen loading in the pulmonary system, which is ultimately more beneficial. After 2-4 days at altitude, cardiac output returns to baseline. Over the following 1-3 weeks, continued (relative) renal hypoxia will trigger the increased renal secretion of erythropoietin. This begins to increase hemoglobin concentration and improves the oxygen-carrying capacity of blood and oxygen delivery to tissues. OTHER: When moving from sea level to a location higher in elevation, a person is exposed to lower partial pressures of oxygen leading to arterial hypoxemia. This decrease in the arterial partial pressure of oxygen (PaO2) is detected by the carotid and aortic bodies activating the peripheral hypoxemia ventilatory drive and increasing minute ventilation. As a result, the arterial and cerebrospinal fluid (CSF) partial pressure of carbon dioxide decreases, and the arterial and CSF pH increases. As the CSF pH becomes alkaline, the ventilatory drive is decreased via the medullary chemoreceptors, balancing out the initial hypoxic respiratory drive. The initial cardiovascular response resulting from hypoxia is an increase in sympathetic activation due to stimulation of the peripheral chemoreceptors. Heart rate and cardiac output thus increase. There is initial vasodilation that predominates for a few hours, but, due to the increase in sympathetic activation, blood pressure begins to increase slowly for several weeks. Even after several days, the cardiac output returns to normal but a new equilibrium is established with a higher heart rate and a lower stroke volume. Hemoglobin increases over the first few days, mainly due to volume contraction from the renal diuretic response. Hemoglobin production is ultimately increased due to an increase in levels of erythropoietin.

Answer 547

Methemoglobinemia and carboxyhemoglobin shifts the oxygen hemoglobin dissociation curve to the LEFT.

Answer 548

Hydroxocobalamin (B12) is first-line therapy for patients with cyanide toxicity. Cyanide is a rapidly acting poison that can be produced by the combustion of synthetic materials. Cyanide toxicity is frequently seen in patients who have had smoke inhalation from residential or industrial fires. Smoke inhalation during a residential or industrial fire remains the leading cause of cyanide toxicity in the United States. Many providers now treat potential cyanide poisoning in all patients who are being treated for carbon monoxide poisoning due to smoke exposure. Cyanide causes its deleterious effects by inactivating cytochrome oxidase, which in turn causes an uncoupling of mitochondrial oxidative phosphorylation and an inhibition of cellular respiration. With aerobic respiration inhibited, cellular metabolism switches from aerobic to anaerobic and causes the production of lactic acid; this results in metabolic acidosis. Patients with cyanide toxicity can present with a myriad of symptoms, which include generalized weakness, neurological symptoms, cardiopulmonary symptoms, and gastrointestinal symptoms. Cyanide toxicity should be on the differential for any patient who presents with a history of smoke exposure or burns secondary to residential or industrial fire. In rare instances, patients with prolonged intravenous (IV) exposure to sodium nitroprusside can exhibit cyanide toxicity. An arterial blood gas analysis in a patient with cyanide toxicity may show normal oxygenation with metabolic acidosis; although depending on the time from exposure, the metabolic acidosis could be masked by respiratory compensation. A venous blood gas may reveal a high oxygen content, which may mirror that of the arterial blood gas because oxygen is not being utilized for cellular respiration. In the inpatient setting, treatment of cyanide toxicity calls for multiple practices: airway control, administration of supportive oxygen, use of vasopressors or fluids for blood pressure control, correction of acidosis, and administration of a cyanide antidote. In 2006, the United States Food & Drug Administration (FDA) approved the use of hydroxocobalamin for use in the treatment of acute cyanide toxicity. Prior to this, the standard of care was the administration of either sodium or amyl nitrite. These substances combined with hemoglobin to produce methemoglobin which has a strong affinity for cyanide. Sodium thiosulfate was administered secondarily to remove the cyanide from the methemoglobin. This process caused the production of thiocyanate which was then excreted in the urine. Though previously a common treatment of cyanide toxicity, this approach had several problems: nitrites can precipitate hypotension and methemoglobinemia, with the latter being toxic. These side effects have made treatment with nitrites fall out of favor with the availability of hydroxocobalamin. Hydroxocobalamin works by combining with cyanide to form cyanocobalamin (vitamin B-12). Cyanocobalamin is cleared via the kidneys. The use of hydroxocobalamin became first-line due to its low adverse risk profile, rapid onset of action, and ease of use in the prehospital setting; all of which help decrease the rate of morbidity and mortality associated with cyanide toxicity.

Answer 549

A standard pulse oximeter generally give measurements approaching **_%** in patients with methemoglobinemia. Methemoglobinemia is an altered state of hemoglobin where the ferrous (Fe2+) form of heme is oxidized to the ferric form (Fe3+). MetHgb is unable to bind new O2, and the oxygen dissociation curve is shifted to the left. The left shift of the oxygen dissociation curve prevents the release of O2 into tissues. Generally, PaO2 levels will remain normal. Methemoglobin absorbs light in both the 660 nm and 930 nm range equally, which corresponds to an SpO2 value of 85%. Normal MetHgb levels are < 1%; thus, this does not often pose a clinical problem unless MetHgb is significantly elevated. Methylene blue (1-2 mg/kg) is the primary pharmacologic treatment for methemoglobinemia. Methylene blue can cause hemolysis in patients with G6PD-deficiency, however. Therefore, ascorbic acid (vitamin C) is the treatment of choice for methemoglobinemia in the setting of G6PD-deficiency. Common acquired causes of methemoglobinemia include prilocaine, benzocaine, metoclopramide, nitrites (including nitric oxide and nitroglycerin), aniline dyes, benzene, chloroquine, dapsone, and sulfonamides.

Answer 550

The oxygen saturation read by a standard two-wave pulse oximeter depends on the differential absorption of **red light** and **infrared light** in tissue. Red light (660nm) Infrared light (940nm) A ratio of the absorbance of red to infrared light is calculated and that calculated number is translated to the oxygen saturation reading. At red wavelengths, DEOXYhemoglobin aborbs MORE light than oxyhemoglobin. At infrared wavelengths, OXYghemoglobin aborbs MORE light than deoxyhemoglobin. NOTE: Dyes (indocyanine green or ICG, indigo carmine, methylene blue), nail polish, ambient light, motion artifacts, vasoconstriction, hypothermia, methemoglobinemia (stuck at 85%), and carboxyhemoglobinemia (falsely elevated) will lead to inaccurate pulse ox readings. Nail polish (esp blue, breen, and black) cause falsely low oxygen saturations by interfering with the differential absorption of 660-940nm light.

Answer 551

What are the three factors associated with relapse in physicians who are treated for substance abuse? Remaining in anesthesiology (#1) Use of opioids as the drug of abuse Personal history of psychiatric illness Family history of substance abuse disorder NOTE: Opioid is the most commonly abused substance amongst anesthesiologists. Prevalence of chemical dependency among physicians is similar to that of the general population (10-13%) The rate of relapse among physicians including anesthesiologists is actually lower than the general populaiton. Review signs/symptoms of SUD among physicians (see picture)

Answer 552

Male (4x incidence than female) Personal history of drug abuse Personal history of psychiatric illness Family history of drug abuse Went to medical school in US NOTE: Early poor performance on in-training exams is NOT associated with increased risk of developing SUD. If you suspect a physician may be impaired you should consult your state physicians health program. Do not confront yourself because it can put provider at risk of suicide.

Answer 553

Storage of packed red blood cells for several weeks results in an decrease in pH (increase H+). Although red blood cell (RBC) metabolism is slowed with refrigeration, packed red blood cells (PRBC) continue to be metabolically active by metabolizing glucose via glycolysis. The pyruvate is then converted via anaerobic metabolism into lactic acid. As lactic acid accumulates, the concentration of hydrogen ions increases, lowering the pH. With the advent of anticoagulant-preservative solutions, PRBCs can now be stored for up to 42 days. Most solutions contain a mixture in different concentrations of the following: citrate, phosphate, dextrose, and adenine. Citrate is used to chelate calcium in the solution, preventing coagulation from occurring; phosphate acts as a buffer to maintain the pH of the storage solution; dextrose (1-2 g) is used to maintain a source of energy because RBCs can undergo only anaerobic glycolysis; adenine maintains a pool of adenosine triphosphate (ATP), preventing the membrane from disintegrating by neutralizing oxidants and keeping the Na+/K+-ATPase pump functioning properly. By day 42, the pH decreases to ~6.5.

Answer 554

Hyperkalemia During storage, anaerobic metabolism converts glucose to lactate resulting in acidosis. Potassium moves out of PRBCs in order to maintain electrochemical gradiant with hydrogen ions that are generated from anaerobic metabolism. After 3 weeks of storage, potassium levels may reach 20-35 mEq/L thought there is usually only 20-30mL of plasma in one unit of PRBCs. By day 42, RBC hemolysis and leakage further contributes to increased potassium. After 4-5 weeks, transfusion of one unit of PRBCs can add 5-7mEq of potassium. Massive transfusions particularly in neonates can lead to hyperkalemia.

Answer 555

Hyponatremia (lack of aldosterone) Hyperkalemia (lack of aldosterone) Hypoglycemia (lack of cortisol) Hyperchloremic metabolic acidosis (HARDASS) Hypercalcemia (decreased GFR, calcium release from bones) Addison disease is diagnosed by noting low blood and urine cortisol levels, even after administration of synthetic ACTH. Patients with primary adrenal insufficiency should have minimal or no response to ACTH, whereas patients with primary hypothalamus or pituitary disorders will have increased cortisol levels in response to ACTH. Skin hyperpigmentation is a classic finding secondary to increased ACTH stimulation with co-released MSH. TrueLearn Insight: Patients with Addison disease on chronic steroids can present in Addisonian crisis if they have abrupt discontinuation of their steroids or in times of stress (e.g. surgery) if not treated with stress dose steroids. The same lab abnormalities as above can be seen, just more pronounced, and patients can also have severe abdominal cramping, nausea, vomiting, hypotension, and even cardiovascular collapse.

Answer 556

11-B Hydroxylase Decreased synthesis of cortisol AND aldosterone.

Answer 557

Dopamine Norepinephrine Epinephrine Tyrosine -> DOPA -> Dopamine -> Norepinephrine -> Epinephrine

Answer 558

Fixed split S2: Atrial septal defect Pulmonary hypertension Right heart failure Split S2 can be heard during inspiration because the decreased intrathoracic pressure will increases VR causing the RV to stay longer in systole and the pulmonic valve to close slightly behind the aortic valve. https://www.youtube.com/watch?v=98HM1fr3cq4

Answer 559

A wide splitting S2 can be heard in patients with a RBBB.

Answer 560

A paradoxical splitting S2 can be heard in patients with a LBBB.

Answer 561

An S3 is associated with CHF and ventricular dilation ("sloshing in", "Kentukcy") An S4 is associated with left ventricular hypertrophy (" a thick heart", "Tennessee") S1 is associated with the closure of the mitral and tricuspid valves and S2 is associated with the closure of the aortic and pulmonary valves. S3 is associated with early ventricular filling and S4 is associated with atrial contraction. S3 and S4 are usually pathologic heart sounds in adults.

Answer 562

1) Posterior fossa craniotomies 2) Sitting position 3) Upper cervical spine The highest venous air embolism (VAE) incidence occurs during neurosurgical procedures. Posterior fossa craniotomies with the patient in the sitting position pose the highest risk for VAE. Venous air embolism can occur during any operative procedure in which the operative site is above the level of the heart and a noncollapsible vein is opened such that a pressure gradient favors air entrainment rather than bleeding. Rarely, a massive VAE may create an “air lock” into the right ventricle, resulting in right ventricular outflow obstruction and cardiovascular collapse. Venous air embolism most commonly occurs when the operative site is above the level of the heart but may also occur when noncollapsible veins are opened in an operative field into which gas has been insufflated under pressure. Additional risk factors for VAE include insufflation during laparoscopic and hysteroscopic procedures, upper cervical spine procedures, supratentorial procedures, excessive ventilation, cardiopulmonary bypass surgeries, central venous catheter insertion/removal, hemodialysis, and penetrating chest injuries.

Answer 563

1) Transesophageal echo (TEE) - most sensitive 2) Precordial doppler 3) ETCO2 4) PA pressures 5) CVP 6) EKG

Answer 564

As little as 100 cc of air entrained into the circulation can cause an airlock in the right ventricle disrupting forward flow and can have devastating consequences for the patient including stroke, MI, cardiac arrest, and/or death. NOTE: Cardiovascular collapse typically occurs with 300cc of entrained air. The fatal dose is around 300-500 cc of air (or 3-5cc/kg). As an example, a 14 guage IV catheter with a 5cm H20 pressure gradient between the atmosphere and the IV space would entrain 100cc of air per second.

Answer 565

Intramedullary nailing of the femur

Answer 566

Phenoxybenzamine (long-acting non-selective α-blocker) A pheochromocytoma is a catecholamine-secreting tumor arising from the adrenal medulla. The tumors generally secrete norepinephrine, epinephrine, and dopamine. The classic triad of a pheochromocytoma is episodic headache, sweating, and tachycardia. They also generally have hypertension, either episodic or persistent. Other characteristics of patients with a pheochromocytoma are tremors, pallor, familial syndrome that predisposes them (e.g. MEN2), adrenal mass, hypertension at a young age and/or resistant hypertension, and an exaggerated catecholamine response to anesthesia or surgery. The diagnosis of pheochromocytoma is typically confirmed by urine total catecholamines, vanillylmandelic acid, and metanephrines. Serum free metanephrine levels may be assessed as well. Metanephrines are the products of catecholamine metabolism within the pheochromocytoma. The measurement of 24-hour urinary excretion of metanephrines is the preferred diagnostic tool, as plasma metanephrine measurement has a lower specificity for pheochromocytoma. The clonidine suppression test is another method to distinguish a pure pheochromocytoma from a false-positive increase in plasma metanephrines. Clonidine is an alpha-2 receptor agonist which suppresses the release of catecholamines from normal neurons, but not from a pheochromocytoma. Therefore measurement of plasma catecholamines and metanephrines before and after a dose of clonidine is given to a patient can prove or disprove the diagnosis. In patients with primary hypertension, the levels of plasma catecholamines and metanephrines decrease, however with a pheochromocytoma they remain elevated. General laboratory features of pheochromocytoma include hyperglycemia, hypercalcemia, and erythrocytosis. Chromogranin A is elevated in case of pheochromocytoma, but is also used as an indicator for carcinoid syndrome. It is associated with paroxysmal episodes of hypertension, which if left untreated can lead to cerebrovascular hemorrhage, arrhythmias, heart failure, and myocardial infarction. These perioperative risks are significantly decreased in patients who are treated with α-blockers prior to surgery. Preoperatively, patients are commonly treated with phenoxybenzamine, which is a long-acting non-selective α-blocker. Selective α1-blockers, such as doxazosin, terazosin, and prazosin, are also commonly used. Beta-blockers without alpha antagonistic properties, like metoprolol, allow for unopposed vascular constriction from excessive catecholamines produced by the pheochromocytoma.

Answer 567

Any RCRI score **> 1 **is considered high-risk for 30-day mortality due to myocardial infarction after noncardiac surgery. Evaluating the patient's functional status by using metabolic equivalents (MET) is also an important part of the preoperative cardiac evaluation. An individual is considered at risk if they cannot achieve a functional level of **4 METs**, at which point the ACC/AHA guidelines recommend additional cardiac evaluation with a stress test to rule out any possible cardiac ischemia.

