NCC Study Guide 2026 Critical Care Topics

Question 1

Arousal definition

Answer 1

wakefulness, largely mediated by the ascending reticular activating system and hypothalamus

Question 2

Awareness

Answer 2

perception of self/environment, which depends on intact arousal

Question 3

Spectrum of Consciousness

Answer 3

Alert: spontaneous arousal, fully interactive and aware
Lethargic: arouses to loud voice or light touch, droswy, slow response, easily drowses off
Obtunded: arouses to light shaking or firm command, sleeps often and slow responses
Stuporous: arouses to vigorous or painful stimulation, minimal movement, quickly lapses
Comatose: not arousable, no voluntary actions, eyes closed

Question 4

For boards, coma generally results from what two things?

Answer 4

1. Bilateral Hemispheric dysfunction or
2. Brainstem dysfunction affecting arousal pathways

Question 5

What is the FOUR score and why is it helpful in the ICU?

Answer 5

The FOUR score is especially useful in the ICU because it is more informative in intubated patients and includes eye response, motor response, brainstem reflexes, and respiration. Studies have generally not shown a major prognostic difference versus GCS, but FOUR gives a more complete neuro-ICU bedside picture, while adding pupillary reactivity improves GCS performance.
GCS is limited in intubated patients due to the impaired verbal score.

Question 6

What are the components of the FOUR score and how many points for each?

Answer 6

Eye Response
Motor Response
Brainstem Reflex
Respiration Pattern
1-4 for each

Question 7

Unilateral fixed dilated pupil source and example?

Answer 7

Compression CN III (ex: uncal herniation)

Question 8

Small reactive pupil source?

Answer 8

Metabolic/toxic
Pontine-related

Question 9

Bilateral fixed pupils source?

Answer 9

Severe brainstem dysfunction
Severe hypoxic-ischemic injury
Drug effect

Question 10

What nerves are involved in the corneal relfex?

Answer 10

Afferent CN V
Efferent CN VII

Question 11

What nerves are involved in the gag reflex and palatal elevation?

Answer 11

CN IX/X

Question 12

What nerves are involved in the pupillary light reflex?

Answer 12

CN II/III

Question 13

What does loss of brainstem reflexes in a comatose patient suggest? What needs to be ruled out?

Answer 13

Structural Brainstem Injury
Advanced Herniation
Rule out: drugs, hypothermia or severe metabolic suppression

Question 14

Decorticate (flexor) posturing suggestion dysfunction where?

Answer 14

Above the red nucleus

Question 15

Decerebrate (extensor) posturing suggests dysfunction where?

Answer 15

At or below the red nucleus (more ominous than decorticate posturing)

Question 16

Cheyne-Stokes Breathing Pattern and localization?

Answer 16

Rhythmic, alternating periods of rapid breathing and apnea (no breathing) associated with bilateral cerebral hemisphere injury or diencephalon dysfunction

Question 17

Central Neurogenic Hyperventilation breathing pattern and localization?

Answer 17

Deep, rapid breaths caused by damage to the midbrain or upper pons.

Question 18

Apneustic Breathing pattern and localization?

Answer 18

Prolonged, gasping inspirations with short, inefficient expirations often indicating injury at the cephalad (upper) pons.

Question 19

Ataxic (Biot’s) Breathing pattern and localization?

Answer 19

Completely irregular breathing patterns (rate and depth) with irregular pauses, pointing to damage in the medulla oblongata.

Question 20

Cluster breathing pattern and localization?

Answer 20

Clusters of rapid breaths followed by irregular periods of apnea, often indicating damage at the lower pons or high medulla.

Question 21

C3-C5 C spine injury damages what and needs what?

Answer 21

Damages phrenic nerve and leads to paralysis of diaphragm and need for mechanical ventillation

Question 22

C5-C7 spine cord injury leads to what?

Answer 22

Reduced lung capacity, weak cough, reliance on accessory muscle use

Question 23

Doctrine that involves brain, blook and csf within fixed skull and ICP changes?

Answer 23

Monro-Kellie

Question 24

Uncontrolled ICP effects?

Answer 24

Reduced cerebral perfusion
Worsens edema
Herniation
Ischemia

Question 25

Normal CSF opening pressure?

Answer 25

8-15 mmHg

Question 26

CPP Equation

Answer 26

MAP - ICP

Question 27

In severe TBI, what is the Brain Trauma Foundation Guidance Recommendations for CPP?

Answer 27

60-70 mmHg

Question 28

What can happen with aggressive attempts to keep CPP >70?

Answer 28

Increased complications like respiratory failure

Question 29

In severe TBI, the Brain Trauma Foundation Guidelines recommend treating ICP above what?

Answer 29

22 mmHg

Question 30

What are the highest-yeild bedside modulators or cerebral blood flow?

Answer 30

PaCO2 MAP/CPP Oxygenation when severe hypoxemia occurs Metabolic demand (ex: fevers, seizures, agitation, sedation, burst supression)

Question 31

What happens with cerebral blood flow with hyperventilation?

Answer 31

Lowers PaCO2 -> cerebral vasoconstriction -> reduced cerebral blood volume -> lower ICP temporarily at risk of reduced CBF

Question 32

What constricts/dilates for cerebral autoregulation?

Answer 32

Arterioles

Question 33

What happenes with elevated PaCO2 to CBF and ICP?

Answer 33

Cerebral vasodilatation -> increased cerebral blood volume -> increased ICP

Question 34

What happens with decreased PaCO2 to CBF and ICP?

Answer 34

Cerebral vasoconstriction -> decreased cerebral blood volume -> lower ICP

Question 35

Brain Trauma Foundation Guildelines for PaCO2?

Answer 35

Avoid prolonged PaCO2 25 mmHg or less, only use temporarily for elevated ICP

Question 36

Goal SpO2 in brain injury?

Answer 36

90% or greater

Question 37

Goal BP in severe TBI?

Answer 37

50-69 years old: at least 100 mmHg 15-49 or over 70: 110 mmHg

Question 38

Steps for Elevated ICP Management

Answer 38

1. Head elevation/optimize venous drainage 2. Analgesia and sedation 3. Treat fevers, agitation and seizures 4. Hyperosmolar therapy 5. CSF drainage when available 6. Brief Hyperventilation only as rescue/bridge 7. Decompressive surgery in selected refractory cases

Question 39

NCC Society Guildeines on Hyperosmolar therapy

Answer 39

Neurocritical Care Society guidance supports hyperosmolar therapy for ICP/cerebral edema across several neurocritical illnesses, though long-term neurologic outcome benefit is less clear. In TBI, the NCS guideline suggests hypertonic sodium solutions over mannitol, while still recognizing mannitol as an effective alternative in appropriate patients.

Question 40

BTF EVD stance?

Answer 40

An external ventricular drain can both measure ICP and lower ICP by drainage. BTF notes that continuous CSF drainage may lower ICP burden more effectively than intermittent use in selected severe TBI patients.

Question 41

Sedatives and Barbiturates in elevated ICP?

Answer 41

Propofol can help control ICP but is not proven to improve long-term outcome. High-dose barbiturates are reserved for refractory intracranial hypertension and require hemodynamic stability.

Question 42

Steroids in elevated ICP?

Answer 42

In severe TBI, steroids are not recommended for improving outcome or lowering ICP, and high-dose methylprednisolone is associated with increased mortality.

Question 43

Functions of CSF?

Answer 43

CSF provides: - mechanical protection - buoyancy - metabolic exchange - waste clearance. CSF reduces the brain’s effective weight from roughly 1500 g to about 50 g, helping protect neural tissue and intracranial vessels

Question 44

CSF Numbers (total volume, in SAH, in ventricles, daily production and turn over rate)

Answer 44

Total volume: 150 cc's SAH: 125 cc's Ventricles: 25 cc's Daily production: 400-600 cc's Turnover: 4-5 times per day in young adults

Question 45

Where is CSF made?

Answer 45

Most CSF is produced by the choroid plexus, with around 80% of production coming from this source. The choroid plexus epithelium and its tight junctions form the blood-CSF barrier

Question 46

What is the blood-CSF Barrier versus the Blood-Brain Barrier?

Answer 46

Blood-CSF: choroid plexus epithelium Blood-Brain: capillary endothelial tight junctions

Question 47

Flow of CSF

Answer 47

Lateral ventricles → foramina of Monro → third ventricle → cerebral aqueduct → fourth ventricle → foramen of Magendie and foramina of Luschka → subarachnoid space.

Question 48

Obstruction of foramen of Monroe causes enlargement of what?

Answer 48

Lateral ventricles enlargement 3rd ventricle normal

Question 49

Obstruction of cerebral aqueduct causes enlargement of what?

Answer 49

Lateral and third ventricles

Question 50

Obstruction of Foramina of Magendie/Luschka/4th ventricle outlet causes enlargement where?

Answer 50

Lateral, third and 4th ventricles

Question 51

Obstruction of the subarachnoid space/basal cistern is also known as what and causes enlargement where?

Answer 51

Communicating Hydrocephalus Fluid cant reach absorption sites from inflammation or scaring from meningitis or hemorrhage Enlargement of ventricles

Question 52

Arachnoid Granulations

Answer 52

Impaired absorption at the sagittal sinus leads to generalized ventricle enlargement

Question 53

Where is CSF absorbed and how?

Answer 53

Classically, CSF was taught to be absorbed primarily through arachnoid villi and granulations into the dural venous sinuses, driven by a pressure gradient between subarachnoid space and venous sinuses. Modern understanding adds that dural lymphatic pathways and other lymphatic/perineural routes appear to be major outflow pathways, including drainage toward cervical lymph nodes and through the cribriform region.

Question 54

CSF versus plasma concentrations or Na, Cl, Mg, K+, Ca, Protein and Cells

Answer 54

Compared with plasma, CSF normally has: higher sodium, chloride, magnesium lower potassium and calcium very low protein and very few cells. Normal cell counts are typically <5 cells/mL

Question 55

What is the glymphatic system?

Answer 55

The glymphatic system is a perivascular fluid clearance network in which CSF enters along periarterial spaces and waste exits along perivenous pathways toward meningeal lymphatics and cervical nodes. This system is increasingly relevant in neurocritical care, edema, and neurodegeneration.

Question 56

Does CSF participate in waste clearance and interstitial fluid homeostasis?

Answer 56

Yes

Question 57

What is obstructive hydrocephalus?

