1
Q
Which CNS structure primarily mediates IMMOBILITY in response to surgical incision?
A
Ventral horn of the spinal cord
**not cortex.
➡ MAC reflects spinal cord depression.
2
Q
What CNS structure is primarily responsible for UNCONCIOUSNESS during general anesthesia?
A
Reticular Activating System (RAS)
(Cortex, Thalamus, Brainstem)
3
Q
Which pathway mediates ANALGESIA during anesthesia?
A
Spinothalamic tract (pain pathway)
4
Q
Which brain structures are responsible for AMNESIA during anesthesia? (2)
A
Amygdala and Hippocampus
5
Q
Heat of vaporisation
A
Is the number of calories required to change 1 gram of liquid into vapor without changing temp
6
Q
Boiling point
A
temperature at which vapor pressure equals atmospheric pressure (760mmHG) at sea level
7
Q
Tech 6 Vaporizer is used for?
A
Desflurane
8
Q
Tech 6 Vaporizer heats desflurane at? #89
A
39 degrees C
9
Q
Tech 6 Vaporizer is a _____ circuit #89
A
Dual Circuit
NOT A VARIABLE BYPASS VAPORIZER
10
Q
Can you fill Tec 6 Vaporizer during use? # 89
A
yes
11
Q
Why does desflurane need special vaporizer?
A
b/c it has a high vapor pressure (669 mmHg)
12
Q
What is MAC?
A
The alveolar concentration at which 50% of patients do NOT move to surgical incision.
13
Q
MAC varies by ____ to ____ among individuals
A
10% - 15%
14
Q
What does MAC mirror?
A
Brains partial pressure
PA ⬄ Pa ⬄ Pbrain
15
Q
What does MAC specifically measure?
A
It measures how POTENT the volatile anesthetic is at preventing movement.
➡ Suppression of movement (spinal cord–mediated response)
16
Q
Lower MAC = ? potency
Higher MAC = ? potency
A
Lower MAC = more potent inhaled anesthetic
Higher MAC = less potent inhaled anesthetic
17
Q
What factors INCREASE MAC? (7) #33
A
- Hyperthermia
- Drugs that increase CNS catecholemines
- Red hair
- Hypernatremia
- Hyperthyroidism
- Chronic ETOH abuse
- Young Age
18
Q
Anything that increases CNS excitability will increase your _____
A
MAC
19
Q
How does hyperthermia increase MAC?
(think CNS metabolic activity)
A
- Higher temperature cause faster biochemical reactions = more synaptic activity.
- Neurons fire faster and more easily
More active CNS → harder to suppress → higher MAC.
20
Q
Why do drugs (cocaine, amphetamines) that increase CNS catecholamines (norepinephrine, dopamine) increase MAC?
A
Increased norepinephrine and dopamine → Increases arousal pathways →
Increase RAS activity →
Increases spinal excitability
21
Q
Why does chronic ethanol abuse increase MAC (while acute ethanol decreases it)?
A
Chronic ethanol exposure produces CNS tolerance through GABA receptor (inhibitory) downregulation and NMDA receptor upregulation → This increases baseline neuronal excitability, making the CNS less sensitive to anesthetics and increasing MAC
v
Acute ethanol, in contrast, acutely depresses CNS activity and lowers MAC.
22
Q
Why does hypernatremia increase MAC?
A
Elevated extracellular sodium enhances neuronal depolarization and action potential generation.
A more easily depolarized nervous system requires greater MAC.
23
Q
MAC potency is directly related to anesthetic gases ______
A
Solubility
24
Q
0.5 MAC of N2O with 0.5 MAC of Sevoflurane will give an effect of …?
A
1 MAC anesthetic
25
MAC amnesia is?
(0.25) 1/4 the MAC
50% of patients will not remember events
***Amnesia happens at lower concentrations than immobility.
26
What end-tidal MAC reduces the risk of awareness/causes AMNESIA? #96
~0.4–0.5 MAC reduces risk of awareness in most pts
27
Why might 0.4–0.5 MAC not always be sufficient? #96
Opioid use, tolerance, young patients, or high-stimulation surgery may require higher concentrations.
28
MAC awake is ?
(0.33) 1/3 the MAC
The alveolar concentration at which 50% of patients will open eyes or respond to command.
29
MAC - BAR (blunt autonomic response) is?
1.5 the MAC
This is the concentration needed to:
- Prevent tachycardia
- Prevent hypertension
- Prevent sympathetic response to incision
30
MAC - Immobility is?