Answer 568

Risk classifications of types of surgeries High-risk: Intrathoracic, intraperitoneal, supra-inguinal vascular procedure, aortic and major vascular surgery Moderate-risk: Head and neck, carotid endarterectomy, orthopedic, urological or gynecological, endovascular aneurysm repair Low-risk: Superficial, outpatient, breast, endoscopic, eye, endocrine (thyroid)

Answer 569

UIndications for ordering a preoperative ECG include: * Symptomatic (chest pain, palpitations, syncope, DOE, orthopnea, peripheral edema) * Murmur on exam * CAD * HF * HTN * CVA Ordering an echocardiogram preoperatively should be considered for patients with a history of heart failure with no prior echocardiogram in the past year, heart failure symptoms, or unknown functional capacity. A stress test is indicated if unable to tolerate >4 metabolic equivalents.

Answer 570

The New York Heart Association classification of heart failure is based on symptoms. The classification is as follows: Class I: no limitation to normal activity Class II: minor limitations, slight symptoms with normal activity Class III: significant limitation to activity, comfortable only at rest Class IV: symptoms at rest, severe limitations

Answer 571

Cromolyn sodium is a mast cell stabilizer. Cromolyn is used to treat allergic rhinitis, controller therapy for asthma, and systemic mastocytosis. Cromolyn is NOT a bronchodilator and is NOT indicated for use in bronchospasm. Cromolyn sodium is a mast cell stabilizer and inhibits mast cell degranulation as well as the release of inflammatory mediators such as histamine and leukotrienes, which otherwise cause allergic symptoms and bronchoconstriction. It is administered orally, intranasally via nebulization, and via ophthalmic route with very little of the drug absorbed systemically by any of these routes. Inhaled cromolyn can be used to reduce hyperreactivity before exposures to exercise, cold air, or antigenic challenge as well as to manage bronchial asthma and allergic rhinitis.

Answer 572

Hyperkalemia Acidosis Liver transplantation is divided into three stages: preanhepatic, anhepatic, and neohepatic. Reperfusion begins the neohepatic stage which is the most precarious stage during liver transplant as there is a large release of potassium (large release of potassium ions during the reperfusion of the donor graft liver and the elevated potassium in the cold storage solution used to preserve the donor graft) and hydrogen ions into the systemic circulation leading to acidosis and hyperkalemia. These metabolic changes can lead to arrhythmias and hemodynamic instability. During reperfusion, there is also an increase in preload and inflammatory mediators which leads to systemic hypotension, pulmonary hypertension, and right heart strain. These symptoms related to reperfusion of the graft are called Postreperfusion Syndrome when severe and occur within 5 minutes of reperfusion. Patients are also at an increased risk of developing hypothermia as the graft is minimally warmed prior to infusion to avoid worsening ischemia. Patients can be especially coagulopathic after reperfusion due to the washout of the accumulated tissue plasminogen activator (tPA) resulting in significant fibrinolysis. Sodium bicarbonate is often given to neutralize the acid load from the graft during reperfusion. Calcium chloride is administered to stabilize the myocardial membranes due to the elevated potassium levels which may be seen as peaked T-waves on electrocardiogram (ECG).

Answer 573

In 1945, the Jehovah's Witness Governing Body banned the use of blood and/or blood-related products for transfusion on the basis of their interpretation of several biblical references. As a result, practicing Jehovah's Witnesses are limited in the products they can receive. The table describes what is generally acceptable for Jehovah's Witness patients.

Answer 574

**Right-to-left shunting Hepatopulmonary syndrome (HPS) is the dysregulation of the vascular tone that controls blood flow through the pulmonary vascular bed that occurs in the setting of cirrhotic liver disease. **This regulation will result in an increase in intrapulmonary right-to-left shunting, which will result in arterial hypoxemia**. Because of the pathophysiology of this hypoxia, this hypoxia is unlikely to respond in a significant fashion to increases in the inspired fraction of oxygen (FiO2). The pathophysiology of cardiopulmonary dysfunction in the setting of hepatic cirrhosis primarily results from the cirrhosis-induced increase in circulating endogenous vasodilators. This systemic vasodilation results in cardiovascular physiology that, on the whole, resembles a large arteriovenous fistula. As the hepatic disease progresses and the amount of circulating vasodilators accumulates, advanced cirrhosis can produce arteriovenous connections throughout many organ systems in the body, including the splanchnic organs, muscle, and skin. It is these communications that are responsible for the gastroesophageal varices that are characteristic of advanced liver disease. This diffuse vasodilation results in both central hypovolemia and splanchnic hyperperfusion and clinically manifests as an attenuated response to exogenously administered vasodilating agents. Just as the rest of the body enters a state of unregulated vasodilation, so, too, does the pulmonary vasculature. The systemic increase in circulating vasodilating agents in the setting of hepatic cirrhosis results in increased right-to-left intrapulmonary shunting. **This occurs through multiple mechanisms, including direct dilation of the pulmonary vasculature, an attenuated response to hypoxic pulmonary vasoconstriction, and development of intrapulmonary arteriovenous shunts**. This increased flow through intrapulmonary shunts allows for the direct movement of mixed venous blood from the pulmonary artery into the pulmonary veins and results in decreased arterial oxygen tension as this shunt fraction increases. This increased blood flow through the lungs also results in a thickening of the walls of the alveolar capillaries. This results in a decreased diffusion of oxygen across the capillary membrane and further worsening of arterial hypoxemia. In addition to all of this, both ascites and pleural effusion are common in advanced cirrhotic liver disease and can further exacerbate the impairment of pulmonary function. The restrictive lung disease that is imparted by both of these on the lung will worsen the ventilatory capacity of the lungs and further compromise gas exchange. Treatment for hepatopulmonary syndrome is primarily focused on improving hepatic function either through medical therapy or through liver transplantation. OTHER: Hepatopulmonary syndrome is defined as intrapulmonary vascular dilatations and increased alveolar-arterial (A-a) oxygen gradient, in the setting of end-stage liver disease. Hypoxia is improved when the patient lies flat (platypnea) and is worsened when the patient stands (orthodeoxia). The intrapulmonary vascular dilations cause increased perfusion relative to ventilation. Standing further worsens this ventilation-perfusion mismatch since gravity causes increased perfusion and pooling in the less-ventilated lower lung segments. Diagnosis requires a room-air, sitting position arterial blood gas indicating an abnormal gas exchange (ie, A-a gradient > 20 mm Hg, PaO2 < 60 mm Hg) and contrast-enhanced echocardiography (CEE) confirming the presence of intrapulmonary vascular dilatations (IPVDs). The presence of IPVDs is confirmed if CEE shows agitated saline bubbles in the left atrium after at least 3-6 cardiac cycles have passed following IV administration. If saline bubbles appear in the left atrium after 1-2 cardiac cycles, the presence of intracardiac shunts (eg, PFO) cannot be ruled out. If the CEE is positive, but there are confounding factors such as cardiopulmonary disease, then a technetium-99m-labeled lung perfusion scan or pulmonary arteriography may help confirm the diagnosis. The pathophysiology of HPS is related to the creation of intrapulmonary vascular dilatations (IPVD). This is due to excessive circulating levels of pulmonary vasodilators, namely nitric oxide (NO). Excess levels of NO are present in patients with hepatic failure, and these levels further increase in the setting of HPS. The IPVDs include dilated precapillary vessels and arteriovenous (AV) connections along the pleura. The IPVDs result in hypoxia due to ventilation-perfusion mismatch, AV shunting, and reducing the transit time of the red blood cells within the alveoli.

Answer 575

What are the four components in calculating a MELD (Model for End-stage Liver Disease) score? INR Bilirubin Na Creatinine "I Crush Several Beers Daily" INR, Creatine, Sodium, Bilirubin, Dialysis If patient is on dialysis then value of 4 is assigned for creatinine

Answer 576

PT/INR Ascites Bilirubin Albumin Encephalopathy "Pour Another Beer At Eleven" NOTE: MELD score "I Crush Several Beers Daily" INR, Creatine, Sodium, Bilirubin, Dialysis (If patient is on dialysis then value of 4 is assigned for creatinine).

Answer 577

Bulbar involvement in combination with respiratory muscle weakness leads to a risk for aspiration and pulmonary complications in patients with amyotrophic lateral sclerosis. Amyotrophic lateral sclerosis (ALS) is characterized by progressive and variable loss of motor neurons within the cerebral cortex, medullary nuclei of cranial nerves, and nuclei of the ventral horn of the spinal cord. The cause of ALS is unknown and many hypotheses have been proposed, including glutamate-induced excitotoxicity and oxidative stress. The diagnosis is made by electrophysiology (electromyography [EMG] and electroneurography) and by neurologic examination, which demonstrates early spastic weakness of the upper and lower extremities, typical subcutaneous muscle fasciculation, and bulbar involvement affecting pharyngeal function, speech, and the facial muscles. No curative treatment is currently available, and patients are therefore treated symptomatically. Patients with ALS generally have a compromised pulmonary status given the natural course of the disease. Bulbar involvement in combination with respiratory muscle weakness leads to a risk for aspiration and pulmonary complications. Of note, these patients also have exaggerated responses to the respiratory depressant effects of opioids and hypnotics. Pulmonary function testing demonstrates a decrease in vital capacity and maximal voluntary ventilation. ALS is an unrelenting disease with 50% of patients dying within 30 months of the onset of symptoms. Riluzole, a glutamate release inhibitor, is the only specific drug for the treatment of ALS. Riluzole modestly improves survival by 3 to 6 months. ND-NMBA: Sensitive Succinylcholine: Sensitive

Answer 578

(see picture) Parkinson disease is a neurodegenerative disorder caused by decreased dopaminergic neurons in the substantia nigra of the midbrain, one of a group of brain structures known as the basal ganglia, which is part of a crucial circuit for coordinating purposeful movement. The disease manifests with progressive motor and nonmotor impairments. Motor symptoms include tremors, muscle rigidity, and bradykinesia. Nonmotor symptoms include cognitive decline in advanced stages of the disease. Degeneration of the substantia nigra occurs in patients with Parkinson disease. This condition results in the disruption of the nigrostriatal pathway and thus decreases the striatal dopamine levels. Unlike dopamine, levodopa can cross the blood-brain barrier (BBB). Levodopa converts to dopamine in both the CNS and periphery. To increase the bioavailability of levodopa and decrease its side effects, it is often administered in combination with peripheral decarboxylase inhibitors (such as carbidopa and benserazide). Dopamine decarboxylase inhibitors prevent the conversion of levodopa to dopamine in the periphery, allowing for more levodopa to cross the BBB. Acetylcholinesterase inhibitors are used to treat tremors (Donepizel, Galantamine, Rivastigmine). Deep brain stimulation in Parkinson disease most commonly targets the subthalamic nucleus and the internal globus pallidus.

Answer 579

Subthalamic nuclei Globus pallidus intermedius

Answer 580

Myotonic dystrophy is a group of hereditary (usually autosomal dominant) diseases resulting in persistent contracture of skeletal muscle (myotonia) following voluntary contraction or external stimulation. This occurs because, following release, calcium does not efficiently return to the sarcoplasmic reticulum and remains available for sustained muscle contraction. In addition to skeletal muscle involvement, certain types of myotonic dystrophy (including the most common, myotonia dystrophica) also affect multiple organ systems. Symptoms and associated findings include: muscle degeneration, cataracts, diabetes mellitus, thyroid dysfunction, adrenal insufficiency, gonadal atrophy, and cardiac abnormalities (e.g. conduction dysfunction, cardiomyopathy, and mitral valve prolapse). Respiratory muscle weakness can lead to a restrictive respiratory pattern and cause mild arterial hypoxemia, reduced ventilatory response to hypoxemia and hypercapnia, and ineffective coughing. Gastrointestinal muscle weakness can lead to delayed gastric emptying, intestinal hypomotility, and pharyngeal muscle weakness. Each of these can contribute to an increased risk of aspiration. Triggers of myotonic episodes should be avoided where possible. These include, but are not limited to: **shivering due to hypothermia, neostigmine, succinylcholine, and direct surgical stimulation of muscle (especially via electrocautery).** To note, neostigmine theoretically can induce myotonia although there is little clinical evidence of this effect, but its use should still be avoided when possible. Treatment of myotonia or myotonic crises includes phenytoin, quinine, and procainamide. These drugs may also be effective as perioperative prophylaxis against perioperative myotonic crises. The drugs work by decreasing sodium influx into skeletal myocytes and delaying the return of membrane excitability following an action potential. In addition, muscle contraction may also be relieved by direct infiltration of the affected muscle with local anesthetic or administering a high concentration of volatile anesthetic (but consider that the myocardial depressant effects may not be well-tolerated). It is important to note that neuromuscular blocking drugs do NOT treat myotonia since they act at the level of the neuromuscular junction, not within the myocyte where the abnormality occurs. Patients with myotonic dystrophy are particularly sensitive to the respiratory- and CNS-depressant effects of anesthetic medications; the smallest effective doses should be given. Similarly, patients with myotonic dystrophy can have an exaggerated response to muscle relaxants. If their use is necessary, small doses of short-acting nondepolarizing drugs should be used. Use of regional anesthesia is effective at reducing or avoiding the above complications, but will not prevent myotonia. NOTE: Phenytoin is useful for treating and preventing myotonic crises in patients with myotonic dystrophy. Succinylcholine administration can cause excessive fasciculations/contractures lasting several minutes which can make intubation coniditons not ideal.

Answer 581

Quadriplegia occurs due to injuries above T1 (between C1-C8) Paraplegia occurs due to injury below T1 (between T1-L5) Paraplegia occurs with injury below the first thoracic spinal levels, meaning within the spinal levels T1-L5. Acute spinal injuries of the cervical spine may result in hypotension secondary to vasodilation (neurogenic shock). Ventilatory support is required for patients with a deficit above C4 because they will lack diaphragmatic function. Patients with injury at the C6 and C7 levels may still need support secondary to loss of chest wall innervation and inability to clear secretions. Paraplegia-level cord injuries vary in presentation based on where the specific injury occurs.

Answer 582

Hepatic clearance of a drug is the amount a drug is removed per unit time and is a product of hepatic blood flow and the extraction ratio. Drugs with a high hepatic extraction ratio are dependent on hepatic blood flow and the fraction of free non-protein-bound drug (eg. Propofol, Fentanyl). Drugs with a low hepatic extraction ratio are dependent on hepatic metabolic function than hepatic blood flow.

Answer 583

1) Hypotension 2) Hyperosmolality 3) Surgical Stress Vasopressin, also known as antidiuretic hormone (ADH) or arginine vasopressin, is a nonapeptide hormone produced in the supraoptic and periventricular nuclei in the hypothalamus. It is transported down axons in inactive carrier proteins called neurophysins that terminate in the posterior pituitary to be stored until released. Vasopressin's main physiologic function is to maintain extracellular fluid volume and plasma osmolality. The major triggers for vasopressin release are hyperosmolality and hypovolemia (hypotension). Surgical stress can also cause increased vasopressin levels for 2-3 days after a surgical procedure. For hyperosmolality, receptors in the hypothalamus sensitive to changes in osmolality induce the secretion of vasopressin when osmolality increases. Vasopressin then functions at the V2 receptor to increase the reuptake of solute-free water by inducing the upregulation of aquaporins in the collecting tubules of the kidney. For hypovolemia (hypotension), the decreased stretch in aortic and carotid baroreceptors stimulates the secretion of vasopressin at much higher levels than the response to hyperosmolality. These high levels preferentially activate the V1 receptor on smooth muscle to activate vasoconstriction and increase blood pressure.