Answer 57

Blockage anywhere in the ventricular outflow pathway can cause upstream ventricular dilation and ICP elevation. The cerebral aqueduct is a classic narrow bottleneck.

Question 58

What is communicating hydrocephalus?

Answer 58

Flow exits the ventricles, but absorption/egress is impaired. Classically this is framed as impaired arachnoid granulation resorption, though newer lymphatic models broaden that concept.

Question 59

What is idiopathic intracranial hypertension?

Answer 59

Elevated ICP without mass lesion, hydrocephalus, or abnormal CSF composition, and one leading theory is impaired CSF absorption.

Question 60

If you suspect SAH, what should you look for on LP?

Answer 60

Xanthochromia and persistent RBCs across tubes

Question 61

Key Points for Cerebral Physiology

Answer 61

Monro-Kellie doctrine CPP = MAP − ICP treat ICP >22 mm Hg in severe TBI CPP target 60–70 mm Hg in severe TBI hyperventilation lowers ICP temporarily but can reduce CBF autoregulation may be impaired in brain injury.

Question 62

Key points for CSF Physiology

Answer 62

150 mL total volume 400–600 mL/day production mostly from choroid plexus flow: lateral → Monro → third → aqueduct → fourth → Luschka/Magendie → subarachnoid classical absorption via arachnoid granulations; modern model includes lymphatic outflow

Question 63

A newly anisocoric, declining ICU patient with extensor posturing most strongly suggests what process?

Answer 63

Impending herniation, especially uncal herniation with brainstem compression

Question 64

CSF Mnemonic

Answer 64

“Little Monkeys Throw Apples For Lucky Monkeys” L – Lateral ventricles M – Foramen of Monro T – Third ventricle A – Aqueduct (cerebral) F – Fourth ventricle L – Foramen of Luschka M – Foramen of Magendie → subarachnoid space “Monkeys THROW apples” → everything before the aqueduct is supratentorial “For Lucky Monkeys” → outlets from the 4th ventricle (Luschka lateral, Magendie midline)

Question 65

Narrowest point for CSF flow?

Answer 65

Aqueduct = common obstruction site

Question 66

Magendie or Luschka, which is midline and which is paired?

Answer 66

Magendie = midline, Luschka = lateral (paired)

Question 67

Normal Pressure Hydrocephalus Symptoms

Answer 67

Mnemonic: “Wet, Wobbly, Wacky” Wet → urinary incontinence Wobbly → gait disturbance (earliest + most prominent) Wacky → cognitive decline 👉 Imaging: ventriculomegaly out of proportion to atrophy

Question 68

Mannitol dose, mechanism, side effects and contraindications?

Answer 68

Dose: 0.25–1 g/kg bolus Causes osmotic diuresis Risks: hypovolemia → ↓ CPP AKI rebound ICP (if BBB disrupted) Contraindicated in hypovolemia/renal failure

Question 69

Hypertonic saline (preferred) concentrations, advantages and risks?

Answer 69

Concentrations: 3%, 7.5%, 23.4% Advantages: expands intravascular volume improves MAP → better CPP Risks: hypernatremia osmotic demyelination (overcorrection)

Question 70

First line in Status?

Answer 70

Benzodiazepines (immediate) Lorazepam IV (preferred) Midazolam IM/IV (if no IV access) 👉 Mechanism: ↑ GABA-A → fast inhibition

Question 71

After benzos, what does status get?

Answer 71

Load a long-acting agent (don’t skip this) Levetiracetam Fosphenytoin/phenytoin Valproate 👉 Even if seizure stops → still load

Question 72

Treatment of refractory status?

Answer 72

Propofol infusion Midazolam infusion Pentobarbital coma 👉 Requires EEG monitoring

Question 73

Keppra/levetiracetam mechanism, pearls, dose, and side effects?

Answer 73

Mechanism: Binds SV2A vesicle protein → modulates neurotransmitter release Dose: load 1–4.5 g IV Side effects: Agitation, mood changes 🔥 Board pearls: favorite in the ICU - No hepatic metabolism issues - Minimal drug interactions - No need for level monitoring - First choice in most ICUs - Safe in liver disease - Adjust in renal failure

Question 74

Phenytoin/Fosphenytoin mechanism, advantages, side effects and board pearls

Answer 74

Mechanism: Blocks voltage-gated sodium channels Fosphenytoin advantages - Safer IV (less tissue injury) - Faster administration Side effects - Arrhythmias - Hypotension - Gingival hyperplasia (chronic) - Stevens-Johnson syndrome 🔥 Board pearls - Avoid in cardiac instability - Strong CYP450 inducer → MANY interactions

Question 75

Valproate mechanism, when to use, avoid in, side effects, board pearls?

Answer 75

Mechanism: ↑ GABA + Na channel effects When to use - generalized seizures - status epilepticus alternative Avoid in: - liver failure - pregnancy Side effects - hepatotoxicity - thrombocytopenia - hyperammonemia 🔥 Board pearls - Good option when phenytoin contraindicated - Watch platelets in ICU

Question 76

Lacosamide mechanism, advantages, risks, and board pearls?

Answer 76

Mechanism: Enhances slow sodium channel inactivation Advantages - Fewer interactions than phenytoin Risks - PR interval prolongation 🔥 Board pearl - Great adjunct in refractory seizures

Question 77

Phenobarbital mechanism, use, and risks?

Answer 77

Mechanism: GABA potentiation Use - refractory seizures - alcohol withdrawal Risks - respiratory depression - hypotension

Question 78

Benzodiazepines in seizures which ones and board pearls?

Answer 78

Drugs - Lorazepam (IV preferred) - Midazolam (IM/IV) - Diazepam (fast onset, shorter duration) 🔥 Board pearls - Lorazepam lasts longer in CNS than diazepam - Midazolam best IM option (prehospital)

Question 79

Propfol in seizures mechanism, benefits, and major risk?

Answer 79

Mechanism: GABA agonist Benefits - ↓ ICP - rapid titration Major risk - Propofol Infusion Syndrome (PRIS) → metabolic acidosis, rhabdo, cardiac collapse

Question 80

Pentobarbital mechanism, use in seizures, risks and goal?

Answer 80

Mechanism: deep GABA suppression Use - super-refractory status epilepticus Risks - hypotension - immunosuppression Goal: burst suppression on EEG

Question 81

Antiepileptics Table

Answer 81

Question 82

High Yield Take Aways Seizure Meds

Answer 82

Benzos first, ALWAYS load second agent Levetiracetam = ICU default Phenytoin = cardiac risk Valproate = liver + platelets Propofol = PRIS risk Refractory status → EEG + burst suppression Always think NCSE in unexplained coma

Question 83

Propofol effect on CMRO2, CBF, ICP and why the boards love it?

Answer 83

Propofol is a short-acting IV hypnotic that reduces CMRO₂, reduces CBF, and often lowers ICP, which is why it is a Neuro ICU favorite for sedation and for refractory status epilepticus. Its rapid onset and short context-sensitive half-life make it especially useful when you need frequent neurologic exams. Why boards love propofol Propofol is often the “best answer” when the question wants an agent that is: rapidly titratable, useful for ventilated neuro patients, compatible with serial exams, and helpful when ICP is elevated.

Question 84

Major adverse effects of propofol and board pearls

Answer 84

Major adverse effects The big complications are hypotension, hypertriglyceridemia, and propofol-related infusion syndrome (PRIS). PRIS is rare but very testable: think metabolic acidosis, rhabdomyolysis, hyperkalemia, acute kidney injury, bradyarrhythmias, and cardiovascular collapse, usually with prolonged high-dose infusions. Board pearls Propofol lowers ICP largely by reducing cerebral metabolism and cerebral blood volume, but it can also lower MAP, which may hurt CPP if you are not simultaneously supporting blood pressure. In other words, propofol may improve ICP while worsening CPP in a hypotensive patient

Question 85

Ketamine mechanism and why boards love it?

Answer 85

Ketamine is an NMDA antagonist. Historically it was avoided in TBI because of concern that it would increase ICP, but more recent reviews and studies have not shown a consistent clinically meaningful ICP increase in controlled, ventilated Neuro ICU settings. Modern evidence supports that ketamine can be used safely in many patients with acute brain injury, including TBI. Why ketamine matters in boards now Ketamine is increasingly favored when you need: sedation or induction in a patient at risk for hypotension, analgesia plus sedation, bronchodilation, or preservation of blood pressure better than propofol would allow. Because it often preserves or raises sympathetic tone, it may help maintain MAP and therefore CPP better than propofol.

Question 86

Ketamine caveats

Answer 86

Ketamine can increase secretions, may cause emergence reactions, and can increase heart rate and blood pressure. In catecholamine-depleted shock, its hemodynamic support may be less reliable. The board-level update is that ketamine is not categorically contraindicated in TBI.

Question 87

Benzo effect on CMRO2/CBF and ICP

Answer 87

Midazolam is more often a sedative than true induction anesthetic in ICU practice, but know that it depresses CMRO2/CBF and can lower ICP, while prolonging wake-up and worsening delirium risk. SCCM PADIS continues to favor non-benzodiazepine sedation over benzodiazepine-based sedation in most mechanically ventilated adults.

Question 88

Volatile anesthetics on CMRO2, CBF and ICP

Answer 88

They decrease CMRO2 but can also cause cerebral vasodilation, which may increase CBF and potentially ICP. In raised ICP, they are generally less attractive than propofol-based approaches.

Question 89

What lowers ICP and is rapid?

Answer 89

Propofol

Question 90

What can be used for hemodynamic instability and induction?

Answer 90

Etomidate

Question 91

What causes sedation/induction and preserves BP?

Answer 91

Ketamine

Question 92

How do you avoid long wake-up and delerium?

Answer 92

Minimize benzodiazepines

Question 93

Nicardipine mechanism and why loved in ICU? Uses and pearls?

Answer 93

Mechanism: Dihydropyridine calcium channel blocker. Why neuro people love it: Smooth titratable infusion, predictable BP lowering, less effect on heart rate/conduction than beta-blockers. Use: ICH, SAH, hypertensive emergency in neuro ICU, post-thrombolysis BP control. Pearls: - Great first-line infusion for many neuro hypertensive emergencies. - Can cause reflex tachycardia, edema, headache. - Nicardipine IV is FDA-labeled for short-term treatment of hypertension when oral treatment is not feasible or desirable.