1 the MAC
If you’re running 1.0 MAC, you may still see HR/BP spike.
31
If des MAC = 6%
....
MAC amnesia = 1.5%
MAC awake = 2%
MAC immobility = 6%
MAC BAR = 9%
32
During induction, what is the direction of anesthetic partial pressure gradient?
(Lungs) Alveoli → Blood → Brain
PA ⬄ Pa ⬄ Pbrain (rising)
33
What partial pressure is changing/rising during induction?
Brain partial pressure rising
Direction of gradient:
Lungs → Brain
34
Explain what happens w/ a:
High blood:Gas Solubility
v
Low blood:Gas Solubility
What happens (step by step):
1. You turn on the vaporizer
2. Start to deliver anesthetic gas into the lungs with inspiration (FI)
3. Gas diffuses into pulmonary capillary blood because there’s a gradient:
PA (alveoli) > Pa (blood) initially
So anesthetic flows into blood.
4. If the agent is highly soluble in blood (high blood:gas) = blood acts like a sponge:
- It can dissolve a LOT of anesthetic
- So a lot leaves the alveoli and disappears into blood
- The alveoli keep getting “drained”
RESULT: PA rises slowly → brain rises slowly → slower induction
OR
4. If the agent is poorly soluble in blood (low blood:gas) = blood acts like a shot glass:
- It cannot dissolve much anesthetic gas
- So it “fills up” (saturates) quickly
- More anesthetic stays in the gas phase (alveoli) and keeps PA high
RESULT: After only a small amount transfers, the blood is essentially “full enough”. It reaches its capacity to hold dissolved anesthetic at that partial pressure very fast.
5. Because blood isn’t soaking it up, alveolar PA rises faster = b/c less anesthetic is being removed from the alveoli
6. Brain partial pressure rises fast because it follows arterial partial pressure
7. And once Pbrain hits the needed threshold → patient loses consciousness.
35
What does Low Blood:Gas solubility mean?
Anesthetic does NOT dissolve (much) in the blood.
36
What factors increase the speed of onset of inhaled anesthetics (aka speed up induction)? (4) #38
High FI
High min ventilation
Low blood solubility = High MAC
Low cardiac output
37
Anything that allows alveolar pressure (PA) to rise quickly will ________ induction
speed up
38
What is minute ventilation equation?
Minute ventilation = Tidal volume × Respiratory rate
39
How does INCREASING minute ventilation affect the speed of induction with inhaled agents? (5)
(step by step)
When you increase ventilation:
1. More fresh anesthetic enters alveoli per minute
2. Faster replacement of anesthetic gas lost to blood
3. Alveolar concentration is maintained or increased = So instead of alveoli being “drained,” they are being refilled quickly.
4. Causes faster rise in alveolar partial pressure
5. Leads to faster brain equilibration
***Minute ventilation = Tidal volume × Respiratory rate
40
How does LOW cardiac output affect the speed of induction with inhaled agents?
(step by step)
1. You turn on the vaporizer.
2. Anesthetic gas accumulates in the alveoli.
3. Low CO = less blood flowing through lungs per minute = less anesthetic is removed from alveoli
4. This causes alveolar concentration to rise faster.
5. Therefore, brain partial pressure rises faster
***Also means higher risk of overdose.
Why? - B/c brain gets high partial pressure quickly
41
Why does LOW cardiac output increase the speed of induction for more soluble agents (ex: isoflurane) than with poorly soluble agents (ex: desflurane)?
Soluble agents (isoflurane) are normally taken up in large amounts by the blood.
When cardiac output decreases = less anesthetic is removed from the alveoli, causing a rapid rise in alveolar partial pressure (PA) and faster brain equililibration.
v.
Poorly soluble agents (desflurane) are minimally taken up by blood regardless of cardiac output, so changes in CO have less impact on induction speed.
42
What is FGF?
What determines it? (2)
#39
FGF = Fresh Gas Flow.
Determined by:
- flowmeter settings (L/min)
- vaporizer concentration (% of servo/iso)
It controls how much anesthetic enters the breathing circuit per minute.
43
Explain how flowmeter and vaporizer work together?
Flowmeter = how much gas moves into pt
Vaporizer = how strong the anesthetic mixture is
Ex:
If FGF = 4 L/min
Vaporizer set to 2% sevo
Then...
2% of 4 L/min = sevo vapor
44
What is FI?
What affects it? (2)
#39 and #42
FI = Inspired anesthetic concentration.