Answer 584

Hypotension!

Answer 585

1) Hyponatremia 2) Hyperkalemia 3) Angiotensin II 4) ACTH

Answer 586

Renin is created and stored by the cells in the afferent arterioles of the kidney. Renin secretion can be caused by 3 different mechanisms: 1) Hyponatremia (chemoreceptors in macula densa) 2) Hypotension (baroreceptors within JGA) 3) B1activity Decreases in blood pressure, such as that displayed by the patient above, would cause a release of renin into the serum by at least one of these mechanisms. Renin then acts by cleaving the peptide angiotensinogen to create angiotensin I. Angiotensin I is then converted to angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II (Ang II) has several effects, which combine to increase systemic perfusion in patients. The most immediate response to Ang II is an increase in blood pressure caused by an increase in systemic vascular resistance. Ang II activates the angiotensin1 (AT1) receptors on vascular smooth muscle cells, causing constriction of the arterioles. Ang II also augments the sympathetic nervous system by inhibiting norepinephrine reuptake into nerve terminals. It also stimulates the release of catecholamines from the adrenal medulla. In addition, Ang II causes a centrally mediated increased thirst and enhances the release of vasopressin. These effects are almost immediate, but are not long-lasting. Ang II also has longer lasting effects in the body. In addition to its effects on blood pressure, it stimulates remodeling of the cardiovascular system, causing hypertrophy of cardiac cells and increased collagen deposition. It also has profound effects on the kidney, causing a decrease in the urinary excretion of both sodium and water. Lastly, Ang II stimulates the adrenal cortex to synthesize and release aldosterone. Aldosterone also acts on the kidneys to decrease the urinary excretion of sodium and water. This ultimately leads to an increase in blood volume and therefore blood pressure.

Answer 587

Hypothalamus (Supraoptic & paraventricular nuclei) Vasopressin is *synthesized* in the hypothalamus and *stored/released *in the posterior pituitary. NOTE: Anterior pituitary- synthesizes FLAT PeG. The mnemonic “FLAT PeG” can be used to recall all of the hormones released by the anterior pituitary. These are follicle stimulating hormone (FSH), luteinizing hormone (LH), adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), prolactin, endorphins, and growth hormone (GH). Posterior pituitary- releases vasopressin (ADH) and oxytocin (but both are synthesized in the hypothalamus supraoptic and paraventricular nuclei)

Answer 588

Anterior pituitary- synthesizes FLAT PeG. The mnemonic “FLAT PeG” can be used to recall all of the hormones released by the anterior pituitary. These are follicle stimulating hormone (FSH), luteinizing hormone (LH), adrenocorticotropic hormone (ACTH), thyroid-stimulating hormone (TSH), prolactin, endorphins, and growth hormone (GH). Posterior pituitary- releases vasopressin (ADH) and oxytocin (but both are synthesized in the hypothalamus supraoptic and paraventricular nuclei)

Answer 589

Vasopressin = antidiuretic hormone (ADH) = arginine vasopressin V1= vasoconstriction, myometrial contractility (decreases blood loss) V2 = increased aquaporins DCT and collecting ducts, release of vWF V3 = found on pituitary gland releases ACTH NOTE: Vasopressin is associated with an increase in platelet aggregation which can result in pseudothrombocytopenia. Vasopressin increases vWF, VIII, and tPA.

Answer 590

Describe Vasopressin's effects on the following blood vessels: Cerebral vasodilation Pulmonary vasodilation (good in pulmonary HTN) Renal vasodilation Mesenteric vasoconstriction (potential for mesenteric ischemia) Peripheral vascular beds vasoconstriction

Answer 591

Milrinone is PDE-III inhibitor resulting in increased intracellular cAMP. Milrinone is considered an inodilator. By increasing the concentration of cAMP, milrinone enhances myocardial contractility (without increasing myocardial O2 demand), promotes myocardial relaxation (lusitropy), and decreases vascular tone in the systemic and pulmonary circulation. NOTE: One adverse effect of Milrinone is development of arrhythmias, both ventricular and supraventricular. The use of Milrinone has been found to be an independent risk factor for the development of post-operative atrial fibrillation after cardiac surgery.

Answer 592

(+) INOTROPE Digitalis is a cardiac glycoside that **inhibits the Na+/K+-ATPase **protein found within the membrane of cardiac myocytes, and this inhibition leads to an increase in intracellular sodium that subsequently increases intracellular calcium via compensatory exchange of intracellular sodium for extracellular calcium. This elevated intracellular calcium is thought to improve contractility in cardiac myocytes. (-) CHRONOTROPE, (-) DROMOTROPE Digitalis also stimulates the vagal nerve to slow conduction through the AV node and prolongs the refractory period in the AV node. Digitalis is an adjunctive therapy reserved for individuals with heart failure with reduced ejection fraction (HFrEF) but can be used to manage rapid ventricular rhythms in patients with heart failure or atrial fibrillation when other therapies have failed. In patients with HFrEF, digitalis causes an improved force and velocity of contraction, increased cardiac output, and improved systolic emptying while causing reduced end-diastolic heart pressure that reduces pulmonary and systemic diastolic pressures.

Answer 593

Frequent ectopic ventricular beats (#1) AV nodal block Sinus bradycardia

Answer 594

Hypokalemia Hypercalcemia Hypomagnesemia Acidosis/alkalosis Low albumin Hypothyroidism Renal insufficiency NOTE: EKG findings include bradycardia, increased PR interval, AV block, downsloping ("scooping") ST segments, QT shortening, PVCs (#1), T-wave inversions or flattening. Thiazide diuretics cause hypokalemia, hypercalcemia, and hypomagnesemia all of which can trigger digoxin toxicity.

Answer 595

Methohexital s the most commonly used induction agent for ECT and is considered the gold standard.

Answer 596

Electroconvulsive therapy (ECT) has been used to manage psychiatric disorders since the 1930s. It can be used to treat mania, affective disorders, depression, and many other psychiatric disorders. It is typically performed three times per week for a total of 6-12 treatments. Weekly or monthly follow-up treatments are used to prevent relapses. An electrical current is applied to the brain, which precipitates a generalized motor seizure. Along with the seizure there is a large surge in the sympathetic nervous system that may result in profound hypertension and tachycardia. Electroconvulsive therapy requires minimum seizure duration of 25-30 seconds to ensure adequate antidepressant efficacy. The anesthetic agent of choice for use during ECT depends on patient factors and length of seizure duration needed for treatment. The key is to use agents that have a neutral or attenuating effects on seizure duration. Methohexital is the “gold standard” however it decreases seizure duration in a dose-dependent manner. Use of methohexital results in longer seizure times (versus propofol), shorter awakening times (versus thiopental), and fewer side effects (versus etomidate). With methohexital there is no change in seizure activity overall, but when compared with saline methohexital decreases the seizure duration. Methohexital will provide some blunting in hypertension and tachycardia that is observed during ECT, which gives it an advantage over other agents. Note, medications that would decrease seizure duration (eg. Propofol, Benzos) should be avoided as an anxiolytic or induction agent during electroconvulsive therapy.

Answer 597

Transcutaneous pacers activate the right ventricle followed by the left ventricle, similar to VOO mode for implantable pacemakers (does not inhibit with the patient's intrinsic rhythm).

Answer 598

The risk of electromagnetic interference causing inappropriate shock from an AICD is significantly decreased when **bipolar** electrocautery is used (versus monopolar). Bipolar configuration decreases the risk because electrical energy is delivered between the two electrodes at the tip of the instrument, where monopolar delivers electricity to the tissue and the path is connected to the return (grounding) pad. The risk decreases with the distance from the EMI source to the pulse generator. Typically, 6 inches is the critical distance. The interference potential is markedly reduced when surgery is below the umbilicus and the grounding pad is situated in a way as to direct the current away from the pulse generator.

Answer 599

The carotid baroreceptors are MORE sensitive than the aortic baroreceptors. The aortic receptors have a higher threshold pressure and are thus less sensitive.

Answer 600

Valsalva involves forced expiration against a clossed glottis. CVP- increases VR- decreases HR- decreases BP- decreases

Answer 601

Phase 4 - slow depolarization, spontaneous inward flow of Na via funny sodium channels Phase 0- fast depolarization, threshold met, T- type calcium channels cause calcium influx Phase 3- repolarization, potassium efflux NOTE: Parasympathetic stimulation -> AcH release -> M2 muscarinic receptors (SA and AV node) --> increased pacemaker cell permeability to K+ --> hyperpolarization -> negative chronotropy, negative dromotropy, negative atria inotropy

Answer 602

The **transgastric midpapillary short-axis (SAX) view** is considered the optimal TEE view when a provider is monitoring for ischemia because the myocardium perfused by the three coronary arteries (left anterior descending, circumflex, and right coronary arteries) can be visualized in a single image. TEE is the most sensitive method for detecting ischemia characterized by left ventricular systolic dysfunction.** Intraoperatively, myocardial ischemia can be detected by TEE quicker than changes on an electrocardiogram (ECG) are detected.** The transgastric midpapillary SAX views are often used when providers are monitoring for ischemia because the myocardium perfused by the three coronary arteries can be visualized in a single image. Ideally, regional wall-motion abnormalities seen in the transgastric midpapillary SAX view are confirmed in other views, including the midesophageal four-chamber, two-chamber, or long-axis planes.

Answer 603

V1-V4 (Precordial Leads) NOTE: The LAD supplies 1/2 of the left atrium (anterior aspect), 1/2 left ventricle (anterior aspect), anterior 2/3 of the interventricular septum, the anterolateral papillary muscle, and the cardiac apex. There are two papillary muslces in the left ventricle. The anterolateral papillary muscle is perfused by both the LAD and LCx. The posteromedial papillary muscle is perfused by the PDA however.

Answer 604

Leads II, III, or aVF NOTE: The RCA provides flow to both the SA and the AV node via the SA nodal and AV nodal branches. The RCA also supplies the lateral right ventricle and the cardiac apex.

Answer 605

The PDA most commonly arises from the RCA (85% Right Dominant), and RCA ischemic changes (leads II, III, aVF) may be seen. Isolated posterior infarctions are difficult to identify with a standard 12-lead ECG but can sometimes be identified with reciprocal changes, such as ST depression, in leads V1-V3. NOTE: The PDA, most commonly arising from the RCA, supplies the posterior 1/3 of the interventricular septum, the posterior inferior aspect of the heart, and the posteromedial papillary muscle.

Answer 606

TEE showing decreased systolic myocardial wall thickening

Answer 607

I, AVL, V5-V6

Answer 608

V5 "V5 keeps the Ventricles alive"

Answer 609

Lead II "Two nodes lead II"

Answer 610

DAPT following DES may be held for time sensitive (non-urgent) noncardiac surgery after three months. NOTE: Studies have shown that the risk of in-stent thrombosis was highest 4-6 weeks after DES placement but remained elevated for up to one year. DES have an anti-restenotic drug (chemotherapeutic agent) which reduces local neointimal hyperplasia but consequently slows endotheliazation (which is why DAPT is needed for 6 months for DES but only 1 month for BMS). BMS are rarely used as DES have been shown to be far more superior.

Answer 611

The SA node and AV node are supplied RCA branches (SA nodal artery, AV nodal artery). In a minority of patients, the SA and AV node may be supplied by the left circumflex. Supply of the SA node does not dependend on coronary dominance of the patient. In patients with right dominant heart (85%), the RCA gives right to the AV nodal artery. The most common cause of AV nodal dysfunction and resulting complete heart block is myocardial infarction, most frequently blockage of the RCA. Revascularization results in prompt resolution of block. Ventricular pacing (transcutaneous, transvenous, or permanent pacemaker) may be needed. Atropine is typically ineffective for high degree AV blocks (Mobitz type II, third degree AV block). Nitroglycerin and morphine should be avoided with inferior MI as they can lead to a decrease in preload and hypotension.

Answer 612

IABP inflates during diastole and deflates during systole. The IABP augments coronary perfusion by inflating during early diastole which improves aortic diastolic pressure. Coronary perfusion pressure (CPP) increases since CPP is the difference between aortic diastolic pressure (AoDP) and left ventricular end diastolic pressure (LVEDP): CPP = AoDP - LVEDP. An IABP also aids in unloading the left ventricle by reducing afterload with deflation at end diastole. The combined effect increases myocardial O2 supply and reduces myocardial O2 demand

Answer 613

AI Aortic Disease (dissection, aneursym, severe plaque, prior grafts) Severe PAD

Answer 614

Common indications for IABP counterpulsation include * Cardiogenic shock (due to ischemia or nonischemic cardiomyopathy) * Severe mitral regurgitation * Bridge to transplantation or ventricular assist device (VAD) placement. * Failure to wean from cardiopulmonary bypass (CPB) * Right ventricular dysfunction (which may acutely appear after CPB)

Answer 615

One of the hallmark features of the arterial waveform tracing in a patient with an intra-aortic balloon pump (IABP) is the **augmented diastolic pressure** tracing after the dicrotic notch.

Answer 616

Aortic valve closure

Answer 617

Higher systolic peak Lower diastolic nadir Lower MAP Delayed and less prominent dicrotic notch

Answer 618

CVP waveform A wave- right atrial contraction C wave- right ventricular contraction w/ bulging of tricuspid valve into right atrium X descent- right atrium relaxation V wave- passive filling of right atrium Y descent- right atrium passive emptying

Answer 619

Adenosine is a purine nucleoside base, most commonly recognized with the molecule adenosine triphosphate, or ATP, and is used thoroughly throughout the entire body in general metabolism. Adenosine’s use as a pharmacological drug works through receptors called purinergic adenosine receptors found throughout the body (A1, A2a, A2B, and A3). Receptors found in the cardiac atrioventricular (AV) nodal tissue and within the peripheral vasculature exhibit clinical manifestations when administering adenosine. Adenosine acts on receptors in the cardiac AV node, significantly slowing conduction time. This effect occurs by activation of specific potassium channels, driving potassium outside of cells, and inhibition of calcium influx, disrupting the resting potential of the slow nodal cardiac myocyte. Driving potassium outside of the cell causes hyperpolarization of the resting membrane potential while slowing calcium influx causes suppression of calcium-dependent action potentials, all requiring a longer time for depolarization to occur and thus slowing down conduction within these cells, which is useful in supraventricular tachycardia (SVT). The side effects of adenosine include hypotension, bronchospasm, and chest discomfort. Adenosine is contraindicated in patients with asthma.

Answer 620

Acquired LQTS usually results from drug therapy, and several patient-specific and medication-related factors can enhance the risk. Causes of acquired LQTS include antiarrhythmic drugs (quinidine, sotalol, dofetilide, ibutilide), psychotropic medications (haloperidol, methadone), erythromycin, cisapride, electrolyte abnormalities (hypokalemia, hypomagnesemia, hypocalcemia), eating disorders, coronary artery disease, and bradyarrhythmias. NOTE: QTc prolongation (>440ms in men, > 460ms in women) QT interval varies with HR. QT is shorter at fast heart rates, QT is longer at slow heart rates. QT interval can be corrected for heart rate: QTc = QT/cardiac cycle (seconds) Volatile anesthetics can prolong QT in a dose-dependent manner should be used with caution in this population.