Question 94

Clevidipine mechanism, use and pearls?

Answer 94

Mechanism: Ultra-short-acting dihydropyridine calcium channel blocker. Use: Same lane as nicardipine, especially when minute-to-minute titration matters. Pearls: - Very rapid onset/offset. Lipid emulsion formulation. - Avoid/consider carefully with egg/soy allergy depending on formulation context and severe lipid metabolism issues. - Can cause reflex tachycardia. FDA labeling states clevidipine is indicated for reduction of BP when oral therapy is not feasible or desirable, and antihypertensive effects diminish within about 5–15 minutes after discontinuation.

Question 95

Labet5alol mechanism, use and pearls?

Answer 95

Mechanism: Alpha-1 and nonselective beta blockade. Use: Bolus or infusion for acute BP control in stroke/ICH, especially if tachycardic. Pearls: - Useful when you want to lower BP and blunt tachycardia. - Avoid/caution in asthma, bradycardia, heart block, decompensated heart failure. - Can make neuro exam harder if significant bradycardia/hypotension develops. - Labetalol IV is labeled for severe hypertension and overdose is characterized by hypotension and bradycardia.

Question 96

Esmolol mechanism, use and pearls?

Answer 96

Mechanism: Ultra-short-acting beta-1 blocker. Use: Tachyarrhythmia, sympathetic surge, aortic syndromes; sometimes adjunct BP control. Pearls: - Best when the issue is heart rate-driven hypertension. - Much less attractive if you need afterload reduction more than chronotropy control. - FDA labeling supports short-term emergent control of tachycardia and hypertension in perioperative/emergent settings.

Question 97

BP management in ICH?

Answer 97

Treat severe hypertension, but avoid reducing MAP so much that CPP suffers.

Question 98

BP management in AIS not receiving thrombolysis?

Answer 98

Permissive hypertension is often acceptable up to higher thresholds.

Question 99

BP management in AIS receiving thrombolysis?

Answer 99

BP must be controlled before and after lytic administration.

Question 100

MC pressors for MAP/CCP?

Answer 100

Norepinephrine

Question 101

Pure vasoconstrictor with risk of reflex bradycardia?

Answer 101

Phenylephrine

Question 102

Catecholamine-sparing vasopressor adjunct?

Answer 102

Vasopressin

Question 103

Dexmedetomidine mechanism and pearls?

Answer 103

Mechanism: Alpha-2 agonist. Effect: Sedation with some analgesic-sparing effect and relatively less respiratory depression. Why exam writers like it: “Cooperative sedation.” Use: Awake yet calm patient, extubation bridge, delirium-prone patients. Downside: Bradycardia and hypotension. FDA labeling describes dexmedetomidine as a relatively selective alpha-2 agonist for ICU/procedural sedation requiring close hemodynamic and oxygen monitoring.

Question 104

Succinylcholine mechanism and pearls?

Answer 104

Mechanism: Persistent depolarization at nicotinic receptor. Onset: Very fast. Duration: Short. Use: RSI. Major contraindications/tests: - Hyperkalemia risk - Burns/crush/denervation after upregulation window - Neuromuscular disease - Malignant hyperthermia susceptibility - Bradycardia Neuro pearl: Sometimes used for emergent RSI, but many neuro patients have reasons to avoid it.

Question 105

Rocuronium pearls

Answer 105

Fast onset at higher RSI dosing, longer duration than succinylcholine. FDA labeling lists 0.6 mg/kg as the recommended initial dose for intubation, with a lower dose sometimes used; higher RSI doses are also used clinically.

Question 106

Vecuronium pearls

Answer 106

Intermediate acting. Useful when you need continued paralysis but not ultra-fast onset.

Question 107

Cisatricurium pearls

Answer 107

Board favorite because it undergoes Hofmann elimination. Good in hepatic/renal failure. Can be used in refractory ICP crises or ventilator dyssynchrony.

Question 108

Alteplase mechanism and pearls?

Answer 108

Mechanism: Converts plasminogen to plasmin, promotes fibrinolysis. AIS dose: 0.9 mg/kg IV, max 90 mg; 10% as bolus over 1 minute, remainder over 60 minutes. FDA labeling for AIS says to administer as soon as possible and within 3 hours after symptom onset, with BP monitoring/control during and after administration.

Question 109

Tenecteplase (TNK) pearls

Answer 109

Mechanism: Fibrin-specific thrombolytic variant with longer half-life than alteplase. AIS dose on current label: weight-based IV bolus over 5 seconds, max 25 mg, started as soon as possible and within 3 hours after symptom onset. FDA labeling now includes AIS dosing.

Question 110

Protamine

Answer 110

Protamine labeling states it is indicated for heparin overdosage; each mg neutralizes at least 100 USP heparin units, and it should be given very slowly with doses not exceeding 50 mg over 10 minutes due to hypotension/anaphylactoid risk.

Question 111

Warfarin reversal

Answer 111

4-factor PCC + vitamin K for major/life-threatening bleeding, especially ICH. Neurocritical Care/SCCM reversal guidance recommends discontinuing vitamin K antagonists, urgently reversing elevated INR, and preferring PCC over FFP when available. Kcentra is FDA-approved for urgent reversal of VKA-associated acquired factor deficiency in adults with acute major bleeding or urgent procedures.

Question 112

Dabigatran mechanism and reversal

Answer 112

Direct thrombin inhibitors` idarucizumab. Praxbind labeling states the recommended dose is 5 g IV, supplied as two 2.5 g/50 mL vials. Backup concepts: activated charcoal if very recent ingestion; dialysis can remove dabigatran because it is not highly protein bound.

Question 113

Direct factor Xa inhibitors and reversal?

Answer 113

Apixaban, rivaroxaban, edoxaban Reversal: andexanet alfa for apixaban/rivaroxaban when reversal is needed for life-threatening or uncontrolled bleeding; otherwise PCC-based approaches are commonly used by protocol. FDA labeling for ANDEXXA specifically indicates reversal for rivaroxaban- or apixaban-treated patients with life-threatening or uncontrolled bleeding and warns of serious thromboembolic/ischemic events. Common alternative by protocol: 4-factor PCC when andexanet is unavailable or not used. Pearl: these patients remain at high thrombosis risk after reversal.

Question 114

Desmopressin (DDAVP)

Answer 114

Often considered to improve platelet adhesion/function in antiplatelet-associated ICH or when urgent neurosurgical intervention is planned. Observational data suggest improved platelet activity after acute ICH, and trauma guidance notes its use is supported more than routine platelet transfusion.

Question 115

If hemorrhage occurs after alteplase/tenecteplase?

Answer 115

Stop lytic infusion if still running. Emergent CT and labs. Use institutional reversal protocol, commonly including cryoprecipitate to replace fibrinogen; antifibrinolytics may also be used depending on protocol.

Question 116

Sedation/anethesia pearls

Answer 116

Propofol: lowers CMRO2/CBF/ICP; fast on/off; hypotension; PRIS. Dexmedetomidine: cooperative sedation; less respiratory depression; bradycardia/hypotension. Midazolam: seizure-friendly; prolonged sedation/delirium. Etomidate: induction with hemodynamic stability. Ketamine: useful when BP support matters; old “ICP contraindication” teaching is oversimplified.

Question 117

BP/CPP Drug Pearls

Answer 117

Nicardipine: titratable neuro antihypertensive. Clevidipine: ultra-short, minute-to-minute titration. Labetalol: good if tachycardic. Norepinephrine: first-line pressor for MAP/CPP support. Phenylephrine: pure alpha, may cause reflex bradycardia. Dobutamine: inotrope for low-output state.

Question 118

Paralytic pearls

Answer 118

Succinylcholine: fast, short, hyperkalemia/MH risk. Rocuronium: fast enough for RSI at appropriate dose, longer action. Cisatracurium: organ-independent breakdown favorite in organ failure.

Question 119

Thrombolysis/reversal pearls

Answer 119

Alteplase: 0.9 mg/kg, max 90 mg; 10% bolus then 60-min infusion. Tenecteplase: single IV bolus, weight-based, max 25 mg for AIS on current label. Warfarin bleed: 4F-PCC + IV vitamin K. UFH bleed: protamine. Dabigatran bleed: idarucizumab. Apixaban/rivaroxaban bleed: andexanet alfa or protocolized PCC approach.

Question 120

Treatment of trigeminal neuralgia

Answer 120

Carbemazepine

Question 121

IABP inflation and deflation timing and effect?

Answer 121

Inflate in diastole -> increase coronary perfusion Deflates in systole -> decrease afterload Net: modest increase in cardiac output (~ 0.5 L/min) and decrease in myocardial oxygen demand

Question 122

Indications for IABP?

Answer 122

Cardiogenic shock (especially ischemic): acute MI with pump failure, bridge to what's next (PCI, CABG, LVAD) Mechanical Complications of MI: papillary muscle rupture (acute MR), ventricular septal rupture (reduces afterload -> improves forward flow) Refractory unstable angina (when not immediately revascularizable) Bridge to: PCI, CABG, LVAD, transplant

Question 123

When is IABP NOT good?

Answer 123

Severe cardiogenic shock needing high output support (choose Impella or VA-ECMO)

Question 124

Contraindications to IABP?

Answer 124

Severe aortic regurgitation Aortic dissection Severe peripheral vascular disease

Question 125

IABP neurocritical care pearls?

Answer 125

May be used in post-cardiac arrest cardiogenic shock Less risk of embolic stroke than more invasive devices

Question 126

What are the 4 main categories of shock?

Answer 126

Hypovolemic, distributive, cardiogenic, obstructive

Question 127

What MAP target is recommended in septic shock?

Answer 127

≥ 65 mm Hg

Question 128

What is the first-line vasopressor in septic shock?

Answer 128

Norepinephrine

Question 129

What is the primary problem in distributive shock?

Answer 129

Decreased systemic vascular resistance

Question 130

What is the primary problem in hypovolemic shock?

Answer 130

Decreased preload

Question 131

What is the primary problem in cardiogenic shock?

Answer 131

Decreased cardiac output

Question 132

What is the primary problem in obstructive shock?

Answer 132

Impaired cardiac filling or outflow

Question 133

Name 3 causes of obstructive shock

Answer 133

Pulmonary embolism, cardiac tamponade, tension pneumothorax

Question 134

What lab is commonly used to assess tissue hypoperfusion?