FI is what the patient actually inhales.
It is determined by:
- Fresh gas flow (L/min)
- Circuit volume
Time = Circuit Volume/Fresh Gas Flow
T = VC/FGF
45
How can you speed up FI (Inspired anesthetic concentration)? (3) # 52
1. increase the FGF
2. increase ventilation
3. decrease functional residual capacity (FRC)
46
What are the 2 ways of speeding up induction?
1. Increasing FI = gets anesthetic into the lungs faster
2. Increasing FA/FI = gets anesthetic from lungs to brain faster.
47
How can you speed up the equilibrium of FA/FI? (4) #52
1. increase the FGF
2. increase min ventilation = (TV x RR)
3. decrease functional residual capacity (FRC)
4. use agent with low solubility
5. mask induction = breathe deeply after apply mask
48
Whats is FRC (Functional Residual Capacity)
The volume of gas remaining in the lungs at end-expiration.
Who has low FRC?
Pediatrics
Obese patients
Supine position
Pregnancy
49
How does decreased FRC affect the speed of inhaled anesthetic induction?
Decreased FRC reduces alveolar gas volume → so each breath replaces a larger fraction of alveolar gas with anesthetic →
This accelerates the rise of FA toward FI →
increasing brain partial pressure faster and →
speeding induction.
50
What is FA?
What determines it? (4)
#39
FA = Alveolar anesthetic concentration (alveolar partial pressure)
FA determines brain partial pressure at equilibrium.
It is determined by:
- Uptake into blood/CO
- Alveolar ventilation (≠ Minute ventilation)
- FI (= high FI accelerates FA)
- Second gas effect
Ex: ARDS pt
51
What is Fa?
What affects it? (3)
#39
Fa = Arterial anesthetic concentration.
Fa reflects what is delivered to the BRAIN.
It is affected by:
- Ventilation = what's moving into alveoli
- Perfusion = what's removed from alveoli
- V/Q mismatch = how efficiently things move from alveoli to arterial blood
52
What delays equilibration of PA(FA)→ Pa(Fa)→ Pbrain? (3)
High blood solubility (aka High Blood:Gas co)
High cardiac output
Hypoventilation = less anesthetic enters alveoli per min
53
What is overpressurization in inhaled anesthesia?
Overpressurization is giving a higher-than-maintenance inspired concentration initially to accelerate the rise of FA (similar to giving an IV bolus).
54
What determines speed of emergence? (4)
1. Blood:Gas solubility
2. Duration of exposure of anesthetic gas
3. Fat accumulation
4. Ventilation
***Low solubility = Faster wake-up
55
Why does fat affect emergence more than induction? #50
Redistribution
Explain:
Fat is poorly perfused (compartment) but highly lipid soluble.
It fills slowly during long cases and redistributes anaesthetic back (into the plasma) slowly during emergence.
56
What tissue group equilibrates first during induction?
Vessel-rich group (VRG)
Ex: Brain, Heart, Liver, Kidneys
57
Vessel-rich group (VRG) organs make up only _____% of your total body weight?
But ____% of all blood pumped by the heart each minute goes to those organs.
And perfusion ml/min/100g is?
10%
75%
55-550
***
If cardiac output is 5 L/min
~3.75 L/min goes to the VRG.
58
Muscle Group? #49
% of Body Mass
% of Cardiac Output
Perfusion ml/min/100g is
% of Body Mass = 50%
% of Cardiac Output = 19%
Perfusion ml/min/100g is = 3 ml/min/100g
59
Fat Group? #49
% of Body Mass
% of Cardiac Output
Perfusion ml/min/100g is
% of Body Mass = 20%
% of Cardiac Output = 6%
Perfusion ml/min/100g is = 1 ml/min/100g
60
Why does INCREASED cardiac output slow induction?
Higher CO removes more anesthetic from alveoli.
Therefore:
→ Slower rise in alveolar partial pressure (PA).
→ Slower brain equilibration.
61
What is the key pharmacokinetic goal of delivering inhaled anesthesia?
Establish and maintain a specific partial pressure in the brain (Pbrain)
***At equilibrium:
PA = Pa = Pbrain
62
What does the Meyer–Overton theory state?
higher lipid solubility = more potency
The more lipid-soluble an inhaled anesthetic is, the more potent it is.
63
What is the Oil:Gas coefficient reflect about an anesthetic agent? (3)
It reflects the anesthestics:
1. LIPID SOLUBILITY
2. POTENCY
3. MAC
64
What does the Blood:Gas coefficient measure?