Answer 621

Nonspecific ß-blockers (Nadolol and propranolol preferred) If medication resistant, then left cardiac sympathetic denervation or pacemaker. If presenting with cardiac arrest (10% of patients), then emergent ICD. NOTE: Congenital long QT syndrome results from a mutation in either cardiac Na or K channels resulting in abnormal ventricular repolarization hence long QT.

Answer 622

Propranolol & Nadolol

Answer 623

Romano-Ward Syndrome Lange Nielsen Syndrome

Answer 624

Second degree, type II, AV block Third degree AV block

Answer 625

Pacemaker indications with the highest evidence as set forth by the American Society of Cardiology: - Sinus node dysfunction with symptomatic bradycardia or sinus pauses that produce symptoms. - Symptomatic sinus bradycardia resulting from chronic required drug therapy - Syncope and sinus dysfunction discovered on electrophysiological studies - Persistent third degree or advanced second degree AV block (high grade AV block) - Symptomatic recurrent SVT which can be terminated by pacing, and ablation/drugs have failed or produce intolerable side effects - Pause dependent ventricular tachycardia - High risk patients with congenital long QT syndrome - Cardiomyopathy benefiting from resynchronization therapy - Can be considered in symptomatic atrial fibrillation not controlled by drug therapy and with coexisting sinus node dysfunction **Pacemakers are NOT indicated in atrial fibrillation without any other indication for placement These indications can be further simplified as: - Symptomatic sinus node disease - Symptomatic atrioventricular node disease, particularly high grade AV block - Long QT syndrome - Hypertrophic obstructive cardiomyopathy - Dilated cardiomyopathy

Answer 626

CRS = Vt / (Pplat - PEEP).

Answer 627

Fluoroscopic studies have shown that the incidence of iatrogenic diaphragmatic paralysis from phrenic nerve blockade occurs in 100% of interscalene blocks using the anatomical approach. Ultrasound approach, even with reduced anesthetic dose, does not guarantee that the phrenic nerve will be missed. As this peripheral nerve block of the cervical spinal roots includes C5 and the phrenic nerve is derived from C3-5, local anesthetic solution can travel up the interscalene sheath and block the origin of the phrenic nerve. It is approximated 10% of patients become symptomatic, particularly those with significant underlying respiratory disease. Healthy patients compensate for this side effect with the sufficient function of the preserved contralateral phrenic nerve. The incidence and effect of phrenic nerve palsy related to interscalene block can be decreased by diluting the local anesthetic solution, decreasing injection volume, or lowering the site of injection (e.g. supraclavicular approach).

Answer 628

Flail chest is a serious traumatic thoracic injury in which 3 or more adjacent ribs are broken in more than one place. This results in a segment of the chest wall that is in discontinuity from the rest of the ribcage. During spontaneous inspiration, the ribcage normally expands to create the intrathoracic negative pressure necessary to draw air into the lungs. In the case of a flail chest, the segment of the chest wall in discontinuity is drawn inwards during inhalation and moves outwards with exhalation. This results in the paradoxical chest wall movement that can be seen in patients with this injury. Additional complications may include decreased lung volume, atelectasis, chronic pain, respiratory failure, need for mechanical ventilation, pneumonia, sepsis, and extended ICU stay. Mortality can be high (5-10% mortality rate if patients reach the hospital alive) due to respiratory complications and the presence of additional serious injuries due to the significant amount of force needed to result in flail chest. The mainstays of treatment include aggressive pulmonary hygiene and adequate analgesia, with thoracic epidural analgesia being effective. Surgical intervention is not routinely performed unless the patient has additional underlying injuries or does not respond to conservative management.

Answer 629

The internal intercostal muscles contract during exhalation and the external intercostal muscles contract during inspiration The muscles of the abdominal wall contract during forced exhalation (external and internal oblique muscles, rectus abdominis, transversus abdominis). Inhalational accessory muscles include the scalene, sternocleidomastoid muscles, pectoralis major, pectoralis minor, serratus anterior, latissimus dorsi, erector spinae, and quadratus lumborum..

Answer 630

In the elderly population, normal age-related pulmonary physiological changes result from respiratory control, lung structure, and pulmonary blood flow alterations. Ventilatory responses to hypoxia, hypercapnia, and mechanical stress are impaired due to reduced central nervous system activity. Pharmacodynamic changes in the elderly include increased sensitivity to the respiratory depressant effects of benzodiazepines, opioids, and volatile anesthetics. Age-related changes in lung structure include a loss of elastic recoil secondary to the reorganization of collagen and elastin in the lung parenchyma, leading to increased lung compliance. This increased lung compliance can result in limited maximal expiratory flow. Decreased lung elasticity is associated with enlargement of alveolar ducts and bronchioles, leading to early collapse of small airways, increasing the risk for air trapping and hyperinflation. Closing capacity (CC), defined as the volume at which small airways begin to collapse during exhalation, increases with age. Lung volume changes in the elderly include increased anatomical dead space, CC, functional residual capacity (FRC) and decreased diffusion capacity, alveolar surface area, vital capacity, forced expiratory volume in the first second, and forced vital capacity. Residual volume increases by approximately 5% to 10% per decade. Despite these changes in lung volumes, total lung capacity is relatively unchanged in the elderly. The physiological changes between the FRC and CC cause an increased ventilation-perfusion mismatch and represent the most important mechanism for the increase in the alveolar-arterial gradient for oxygen seen in aging. The age-related decrease in height and calcification of the vertebral column and rib cage leads to a barrel chest appearance with associated diaphragm flattening. The flattened diaphragm is less efficient, and the age-related muscle mass decrease further impairs its function. Hypoxic pulmonary vasoconstriction is blunted in the elderly (> 65 years) population, and this can cause difficulty with one-lung ventilation.

Answer 631

1) Increased closing capacity The closing capacity (CC) is the volume in the lungs at which its smallest airways, the respiratory bronchioles, collapse. With aging, a loss of elasticity secondary to a reorganization of collagen and elastin in the lung parenchyma causes an increase in the tendency for small airways to collapse during exhalation. This increases the residual volume (RV) and CC. The progressive increase in CC with aging is more rapid than the slow progressive increase in functional residual capacity (FRC). After age 65, the CC is greater than the FRC in the upright position. When CC is greater than FRC, small airways close during normal tidal breathing, creating a V/Q mismatch in the dependent lung regions. This V/Q mismatch, related to an increased CC, is a significant factor in the progressive decrease in PaO2 seen with aging. 2) Decreased alveolar surface area Also contributing to the decrease in PaO2 is decreased alveolar surface area. PaO2 decreases by 0.35-0.5 mm Hg per year between the ages of 40-75. After the age of 75, PaO2 remains relatively constant, around 80-85 mmHg.

Answer 632

A 1.36% concentration of sevoflurane produces 1 minimal alveolar concentration (MAC) at sea level in an 80-year-old patient because MAC decreases 6% per decade after the age of 40 years: 1.8% × (1 − [4 × 6%]) = 1.36%.

Answer 633

Obesity has long been recognized as significantly affecting respiratory function, including a higher respiratory rate to meet the heightened demand for ventilation in the setting of increased CO2 production and respiratory muscle inefficiency. xcess body weight can decrease both chest wall and lung compliance. This results in a decreased functional residual capacity (FRC), vital capacity, and total lung capacity. FRC is the volume of air that remains in the lungs after a normal expiration. FRC is the sum of residual volume and expiratory reserve volume (ERV). Reduced FRC is primarily at the expense of decreased ERV while residual volume and closing capacity are unchanged. This results in lung volumes that fall below closing capacity during normal tidal volume ventilation leading to small airway collapse, ventilation-perfusion mismatch, right-to-left shunt, and arterial hypoxemia. In the supine position under general anesthesia, this effect is multiplied. Forced vital capacity (FVC) and forced expiratory volume in one second (FEV1) may be decreased in obesity (restrictive pattern) but are usually within normal limits. FVC/FEV1 ratio is unchanged in obesity.

Answer 634

In patients with FEV1/FVC <0.7 GOLD 1 - mild: FEV1 ≥80% predicted GOLD 2 - moderate: 50% ≤ FEV1 <80% predicted GOLD 3 - severe: 30% ≤ FEV1 <50% predicted GOLD 4 - very severe: FEV1 <30% predicted. Preoperative spirometry has not been shown to predict postoperative pulmonary outcomes in patients with COPD undergoing non-cardiothoracic surgery better than a routine clinical encounter with a history and physical examination.

Answer 635

The trachea can be anesthetized (translaryngeal/transtracheal block) by injecting local anesthetic transtracheally through the cricothyroid membrane. Cough may occur with the injection, and this will help spread the local anesthetic. Sensory, motor, and parasympathetic innervation of the trachea is via the recurrent laryngeal nerve.

Answer 636

The alveolus is the primary site for gas exchange in the lungs. The alveolus is primarily composed of type I alveolar cells, which cover 80% of the alveolar surface. Type I alveolar cells are squamous cells that are flat in nature, with flattened nuclei and thin cytoplasmic extensions that provide the surface area required for gas exchange. These cells are extremely susceptible to damage, highly differentiated, and metabolically limited. When they are damaged, type I alveolar cells are not replaced by other type I alveolar cells but rather by type II alveolar cells. These type II alveolar cells are interspersed among type I alveolar cells, predominantly at the alveolar-septal junctions. Unlike type I alveolar cells, type II alveolar cells are metabolically active and secrete the lung surfactant. Type II alveolar cells also play a role in pulmonary defense through the secretion of inflammatory mediators. Type III alveolar cells function as part of the immune system of the lung. They are able to migrate and ingest foreign material in the lungs.

Answer 637

Fixed obstruction A fixed obstruction refers to an airway obstruction that is static and does not change with inspiration or expiration. Examples include tracheal stenosis or a large goiter. A fixed obstruction reduces flow in both the inspiratory and expiratory phases. In both phases, the flow will reach a plateau represented by a flattening of the flow-volume loop, i.e., the maximum flows during both phases will be reduced compared to a normal flow-volume loop. Note that a fixed obstruction, whether it is intrathoracic or extrathoracic, will produce a similar pattern on the flow-volume loop. NOTE: Flow-volume loops plot lung volume on the x-axis and flow on the y-axis. A positive value on the y-axis indicates expiration, while a negative value indicates inspiration. A continuous flow loop is formed traveling in a clockwise direction. Flow is positive as it goes towards the device during expiration, then negative as it travels away from the device (towards the patient) during inspiration.

Answer 638

Extrathoracic obstruction Flow-volume loop illustrates a variable extrathoracic obstruction. Expiratory flow is relatively preserved while flow during inspiration is reduced with a plateau during this phase on the flow-volume loop.

Answer 639

Intrathoracic obstruction Flow-volume loop illustrates a variable intrathoracic obstruction. Inspiratory flow is relatively preserved while flow during expiration is reduced with a plateau during this phase on the flow-volume loop.

Answer 640

Continuous mandatory ventilation is the very first vent mode. It simply provides the set number of breaths and the set volume/pressure for a set time on the basis of the inspiratory/expiratory ratio. If a patient attempts to inhale between the scheduled breaths, they will not be able to draw any air, just as if they are breathing against a clamped tube. Intermittent mandatory ventilation is the next vent mode. It is an improvement compared with CMV in that, if the patient attempts to inhale between the scheduled breaths, the patient will be able to draw air. However, the breath is unsupported, and the fact that this spontaneous breath occurred does not affect the occurrence of the scheduled breaths. Both CMV and IMV are now antiquated and are no longer routinely used with modern ventilators. Synchronized intermittent mandatory ventilation is an improvement compared with IMV in two ways. First, spontaneous breaths are supported in SIMV, either as controlled breaths or as pressure-supported breaths. Second, SIMV accounts for spontaneous breaths when mandatory breaths are scheduled. For example, if an RR of 10 is set and a patient has initiated a spontaneous breath within a six-second window after the last breath, then the spontaneous breath will be fully supported as a controlled breath (on the basis of the set volume/pressure setting) and will replace the originally scheduled breath. If a spontaneous breath has not occurred within the window, then the scheduled breath will occur at the end of the six seconds. If a second breath is attempted within the six-second window, then that breath will only be given pressure support but will not be a fully controlled breath. If the patient attempts to breathe 20 times per minute when an RR of 10 is set, then half of the breaths will consist of controlled breaths, and the other half of the breaths will be pressure-supported breaths. Assist control is the newest vent mode. It can be easily identified because all breaths initiated by the patient will be fully supported as controlled breaths (with the set volume/pressure). It has been argued that AC is more comfortable than SIMV for the patient because, in AC mode, each of the breaths is identical and without variation. However, if the patient triggers 20 breaths per minute when 10 breaths are intended, 20 fully supported controlled breaths will be given, which may result in unintended hyperventilation. Because AC is the most commonly used vent mode, some vents abbreviate the combination of AC VC, AC PC, and AC PRVC as simply VC, PC, and PRVC, respectively; however, it is important to realize that these are actually AC vent modes.

Answer 641

Obstructive pattern Flow-volume loop illustrates an obstructive pattern, such as in chronic obstructive pulmonary disease or bronchitis. This refers to lower airway obstruction and flow during expiration is lower than normal.

Answer 642

NOTE: ASA physical status classification was originally created to compare anesthetic data. Nowaways is used to assess and communicate the medical comorbidities of patients. **It is NOT predictive of perioperative risk.**

Answer 643

Predictors of difficult intubation * Short/thick neck * Limited cervical mobility (cannot touch the tip of the chin to chest or extend the neck) * Short thyromental distance (<3 fingerbreaths, < 6.5cm) * Small mouth opening (< 2 fingerbreaths, < 3cm) * Long upper incisors * Prominent overbite * Inability to protrude the mandible/bite upper lip * High, arched palate * Mallampati score of III or IV NOTE: ASA defines difficult intubation as 3 or more attempts that takes over 10min. Short thyromental space (<6.5cm or 3 fingerbreaths) inidicates small mandibular space for displacement of tissues during direct laryngoscopy) A highly arched palate is associated with various congenital abnormalities and results in a more narrow and longer oropharynx, making laryngoscopy more challenging.

Answer 644

Upper lip bite test 96% specificity 80% sensitivity This finding is associated with >60% incidence of difficult intubation.

Answer 645

Vital signs Airway exam Assessment of heart Assessment of lungs (auscultation required) NOTE: There are no examples of what is required within these components other than the inclusion of auscultation of the lungs.