Answer 134

Lactate

Question 135

Does normal blood pressure rule out shock?

Answer 135

No

Question 136

What is the priority before vasopressors in hypovolemic shock?

Answer 136

Volume resuscitation

Question 137

What is the preferred nutrition route in ICU patients?

Answer 137

Enteral nutrition if the gut is functional

Question 138

When should enteral nutrition be started in ICU patients?

Answer 138

Within 24–48 hours

Question 139

Name 3 contraindications to enteral feeding

Answer 139

Bowel ischemia, obstruction, uncontrolled shock

Question 140

When is parenteral nutrition used?

Answer 140

When enteral feeding is not possible or insufficient

Question 141

What electrolyte abnormality defines refeeding syndrome?

Answer 141

Hypophosphatemia

Question 142

What other abnormalities occur in refeeding syndrome?

Answer 142

Hypokalemia and hypomagnesemia

Question 143

Why is fever harmful in neuro ICU patients?

Answer 143

Increases cerebral metabolic demand and worsens brain injury

Question 144

What is the main goal of temperature management in neuro ICU?

Answer 144

Prevent fever (maintain normothermia)

Question 145

What must be treated during targeted temperature management?

Answer 145

Shivering

Question 146

What tidal volume is used for lung-protective ventilation?

Answer 146

4–8 mL/kg predicted body weight

Question 147

What is the preferred DVT prevention strategy in ICU patients?

Answer 147

Pharmacologic prophylaxis if no contraindication

Question 148

Who should receive stress ulcer prophylaxis?

Answer 148

High-risk ICU patients

Question 149

What medications are used for stress ulcer prophylaxis?

Answer 149

PPI or H2 blocker

Question 150

What are key pressure ulcer prevention strategies?

Answer 150

Repositioning, skin care, adequate nutrition

Question 151

What is the best CAUTI prevention strategy?

Answer 151

Avoid unnecessary Foley and remove early

Question 152

What are key VAP prevention measures?

Answer 152

Head-of-bed elevation, oral care, minimize sedation, early extubation

Question 153

What is the best delirium prevention strategy?

Answer 153

Light sedation and early mobility

Question 154

Which sedatives increase delirium risk?

Answer 154

Benzodiazepines

Question 155

What is the first step in trauma evaluation?

Answer 155

Primary survey (ABCDE)

Question 156

Name immediately life-threatening chest injuries

Answer 156

Tension pneumothorax, tamponade, massive hemothorax

Question 157

What is the best initial test in unstable trauma patients?

Answer 157

FAST exam

Question 158

What is the best imaging test in stable trauma patients?

Answer 158

CT scan

Question 159

What is the classic triad of fat embolism syndrome?

Answer 159

Respiratory distress, neurologic changes, petechial rash

Question 160

What is the first priority in burn patients?

Answer 160

Airway assessment

Question 161

What is a key complication of electrical injury?

Answer 161

Arrhythmias and rhabdomyolysis

Question 162

What is a major delayed complication of hanging/strangulation?

Answer 162

Airway edema

Question 163

What determines oxygenation in pulmonary physiology?

Answer 163

FiO2, PEEP, V/Q matching

Question 164

What determines CO2 elimination?

Answer 164

Ventilation

Question 165

What is the key ventilator strategy in ARDS?

Answer 165

Low tidal volume ventilation

Question 166

What tidal volume is used in ARDS?

Answer 166

4–8 mL/kg predicted body weight

Question 167

What intervention improves survival in severe ARDS?

Answer 167

Prone positioning

Question 168

What type of shock does massive pulmonary embolism cause?

Answer 168

Obstructive shock

Question 169

Which chamber fails in massive pulmonary embolism?

Answer 169

Right ventricle

Question 170

What are first-line treatments for COPD exacerbation?

Answer 170

Bronchodilators and steroids

Question 171

When is noninvasive ventilation used in COPD exacerbation?

Answer 171

Hypercapnic respiratory failure

Question 172

What is first-line therapy for asthma exacerbation?

Answer 172

Short-acting beta agonists and steroids

Question 173

What adjunct is used in severe asthma exacerbation?

Answer 173

Magnesium sulfate

Question 174

What is a major ventilator risk in asthma?

Answer 174

Auto-PEEP (air trapping)

Question 175

What is the main ICU issue in pulmonary hypertension?

Answer 175

Right ventricular failure

Question 176

Why should excessive fluids be avoided in pulmonary hypertension?

Answer 176

Worsens right ventricular dilation and failure

Question 177

What is the difference between aspiration pneumonitis and pneumonia?

Answer 177

Pneumonitis is chemical injury; pneumonia is infectious

Question 178

What causes neurogenic pulmonary edema?

Answer 178

Catecholamine surge after CNS injury

Question 179

What are common uses of bronchoscopy in ICU?

Answer 179

Airway clearance, BAL, bleeding localization

Question 180

What is a major risk of bronchoscopy?

Answer 180

Hypoxemia

Question 181

What type of problem is ARDS?

Answer 181

Shunt and compliance problem

Question 182

What type of problem are asthma and COPD?

Answer 182

Airflow resistance problem

Question 183

Can shock exist with normal blood pressure?

Answer 183

Yes

Question 184

What is the most important concept in ICU prophylaxis?

Answer 184

Use of bundles rather than single interventions

Question 185

What is the primary function of an intra-aortic balloon pump (IABP)?

Answer 185

Inflates in diastole to increase coronary perfusion and deflates in systole to reduce afterload

Question 186

How much cardiac output support does IABP provide?

Answer 186

Modest (~0.5 L/min increase)

Question 187

What is a key indication for IABP?

Answer 187

Cardiogenic shock (especially ischemic)

Question 188

What mechanical complications of MI are indications for IABP?

Answer 188

Papillary muscle rupture, ventricular septal rupture

Question 189

Why does IABP help in acute MR or VSD?

Answer 189

Reduces afterload, improving forward flow

Question 190

When is IABP used as a bridge?

Answer 190

Bridge to PCI, CABG, LVAD, or transplant

Question 191

What is a major limitation of IABP?

Answer 191

Insufficient support in severe cardiogenic shock

Question 192

What are contraindications to IABP?

Answer 192

Aortic regurgitation, aortic dissection, severe peripheral vascular disease

Question 193

What devices provide temporary ventricular support?

Answer 193

Impella, TandemHeart, RVAD

Question 194

What is the main advantage of Impella over IABP?

Answer 194

Greater cardiac output support

Question 195

What is a key indication for Impella?

Answer 195

Severe cardiogenic shock

Question 196

What is a common use of temporary VADs in procedures?

Answer 196

High-risk PCI

Question 197

What condition is a classic board indication for temporary VAD?

Answer 197

Fulminant myocarditis

Question 198

What type of failure requires RVAD?

Answer 198

Right ventricular failure

Question 199

Which device is best for biventricular failure?

Answer 199

VA ECMO

Question 200

What does VV ECMO support?

Answer 200

Lungs only

Question 201

What is the primary indication for VV ECMO?

Answer 201

Severe ARDS

Question 202

What physiologic problem does VV ECMO treat?

Answer 202

Hypoxemia and/or hypercapnia

Question 203

Is cardiac function supported in VV ECMO?

Answer 203

No

Question 204

What is a common VV ECMO indication in modern exams?

Answer 204

Severe viral pneumonia (e.g., COVID)

Question 205

What does VA ECMO support?

Answer 205

Heart and lungs

Question 206

What is the primary indication for VA ECMO?

Answer 206

Cardiogenic shock

Question 207

What is ECPR?

Answer 207

Extracorporeal CPR using VA ECMO

Question 208

What condition is VA ECMO used for after cardiac arrest?

Answer 208

Refractory cardiac arrest

Question 209

What PE scenario is VA ECMO used for?

Answer 209

Massive PE with hemodynamic collapse

Question 210

What is Harlequin syndrome in VA ECMO?

Answer 210

Differential hypoxia (upper body hypoxic, lower body oxygenated)

Question 211

What is the key difference between VV and VA ECMO?

Answer 211

VV supports lungs only; VA supports heart and lungs

Question 212

Which ECMO type has higher stroke risk?

Answer 212

VA ECMO

Question 213

Which ECMO type is used for ARDS?

Answer 213

VV ECMO

Question 214

Which ECMO type is used for cardiogenic shock?

Answer 214

VA ECMO

Question 215

What is the most common neurologic complication of LVAD?

Answer 215

Ischemic stroke

Question 216

Why do LVAD patients get ischemic strokes?

Answer 216

Thromboembolism, pump thrombosis, atrial fibrillation

Question 217

Why are LVAD patients at risk for intracranial hemorrhage?

Answer 217

Anticoagulation, platelet dysfunction, acquired vWD

Question 218

What is a key board concept for LVAD complications?

Answer 218

Simultaneous risk of thrombosis AND bleeding

Question 219

What type of hemorrhage is common in LVAD patients?

Answer 219

Intraparenchymal hemorrhage, subdural hematoma

Question 220

Why do LVAD patients develop GI bleeding?

Answer 220

AV malformations from shear stress

Question 221

How can LVAD infections cause neurologic complications?

Answer 221

Septic emboli → stroke

Question 222

What is the most important neurologic complication of ECMO?

Answer 222

Intracranial hemorrhage

Question 223

Why does ECMO cause intracranial hemorrhage?

Answer 223

Systemic anticoagulation and coagulopathy

Question 224

Which ECMO type has highest hemorrhage risk?

Answer 224

VA ECMO

Question 225

What causes ischemic stroke in ECMO patients?

Answer 225

Thromboembolism from circuit or low flow

Question 226

What is the most common brain injury mechanism after ECMO for cardiac arrest?

Answer 226

Hypoxic-ischemic injury

Question 227

When does most hypoxic brain injury occur in ECMO patients?

Answer 227

Before ECMO initiation

Question 228

What type of seizures are common in ECMO patients?

Answer 228

Nonconvulsive seizures

Question 229

What monitoring is often required for ECMO patients?

Answer 229

Continuous EEG

Question 230

What causes cerebral edema in ECMO patients?

Answer 230

Hypoxia and reperfusion injury

Question 231

What rare but catastrophic complication can occur in ECMO circuits?

Answer 231

Air embolism

Question 232

Rank devices by increasing neurologic risk

Answer 232

IABP < VAD/Impella < VV ECMO < VA ECMO

Question 233

Which device is best for mild cardiogenic shock?