It measures how well the anesthetic dissolves in blood compared to alveolar gas.
65
Why does lipid solubility determine potency? (3)
If a drug dissolves easily into lipid:
1. It accumulates in brain + spinal cord
2. It produces effect at lower alveolar partial pressure (PA)
3. You need less alveolar concentration
66
Oil:Gas Coefficient → determines ?
Blood:Gas Coefficient → determines ?
Oil:Gas Coefficient → determines SOLUBILITY, POTENCY and MAC
Blood:Gas Coefficient → determines SPEED of induction
67
High Oil:Gas Relationship →
? Solubility
? Potency
? MAC
High Oil:Gas
→ High lipid solubility
→ High potency
→ Low MAC
68
Low Oil:Gas Relationship →
? Solubility
? Potency
? MAC
Low Oil:Gas
→ Low lipid solubility
→ Low potency
→ High MAC
69
What happens to MAC as lipid solubility increases?
MAC decreases.
***Greater lipid solubility = lower MAC.
***MAC = the alveolar concentration needed to prevent movement in 50% of patients
70
Does MAC measure unconsciousness or immobility?
Immobility (spinal cord mediated).
71
How does isoflurane compare to desflurane in potency? Why?
Isoflurane is more potent (lower MAC) due to higher lipid solubility.
72
MAC % (potency) for:
Nitrous ≈
Isoflurane ≈
Sevoflurane ≈
Desflurane ≈
Nitrous ≈ 105 (not potent alone)
Isoflurane ≈ 1.15 - 1.2 → most potent
Sevoflurane ≈ 2
Desflurane ≈ 5.8
73
What is Saturated Vapor Pressure (SVP)?
How volatile the liquid anesthetic is at room temperature.
74
Blood:Gas Partition Coefficient
This determines the speed of induction
75
Saturated Vapor Pressure (SVP) for:
Nitrous ≈
Isoflurane ≈
Sevoflurane ≈
Desflurane ≈
Nitrous ≈ gas
Isoflurane ≈ 238mmHg
Sevoflurane ≈ 157mmHg
Desflurane ≈ 669mmHg
76
Blood:Gas Partition Coefficient for:
Nitrous ≈
Isoflurane ≈
Sevoflurane ≈
Desflurane ≈
Nitrous ≈ 0.47
Isoflurane ≈ 1.4 → slowest
Sevoflurane ≈ 0.6 -0.65
Desflurane ≈ 0.42 → fastest
77
What determines DEPTH OF ANESTHESIA according to Meyer–Overton?
The number of anesthetic molecules dissolved in the brain.
78
HIGH MAC Relationship →
? Solubility
? Potency
? Oil:Gas Relationship
HIGH MAC →
Lower Lipid Solubility
Less Potency
Lower Oil:Gas Relationship
79
LOW MAC Relationship →
? Solubility
? Potency
? Oil:Gas Relationship
LOW MAC →
Higher Lipid Solubility
Higher Potency
Higher Oil:Gas Relationship
80
High Blood:Gas →
? Solubility
? Rise in PA
? Induction
High Blood:Gas →
High blood solubility
Slower rise in PA
Slow induction
81
Low Blood:Gas →
? Solubility
? Rise in PA
? Induction
Low Blood:Gas →
Low blood solubility
High rise in PA
High induction
82
What Guedal's 4 Stages of Anesthesia?
1️⃣ Stage I – Induction (awake → loss of consciousness)
2️⃣ Stage II – Excitement / Delirium
3️⃣ Stage III – Surgical anesthesia
4️⃣ Stage IV – Overdose / Medullary depression
83
What happens in Stage I of Guedel’s anesthesia?
Induction to loss of consciousness
84
What happens in Stage II of Guedel’s anesthesia? (5)
Delerium w a period of Excitement
1. Increased HR
2. Increased RR
3. Dilated pupils
4. Disconjugate gaze
5. High risk of laryngospasm/bronchospasm
85
What happens in Stage III of Guedel’s anesthesia? (3)
Surgical anesthesia/Maintenance period
1. Fixed gaze
2. Constricted pupils
3. No movement to incision
86
What happens in Stage IV of Guedel’s anesthesia? (4)
Overdose
1. Absent or shallow irregular RR
2. Hypotension
3. Profound cardiovascular collapse
4. Dilated, nonreactive pupils
87
What Is an Inhalational Induction?
You use anesthetic gas through a mask to put the patient to sleep, instead of giving IV medication first.