Answer 646

Stage 1: Analgesia * Stage 1 of anesthetic depth, often referred to as the induction stage, begins with the first administration of any anesthetic drug and ends with the loss of consciousness. * During stage 1, the patient remains in a state of analgesia and disorientation with or without amnesia. * Patients in stage 1 will demonstrate slow and regular respirations and should be able to maintain a conversation. Stage 2: Excitement/Delirium * Stage 2 of anesthetic depth is characterized by the loss of consciousness and continues to the onset of autonomic breathing. Disinhibition, uncontrolled movement, and airway hypersensitivity are characteristics of stage 2. * Patients in stage 2 are at the highest risk of laryngospasm, and airway stimulation should be avoided. * Hypertension, tachycardia, irregular respiration, and nonpurposeful response to painful stimulus, may all indicate that a patient is in stage 2 of an anesthetic. * Eye examination during stage 2 is characterized by loss of the eyelash reflex, divergent gaze, and reflex pupillary dilatation. * Patients receiving a total intravenous anesthetic may exhibit fewer, if any, of the characteristic signs of stage 2 of anesthetic depth. Stage 3: Surgical Anesthesia * The resumption of regular, spontaneous respiration marks the entrance into stage 3 of anesthetic depth, which continues until respiratory paralysis. * Stage 3 is the depth of anesthesia that is most desirable for surgical incision. * During stage 3, airway reflexes become suppressed, allowing for safe airway manipulation, including insertion and removal of an endotracheal tube. * Stage 3 can be divided into 4 separate planes of anesthesia. * Plane I is marked by spontaneous breathing and central, constricted pupils with loss of the eyelid and conjunctival reflexes. * Plane II is characterized by intermittent cessation of respiration along with the loss of ocular movement and laryngeal reflexes. * Plane III is marked by the loss of function of the intercostal and abdominal musculature and the loss of the pupillary light reflex. Plane III is considered “true surgical anesthesia” and is ideal for most surgeries. * Plane IV is demonstrated by irregular respiration and, eventually, full diaphragm paralysis, resulting in apnea. The carinal reflex is also lost in plane IV of stage 3. Stage 4: Overdose * Stage 4 of anesthetic depth is marked by apnea. Anesthetic overdose is the characteristic feature of stage 4. * During stage 4, the patient’s pupils become fixed and dilated, and all reflexes and skeletal muscle tone are lost. Hypotension and bradycardia can occur, indicating brainstem and cardiovascular suppression. * A patient in stage 4 should have anesthetic depth reduced as soon as possible or risk cardiovascular injury, neurologic injury, and death.

Answer 647

Standard #1) For all general anesthetics, MAC, and regional anesthetics, qualified anesthesia personnel should be in the room at all times. Standard #2) During all anesthetics- oxygenation, ventilation, circulation, and temperature shall be continually monitored. Within the second standard are the monitored parameters which are required to have an alarm associated with them. Two for oxygenation and two for ventilation. Two for oxygenation are low oxygen concentration limit alarm and pulse oximetry low threshold alarm. Two for ventilation is a circuit disconnection alarm and a low ETCO2 alarm.

Answer 648

In 2011, a large meta-analysis (involving 55 studies and over 177,000 subjects) was published to evaluate the use of the modified Mallampati score as a prognostic test. When used as a stand-alone test, a high risk (class III or IV) modified Mallampati score demonstrated a sensitivity of 35% in predicting difficult intubation or laryngoscopy. Like many screening tests, its specificity was much higher, determined to be 91% in this large study. So basically cant use it to rule out disease better at ruling it in.

Answer 649

Minimal Sedation * Normal response to verbal stimulation * Airway reflexes, spontaneous ventilation, and cardiovascular function are all unaffected Moderate Sedation * Purposeful response to verbal or tactile stimulation * Spontaneous ventilation is adequate and no airway intervention is required * Cardiovascular function is usually maintained Deep Sedation * Purposeful response to repeated or painful stimulation (reflex withdrawal from a painful stimulus is NOT considered purposeful response) * Spontaneous ventilation may be inadequate and airway intervention may be required * Cardiovascular function is usually maintained General Anesthesia * Unable to arouse even with painful stimulus * Spontaneous ventilation is frequently inadequate and airway intervention is often required * Cardiovascular function may be impaired NOTE: The patient's level of conciousness marks the difference between general anesthesia and moderate/deep sedation. If a patient makes purposeful movements to repeated or painful stimuli, they can be considered to be in a plane of moderate or deep sedation respectively. Regardless of airway intervention, if a patient does not make purposeful actions to repeated or painful stimuli they are considered to be in a plane of general anesthesia.

Answer 650

Patient under moderate sedation will exhibit purposeful response to **verbal or tactile stimulation**

Answer 651

Patient under deep sedation will exhibit purposeful response to **repeated or painful stimulation** (reflex withdrawal from a painful stimulus is NOT considered purposeful response)

Answer 652

Atlantoaxial instability is seen in trauma, Rheumatoid Arthritis, Lupus, Down Syndrome, achondroplasia. Estimated 25% of patients with RA have some degree of atlantoaxial subluxation. May cause spinal cord trauma with neck manipulation.

Answer 653

Manual in-line stabilization (MILS) is recommended during direct laryngoscopy and intubation in patients with known or suspected cervical spine instability. When one initially evaluates a patient with a suspected spine fracture, the presence of any of the following indicates a high risk of injury: * High-speed (> 35 miles per hour) motor vehicle collision * Death at the scene of a motor vehicle collision * Fall from a height > 10 feet * Significant closed head injury of intracranial hemorrhage seen on computed tomography * Neurologic symptoms or signs referred to the cervical spine * Pelvic or multiple extremity fractures

Answer 654

**Mitral regurgitation and aortic regurgitation **are the most common valvular manifestations of rheumatoid arthritis (RA). Stenotic valvular lesions are not typically associated with RA.

Answer 655

End-tidal carbon dioxide values between 10-20 mmHg support adequate circulation during CPR and appropriate mechanical technique. Sudden increases in value to greater than 30 mmHg may indicate ROSC.

Answer 656

Hypercalcemia causes QT shortening. Hypocalcemia causes QT prolongation. NOTE: QTc prolongation (>440ms in men, > 460ms in women) QT interval varies with HR. QT is shorter at fast heart rates, QT is longer at slow heart rates. QT interval can be corrected for heart rate: QTc = QT/cardiac cycle (seconds)

Answer 657

In the anhepatic phase of liver transplantation, **hypocalcemia** is a common electrolyte abnormality that can occur secondary to rapid infusion of blood products with citrate. Hypocalcemia can manifest as hypotension that is unresponsive to beta agonists. Because patients with end-stage liver disease can be coagulopathic at baseline, the rapid administration of fresh frozen plasma is often given to maintain an INR less than or equal to 1.5 or to control excessive surgical bleeding. However, INR does not necessarily correlate with bleeding risk in this patient population. A goal hematocrit for liver transplantation usually ranges between 26-32%. This allows for adequate delivery of oxygen and helps to prevent hepatic artery thrombosis. Because citrate is often added to stored blood products to prevent clotting, a rapid transfusion of fresh frozen plasma also means a rapid transfusion of citrate. Citrate acts as a calcium chelating agent which can cause hypocalcemia and metabolic alkalosis. Hypocalcemia secondary to citrate toxicity is more likely in patients with underlying liver dysfunction when the rate of infusion of blood product is greater than 50 mL/min. Because these two factors are often seen during liver transplantation, hypocalcemia is a common occurrence.

Answer 658

Hypocalcemia Patients with liver dysfunction who receive multiple blood transfusions can develop hypocalcemia due to the calcium chelation by citrate (which is metabolized by the liver). Hypocalcemia may manifest as prolonged QT interval.

Answer 659

Hypermagnesemia causes QT prolongation.

Answer 660

Fatty acids from triglycerides are converted to acetyl-coenzyme A prior to metabolism into ATP. Triglycerides, the main constituent of fat in the human body, consist of one glycerol attached to three chains of fatty acids. These fatty acids undergo metabolism primarily in the liver, where they are converted to acetyl-CoA, then undergo the citric acid cycle to yield ATP. Excess acetyl-CoA is converted to ketone bodies, which can be used as an alternative energy source.

Answer 661

LDL is a lipoprotein that delivers cholesterol from the liver to the peripheral tissues.

Answer 662

VLDL is a lipoprotein that delivers triglycerides from the liver to the peripheral tissues.

Answer 663

HDL is a lipoprotein that delivers cholesterol from the rest of the body to the liver. TrueLearn Insight: Cholesterol synthesis occurs in the cytoplasms of the hepatocytes and intestinal epithelial cells. The starting substrate is acetyl-CoA, and the rate-limiting step is the conversion of 3-hydroxy-3-methylglutaric acid coenzyme A (HMG-CoA) to mevalonate by HMG-CoA reductase, the target of statins. HMG-CoA reductase is also activated by estrogen, insulin, and thyroxine and is inhibited by cholesterol and glucagon. It is worth noting that statins increase the ratio of HDL to LDL.

Answer 664

Five GLUTs facilitate the movement of glucose across the cellular membrane. Glucose transporters 1, 2, 3, and 5 are insulin-independent transporters, while GLUT4 is the only insulin-dependent transporter. Glucose transporter 4 is responsible for most glucose uptake into adipocytes and striated muscle (skeletal and cardiac), and GLUT 2 is responsible for the uptake of glucose into the pancreas.

Answer 665

Most blood product preservative solutions contain a mixture of citrate, phosphate, dextrose, and adenine. Citrate is used to chelate calcium in the solution preventing coagulation from occurring. Phosphate acts as a buffer to maintain the pH of the storage solution. Dextrose is used to maintain a source of energy as RBCs as they are only able to undergo anaerobic glycolysis Adenine maintains a pool of ATP for cell membrane integrity. At two weeks of storage, metabolic changes occur, such as depletion of 2,3-diphosphoglycerate, which shifts the oxygen dissociation curve to the left, increasing oxygen affinity. By day 42, the pH decreases to 6.5, potassium concentration increases to 50 mmol/L due to RBC hemolysis and leakage, and 15-20% of RBCs are no longer viable.

Answer 666

Hypocalcemia (chelates) Metabolic alkalosis (citrate converted to bicarb by liver) Hypokalemia (H/K exchanger response to alkalosis)

Answer 667

Isoproterenol MOA: B1 & B2 agonist (structurally similar to epinephrine) Effects: Increased HR and contractility, peripheral vasodilation, bronchodilation Indications: Bradycardia in third degree AV block Denervated heart after recent cardiac transplant

Answer 668

Femoral nerve (impingement by inguinal ligament) Obturator nerve (impingement by inguinal ligament) Lateral femoral cutaneous nerve (impingement by inguinal ligament) Sciatic nerve (stretch injury) Saphenous nerve (compression against the medial condyle of the tibia with improper padding or positioning) Common peroneal nerve (compression at the fibular head) These injuries are associated with prolonged positioning (>2hrs) NOTE: Tibial Nerve = Plantarflexion + Inversion Peroneal Nerve = Dorsiflexion + Eversion "TIP PED"

Answer 669

The most commonly injured nerve in patients undergoing surgery in lithotomy position is the common peroneal nerve. It originates between L4-S2. It is due to stretching and/or compression of the nerve between the lateral head of the fibula and the bar holding the legs. The injury is associated with a low BMI and prolonged surgery. The common peroneal nerve is responsible for foot dorsiflexion and toe extension. The injury leads to isolated foot drop.

Answer 670

The most common injuries during anesthesia in the lateral position are **brachial plexus injuries (brachial plexus neuropraxias). ** Cause: Axilla and neck compression (occurs when one shoulder or arm remains dependent under the ribcage or excessive lateral flexion at neck) S/S: Loss of sensation in the affected extremity, with inability to flex the elbow, supinate the arm, or abduct and rotate the shoulder. Prevention: In an effort to mitigate compression of the dependent side, thoracic padding (called an "axillary roll", an unfortunate misnomer) is used to ensure that the weight of the upper body lies on the thorax and not the dependent arm. The roll is placed under the dependent rib cage, 10 cm distal to the axillary folds, at the seventh to ninth rib. Should this padding migrate cranially into the axilla, it may actually exacerbate pressure on the brachial plexus and promote a compression injury on the dependent side. The cervical spine should also be kept in a neutral position using extra bedsheets/blankets under the head pillow, taking care to avoid flexion on the spine in either lateral direction. This can exacerbate brachial plexus injury and is best characterized by viewing the patient from the side prior to the placement of surgical drapes. OTHER: Traction injuries on the nondependent brachial plexus occur most frequently when the patient sags into a semi-supine posture following initial positioning. As the non-dependent arm is usually fixed to an arm board support this motion places tension on the shoulder joint and can cause traction injury. Another common injury in the nondependent upper extremity is a suprascapular nerve injury that results from anterior flexion of the arm across the chest. This places tension on the suprascapular nerve and can result in deep and poorly characterized pain about the nondependent shoulder.

Answer 671

According to the Anesthesia Closed Claims Project database, the **ulnar** nerve is the most commonly injured peripheral nerve perioperatively. Ulnar can occur from malpositioning or compression such as flexion of the elbow > 110° for extended periods of time during surgery (eg positioning arm over chest). Patients with ulnar nerve injuries can present with numbness, tingling, or pain at the dorsal and palmar surface of the medial one-and-a-half fingers. Motor dysfunction can include weakness of wrist flexion, flexion of the fifth digit, abduction of the fifth and fourth digit, and adduction of the thumb. OTHER NERVE INJURIES: A radial nerve injury can present with sensory deficits of the dorsal forearm, dorsal aspect of the first through the lateral aspect of the fourth digit. Motor dysfunction can affect extension of the forearm at the elbow. It can also present with wrist drop and decreased grip strength, depending on the location of the injury. A musculocutaneous nerve injury would present with sensory deficits in the lateral forearm and from the elbow to the base of the thumb. Motor deficits can affect elbow flexion and forearm supination. A median nerve injury would present with numbness of the palmar aspect of the first four digits, medial forearm, medial arm. Weakness with wrist flexion, first four digit finger flexion, opposition of the thumb, and pronation. An axillary nerve injury would present with a sensory deficit over the lower part of the deltoid and lateral arm. Motor deficits can affect shoulder abduction above 15° and external rotation of the arm.

Answer 672

A median nerve injury can occur due to overextension of the elbow. Symptoms: Numbness of the palmar aspect of the first four digits, medial forearm, medial arm. Weakness with wrist flexion, first four digit finger flexion, opposition of the thumb, and pronation

Answer 673

A median nerve injury would present with numbness of the palmar aspect of the first four digits, medial forearm, medial arm. Weakness with wrist flexion, first four digit finger flexion, opposition of the thumb, and pronation. NOTE: Can occur with overextension of the elbow.

Answer 674

A radial nerve injury can present with sensory deficits of the dorsal forearm, dorsal aspect of the first through the lateral aspect of the fourth digit. Motor dysfunction can affect extension of the forearm at the elbow. It can also present with wrist drop and decreased grip strength, depending on the location of the injury.

Answer 675

A musculocutaneous nerve injury would present with sensory deficits in the lateral forearm and from the elbow to the base of the thumb. Motor deficits can affect elbow flexion and forearm supination.

Answer 676

An axillary nerve injury would present with a sensory deficit over the lower part of the deltoid and lateral arm. Motor deficits can affect shoulder abduction above 15° and external rotation of the arm.

Answer 677

A musculocutaneous nerve injury would present with sensory deficits in the lateral forearm and from the elbow to the base of the thumb. Motor deficits can affect elbow flexion and forearm supination.

Answer 678

A SAH is defined by bleeding into the subarachnoid space, which makes about 5% of all strokes. The most common cause of a SAH is a ruptured cerebral aneurysm. Risk factors for aneurysms include hypertension, polycystic kidney disease, fibromuscular dysplasia, and cerebral aneurysm in a first-degree relative. SAH presents clinically with a variety of signs and symptoms, including severe headache, stiff neck, photophobia, decreased level of consciousness, and focal neurologic changes. The Hunt-Hess classification system grades the severity of SAH based on history and physical exam. This scale uses clinical features to approximate prognosis and mortality. Modified Hunt-Hess Scale Grade 0: Unruptured aneurysm Grade 1: Asymptomatic or mild headache Grade 2: Moderate-to-severe headache and/or cranial nerve palsy only Grade 3: Mild focal deficit and/or confusion/lethargy Grade 4: Hemiparesis and/or stupor Grade 5: Coma or decerebrate posture NOTE: Rebleeding peaks in first 24 hours. Vasospasm peaks at 7 days.