Answer 233

IABP

Question 234

Which device is best for severe LV failure?

Answer 234

Impella or VAD

Question 235

Which device is best for respiratory failure only?

Answer 235

VV ECMO

Question 236

Which device is best for combined cardiac and respiratory failure?

Answer 236

VA ECMO

Question 237

What is the most feared complication in an ECMO patient with acute neuro decline?

Answer 237

Intracranial hemorrhage

Question 238

What are the two most likely diagnoses in an LVAD patient with acute neuro deficit?

Answer 238

Ischemic stroke or intracranial hemorrhage

Question 239

What is the most important determinant of neurologic outcome in ECMO patients?

Answer 239

Pre-ECMO hypoxic injury

Question 241

Front

Answer 241

Back

Question 242

What is the equation for cardiac output (CO)?

Answer 242

CO = heart rate × stroke volume

Question 243

What is the relationship between MAP, CO, and SVR?

Answer 243

MAP ≈ CO × SVR

Question 244

What is the equation for cerebral perfusion pressure (CPP)?

Answer 244

CPP = MAP − ICP

Question 245

Why can a normal MAP still be inadequate in Neuro ICU patients?

Answer 245

Elevated ICP can reduce CPP despite normal MAP

Question 246

What are the four determinants of cardiac output?

Answer 246

Preload, afterload, contractility, heart rate

Question 247

What is preload?

Answer 247

Ventricular filling before contraction

Question 248

What is afterload?

Answer 248

Resistance the ventricle ejects against

Question 249

What is contractility?

Answer 249

Intrinsic myocardial pump strength

Question 250

Which ventricle is more sensitive to afterload changes?

Answer 250

Right ventricle

Question 251

What happens to the RV in pulmonary embolism?

Answer 251

Acute afterload increase → RV failure

Question 252

What cardiovascular effects can acute brain injury cause?

Answer 252

Arrhythmias, stress cardiomyopathy, BP lability, troponin elevation, pulmonary edema

Question 253

What is stress-induced cardiomyopathy also called?

Answer 253

Takotsubo cardiomyopathy

Question 254

What triggers stress cardiomyopathy in Neuro ICU?

Answer 254

SAH, seizures, stroke, acute neurologic injury

Question 255

What is the pathophysiology of stress cardiomyopathy?

Answer 255

Catecholamine-mediated myocardial stunning

Question 256

What are typical echo findings in Takotsubo?

Answer 256

Regional wall motion abnormalities not limited to a single coronary territory

Question 257

What is the classic wall motion abnormality in Takotsubo?

Answer 257

Apical ballooning

Question 258

What ECG findings can occur in Takotsubo?

Answer 258

ST changes, T-wave inversion, QT prolongation

Question 259

What is typical troponin pattern in Takotsubo?

Answer 259

Mild elevation relative to degree of dysfunction

Question 260

What are complications of stress cardiomyopathy?

Answer 260

Cardiogenic shock, pulmonary edema, arrhythmias, LV thrombus

Question 261

What key board clue suggests Takotsubo over ACS?

Answer 261

Wall motion abnormalities beyond a single coronary territory

Question 262

What defines acute coronary syndrome (ACS)?

Answer 262

Plaque rupture or thrombosis causing myocardial ischemia

Question 263

What are the 3 types of ACS?

Answer 263

Unstable angina, NSTEMI, STEMI

Question 264

What distinguishes STEMI from NSTEMI?

Answer 264

STEMI has ST elevation and complete occlusion; NSTEMI does not

Question 265

What is the major treatment priority in STEMI?

Answer 265

Rapid reperfusion

Question 266

What is ischemic cardiomyopathy?

Answer 266

Chronic LV dysfunction due to coronary artery disease

Question 267

What echo finding suggests ischemic cardiomyopathy?

Answer 267

Regional wall motion abnormality in coronary distribution

Question 268

What is a key Neuro ICU challenge with troponin elevation?

Answer 268

Distinguishing ACS from stress cardiomyopathy or demand ischemia

Question 269

What is the hemodynamic feature of aortic stenosis?

Answer 269

Fixed outflow obstruction

Question 270

Why are aortic stenosis patients preload dependent?

Answer 270

Fixed obstruction limits ability to increase cardiac output

Question 271

What murmur is associated with aortic stenosis?

Answer 271

Harsh systolic murmur radiating to carotids

Question 272

What happens in acute aortic regurgitation?

Answer 272

Rapid volume overload → pulmonary edema and shock

Question 273

What is a key feature of chronic aortic regurgitation?

Answer 273

Wide pulse pressure

Question 274

What causes acute mitral regurgitation?

Answer 274

Papillary muscle dysfunction, often after MI

Question 275

What is the clinical consequence of acute MR?

Answer 275

Pulmonary edema and reduced forward output

Question 276

What is a key complication of mitral stenosis?

Answer 276

Atrial fibrillation

Question 277

What is the hemodynamic issue in mitral stenosis?

Answer 277

Elevated left atrial pressure → pulmonary congestion

Question 278

What arrhythmia is most common in ICU patients?

Answer 278

Atrial fibrillation

Question 279

What are ECG findings in atrial fibrillation?

Answer 279

Irregularly irregular rhythm, no P waves

Question 280

What is the major complication of AF?

Answer 280

Thromboembolic stroke

Question 281

What is the first step in stable AF management?

Answer 281

Rate control

Question 282

What is the treatment for unstable AF?

Answer 282

Synchronized cardioversion

Question 283

What defines ventricular tachycardia?

Answer 283

Wide-complex tachycardia originating from ventricles

Question 284

What is the rule for wide-complex tachycardia?

Answer 284

Assume VT until proven otherwise

Question 285

What is treatment for unstable VT?

Answer 285

Synchronized cardioversion

Question 286

What is treatment for pulseless VT?

Answer 286

Defibrillation

Question 287

What is torsades de pointes?

Answer 287

Polymorphic VT associated with prolonged QT

Question 288

What is first-line treatment for torsades?

Answer 288

Magnesium

Question 289

What are causes of QT prolongation?

Answer 289

Drugs, hypokalemia, hypomagnesemia, bradycardia

Question 290

What arrhythmias are common in SAH?

Answer 290

QT prolongation, AF, PVCs, ventricular arrhythmias

Question 291

What defines symptomatic bradycardia?

Answer 291

Low heart rate causing hypotension, AMS, chest pain, or shock

Question 292

What is first-line treatment for symptomatic bradycardia?

Answer 292

Atropine

Question 293

What are indications for temporary pacing?

Answer 293

Unstable bradycardia, high-grade AV block, bridge to permanent pacemaker

Question 294

What are indications for permanent pacemaker?

Answer 294

Symptomatic sinus node dysfunction, high-grade AV block

Question 295

What AV blocks require permanent pacemaker?

Answer 295

Mobitz II and complete heart block

Question 296

What is an important pacing principle?

Answer 296

Treat reversible causes before placing permanent pacemaker

Question 297

What reversible causes of bradycardia must be ruled out?

Answer 297

Hyperkalemia, drug toxicity, ischemia, infection

Question 298

What is aortic dissection?

Answer 298

Intimal tear with blood creating a false lumen

Question 299

What are Stanford types of aortic dissection?

Answer 299

Type A (ascending), Type B (not ascending)

Question 300

Which aortic dissection requires surgery?

Answer 300

Type A

Question 301

What are classic symptoms of aortic dissection?

Answer 301

Sudden tearing chest/back pain, pulse deficit

Question 302

What neuro symptoms can aortic dissection cause?

Answer 302

Stroke from branch vessel involvement

Question 303

What is first step in medical management of aortic dissection?

Answer 303

Control heart rate with beta blocker

Question 304

What HR target is used in aortic dissection?

Answer 304

~60 bpm

Question 305

What is goal of BP control in aortic dissection?

Answer 305

Reduce shear stress while maintaining perfusion

Question 306

Why is aortic dissection dangerous in stroke patients?

Answer 306

tPA can be fatal if dissection is present

Question 307

What are the main goals of cardiac ultrasound in ICU?

Answer 307

Assess LV function, RV function, effusion, volume status

Question 308

What are basic echo views?

Answer 308

Parasternal long, parasternal short, apical 4-chamber, subcostal, IVC

Question 309

What finding suggests tamponade on echo?

Answer 309

Pericardial effusion with RV diastolic collapse

Question 310

What are echo signs of tamponade?

Answer 310

RA/RV collapse, plethoric IVC, effusion

Question 311

What does hyperdynamic LV suggest?

Answer 311

Low preload or hypovolemia

Question 312

What are echo findings of RV strain?

Answer 312

RV dilation, septal flattening, RV > LV

Question 313

What condition causes RV strain on echo?

Answer 313

Pulmonary embolism

Question 314

What are limitations of IVC assessment?

Answer 314

Affected by ventilation, RA pressure, TR

Question 315

What is key concept of POCUS in ICU?

Answer 315

Answer focused binary questions quickly

Question 316

What are 3 key binary POCUS questions?

Answer 316

Effusion? LV function? RV strain?

Question 317

What is a major limitation of cardiac POCUS?

Answer 317

Cannot replace full echocardiography

Question 318

What is the most important cardiovascular concept in Neuro ICU?

Answer 318

CPP depends on MAP and ICP

Question 319

What is a key board trap with troponin elevation in Neuro ICU?

Answer 319

Assuming all elevations are ACS

Question 320

What is a key hemodynamic principle in RV failure?

Answer 320

Avoid high afterload and excessive fluids

Question 321

What is a key management principle in cardiogenic shock?

Answer 321

Support perfusion and treat underlying cause

Question 322

What is the relationship between preload and stroke volume?

Answer 322

Increases until plateau (Frank-Starling)

Question 323

What happens with excessive preload?

Answer 323

Pulmonary edema, RV failure

Question 324

What is a key complication of stress cardiomyopathy?

Answer 324

LV thrombus

Question 325

What echo pattern suggests Takotsubo instead of ACS?

Answer 325

Wall motion abnormality not in single vascular territory

Question 326

What is the standard RBC transfusion threshold in stable ICU patients?

Answer 326

Hemoglobin <7 g/dL

Question 327

When is a higher transfusion threshold (≈8 g/dL) reasonable?

Answer 327

Cardiovascular disease, cardiac surgery, or symptomatic ischemia

Question 328

What is the key physiologic concern of anemia in neuro patients?