Awake → breathing anesthetic → asleep.
88
What are the 2 ways to do Inhalational Induction?
1. Tidal Volume Breathing = Patient breathes normally in and out.
2. Vital Capacity Breath = Patient takes a big deep breath and holds it.
89
Is Inhalational Induction slower or faster than IV?
Slower
IV Induction > Vital Capacity Breath > Tidal Volume Breathing
90
How does Nitrous speed up induction?
Second gas effect
91
What is Second gas effect? #57
Nitrous leaves the alveoli fast, shrinks alveolar volume, and concentrates the second gas.
step by step:
1. We give a high concentration of nitrous oxide (like 70%).
2. Nitrous is absorbed very rapidly and in large amounts into the blood.
3. Because so much nitrous leaves the alveoli quickly, the total gas volume inside the alveoli shrinks.
4. When the alveolar volume shrinks, the remaining gases (like sevoflurane) become more concentrated.
5. That increase in alveolar concentration makes the second gas reach the brain faster.
92
Does second gas effect change potency (MAC) or speed?
Speed of induction
Why? - b/c it increases the rate of rise of alveolar partial pressure (PA) of the second gas.
93
If the second gas was Desflorene, would the "second gas effect" speed up induction?
Compare to sevo/iso.
Yes. But, less dramatically than with sevo or iso.
Why? - B/s desflurane already has:
- Very low Blood:Gas solubility
- Rapid PA rise on its own
The second gas effect is more noticeable with more soluble
94
Can you use Desflurase for mask intubation?
No, it is an irritant
95
Volatile agents are able to .... the airway? (2)
Relax smooth airway
Brochodilation
96
Patients undergoing inhalation induction exhibit ALL the stages of anesthesia, especially _______?
Why?
Stage 2 - Excitement/Delerium Phase
= in this phase the brain is partially depressed, the higher centers start to turn off (cortex) but the lower centers (brainstem + spinal cord) are still active.
Why?
B/c inhalational induction moves through Stage 2 more slowly.
The anesthetic must build up in alveoli → blood → brain
97
If a pt starts to have brochospasm, what can you do?
Increase inhalation agent to cause bronchodilation
Which one?
Sevo or Iso
Not?
Desflurane (b/c irritant) or Nitrous (not a bronchodilator)
98
Why do inhaled anesthetics allow rapid emergence?
Because they are eliminated via exhalation
99
Why do inhaled anesthetics diffuse rapidly?
Nonionized, low molecular weight.
100
What 2 major factors determine speed of emergence from inhaled anesthesia? #59
1. Agent solubility
2. FGF rate
101
How does high (agent) blood solubility affect recovery?
Greater tissue storage (in fats) and slower elimination, prolonging recovery
102
Why should fresh gas flow be increased during emergence?
To prevent rebreathing of exhaled anesthetic and accelerate washout from the lungs
103
What factors affect (emergence) WAKE UP from inhaled anesthesia? (6) #60
1. Inhalation agent used (solubility)
2. Alveolar ventilation
3. Length of procedure
4. Patient factors (age, mental status, medical conditions, medications)
5. Obesity (fat depot storage)
6. Airway issues (OSA, obstruction)
***Anything that increases tissue storage or reduces washout will delay emergence.
104
How can carbon monoxide (CO) be produced in the anesthesia circuit?
When volatile anesthetics (Desflurane and isoflurane) degrade in dry or desiccated CO₂ absorbents.
105
What is soda lime primarily composed of?
Calcium hydroxide (Ca(OH)₂)
+
Small amounts of:
Sodium hydroxide (NaOH) and
Potassium hydroxide (KOH)
106
What happens when CO₂ reacts with soda lime?
CO₂ is chemically absorbed and converted into:
1. Calcium carbonate (CaCO₃)
2. Water (H₂O)
3. Heat
107
Soda lime reaction is ...
Exothermic
CO₂ + Ca(OH)₂ → CaCO₃ + H₂O + heat
108
How do you know when the absorbant has been exhausted? #78
ethyl violet
rising ETCO₂
109
Why is Compound A clinically concerning?
It is nephrotoxic (kidney toxic).
110
Which anesthetic is associated with Compound A formation?
Sevo
111
Colors of ansthetic gases
iso - purple
sevo - yellow
des - blue
112
What is Coronary steal?
Redistribution of blood flow away from ischemic myocardium to normal myocardium due to vasodilation.