Answer 679

ASA Practice Guidelines Preoperative Fasting "Minimum fasting periods" Clear liquids: 2hrs Carbohydrate drink: 2hrs Light meals: 6hrs Regular meals: 8hrs NOTE: Clear liquids are eliminated in the stomach in an exponential fasion. Liquids are thought to empty secondary to the pressure gradient between the stomach and duodenum. Solid foods are eliminated in the stomach in a linear fashion. Solids are emptied from the stomach only when they have been digested to essentially liquid. Elimination of non-clear liquids depends on multiple considerations- amount of milk ingested, caloric content, ratio of fat, and amino acids. Higher fat content will take longer to eliminate.

Answer 680

1- Decreases thirst & hunger 2- Optimizes intravascular volume status 3- Decreases insulin resistance, better blood glucose control/stability 3- Decreases risk of aspiration NOTE: Patients benefited from reduced thirst/hunger when carbohydrate-containing clear liquids were ingested up to two hours before surgery (compared to both fasting and ingestion of noncaloric clear liquids). Strong evidence exists that when clear liquids are given to patients 2-4 hours before surgery (compared to NPO > 8hrs) these patients have a decreased risk of aspiration as evidenced by lower gastric volumes and higher gastric pH at time of induction. No difference established in PONV between the groups (compared to 8 hr fast).

Answer 681

If not already intubated, then hold enteric feeding 8 hours before surgery. If intubated, can continue perioperatively. NOTE: Postpyloric feeding does NOT reduce risk of aspiration.

Answer 682

Smoking contributes to numerous perioperative complications, but the worst are pulmonary, cardiovascular, and impaired healing of surgical wounds/bone. The duration of smoking cessation that is required to see any benefit is arguable, and it depends on the complication considered. PULMONARY Inhaling cigarette smoke singes off the mucociliary cells. When these cells are functioning properly, they act to help clear secretions; thus, destruction leads to impaired secretion management. Hyperplasia of mucous-producing goblet cells also increases mucous production, compounding the problem. Alveolar macrophage function is impaired, weakening normal defense mechanisms against infection. CARDIOVASCULAR The cardiovascular system is significantly impacted by smoking because smoking increases atherosclerosis by altering lipid metabolism and producing endothelial damage through free radical generation. Even short-term exposure causes increased vascular events due to increased coagulability, increased sympathetic tone, and decreased oxygen-carrying capacity. WOUND HEALING Compromised wound healing occurs secondary to decreased tissue oxygenation from vasoconstriction and carboxyhemoglobin production. Cigarette smoke produces carbon monoxide when the tobacco is burned incompletely. Incomplete burning occurs when there is not enough oxygen to convert all the carbon in the tobacco to carbon dioxide. Several case reports describing carbon monoxide poisoning in cigarette smokers have been published. Even nonsmokers have some degree of carbon monoxide in their blood; smokers generally have three to four times the amount of carbon monoxide compared with nonsmokers. In people who smoke two or more packs per day, this level can rise to fifteen times and cause carbon monoxide toxicity. EFFECT ON DRUG METABOLISM Metabolism of anesthesia medications and volatile anesthetics may be altered in the smoker. Nicotine and the polycyclic aromatic hydrocarbons in cigarettes induce the cytochrome p450 system. Most narcotic medications have an increased dose requirement because of ramping up of these liver enzymes, resulting in quicker metabolism. The same is possibly true of the muscle relaxants rocuronium and vecuronium. Ropivacaine has enhanced metabolism in smokers; however, use of lidocaine seems to result in no significant alteration. EFFECTS ON PAIN Another, less expected perioperative implication of smoking is the experience of pain. Results of several studies have provided evidence that smokers tend to have higher pain scores and, thus, opiate consumption in the postoperative period. Several theories have been proposed to explain this. One theory is that smokers experience acute nicotine withdrawal, which makes them more likely to require pain medication. Another theory is secondary to the metabolism changes discussed above. This does not seem to be unique to the immediate postoperative period; results of several studies have provided evidence that this continues for several months postoperatively.

Answer 683

Blood: Gas Partition Coefficients: Halothane: 2.54 Isoflurane: 1.46 Sevoflurane: 0.69 Desflurane: 0.42 Nitrous Oxide: 0.46 The higher the coefficient, the more potent the agent. Inhalational anesthetics reach equilibrium when the anesthetic partial pressures of the alveolus, blood, and CNS become equal. The faster the alveolar fraction (FA) of inhaled agent approaches the fraction of inspired (FI) agent, the faster the agent will reach equilibrium. Insoluble agents (e.g. desflurane, nitrous oxide) have a low blood to gas partition coefficient. Therefore, their partial pressures quickly build in the alveoli. More soluble anesthetics (e.g. halothane, isoflurane) will diffuse across the alveoli and into the alveolar capillary bed more readily, thereby increasing the time needed reach this equilibrium.

Answer 684

Volatile anesthetics with a lower blood:gas partition coefficients have a faster rate of alveolar uptake (thus a slower onset/offset) Blood: gas partition coefficient is inversely proportional to the speed of alveolar uptake. The higher the blood:gas partition coefficient, the slower the alveolar uptake (and longer the time of onset/offset). A larger coefficient means that the gas has a higher solubility in the blood but a slower onset of action because more anesthetic must be dissolved before it equilibriates with the tissue of the CNS. Blood solubility, which is often described in terms of the blood:gas partition coefficient, is one of the principal determinants concerning the uptake and speed of onset of the inhaled volatile agents. The partition coefficient describes how the anesthetic is split between the two phases (blood and gas). Alveolar concentration of an anesthetic (FA) divided by the inspired concentration (FI) yields a ratio that can be used to assess the relationship of the delivered anesthetic by ventilation and the degree of anesthetic uptake/removal. Therefore, inhaled agents with a high FA/FI ratio are associated with a low solubility, while higher blood solubility values are associated with a lower FA/FI ratio. NOTE: Potency is different. Potency is primarily determined by a volatile anesthetics lipid solubility (oil:gas partition coefficient)

Answer 685

Decreases intracellular calcium

Answer 686

Changes in CO has the greatest effect on the rate of rise of FA/Fi with which anesthetics? SOLUBLE volatile anesthetics > Insobule volatile anesthetics The uptake of volatile anesthetics is directly proportional to cardiac output, solubility, and arterial venous partial pressure difference. Greater uptake into the blood may imply faster distribution within the body, but this means the partial pressure of anesthetic in the blood is lower. This in turn causes the gas to take longer to reach and equilibirum between the alveoli and the brain thereby slowing induction. Variation in CO will have a limited effect on FA/Fi rate of rise during the initial transfer for insoluble agents (eg. Desflurane) as compared to soluble agents since they have decreased blood uptake and faster induction.

Answer 687

Minute ventilation Alveolar blood flow (ie CO) Blood:gas partition coefficient Difference in alveolar vs. venous partial pressures NOTE: Increase rate of rise of FA/Fi include: * High minute ventilkation * Low cardiac output * Relatively low blood:gas partitiion coefficients (less soluble) * Low Parterial-Pvenous (meaning less blood uptake)

Answer 688

Factors that speed recovery (or emergence) from inhalational anesthetics? High FGFs Increased ventilation Decreased solubility of agent Elimination of rebreathing Low anesthetic circuit volume Low absorption by the circuit High CBF NOTE: These factors also increase speed of induction.

Answer 689

Why does the FA/Fi curve rise faster for Nitrous Oxide than Desflurane, despite the fact that Desflurane having a lower blood:gas partition coefficient (less-soluble) than Nitrous Oxide? Concentration Effect NOTE: The cocentration effect describes the concentration of NO itself in the alveoli after its uptake into the circulation. NO is drawn into the trachea as NO is moved from the lung into the circulation further increasing the amount of NO. This effect explains why the rate of FA/Fi rise for NO is faster than desflurane, despite having a higher blood:gas partition coefficient. The second gas effect describes how the rapid diffusion and uptake of NO concentrates the potent anesthetic (Sevoflurane) that is left behind in the alveoli.

Answer 690

The cocentration effect describes the concentration of NO itself in the alveoli after its uptake into the circulation. NO is drawn into the trachea as NO is moved from the lung into the circulation further increasing the amount of NO. This effect explains why the rate of FA/Fi rise for NO is faster than desflurane, despite having a higher blood:gas partition coefficient. The second gas effect describes how the rapid diffusion and uptake of NO concentrates the potent anesthetic (Sevoflurane) that is left behind in the alveoli.

Answer 691

At sea level (barometric pressure 760 mm Hg), oxygen has a partial pressure (PO2) of approximately **160 mm Hg **(21% of 760, with the variation due to water vapor pressure).

Answer 692

Rank the following volatile gases from highest to lowest vapor pressure: NO- 38,770 mmHg Desflurane- 669 mmHg Isoflurane- 238 mmHg Sevoflurane- 157 mmHg These vapor pressures are at 20 degrees celcius and 1 atm. At 20 degrees celcius and 1 atm all inhalation anesthetics exist in the liquid form except NO (which has a boiling point of -88 degree celicius). Although most of the inhalational anesthetics may be liquid in form, they equilibrate between the liquid and gas phases in a closed container. Vapor pressure is proportional to temperature. As the temperature rises, the kinetic energy of the liquid increases which raises the number of molecules in the gaseous state and increases the vapor pressure. After the temperature is raised sufficiently such that the vapor pressure exceeds the atmospheric pressure in an open container, it will have reached its boiling point.

Answer 693

Hepatitis B

Answer 694

In emergencies where an aseptic technique cannot be guaranteed, CVC's should be replaced within **48 hours.**

Answer 695

The list of patients who should receive prophylaxis is below: - Patients with a prosthetic cardiac valve - Patients who have previously had IE - Patients with unrepaired cyanotic congenital heart disease (including palliative shunts/conduits) - Patients with congenital heart defects which were repaired with prosthetic material within 6 months of the procedure - Patients with repaired congenital heart disease with residual defects at the site, or adjacent to the site, of a prosthetic patch or device - Cardiac transplantation recipients who develop cardiac valvulopathy (substantial leaflet pathology and regurgitation) Of note, prophylaxis only applies to certain surgical procedures: - Dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa - Invasive respiratory tract procedures that involve incision or biopsy of the respiratory mucosa (e.g. tonsillectomy, adenoidectomy, bronchoscopy with biosy, wedge resection) - Infected skin, skin structure, or musculoskeletal tissue (eg. incision of abscess) Antibiotics are no longer recommended for endocarditis prophylaxis for patients undergoing genitourinary or gastrointestinal tract procedures (UNLESS surgery is done on these areas and their is an active infection). The preferred prophylactic regimen is Amoxicillin 2 g given as a one time oral dose 30-60 min before the procedure.

Answer 696

Etomidate Ketamine NO Succinylcholine Anesthetic drugs to avoid in the event of an ocular trauma include etomidate, ketamine, and nitrous oxide. Etomidate is relatively contraindicated in emergent ocular surgery because it may induce myoclonus severe enough to increase IOP. Ketamine can cause nystagmus and blepharospasm and adversely affect surgical conditions. Ketamine was previously thought to increase IOP due to its sympathomimetic effects; however, recently, researchers have refuted this theory. Nitrous oxide should be avoided in ocular surgeries if there is a planned or if there has been a recent injection of gas to create an intraocular bubble or if there is a risk for vascular air embolism or pneumothorax. Succinylcholine can cause a transient increase in IOP that persists for 5 to 10 minutes after administration. The proposed mechanisms include choroidal vascular dilatation or prolonged tonic contractions of the extraocular muscles. Although patients with treated glaucoma are at minimal risk, the administration of succinylcholine to patients with recent ocular incisions or with penetrating eye injuries may result in vitreous expulsion and vision loss. Available data regarding pretreatment with nondepolarizing muscle relaxants to prevent succinylcholine-induced elevations in IOP are contradictory; however, pretreatment with dexmedetomidine, nifedipine, or lidocaine (1 to 1.5 mg/kg) may attenuate the increase in IOP after succinylcholine administration and intubation. OTHER: When making an anesthetic plan for patients with open globe injuries, several steps should be taken to avoid further injury to the eye: - Ensure adequate depth of anesthesia prior to laryngoscopy. Coughing and bucking cause a large increase in IOP and should be avoided. - Avoid succinylcholine, if possible, as it can increase IOP. - Propofol is preferred over etomidate or ketamine since the latter two drugs can cause myoclonus and nystagmus, respectively. - Avoid nitrous oxide as it can cause enlargement of intraocular gas bubbles and increase IOP. - Use caution with retrobulbar blocks as large volumes of local anesthetic behind the eye can increase IOP. - Attempt to avoid coughing and bucking with emergence.

Answer 697

Anterior Ischemic Optic Neuropathy (AION)- typically presents with unilateral painless visual loss that may not be present until after the first postoperative day. Results of physical examination will include findings of an afferent pupillary defect, altitudinal field defects, and optic pallor or disc edema. Anterior ischemic optic neuropathy is thought to be due to temporary hypoperfusion/nonperfusion of the blood vessels supplying the anterior aspect of the optic nerve. Cardiovascular disease, CABG, and spine surgery are risk factors. It is also thought that increased intraocular pressure due to crystalloid infusion and cardiopulmonary bypass machine priming solution can lead to ischemia. Vision loss is usually painless and the prognosis is often poor. Posterior Ischemic Optic Neuropathy (PION)-sudden, painless vision loss with an afferent pupillary defect. PION is thought to result from a reduction in oxygen supply to the retrolaminar aspect of the optic nerve. When an ischemic insult occurs, the resulting damage ensues slowly, leading to a symptom-free period followed by vision loss. Patients will often present with an afferent pupillary defect or nonreactive pupil. **Disc edema is absent in PION, while it is present in anterior ischemic optic neuropathy (AION)- important distuinguising feature.** Posterior ischemic optic neuropathy is often associated with spine surgeries that render the optic nerve vulnerable to ischemia due to its poor collateral flow. Posterior ischemic optic neuropathy more commonly affects men and is associated with surgeries involving the nose, neck, sinuses, or spine. **Bilateral blindness occurs more often with PION than with AION.** Posterior is more common than anterior ION! Risk factors include male sex, obesity, use of a Wilson frame, prolonged anesthetic, increased blood loss, and lower percent colloid administration. Although controlled hypotension has not been found to be an independent risk factor for ION, its routine use is not recommended and should be determined on a case-by-case basis. Central Retinal Artery Occlusion (CRAO)- presents as a sudden, painless loss of vision in one eye. A relative afferent pupillary defect is present. Ophthalmoscopic findings include a cherry-red spot at the fovea centralis, grayish-white discoloration of the retina, retinal plaques/emboli, and narrowing of all retinal vessels. Corneal abrasions- pain, tearing, photophobia, and a foreign body sensation. The pain is worsened by blinking and ocular movement and is typically present immediately after emergence from anesthesia.

Answer 698

Foreign body sensation Pain with blinking Pain with eye movement Tearing NOTE: Always tape eyes BEFORE masking as the mask can push high flow oxygen to eyes drying them out and mask can directly cause corneal abrasion. Under general anesthesia, corneal reflexes are obviously impaired and they also have decreased tear production.

Answer 699

Anterior ION: + disc edema Posterior ION: - disc edema Anterior is typically unilateral. Posterior is commonly bilateral.