Answer 328

Decreased cerebral oxygen delivery

Question 329

Does neuro injury automatically require liberal transfusion?

Answer 329

No, restrictive strategy is still standard unless instability

Question 330

When should RBC transfusion be given regardless of Hgb threshold?

Answer 330

Active bleeding, shock, symptomatic anemia, ischemia

Question 331

What is TACO?

Answer 331

Transfusion-associated circulatory overload

Question 332

What is TRALI?

Answer 332

Transfusion-related acute lung injury

Question 333

What electrolyte abnormalities occur in massive transfusion?

Answer 333

Hyperkalemia and hypocalcemia

Question 334

Platelet transfusion threshold for prophylaxis in hypoproliferative thrombocytopenia?

Answer 334

≤10,000/µL

Question 335

Platelet threshold for neurosurgery or CNS procedures?

Answer 335

>100,000/µL

Question 336

Should platelets be given for nonoperative ICH with platelet count >100k?

Answer 336

No

Question 337

Do antiplatelet drugs affect platelet count or function?

Answer 337

Function (count may be normal)

Question 338

Key board concept for platelet transfusion in ICH?

Answer 338

Do NOT reflexively transfuse platelets

Question 339

What are major causes of acute coagulopathy in ICU?

Answer 339

Trauma, massive transfusion, liver failure, uremia, drugs, DIC

Question 340

What is the “lethal triad” in trauma?

Answer 340

Hypothermia, acidosis, coagulopathy

Question 341

What additional factor is often added to form the “lethal diamond”?

Answer 341

Hypocalcemia

Question 342

What is the earliest clotting factor deficiency in massive bleeding?

Answer 342

Fibrinogen

Question 343

What fibrinogen level should generally be maintained in bleeding?

Answer 343

>150–200 mg/dL

Question 344

What causes uremic bleeding?

Answer 344

Platelet dysfunction

Question 345

Treatment for uremic platelet dysfunction?

Answer 345

Desmopressin (DDAVP)

Question 346

What is DIC?

Answer 346

Systemic activation of coagulation causing clotting and bleeding

Question 347

Common triggers of DIC?

Answer 347

Sepsis, trauma, malignancy, obstetric emergencies

Question 348

Platelet count in DIC?

Answer 348

Low

Question 349

PT and aPTT in DIC?

Answer 349

Prolonged

Question 350

D-dimer in DIC?

Answer 350

Elevated

Question 351

Fibrinogen in DIC?

Answer 351

Low (especially severe DIC)

Question 352

Primary treatment of DIC?

Answer 352

Treat underlying cause

Question 353

When are blood products given in DIC?

Answer 353

Only if bleeding or procedures needed

Question 354

How does chronic vs acute DIC differ?

Answer 354

Chronic = thrombosis; acute = bleeding

Question 355

Major risk factor for DVT in neuro ICU patients?

Answer 355

Immobility

Question 356

First-line DVT prophylaxis if anticoagulation unsafe?

Answer 356

Mechanical prophylaxis (compression devices)

Question 357

When should pharmacologic DVT prophylaxis be started?

Answer 357

Once bleeding risk is acceptable

Question 358

First-line treatment of DVT?

Answer 358

Anticoagulation

Question 359

When is an IVC filter considered?

Answer 359

When anticoagulation is contraindicated

Question 360

What neuropathy is associated with vincristine?

Answer 360

Peripheral and autonomic neuropathy

Question 361

Methotrexate neurotoxicity presents as what?

Answer 361

Encephalopathy, seizures, stroke-like symptoms

Question 362

Cytarabine toxicity causes what neurologic syndrome?

Answer 362

Cerebellar dysfunction (ataxia, dysarthria)

Question 363

Ifosfamide causes what neuro complication?

Answer 363

Encephalopathy

Question 364

What neurologic complications occur with checkpoint inhibitors?

Answer 364

Encephalitis, myasthenia gravis, neuropathy

Question 365

Blinatumomab neurotoxicity includes what?

Answer 365

Encephalopathy, seizures, tremor

Question 366

Key concept for immunotherapy toxicity?

Answer 366

Autoimmune-mediated neurologic injury

Question 367

What is the most classic neurologic complication of HSCT?

Answer 367

PRES

Question 368

What drugs commonly cause PRES in transplant patients?

Answer 368

Tacrolimus and cyclosporine

Question 369

Symptoms of PRES?

Answer 369

Seizures, headache, visual changes, encephalopathy

Question 370

Major cause of neurologic complications after HSCT?

Answer 370

Infection

Question 371

What type of stroke risk exists after HSCT?

Answer 371

Hemorrhagic and ischemic

Question 372

What is ICANS?

Answer 372

Immune effector cell-associated neurotoxicity syndrome

Question 373

Early signs of ICANS?

Answer 373

Aphasia, confusion, inattention

Question 374

Severe ICANS symptoms?

Answer 374

Seizures, coma, cerebral edema

Question 375

When does ICANS typically occur?

Answer 375

Within days to 1 week after CAR-T

Question 376

What scoring system is used for ICANS?

Answer 376

ICE score

Question 377

Primary treatment for ICANS?

Answer 377

Corticosteroids

Question 378

Does tocilizumab treat ICANS effectively?

Answer 378

No (better for CRS)

Question 379

What is the most important neurologic complication of sickle cell disease?

Answer 379

Stroke

Question 380

What should be assumed in SCD with acute neurologic deficit?

Answer 380

Stroke until proven otherwise

Question 381

First-line treatment for SCD stroke?

Answer 381

Exchange transfusion

Question 382

Why avoid simple transfusion in high Hgb SCD patients?

Answer 382

Risk of hyperviscosity

Question 383

What screening tool predicts stroke risk in SCD?

Answer 383

Transcranial Doppler

Question 384

Classic pentad of TTP?

Answer 384

Thrombocytopenia, MAHA, neurologic symptoms, renal dysfunction, fever

Question 385

What enzyme deficiency causes TTP?

Answer 385

ADAMTS13 deficiency

Question 386

Coagulation labs in TTP?

Answer 386

Usually normal PT/aPTT

Question 387

Key neurologic features of TTP?

Answer 387

Confusion, seizures, stroke

Question 388

First-line treatment for TTP?

Answer 388

Plasma exchange

Question 389

What medication is added for TTP?

Answer 389

Steroids ± caplacizumab

Question 390

Should platelets be transfused in TTP?

Answer 390

No (unless life-threatening bleeding)

Question 391

What differentiates HUS from TTP?

Answer 391

HUS has more severe renal failure

Question 392

What causes typical HUS?

Answer 392

Shiga toxin infection

Question 393

What causes atypical HUS?

Answer 393

Complement dysregulation

Question 394

DIC vs TTP – PT/aPTT findings?

Answer 394

DIC prolonged, TTP normal

Question 395

DIC vs TTP – primary issue?

Answer 395

DIC = consumptive coagulopathy; TTP = platelet microthrombi

Question 396

TTP vs HUS – dominant organ involvement?

Answer 396

TTP = brain; HUS = kidneys

Question 397

Most important lab abnormality in DIC

Answer 397

Elevated D-dimer

Question 398

Most important treatment in DIC

Answer 398

Treat underlying cause

Question 399

Most dangerous neurologic chemo toxicity pattern

Answer 399

Methotrexate stroke-like syndrome

Question 400

Most tested transplant neuro complication

Answer 400

PRES

Question 401

Most important CAR-T neuro complication

Answer 401

ICANS

Question 402

Most important hematologic emergency with neuro symptoms

Answer 402

TTP → plasma exchange immediately

Question 403

Front

Answer 403

Back

Question 404

What are the major physiologic functions of the kidneys?

Answer 404

Regulate volume status, osmolality, electrolytes, acid-base balance, and excretion of nitrogenous waste and many drugs

Question 405

What determines glomerular filtration rate (GFR) at the board level?

Answer 405

Renal blood flow and filtration pressure across the glomerulus

Question 406

What conditions commonly reduce renal perfusion in ICU patients?

Answer 406

Hypovolemia, shock, severe vasoconstriction, abdominal compartment syndrome, and low cardiac output

Question 407

Why is renal hypoperfusion especially important in neurocritical care?

Answer 407

Hypotension can reduce both renal perfusion and cerebral perfusion, especially when ICP is elevated

Question 408

What are the 3 major AKI categories?

Answer 408

Prerenal, intrinsic, and postrenal

Question 409

What is prerenal azotemia?

Answer 409

Decreased kidney perfusion with initially intact tubular function

Question 410

What is intrinsic AKI?

Answer 410

Parenchymal kidney injury, most commonly acute tubular injury/necrosis in ICU patients

Question 411

What is postrenal AKI?

Answer 411

Kidney injury caused by urinary tract obstruction

Question 412

What hormonal systems are closely linked to renal physiology in neuro ICU patients?

Answer 412

ADH, aldosterone, natriuretic peptides, and the renin-angiotensin-aldosterone system

Question 413

How does KDIGO define acute kidney injury?

Answer 413

By a rise in creatinine, reduced urine output, or both

Question 414

What are common prerenal causes of AKI?

Answer 414

Hypovolemia, shock, hemorrhage, sepsis, and overdiuresis

Question 415

What are common intrinsic causes of AKI?

Answer 415

Acute tubular injury, interstitial nephritis, glomerular disease, and pigment nephropathy

Question 416

What are common postrenal causes of AKI?

Answer 416

Foley obstruction, bilateral ureteral obstruction, and outlet obstruction

Question 417

What should the ICU AKI workup include?

Answer 417

Hemodynamics, fluid balance, medication review, urinalysis/microscopy, urine output trend, Foley/bladder assessment, and renal ultrasound if obstruction is possible

Question 418

What is an important early clue to AKI before creatinine rises?

Answer 418

Oliguria

Question 419

Why can a normal creatinine be misleading in severe AKI?

Answer 419

Low muscle mass can mask severity

Question 420

What are common ICU causes of AKI?

Answer 420

Sepsis and ischemic tubular injury

Question 421

What postrenal cause of abrupt oliguria must not be missed?

Answer 421

Urinary obstruction

Question 422

What are the major management steps in AKI?

Answer 422

Restore perfusion if prerenal, treat shock/sepsis, stop nephrotoxins, adjust drug doses, manage hyperkalemia/acidosis/volume overload, and start RRT when indicated

Question 423

What is the structured approach to acid-base disorders?