Ex: CAD, multi-vessel disease, stenosis, MI
113
Isoflurane (7) #86
Most potent = low MAC (1.2)
High solubility = Blood:Gas Co (1.4 - 1.46)
Vapor Pressure = 238
↓ SVR → ↓ MAP
↑ CBF
Coronary steal
Pungent → no mask induction
114
Sevoflurane (5) #87
Non-pungent → good for mask induction
Compound A
Bronchodilator
Low solubility = Blood:Gas Co (0.6 - 0.65)
Vapor pressure = 157 - 160
MAC = 2
115
Desflurane (6) #88
Lowest solubility = Blood:Gas Co (0.42)
Vapor pressure = 669 → heated vaporizer
Fastest induction and emergence
Pungent → no mask induction
SNS stimulation = ↑ HR + ↑ BP
Carbon monoxide risk
116
All volatile anesthetic agents increase incedence of _____ and the risk increases with the duration of exposure to the anesthetic
#90
PONV
117
Which inhaled agents are non-pungent?
Sevoflurane
Halothane
Nitrous oxide
118
How do volatile anesthetics affect respiratory rate and tidal volume?
Dose dependent
↑ Respiratory rate
↓ Tidal volume
119
How do inhaled anesthetics affect the ventilatory response to CO₂?
Dose-dependent depression of the response to hypercarbia → PaCO₂ increases.
120
How do volatile inhalational agents affect MAP?
Dose-dependent decrease
121
How do inhalational anesthetics lower blood pressure?
They relax vascular smooth muscle → ↓ SVR (Vasodilation) → ↓ BP.
122
How do inhalational agents affect CO and CI?
Dose-dependent decrease
123
How does Nitrous Oxide affect the sympathetic nervous system and on hemodynamics?
Activates SNS → ↑ SVR.
↑ CVP
↑ Arterial pressure
124
Key difference: Volatiles vs N₂O on SVR?
Volatiles = Vasodilate → ↓ SVR → ↓ MAP
N₂O = SNS activation → ↑ SVR → ↑ BP
125
What happens to heart rate with RAPID increases in Isoflurane or Desflurane?
HR and BP increase due to sympathetic stimulation.
126
Which causes more initial tachycardia when rapidly increased: Desflurane or Isoflurane?
Desflurane > Isoflurane.
127
Which volatile is most likely to cause tachycardia? Why?
Desflurane
Airway irritation → sympathetic activation → tachycardia
128
How does Sevoflurane affect heart rate?
Minimal effect on HR.
129
How can you blunt the tachycardia caused by volatiles?
Use opioids (fentanyl) or beta-blockers ( esmolol).
130
How do inhaled anesthetics affect myocardial oxygen supply vs demand?
They increase coronary blood flow more than myocardial oxygen demand.
131
How do volatile anesthetics affect cerebral blood flow (CBF) and ICP?
Dose-dependent increase in CBF due to direct cerebral vasodilation.
↑ CBF → ↑ intracranial blood volume → ↑ ICP.
132
How can you blunt volatile-induced increases in ICP?
Hyperventilation (↓ PaCO₂ → cerebral vasoconstriction).
133
How do volatiles affect cerebral metabolic rate of oxygen (CMRO₂)?
Dose-dependent decrease in CMRO₂.
134
Which volatile is generally preferred in neurosurgical cases requiring smoother hemodynamics?
Sevoflurane (less sympathetic stimulation than Desflurane).
135
How do inhaled anesthetics affect renal blood flow?
↓ Systemic BP → ↓ renal perfusion → ↓ GFR.
136
How are inhalational anesthetics different from IV anesthetics in terms of metabolism?
Undergo minimal hepatic metabolism — most is eliminated unchanged via the lungs.
137
What effect do inhaled anesthetics have on skeletal muscle?
Dose-dependent skeletal muscle relaxation.
138
How do inhaled anesthetics interact with neuromuscular blockers?
They (SYNERGISTICALLY) potentiate both depolarizing and nondepolarizing NMBA.
Additive = 1 + 1 = 2
Synergistic = 1 + 1 > 2
139
How do inhaled anesthetics enhance NMBA?
Decrease CNS motor output
Increase postsynaptic sensitivity at the NMJ
Decrease presynaptic ACh release
140
What is the blood:gas coefficient of N₂O? What does that mean?
0.46 → low solubility → rapid onset and rapid offset.
141
Does N₂O trigger malignant hyperthermia?
No
142
What are the cardiovascular effects of N₂O?
Minimal CV depression; may slightly increase BP via sympathetic stimulation.