Answer 700

Posterior ION Spine surgery renders the optic nerve vulnerable to ichemia due to its poor collateral flow. Think "posterior" is closer to the spinal cord.

Answer 701

Cardiac surgery

Answer 702

Prone position (eg. spine surgery)

Answer 703

Male Obese External occular compression Prone positioning (eg. spine surgery) Wilson frame Long surgery (>5hrs) SIgnificant blood loss

Answer 704

There is controversy surrounding the transient effect of ketamine on increasing IOP, but it can also cause **rotary nystagmus** and **blepharospasm** and should be avoided in ophthalmologic surgery. Succinylcholine, hypoxia, hypoventilation, straining, coughing, and retching can all increase IOP. Direct laryngoscopy and endotracheal intubation with inadequate anesthesia can prove disastrous to the injured eye if a patient is not adequately anesthetized or paralyzed.

Answer 705

Ischemic heart disease Pulmonary hypertension Aortic dissections Vascular aneurysms

Answer 706

Contact dermatitis is an example of a type IV hypersensitivity reaction.

Answer 707

The most significant route of latex exposure is through contact at mucosal surfaces.

Answer 708

Autoimmune hemolytic anemia is an example of a type II hypersensitivity reaction.

Answer 709

Anaphylaxis, food, drug, and seasonal allergies are all examples of a type I hypersensitivity reaction.

Answer 710

In patients with a Penicillin allergy, the cross-reactivity with Cephalosporins is approximately < 1 %. NOTE: Anaphylactic reaction to cephalosporins is uncommon with estimates being 0.0001% to 0.1%. An alternative may be sought if there is history of severe allergic reaction or anaphylaxis to Penicillin.

Answer 711

Ester local anesthetics

Answer 712

Clindamycin or Vancomycin NOTE: In patients with a Penicillin allergy, the cross-reactivity with Cephalosporins is approximately < 1 %. Anaphylactic reaction to cephalosporins is uncommon with estimates being 0.0001% to 0.1%.

Answer 713

Various factors and allergies are associated with an increased risk of anaphylaxis to latex. Healthcare worker Having a history of spina bifida or urogenital anomalies (due repeated exposure to latex foleys) Certain food allergies (avocados, apples, bananas, tomatoes, pineapples, peaches, melons, kiwis, papayas, carrots, celery, chestnuts, buckwheat, and white potatoes)

Answer 714

Steroidal NMBAs (RVP)

Answer 715

By maintaining the fraction of inspired oxygen (FiO2) **< 30%,** the risk of operating room items becoming flammable is decreased significantly. For an operating room fire to occur, the fire triad must be present—ignition source, oxidizer, and fuel. The ignition sources are numerous and include lasers, electrosurgical units, and fiber optic cables. The oxidizers in operating room fires are either oxygen or nitrous oxide. Oxygen is a component of room air and can be more present with supplemental oxygen administered during anesthesia. Nitrous oxide is equally as efficacious as an oxidizer as oxygen and may be administered during an anesthetic. Fuel sources include gauze dressings, endotracheal tubes, mattress pads, body/facial hair, and drapes. The key to prevention is minimizing the components in the triad.

Answer 716

An upper extremity tourniquet should be inflated to at least 50 mm Hg above the systolic blood pressure. A lower extremity tourniquet should be inflated to at least 100 mm Hg above the systolic blood pressure.

Answer 717

Tourniquets can be used safely for 2 hour(s). When inflation times are too long or tourniquet pressures are too high, damage can occur to the tissues beneath (blood vessels, nerves, muscles, and skin). Tourniquet pain does not respond well to opioids or deepening of the anesthetic! Tourniquet deflation is the only definitive treatment of tourniquet pain. To increase the duration of the tourniquet use, a perfusion break can occur. When the cuff is deflated, several physiological events occur such as transient metabolic acidosis, increased carbon dioxide levels, increased potassium, and a drop in systemic blood pressure. Care should be taken when the cuff is deflated in patients who are at risk of complications. The cuff should be inflated to 50 mmHg above the systolic blood pressure when a tourniquet used in the arm and to 100 mmHg above the systolic blood pressure when a tourniquet is used in the leg.

Answer 718

At least 5 minutes NOTE: In general, it is recommended to give antibiotics 30-60 minutes prior to start of procedure.

Answer 719

YES Antibiotics should be redosed if significant blood loss (>1500cc).

Answer 720

A pulse pressure variation (PPV) **< 10%** is evidence that the patient is no longer fluid responsive, so further crystalloid administration should be avoided to prevent hypervolemia.

Answer 721

Testes, ovaries, bone marrow, lymphoid tissues, and small intestines

Answer 722

When a person is exposed to ionizing radiation, damage to cells and deoxyribonucleic acid can occur, and the radiation effects can be divided into deterministic or stochastic effects (Table 1). Deterministic effects are short-term effects that occur only after a threshold dose is reached, and, if the dose is below the threshold, no effect should occur. For deterministic effects, a larger dose results in worse severity. Stochastic effects do not have a threshold and occur by statistical chance; a larger dose results in a greater chance of experiencing that effect. For stochastic effects, severity does not depend on the dose. The stochastic health effects can occur from either a short or a long exposure period.

Answer 723

The majority of occupational exposure of the anesthesiologist to ionizing radiation from fluoroscopy comes from **x-rays reflected off the patient.** OTHER: The maximal annual exposure mandated by multiple national organization is no more than 5rem (single CXR = 25milirem, single CT A/P = 1rem). Six feet of air between the provider and the radiation source provides approximately the same protection as 9in of concrete or 2.5mm of lead (standard lead approns have 0.5mm lead). This is because radiation intensity is inversely proportional to the square of the distance from the radiation source.

Answer 724

A variety of low-flow systems (e.g. nasal cannulas, simple face masks, partial rebreathing masks, and nonrebreathing masks) are used perioperatively to provide patients with supplemental oxygen. A low-flow system is one which delivers 100% oxygen at flows less than a patient’s inspiratory flow rate. It is important to realize that although the delivered oxygen is 100%, the actual inspired oxygen (FiO2) is less than 100% as it is diluted with room air. The FiO2 can be increased by increasing the oxygen flow rate, but each system does have a maximum FiO2 that can typically be provided. Nasal cannulas provide an FiO2 of 25-40% with flow rates up to 6 L/min. Simple face masks provide an FiO2 of approximately 35-50% with oxygen flows of 5-10 L/min. Nonrebreathing mask can provide an FiO2 of 60-80% with oxygen flows of 10-15 L/min.

Answer 725

2.5mg/kg IV over one minute which can be repeated every 5-10 minutes as necessary up to 10 mg/kg. After the acute phase has resolved, dantrolene should be continued for 24-48 hours either as a 1 mg/kg bolus every 4-6 hours, or as an infusion of 0.25 mg/kg/hr to prevent recrudescence. The only treatment for malignant hyperthermia remains dantrolene, which is believed to suppress the release of calcium ions from the sarcoplasmic reticulum. The moment malignant hyperthermia is suspected, all triggering agents should be stopped, 100% oxygen should be flushed through the system, and dantrolene should be immediately administered.

Answer 726

Central Core Disease Multiminicore Disease King-Denborough Syndrome NOTE: Duchenne, Becker, Myotonic Dystrophy are NOT associated with MH but succinylcholine should be avoided due to potential for hyperkalemia.

Answer 727

Autosomal Dominant (w/ variable penetrance) NOTE: MH is a disorder resulting from mutations in the RYR1 gene coding for the ryanodine receptor. The ryanodine receptor regulates the release of calcium ions from the sarcoplasmic reticulum during the muscle contraction. Mutations affecting this receptor result in an abnormal unregulated release of calcium ions causing the symptoms of MH (muslce rigidity, increased ETCO2, lactic acidosis, rhabdo, hyperkalemia, elevated serum creatinine kinase, myoglobinuria).

Answer 728

Turn off vaporizer Bag mask patient Flush circuit at 10L/min for 90 seconds Change out breathing circuit and bag Apply charcoal filters on inspiratory and expiratory limb (replace every hour) Increase FGF to 10L/min w/ 100% FiO2 Hyperventilate patient Dantrolene (2.5mg/kg over a minute repeat every 5-10minutes up to max dose of 10mg/kg)

Answer 729

Malignant Hyperthermia POI: AD Mutated Gene: RYR1 gene coding for the ryanodine receptor which regulates the release of calcium ions from the sarcoplasmic reticulum during muscle contraction Triggers: Succinylcholine and all volatile anesthetics Symptoms: muscle rigidity, masseter rigidity, increased carbon dioxide production, adenosine triphosphate consumption, anaerobic glycolysis, hyperthermia, lactic acidosis, rhabdomyolysis, elevated levels of CK, hyperkalemia, myoglobinuria.

Answer 730

The **halothane-caffeine contracture test** has the highest sensitivity (97%) and is considered the current gold standard for the diagnosis of malignant hyperthermia. Specificity, however, is 78% so some false positives may occur. NOTE: Halothane-caffeine contracture test requires a muscle biopsy. Muscle is exposed to halothane and caffeine and the extent of muscle contraction is tested. While genetic testing for mutations of the ryanodine receptor has become increasingly common, not all genetic defects representing MH have been identified. Genetic testing is less sensitive.

Answer 731

Presentation: Fever Confusion Tachcyardia Congestive heart failure Onset: 6-18hrs after inciting event Treatment: Propranolol Methimazole or PTU Hydrocortisone Pressors/inotropes (send to ICU)

Answer 732

20% Intravenous Lipid Emulsion (ILE) Initial bolus 1.5cc/kg (over several minutes) Followed by an infusion at 0.25cc/kg/min (over 30-60min or until hemodynamic stability is achieved) The hypothesis for ILE's efficacy in treating cardiotoxicity is the formation of an intravascular lipid phase that absorbs the lipophillic drug. This redues the amount of free drug available to bind to the myocardium and exert negative effects. LAST manifests as CNS excitation to CNS depression followed by CV excitation to CV depression: CNS Agitation, auditory change, metallic taste Seizures, CNS depression CV Dysrhythmias Bradycardia, AV block, asystole, diminished contractility

Answer 733

The maximum acceptable dose of lidocaine during tumescent anesthesia is 35 to 55 mg/kg. Tumescent anaesthesia describes the practice of injecting a very dilute solution of local anaesthetic combined with epinephrine and sodium bicarbonate into tissue until it becomes firm and tense (tumescent). It was initially described in the field of liposuction but now surgical applications for the technique are widely varied ranging across vascular surgery, breast surgery, plastic surgery and ENT procedures. Patients are at risk of LAST and fluid overload/pulmonary edema in these surgeries.

Answer 734

Normal saline, with a supranormal chloride concentration of 154 mEq/L, can cause hyperchloremic *non–anion gap* acidosis if it is given in high volumes. Normal saline solution, originally introduced in the 19th century at the time of chlolera outbreaks, was labeled normal as a result of flawed research. Normal saline, which has been the most widely used fluid for more than a century despite minimal research providing evidence of clinical efficacy and safety, has been increasingly scrutinized since the year 2000. Rapid and large-volume normal saline administration will cause hyperchloremic non–anion gap metabolic acidosis. Normal saline contains 154 mEq/L of both sodium and chloride, which is higher than physiologic concentrations of both, but especially for chloride. **Excessive chloride impairs bicarbonate reabsorption in the kidneys, and the serum bicarbonate concentration will decrease with the use of normal saline.** This decrease in bicarbonate compensates for the increase in chloride and maintains electroneutrality, causing non–anion gap acidosis.

Answer 735

The lactate in lactated ringers solution is converted to pyruvate by lactate dehydrogenase (LDH) in the liver. Pyruvate then enters the citric acid cycle to produce H2O, CO2, and **bicarbonate**. Lactate in lactated ringers DOES NOT increase lactic acid levels and DOES NOT cause acidosis because it is the base conjugate of lactic acid.

Answer 736

Acetate is metabolized by the liver, muscle, and heart to bicarbonate. Gluconate is converted to glucose by the liver which can then be used for glycolysis and citric acid cycle.

Answer 737

Methadone (Dolophine, Methadose)- full μ-opioid agonist, NMDA anatagonist, also acts like an SSRI in that it inhibits the serotonin transporter (SERT) .

Answer 738

Buprenorphine (Suboxone)- partial μ-opioid agonist, κ-antagonist

Answer 739

QT prolongation

Answer 740

Administer half the dose in IV form. Example: 30mg Methadone daily = 15mg Methadone IV

Answer 741

Full μ-opioid agonist NMDA anatagonist SSRI NOTE: High oral bioavailablility, high potency, long duration of action. No active metabolites.

Answer 742

Nalbuphine (Nubain) Partial mu-opioid receptor antagonist Kappa-opioid receptor agonist NOTE: Analgesic properties are mediated specifically through agonist activity at the kappa-opioid receptor. Although nalbuphine can result in respiratory depression, due to its antagonism of the mu-opioid receptor, it antagonizes the respiratory depressant effects of other opioid medications while concomitantly adding to the analgesic activities of these drugs. Non-FDA approved uses of nalbuphine do exist such as treatment of labor pain, opioid-induced urinary retention, opioid-induced respiratory depression, and **pruritus associated with neuraxial opioid use (2.5mg Q10-15min, more effective than Zofran or Benadryl)**

Answer 743

Mu opioid agonist & antagonist (mixed) Partial kappa agonist Used in treating pain, post-operative shivering, and neuraxial opioid-induced pruritis. It is also the only opioid that does not cause sphincter of oddi contraction and increased CBD tone.

Answer 744

40mcg every 5 minutes (until apnea or pronounced hypoapnea is resolved) Dilute Naloxone from 0.4mg/cc to 0.04mg/cc (40mcg). Recommend 40mcg dose to avoid adverse effects such as **increased heart rate, increased blood pressure, and potentially pulmonary edema. ** NOTE: Naloxone has a greater affinity for mu opioid recepots but also has some activity at the delta and kappa receptors. Can also reverse the nausea, vomiting, pruritis, and urinary retention effects of opioids. Duration of action: 30-60minutes Renarcotization can occur with long-acting opioids such as morphine and dilaudid. Naloxone is thus ideally used to reverse fentanyl or alfentanil. Repeated doses or infusion may be needed for long-acting opioids. Naltrexone is a longer-acting opioid antagonist that is better suited for longer acting opioids.

Answer 745

Mu agonist (weak) SNRI NOTE: Tramadol is a prodrug metabolized by CYP 2D6 Tramadol's mu opioid affinity is 1/6000 that of Morphine and 1/10 that of Codeine. Risk of serotonin syndrome when combined with SSRIs or MAOi.

Answer 746

NMDA receptor antagonists include: - Ketamine - Nitrous Oxide - Methadone - Tramadol - Dextromethorphan (Robitussin) - Memantine (Alzheimer med) The NMDA receptor is an ionotropic glutamate receptor that functions as a non-specific ion channel when activated. Unlike most other receptor types which are either voltage-dependent or ligand-gated, the NMDA receptor is both. The two primary receptor agonists are glutamate and glycine and the receptor contains specific binding sites for each. In addition, the receptor can only be activated when the cell is depolarized. At resting membrane potential (non depolarized state), the ion channel is blocked by magnesium. Depolarization removes the magnesium. Therefore, both of the following two conditions must be met for the NMDA receptor to become activated: 1) Glutamate (or glycine) must be bound (ligand-gated) and 2) The cell must be depolarized (voltage-gated) The receptor will not be active if only one of these conditions is met. When the receptor is activated, the ion channel opens and allows sodium and calcium entry into the cell and potassium out of the cell. However, it is the calcium influx (C) that is the primary mediator of the effects of NMDA receptor activation since it acts as a second messenger for a variety of signaling pathways.