Answer 423

Determine if primary disorder is metabolic or respiratory, assess pH, assess compensation, calculate anion gap if metabolic acidosis, and look for mixed disorders

Question 424

What are common causes of high anion gap metabolic acidosis?

Answer 424

Lactic acidosis, ketoacidosis, renal failure, and toxins

Question 425

What are common causes of normal anion gap metabolic acidosis?

Answer 425

Diarrhea, renal tubular acidosis, and saline load

Question 426

What are common causes of metabolic alkalosis?

Answer 426

Vomiting, diuretics, contraction alkalosis, and mineralocorticoid excess

Question 427

What causes respiratory acidosis?

Answer 427

Hypoventilation, CNS depression, severe COPD/asthma, and neuromuscular weakness

Question 428

What causes respiratory alkalosis?

Answer 428

Hyperventilation, pain, anxiety, sepsis, pregnancy, and liver failure

Question 429

Why are acid-base disorders especially important in the Neuro ICU?

Answer 429

Changes in PaCO2 alter cerebral blood flow and ICP

Question 430

What is the first step in evaluating hyponatremia?

Answer 430

Determine whether it is hypotonic hyponatremia, then assess symptoms and volume status

Question 431

What is the immediate treatment for severe symptomatic hyponatremia?

Answer 431

Hypertonic saline

Question 432

What major complication results from overcorrection of chronic hyponatremia?

Answer 432

Osmotic demyelination syndrome

Question 433

What usually causes hypernatremia in ICU patients?

Answer 433

Water deficit from diabetes insipidus, inadequate free water, or excessive water loss

Question 434

What is the major principle in treating hypernatremia?

Answer 434

Correct the underlying cause and replace free water carefully

Question 435

What is the danger of correcting chronic hypernatremia too rapidly?

Answer 435

Cerebral edema and neurologic injury

Question 436

Why are potassium disorders important in the ICU?

Answer 436

Both hypo- and hyperkalemia can cause life-threatening arrhythmias

Question 437

Why can hypokalemia be refractory to treatment?

Answer 437

Concurrent hypomagnesemia

Question 438

What is the emergency treatment sequence for hyperkalemia with ECG changes?

Answer 438

Stabilize myocardium, shift potassium intracellularly, then remove potassium from the body

Question 439

Why is magnesium important in critically ill patients?

Answer 439

Low magnesium predisposes to torsades, arrhythmias, seizures, and refractory hypokalemia

Question 440

What are major manifestations of hypocalcemia?

Answer 440

Tetany, seizures, and QT prolongation

Question 441

What are major manifestations of hypercalcemia?

Answer 441

Altered mental status, ileus, nephrogenic DI, and arrhythmias

Question 442

Why is hypophosphatemia dangerous in ICU patients?

Answer 442

It impairs diaphragmatic function, cardiac function, and oxygen delivery

Question 443

What are the classic urgent indications for renal replacement therapy?

Answer 443

Refractory hyperkalemia, severe acidosis, severe volume overload, symptomatic uremia, and certain toxins

Question 444

What is the general board mnemonic for urgent dialysis indications?

Answer 444

AEIOU

Question 445

What is intermittent hemodialysis best characterized by?

Answer 445

Rapid solute and fluid removal

Question 446

What is CRRT best characterized by?

Answer 446

Slower, steadier solute and fluid removal

Question 447

When is CRRT often preferred over intermittent dialysis?

Answer 447

In hemodynamic instability or intracranial pathology

Question 448

Why is CRRT often preferred in neurocritical care patients?

Answer 448

Rapid osmotic shifts and abrupt BP changes from intermittent dialysis can worsen cerebral edema or perfusion

Question 449

What is SLED/PIRRT?

Answer 449

A hybrid renal replacement modality between intermittent dialysis and CRRT

Question 450

How does AKI affect drug handling?

Answer 450

By reducing renal clearance and often altering volume of distribution and protein binding

Question 451

What are common pharmacologic implications of AKI?

Answer 451

Drug accumulation, toxicity, need for dose reduction, and increased vulnerability to nephrotoxins

Question 452

What antiseizure medication commonly requires renal dose adjustment?

Answer 452

Levetiracetam

Question 453

What neuropathic pain drugs commonly accumulate in renal failure?

Answer 453

Gabapentin and pregabalin

Question 454

How can LMWH be affected by renal failure?

Answer 454

It can accumulate

Question 455

Which antibiotics are especially important to monitor/dose-adjust in AKI?

Answer 455

Vancomycin, aminoglycosides, and many beta-lactams

Question 456

What is a core medication principle in AKI and CRRT?

Answer 456

Adjust doses based on renal function and modality

Question 457

What is sepsis?

Answer 457

Life-threatening organ dysfunction caused by a dysregulated host response to infection

Question 458

What is septic shock?

Answer 458

A subset of sepsis with profound circulatory and metabolic abnormality, typically requiring vasopressors to maintain MAP ≥65 mm Hg and often associated with elevated lactate despite fluids

Question 459

What are the first management priorities in severe sepsis or septic shock?

Answer 459

Recognize infection, obtain cultures if feasible, start antibiotics rapidly, give crystalloids, start vasopressors if needed, and pursue source control

Question 460

How quickly should antimicrobials ideally be started in septic shock?

Answer 460

Within 1 hour

Question 461

What initial fluid strategy is commonly recommended in septic shock?

Answer 461

At least 30 mL/kg of crystalloid within the first 3 hours for sepsis-induced hypoperfusion or septic shock

Question 462

What is the first-line vasopressor in septic shock?

Answer 462

Norepinephrine

Question 463

What is the MAP target in septic shock?

Answer 463

About 65 mm Hg

Question 464

What is the role of lactate in sepsis?

Answer 464

It helps assess hypoperfusion, but normal lactate does not exclude dangerous infection

Question 465

What is a major fluid resuscitation trap in septic shock?

Answer 465

Giving endless fluid despite persistent hypotension instead of starting vasopressors

Question 466

What is infective endocarditis?

Answer 466

Infection of the endocardial surface, usually involving heart valves

Question 467

What neurocritical care complications of infective endocarditis are high yield?

Answer 467

Embolic stroke, intracranial hemorrhage from mycotic aneurysm, acute valvular failure, conduction abnormalities, and persistent bacteremia

Question 468

When should infective endocarditis be suspected?

Answer 468

In patients with bacteremia, new murmur, embolic phenomena, stroke plus fever or positive cultures, prosthetic valves, or intracardiac devices

Question 469

What is the basic diagnostic approach to infective endocarditis?

Answer 469

Multiple blood cultures, echocardiography, and Duke-style clinical reasoning

Question 470

When is TEE especially useful in infective endocarditis?

Answer 470

When suspicion is high or TTE is insufficient

Question 471

What antithrombotic board issue is important in infective endocarditis with stroke?

Answer 471

Risk of hemorrhagic transformation and mycotic aneurysm complicates antithrombotic use

Question 472

What are the core principles of antimicrobial use in critical care?

Answer 472

Get cultures when feasible, start early empiric therapy for serious infection, cover likely pathogens based on source/host factors, de-escalate when data return, use the shortest effective duration, adjust for organ dysfunction, and achieve source control

Question 473

What is de-escalation of antibiotics?

Answer 473

Narrowing therapy once culture and clinical data identify the likely pathogen(s)

Question 474

What are common antimicrobial stewardship board traps?

Answer 474

Continuing broad-spectrum therapy without data, failing to dose-adjust in AKI, ignoring source control, and not narrowing after cultures return

Question 475

Why is source control essential in severe infection?

Answer 475

Antibiotics alone often fail without drainage, debridement, or removal of the infected source

Question 476

What makes infection in immunosuppressed patients different?

Answer 476

They can deteriorate quickly, present atypically, and develop unusual or opportunistic pathogens

Question 477

What is a key principle in neutropenic fever?

Answer 477

Fever may be the only sign of severe infection and empiric therapy must be prompt

Question 478

When should fungal disease be considered earlier?

Answer 478

In prolonged neutropenia or persistent nonresponse to antibacterial therapy

Question 479

What is a major treatment principle in unstable immunosuppressed patients?

Answer 479

Start broad enough early and narrow later once data return

Question 480

What endocrine systems are most important in neurocritical care?

Answer 480

Pituitary, thyroid, adrenal, and ADH/water balance systems

Question 481

Why is endocrine physiology important in Neuro ICU boards?

Answer 481

Endocrine failure or excess alters hemodynamics, sodium, urine output, and mental status

Question 482

What is pituitary apoplexy?

Answer 482

Acute hemorrhage or infarction of the pituitary, often in a pituitary adenoma

Question 483

What is the classic presentation of pituitary apoplexy?

Answer 483

Sudden severe headache, visual loss or diplopia, ophthalmoplegia, altered mental status, and acute adrenal insufficiency

Question 484

What imaging test is preferred for pituitary apoplexy?

Answer 484

MRI

Question 485

What is the life-saving early treatment in unstable pituitary apoplexy?

Answer 485

IV hydrocortisone

Question 486

Why is pituitary apoplexy a board emergency?

Answer 486

Because acute secondary adrenal insufficiency can be fatal

Question 487

What is central diabetes insipidus?

Answer 487

Deficiency of ADH causing inability to concentrate urine

Question 488

What are classic findings in central DI?

Answer 488

Polyuria, rising serum sodium, high serum osmolality, and inappropriately dilute urine

Question 489

What causes central DI in Neuro ICU patients?

Answer 489

Pituitary surgery, severe brain injury, and hypothalamic-pituitary damage

Question 490

What is the treatment of central DI?

Answer 490

Careful free water replacement and desmopressin (DDAVP)

Question 491

What should be closely monitored during DI treatment?

Answer 491

Sodium, urine output, and osmolality

Question 492

What endocrine pearl links adrenal insufficiency and DI?

Answer 492

Untreated adrenal insufficiency can mask DI, and starting glucocorticoids can unmask it

Question 493

What is panhypopituitarism?

Answer 493

Deficiency of multiple pituitary hormones

Question 494

What is the most dangerous component of panhypopituitarism in the ICU?

Answer 494

Secondary adrenal insufficiency

Question 495

What replacement-sequence pearl is critical in panhypopituitarism?

Answer 495

Replace glucocorticoids before thyroid hormone

Question 496

Why must steroids be given before thyroid hormone in combined pituitary failure?