143
How does N₂O affect ventilation?
↑ Respiratory rate
↓ Tidal volume
Minute ventilation = Tidal volume × Respiratory rate
144
Does N₂O provide muscle relaxation?
No
145
Does N₂O provide muscle relaxation?
Yes
146
Why does N₂O expand closed air spaces?
It diffuses into spaces faster than nitrogen can leave (34× more soluble than N₂).
147
What effect does N₂O have on compliant vs noncompliant spaces? #93
Compliant space → Volume increases
Noncompliant space → Pressure increases
148
In what situations should N₂O be avoided?
* Pneumothorax
* Bowel obstruction
* Venous air embolism
* Middle ear surgery
* Retinal gas bubble
* Long cases with ETT cuff
149
What vitamin pathway is affected by N₂O?
B12 inhibition
150
What patients are at risk from prolonged N₂O exposure?
* B12 deficiency
* Malnourished
* Vegan
* Elderly
* Chronic exposure
151
What is diffusion hypoxia?
Explain.
Hypoxemia that occurs when nitrous oxide is discontinued abruptly.
N₂O leaves blood quickly → floods alveoli → dilutes alveolar oxygen → ↓ PAO₂ → ↓ PaO₂.
152
How do you prevent diffusion hypoxia?
Explain.
Administer 100% oxygen for at least 5 minutes after discontinuing N₂O.
Administering 100% oxygen offsets dilutional drop in PAO₂ caused by rapid N₂O efflux.
153
Which patient is at highest risk for diffusion hypoxia?
Patients breathing room air immediately after stopping N₂O.
154
What are major risk factors for intraoperative awareness? (5)
* Use of neuromuscular blockers
* Substance abuse (↑ anesthetic requirement)
* High-risk surgeries (cardiac, trauma, C-section)
* Inadequate anesthetic delivery
* Poor machine maintenance
155
What drug is commonly used to reduce risk of recall in high-risk patients?
Midazolam (Versed).
156
What is the underlying mechanism of malignant hyperthermia (MH)?
What is the underlying mechanism of malignant hyperthermia (MH)?
Sustained muscle contraction → massive ATP consumption → heat production → hypermetabolism.
157
Which receptor is mutated in MH?
Which receptor is mutated in MH?
158
What triggers malignant hyperthermia? (2)
1. Volatile inhalational anesthetics
2. Succinylcholine
***NOT nitrous oxide
159
What is the earliest and most sensitive sign of MH?
Unexplained rise in ETCO₂
Why? - Massive increase in CO₂ production due to hypermetabolism.
160
Is fever an early sign of MH?
No. Hyperthermia is a late sign.
161
What cardiovascular sign commonly accompanies early MH?
Tachycardia
162
What acid-base disturbance occurs in MH?
metabolic + respiratory acidosis
163
Why does hyperkalemia occur in MH?
Muscle breakdown (rhabdomyolysis) releases potassium.
164
Which volatile agents have greater environmental impact?
Desflurane
N₂O
165
Which volatile agents are preferred when considering short-term environmental impact?
Sevoflurane and isoflurane (lower global warming potential than desflurane).
166
What is low-flow anesthesia?
Using low fresh gas flows (≤1 L/min) during maintenance.
167
What is the benefit of low-flow anesthesia?
Can reduce volatile anesthetic use by up to 80%.
168
What types of anesthesia eliminate volatile greenhouse gas emissions?
Total intravenous anesthesia (TIVA)
Regional = Spinal, epidural, and peripheral nerve blocks
169
What are the 5 AANA Monitoring Standards?
1. Oxygenation
2. Ventilation
3. Circulation
4. Temperature
5. Neuromuscular
170
What does Standard 1 (Oxygenation) require during anesthesia?
Continuous monitoring of:
1. Oxygenation by clinical observation
2. Pulse oximetry
171
Is pulse oximetry optional?
Pulse ox is NOT optional. It is continuous.
172
Why must oxygen concentration (FiO₂ %) be continuously monitored in the anesthesia machine?
To detect:
1. Hypoxic gas mixtures
2. Pipeline crossover
3. Accidental delivery of low FiO₂ (= measured oxygen concentration in the circuit)
173
What device detects hypoxic gas mixtures on the anesthesia machine?
#7
Oxygen analyzer aka Oxygen Sensor
174
What is the minimum safe FiO₂ reading?
21-25%
175
How much FiO2 for induction and emergence?
v
General FiO2 range throughout case?