Answer 747

Intrathoracic Obstruction Spirometry produces flow-volume loops. Different types of lung disease create stereotypical patterns on these flow-volume loops. An intrathoracic obstructive pattern is often described as having an expiratory pattern that resembles a "boot shape." This is commonly seen in patients with chronic obstructive pulmonary disease and asthma. It is thought to be secondary to the narrowing of the upper airways and loss of elastic recoil in the lower airways.

Answer 748

A patient that is being mechanically ventilated (not spontaneous) Tidal volumes must be 8-10 mL/kg PEEP > 5 Sinus rhythm Closed intrathoraic cavity with normal intrathoracic pressures Closed abdomen with normal intraabdominal pressures NOTE: Arterial waveform analysis, in which variation in pulse pressure, systolic pressure, or stroke volume **> 10% is considered fluid responsive**, is one of the most popular mechanisms used in a GDT protocol.

Answer 749

SHORT ACTING Midazolam (Versed) INTERMEDIATE TO LONG ACTING Alprazolam (Xanax) Lorazepam (Ativan) Diazepam (Valium) Chlordiazepoxide (Librium) NOTE: Midazolam has an elimination half-life of 1.5–3 h. The duration of action is 60–120 min. All benzodiazepines are metabolized by the liver and excreted by the kidneys.

Answer 750

0.25-1mg/kg (max 20mg) Younger children should be given higher starting dose (0.5mg/kg-1.0mg/kg) due to their high volume of distribution. Older children (6-16 y/o) should be given a lower initial dose (0.25mg/kg) Adequate anxiolysis occurs in approximately 20min after oral administration. Elimination half-life of approximately 2 hours.

Answer 751

**Positive allosteric modulators of the GABA-A receptor. ** Benzodiazepines increase the total conduction of chloride ions across the neuronal cell membrane while the endogenous ligand GABA is already bound. Thus, they are considered a positive allosteric modulator *rather than an agonist* as they do not directly bind to the receptor site for GABA.

Answer 752

Floppy infant syndrome Neonatal withdrawal syndrome NOTE: In general, benzos should also be avoided in the first trimester when anatomical structures are forming. Single dose of benzos has not been associated with teratogenicity.

Answer 753

Increases in PaCO2 and decrease in pH shift the oxygen dissociation curve to the RIGHT which is called the Bohr effect. This leads to hemoglobin offloading oxygen to the tissues. Increases oxygen delivery to acidotic and hypoxic tissues.

Answer 754

In hypoxic states hemoglobin has an increased affinity for CO2 which is called the Haldane effect.

Answer 755

Rightward shift of hemoglobin P50. Results in better oxygen delivery to the tissues. The P50 of hemoglobin is the partial pressure of oxygen at which hemoglobin is 50% saturated with oxgyen. NOTE: It is recommended that patients stop smoking 8 weeks prior to surgery to help reduce postoperative pulmonary morbidity.

Answer 756

1) Blunts hypoxic pulmonary vasoconstriction High FiO2 increases shunt fraction and blunts hypoxic pulmonary vasoconstriction. 2) Microatelectasis High concentrations of FiO2 causes microatelectasis. This is because when using high concentrations of oxygen there is less nitrogen is the alveoli which normally helps stent open the alveoli. Less nitrogen results in more alveolar collapse which is called microatelectasis.

Answer 757

NOTE: Nitroprusside and nitroglycerin produce nitric oxide and cause systemic as well as pulmonary vasodilation. Pulmonary vasodilation will blunt HPV at hypoxic alveoli. Calcium channels blockers (eg. nicardipine) inhibits HPV by preventing calcium influx into cells.

Answer 758

Variable intrathoracic airway obstruction Plateaued expiratory curve

Answer 759

Fixed upper airway obstruction Plateaued inspiratory AND expiratory curve

Answer 760

Metabolic acidosis Hypoxia A left shift amplies the patients respiratory drive and leads to hyperventilation to improve alveolar ventilation.

Answer 761

Deep anethesia Volatile anesthetics Propofol Benzodiazepines Opioids NOTE: The slope of the carbon dioxide response curve represents carbon dioxide sensitivity which is primarily a function of chemoreceptor thresholds. At increasing partial pressures of arterial CO2 an awake and unmedicated patient will generally respond with approximately linear increases in alveolar ventilation in order to compensate and return to normocapnia. This response may be profoundly blunted when sedative-hypnotics, opioids, or other anesthetic medications are administered because these drugs tend to impair chemoreceptor activation and signaling. The end result is that significantly higher arterial CO2 tensions will be required to provoke an equivalent ventilatory response and patients will therefore tend to hypoventilate despitre progressive hypercapnia.

Answer 762

Profound hypercarbic narcosis can be seen at partial pressures of 100-120mmHg. NOTE: Corresponding acidosis will cause hypotension and arrhythmias. Also will get increased ICP which can be detrimental if patient already has elevated ICP.

Answer 763

LEFT Fetal hemoglobin Carboxyhemoglobin Methemoglobin Sickle hemoglobin RIGHT Sulfhemoglobin

Answer 764

Storage of PRBCs shifts the oxygen-hemoglobin dissociative curve to the LEFT. 2,3 DPG is an intermiate step in the glycolytic pathway and this product of cellular metabolism is a factor in shifting of the oxygen hemoglobin dissociation curve. Storage of PRBCs depletes 2,3 DPG as the RBCs are using this intermediate to create energy in storage. Decrease in 2,3DPG shifts the curve to the left.

Answer 765

Peak Inspiratory Pressure (PIP) = Resistance Pressure (Pr) + pressure from overcoming respiratory system complaice (Pc) + positive end expiratory pressure (PEEP) If PIP is increased a differential includes: 1) Increased resistance (kinked tube, mucus plug, bronchospasm) 2) Decreased compliance (insufflation, bronchial intubation, pumonary edema, tension pneumothorax)

Answer 766

By adjusting the splitting ratio (see picture).

Answer 767

Dead space is the portion of the lung volume that is not involved in perfusion and therefore not involved in gase exchange. Physiological dead space = anatomical dead space (oronasopharynx, trachea, bronchi, bronchioles) + alveolar dead space (alveoli that is not perfused) In healthy individuals 30% of minute ventilation is spent on dead space ventilation. Physiological dead space is approximately 2mL/kg in the adult patient. When minute ventilation decreases below 2.1L/min ventilation is no longer effective for CO2 removal (see picture). This means that in a healthy individual of an average 500mL TV a total of 150mL goes to the conduction airways (anatomic deadspace) and alveoli that are not perfused (alveolar dead space) and only 350mL actually participates in alveolar ventilation. In a patient with rapid shallow breathing, when titdal volumes approach 150mL most of that volume goes to dead space ventilation and despite the apparent presence of minute ventilation the alveolar ventilation is close to zero. To put it in another way, not all minute ventilation is created equal.

Answer 768

Bohr Formula VD = VT (PACO2 - PECO2) / PACO2

Answer 769

INCREASE General anesthesia (multifactorial, including loss of skeletal muscle tone and bronchoconstrictor tone) Positive pressure ventilation (decreases VR/CO thus decreasing pulmonary perfusion) Artificial airways/ anesthesia circuit Upright position (apices of lungs are essentially nonperfused in the upgright position due to the effects of gravity on blood flow distribution) Neck extension (increases length thus volume of upper airway) Bronchodilators Anticholinergics Low cardiac output states (shock, heart failure) COPD (increases pulmonary vasculature resistance) DECREASE Supine position Neck flexion Spontaneous breathing

Answer 770

Mechanical dead space is the area within the circuit that does not participate in gas exchange. Mechanical dead space within the circle system is distal to the Y-piece. It is in effect an external extension of the physiological dead space. Areas of mechanical dead space in a typical anesthesia machine circle system are: 1) Portion of the ETT which extends out of the tracha 2) Breathing circuit elbow connector 3) Any connector used between the ETT and the breathing circuit (eg. HME). 4) The Y-piece NOTE: The expiratory limb, inspiratory limb, and reservoir bag DO NOT add mechanical dead space as they are still within the breathing system. Extending the length of the inspiratory and/or expiratory limb DOES NOT add dead space as this is still within the circle breathing system. The one-way valves prevent inspiration of exhaled air or expiration into the inspiratory limb regardless of the length of the tubing present.

Answer 771

FRC represents the volume at which the lungs natural tendency to recoil equals the chest's tendency to expand. FRC = ERV + RV.

Answer 772

ETCO2 is always lower than PaCO2 as a result of dead space ventilation. ETCO2 is 5-10mmHg lower than PaCo2 NOTE: Acute increases in the gradient between the two should raise concern of increased dead space ventilation- most commonly decreased CO but other potential causes include PEs, high PEEP, right to left intracardiac shunts, etc.

Answer 773

Atelectasis develops in about 90% of patients who are anesthetized and can persist for several days in the post-operative period. Atelectasis is believed to be caused by a combination of: 1) Changing patient from an upright to supine position (decreases FRC) 2) Loss of muscle tone from volatile gases, & NMBAs (decreases FRC) 3) Loss of surfactant 4) Compression atelectasis (diaphragm relaxation and cephalad displacement pushing on lungs, worse in supine positioning) 5) Absorption atelectasis (occurs when less gas enters the alveolus than is removed by uptake by the blood.

Answer 774

Phenomenom where complete absorption of oxygen results in collapse of alveoli. Hence why recommennded to keep FiO2 lowest possible while maintaining O2 sats > 90%

Answer 775

In order to prevent acute lung injury (ALI), plateau pressures should be kept under 30cm H20.

Answer 776

According to the law of Laplace the pressure in a spherical structure (eg. alveoli) is equal to: P= 2 x h x T / R h = wall thickness T = wall tension R = sphere's radius Surfactant reduces surface tension preventing the collapse of small alveoli at low lung volumes. Surfactant is made up of phospholipids and glycoproteins. Surfactant is produce by type II alveolar epithelial cells. As alveoli become smaller during expiration, the surface phospholipid layer thickens and the cocentrations of surfactant at the surface increases more effectively reducing surface tension. The reduction in surface tension, proportional to the reduction in radius, prevents the wall tension from overcoming the critical collapsing pressure, which would otherwise lead to the collapse of small alveoli and atelectasis.

Answer 777

Determinants of myocardial oxygen supply? 1) CBF 2) Arterial oxygen content (CaO2) 3) Ability of myocardium to extract O2 (eg. decreased capillary density in hypertrophied hearts, changes in oxyhemoglobin dissociation curve) Determinants of myocardial oxygen demand? 1) HR 2) Contractility 3) Wall Stress ("Laplace law", wall stress = pressure x radius /(2* thickness)

Answer 778

WOB = ventilatory rate x (airway resistance/lung compliance) NOTE: If airway resistance increases or lung compliance decreases there will be an increased WOB.

Answer 779

Surfactant production begins at 24 weeks gestational age and reaches adequate levels at 34 weeks gestational age. Premature infants born before 34 weeks gestational age have a surfactant deficiency that leads to increased surface tension, reduced FRC, and increased WOB. This culiminates in atelectasis, pulmonary edema, and hypoxemia. This is the basis of Respiratory Distress Syndrome (RDS) which is also known as surfactant deficiency disorder.

Answer 780

A right-to-left intrapulmonary shunt will slow inhalation induction. The rate of rise for the alveolar concentration to inspired concentration (FA/Fi) will decrease. This is due to the dilution of the anesthetic agent when the venous blood that has bypassed the lungs mixes with arterial blood.

Answer 781

A right-to-left intracardiac shunt affect decreases speed of inhalational induction (mixing of anesthetic poor and rich blood). A right-to-left intracardiac shunt affect increases speed of IV induction (bypasses pulmonary circulation).

Answer 782

Minimal/no effect for both inhalational and IV induction.

Answer 783

ACLS medications that have been effectively administered via the ETT route include epinephrine, naloxone, atropine, and lidocaine. “LEAN” NOTE: When medications are administered via the ETT route, higher doses (approximately 2 to 2.5 times the intravenous dose) are required. In addition, to produce a larger surface area within the bronchoalveolar space, these drugs are diluted in a 5 to 10 cc solvent such as isotonic saline or distilled water before application through the end of the ETT.

Answer 784

Risk factors include increased intraocular pressure (IOP) or orbital venous pressure (OVP); hypotension and hemodilution during surgeries; and procedures such as coronary artery bypass grafting, spine surgery, and thoracoabdominal aortic surgeries. Increased IOP due to external compression can lead to a decrease in retinal blood flow, injuring the retinal and optic nerves. Thus, the amount of time spent in the prone position should be minimized, and the patient's eyes should be checked periodically to ensure that there is no pressure on the eyes. When OVP is increased, there is a decreased perfusion pressure gradient to the optic nerve head, resulting in ischemia. Patients will typically present with a sudden, unilateral, painless loss of vision, altitudinal field defects, optic disc edema or pallor, and afferent pupillary defects

Answer 785

MAP (most accurate) Systolic (underestimated) - least accurate Diastolic (overestimated) NOTE: BP cuff measures MAP, but systolic and diastolic are calculated. Bladder of the cuff should cover 40% of the upper arm's circumference and 80% of the length of the upper arm.

Answer 786

Ideal BP cuff bladder length is > 80% of patient’s arm circumference. Using a cuff that is TOO SMALL will result in an OVERESTIMATION of BP Using a cuff that is TOO LARGE will result in an UNDERESTIMATION of BP

Answer 787

Corneal reflex Afferent: V (opthalmic division, V1) Efferent: VII (stimulates orbicularis oculi muscle) During induction of anesthesia, corneal reflex is first to be lost.

Answer 788

MOA a1- antagonist b1- antagonist b2- antagonist AND partial agonist (overall, arteriolar vasodilation) Onset- 5 min Peak effect- 15 min Half life- 6 hours Duration- 16-18hrs

Answer 789

Selective B1 antagonist

Answer 790

Slower induction speed

Answer 791

What effect does an right-to-left intracardiac shunt have on speed of inhalational induction? > Slower induction speed What effect does an right-to-left intracardiac shunt have on speed of IV induction? > Faster induction speed

Answer 792

Shortens/attenuates

Answer 793

Prolongs/potentiates

Answer 794

Magnesium May modulate ventricular response rate and promote conversion to sinus rhythm when weaning from CPB.

Answer 795

Bivalirudin

Answer 796

Idarucizumab

Answer 797

Andexanet Alfa

Answer 798

CO increased SVR decreased

Answer 799

Doxorubicin Cyclophosphamide Paclitaxel Rituximab 5-Flourouracil NOTE: Careful attentionn must be paid to fluid administration to avoid the complications associated with heart failure such as pulmonary edema.

Answer 800

Bleomycin Bleomycin keep FiO2 BElow

Answer 801

HR >10bpm SBP > 15-25mmHg They would also experience numbness in a minute and weakness after 3 minutes. Analgesic effect of an epidural typically takes 10 minutes.

Answer 802

Must have condition + procedure Oral Amoxicillin 2g 30-60min prior to procedure

Answer 803

Men Age > 55 BMI > 30 Mallapatti 3 or 4 No neeth (endentulous) Bearded OSA/snoring

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