Answer 496

Thyroid replacement can precipitate adrenal crisis if cortisol deficiency is untreated

Question 497

What is SIADH?

Answer 497

Syndrome of inappropriate antidiuretic hormone secretion causing water retention and euvolemic hypotonic hyponatremia

Question 498

What are typical lab features of SIADH?

Answer 498

Hypotonic hyponatremia, concentrated urine, and inappropriately elevated urine sodium in the right context

Question 499

What is the treatment of severe symptomatic SIADH?

Answer 499

Hypertonic saline

Question 500

What is the treatment of chronic or less symptomatic SIADH?

Answer 500

Fluid restriction and treatment of the underlying cause

Question 501

What major treatment danger exists in SIADH?

Answer 501

Overcorrection of hyponatremia

Question 502

What is cerebral salt wasting?

Answer 502

A neuro-associated syndrome of renal sodium loss causing hyponatremia with true volume depletion

Question 503

What are typical features of cerebral salt wasting?

Answer 503

Hyponatremia, high urine sodium, hypovolemia, and often high urine output

Question 504

What is the key volume-status difference between SIADH and cerebral salt wasting?

Answer 504

SIADH is euvolemic or slightly hypervolemic; CSW is hypovolemic

Question 505

How is cerebral salt wasting treated?

Answer 505

Volume and sodium replacement, sometimes fludrocortisone

Question 506

What is the key treatment contrast between SIADH and CSW?

Answer 506

SIADH is treated with fluid restriction; CSW is treated with salt and volume replacement

Question 507

What important diagnostic caution applies to cerebral salt wasting?

Answer 507

It is probably overdiagnosed; SIADH and adrenal insufficiency are often more common

Question 508

What is thyroid storm?

Answer 508

Life-threatening severe thyrotoxicosis with hyperthermia, tachyarrhythmia, delirium, GI symptoms, and cardiovascular collapse

Question 509

What is the treatment sequence for thyroid storm?

Answer 509

Beta-blocker, thionamide, iodine after thionamide, steroids, and supportive care

Question 510

Why must iodine be given after thionamide in thyroid storm?

Answer 510

To avoid providing substrate before blocking new hormone synthesis

Question 511

What is myxedema coma?

Answer 511

Severe decompensated hypothyroidism with altered mental status and multisystem failure

Question 512

What are classic features of myxedema coma?

Answer 512

Hypothermia, bradycardia, hypotension, hypoventilation, altered mental status, and often hyponatremia

Question 513

What is the treatment of myxedema coma?

Answer 513

Thyroid hormone replacement, stress-dose steroids until adrenal insufficiency is excluded, and aggressive supportive care

Question 514

What is acute adrenal insufficiency or adrenal crisis?

Answer 514

A life-threatening state of cortisol deficiency causing shock and metabolic abnormalities

Question 515

What are classic findings in adrenal crisis?

Answer 515

Hypotension or shock, hyponatremia, hyperkalemia in primary disease, hypoglycemia, abdominal pain, weakness, vomiting, and altered mental status

Question 516

What is the key management principle in suspected adrenal crisis?

Answer 516

Do not wait for confirmatory testing in an unstable patient

Question 517

What is the immediate treatment of adrenal crisis?

Answer 517

IV hydrocortisone and fluids

Question 518

Why must glucose always be checked in acute neurologic change?

Answer 518

Hypoglycemia can mimic stroke, seizure, or encephalopathy

Question 519

What is the immediate treatment of severe hypoglycemia?

Answer 519

IV dextrose

Question 520

What are the major hyperglycemic emergencies?

Answer 520

Diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS)

Question 521

What are the treatment pillars of DKA and HHS?

Answer 521

Fluids, insulin, potassium-aware management, and treatment of the precipitating cause

Question 522

What glycemic control principle is important in ICU patients?

Answer 522

Avoid both severe hyperglycemia and hypoglycemia; very tight control is not favored

Question 523

What are the major physiologic roles of the GI system?

Answer 523

Motility, digestion, absorption, barrier function, and splanchnic blood flow

Question 524

How does critical illness affect GI physiology?

Answer 524

It impairs motility, barrier function, absorption, and perfusion, predisposing to ileus, stress injury, bacterial translocation, and abdominal hypertension

Question 525

Why is the gut vulnerable in shock?

Answer 525

Splanchnic perfusion falls early in shock states

Question 526

What is an acute abdomen?

Answer 526

A syndrome of potentially dangerous abdominal pathology requiring urgent evaluation

Question 527

What dangerous causes of acute abdomen are high yield?

Answer 527

Perforation, mesenteric ischemia, bowel obstruction with strangulation, ischemic bowel, and intra-abdominal sepsis

Question 528

What are the main management priorities in acute abdomen?

Answer 528

Resuscitation, early imaging when feasible, broad antibiotics if infection/perforation is likely, urgent surgical consultation, and source control

Question 529

What are the initial priorities in acute upper GI bleeding?

Answer 529

Resuscitation first, then localization and definitive therapy

Question 530

What is a key endoscopy timing fact in upper GI bleeding?

Answer 530

Endoscopy is generally performed within 24 hours in hospitalized UGIB patients

Question 531

What medication is commonly used after endoscopic hemostasis in ulcer bleeding?

Answer 531

High-dose proton pump inhibitor therapy

Question 532

What medication may improve visualization before UGIB endoscopy?

Answer 532

Erythromycin

Question 533

What is an important board pearl about brisk hematochezia?

Answer 533

It can still come from an upper GI source

Question 534

What is a key imaging test for significant acute lower GI bleeding?

Answer 534

CT angiography

Question 535

What is a board-level colonoscopy pearl in lower GI bleeding?

Answer 535

Stable patients do not necessarily benefit from urgent colonoscopy within 24 hours

Question 536

What is adynamic ileus?

Answer 536

Impaired bowel motility without a mechanical transition point

Question 537

What commonly causes adynamic ileus?

Answer 537

Surgery, opioids, sepsis, electrolyte derangements, and critical illness

Question 538

How is adynamic ileus treated?

Answer 538

Supportive care and correction of the underlying cause

Question 539

What is the major concern with mechanical bowel obstruction?

Answer 539

Progression to strangulation, ischemia, and perforation

Question 540

What finding distinguishes mechanical obstruction from simple ileus on imaging?

Answer 540

A transition point

Question 541

What are the classic clues to GI perforation?

Answer 541

Sudden severe abdominal pain, peritoneal signs, free air, and sepsis physiology

Question 542

What is the treatment of acute GI perforation?

Answer 542

Resuscitation, broad-spectrum antibiotics, and urgent source control, often surgical

Question 543

What is a hallmark symptom of acute mesenteric ischemia?

Answer 543

Abdominal pain out of proportion to the physical exam

Question 544

What risk factors commonly suggest acute mesenteric ischemia?

Answer 544

Atrial fibrillation, embolic risk, shock, vasoconstrictor states, and hypercoagulability

Question 545

What is the key diagnostic test in suspected acute mesenteric ischemia?

Answer 545

CT angiography

Question 546

Why is acute mesenteric ischemia so dangerous?

Answer 546

Delays in diagnosis and revascularization are often lethal

Question 547

What is intra-abdominal hypertension?

Answer 547

Sustained or repeated intra-abdominal pressure ≥12 mm Hg

Question 548

What is abdominal compartment syndrome?

Answer 548

Sustained intra-abdominal pressure >20 mm Hg associated with new organ dysfunction, with or without abdominal perfusion pressure <60 mm Hg

Question 549

What organ effects can abdominal compartment syndrome cause?

Answer 549

Reduced venous return, worse ventilation, decreased renal perfusion/oliguria, bowel ischemia, and reduced cardiac output

Question 550

What is the standard bedside method for measuring intra-abdominal pressure?

Answer 550

Bladder pressure measurement

Question 551

What is the treatment principle for abdominal compartment syndrome?

Answer 551

Decompression/supportive measures first, but overt ACS may require decompressive laparotomy

Question 552

What is acute liver failure?

Answer 552

Acute liver injury with coagulopathy and encephalopathy in a patient without preexisting cirrhosis

Question 553

What major neurologic complication is a leading cause of death in acute liver failure?

Answer 553

Cerebral edema

Question 554

What is a major mechanism of brain edema in acute liver failure?

Answer 554

Ammonia-driven astrocyte swelling

Question 555

What are key management principles in acute liver failure?

Answer 555

ICU monitoring, identify the cause, early transplant-center involvement, manage cerebral edema and secondary injury, and treat renal failure/infection/coagulopathy/glucose abnormalities

Question 556

What systemic factors should be avoided in acute liver failure with cerebral edema?

Answer 556

Hypoxia, hypotension, fever, and hyponatremia

Question 557

What neurocritical care principle applies to brain edema in acute liver failure?

Answer 557

Maintain perfusion, avoid secondary injury, and use ICP-directed supportive measures while treating the liver failure

Question 558

What is acute decompensation of cirrhosis?

Answer 558

Development or worsening of complications such as ascites, encephalopathy, GI bleeding, bacterial infection, and renal dysfunction

Question 559

What are common precipitants of acute decompensation of cirrhosis?

Answer 559

Infection, bleeding, alcohol-related hepatitis, and other acute insults

Question 560

What is an important infection to consider in cirrhosis with ascites?

Answer 560

Spontaneous bacterial peritonitis

Question 561

What is a key board pearl in hepatic encephalopathy?

Answer 561

Search for and treat the precipitating trigger, not just the encephalopathy itself

Question 562

What is an important renal board pearl in cirrhosis?

Answer 562

Renal failure is not always just dehydration; hepatorenal physiology may be involved

Question 563

How does liver failure alter drug handling?

Answer 563

By reducing hepatic extraction, altering protein binding, causing portosystemic shunting, and changing volume of distribution

Question 564

What are the pharmacologic implications of altered hepatic clearance?

Answer 564

Exaggerated or prolonged drug effects, especially with sedatives, opioids, benzodiazepines, and other hepatically metabolized drugs

Question 565

Why is oversedation especially dangerous in liver disease?

Answer 565

It can worsen hepatic encephalopathy and obscure neurologic assessment

Question 566

What general medication principles apply in severe liver disease?

Answer 566

Use caution with hepatotoxic drugs, anticipate prolonged sedation, and reassess anticoagulant/bleeding decisions carefully