100%
50-60%
176
All oxygen analyzer must have a ...?
low level alarms
177
What must be continuously monitored under Standard 2 (Ventilation)?
Continuous Capnography (ETCO₂)
How?
1. GA with ETT → inline capnography
2. LMA → inline capnography
3. Mask GA → sampling line
4. MAC/deep sedation → nasal ETCO₂
178
Can you rely on SpO₂ alone during MAC?
No
179
What disappears first in apnea?
ETCO₂ waveform.
180
Under Standard 3, what must be continuously monitored? (2)
Via?
1. Heart rate
2. Cardiovascular status
via...
1. ECG
2. BP monitoring (at least every 5 min)
181
When must temperature be monitored?
If using volatile anesthetics
MH triggering agents are used
If significant temperature changes are intended or suspected
182
When must neuromuscular function be monitored?
Whenever NMBA are used
183
A sedated patient refuses oxygen during MAC. What is your responsibility?
Still maintain monitoring standards
Document pts refusal
***Standard of care does NOT disappear because the patient refuses.
184
Why are AANA Monitoring Standards important legally?
They define:
- Minimum standard of care
- What is considered safe practice
- Foundation for malpractice review
185
What does a pulse oximeter:
Directly measure vs estimates?
Directly measure:
1. Light absorbance
2. Pulse rate
Estimates:
1. Arterial oxygen saturation (SaO₂) of Hgb
186
What physical law does pulse oximetry rely on?
Beer-Lambert Law
187
What is the key principle of Beer-Lambert Law?
There is a LINEAR relationship between:
Concentration of solute ↔ Light absorbance
Explain:
More hemoglobin absorbing light → More absorbance → Less transmitted light
188
What two wavelengths does a pulse oximeter use?
1. Red light (~660 nm) → absorbed more by deoxyhemoglobin
2. Infrared light (~940 nm) → absorbed more by oxyhemoglobin
189
Pulse Ox Assumption # 1:
What two light absorbers does pulse oximetry assume are present in the body?
1. Oxyhemoglobin (infrared light)
2. Deoxyhemoglobin (red light)
190
Pulse Ox Assumption # 2:
What portion of blood flow does the pulse ox analyze?
Only pulsatile arterial blood flow
191
Pulse Ox Assumption # 3:
How is SpO₂ calculated?
Is it a direct measurement?
Using an empirically derived calibration curve
Based on healthy volunteers.
It is NOT a direct physiologic measurement.
192
How does CO affect pulse oximeter readings?
Carboxyhemoglobin absorbs light like oxyhemoglobin (infrared light = 660 nm)
SpO₂ appears falsely normal.
193
Why does hypotension affect pulse ox accuracy?
B/c Pulse ox depends on pulsatile arterial flow.
Hypotension → Low perfusion → weak signal → inaccurate reading
194
If SpO₂ is 100%, what is NOT guaranteed? (3)
Adequate:
1. Oxygen delivery to tissues
2. Oxygen utilization by tissues
3. Ventilation
195
How delayed can pulse ox detection be?
Up to ~20 seconds (or more)
196
Why does methylene blue cause SpO₂ to drop into the 70s?
Methylene blue absorbs red light (~660 nm).
Pulse ox interprets this as deoxygenated hemoglobin.
197
Which IV dyes interfere with pulse ox? (3)
Methylene blue
Indigo carmine
Indocyanine green
198
Why do nail polish and movement affect pulse ox readings?
They interfere with:
- Light transmission
- Pulsatility detection
Leads to inaccurate SpO₂.
199
What is Methemoglobinemia?
In methemoglobinemia:
Iron becomes Fe³⁺ (ferric) → cannot bind oxygen = making Hgb molecule useless for oxygen transport.
Normally:
Hemoglobin iron = Fe²⁺ (ferrous) → binds oxygen
200
In methemoglobinemia you’ll see..?
SpO₂ stuck around 85%
Chocolate-colored blood
Treated w: Methylene blue
201
SpO₂
SaO₂
PaO₂
CaO₂
SpO₂ = Peripheral Oxygen Saturation = Estimated percentage of hemoglobin saturated with oxygen = pulse ox
SaO₂ = Arterial Oxygen Saturation = True percentage of hemoglobin saturated with oxygen in arterial blood = ABG = GOLD STANDARD
PaO₂ = Arterial Oxygen Partial Pressure = The pressure exerted by dissolved oxygen in arterial plasma = ABG = reflects lung oxygenation
CaO₂ = Total oxygen in blood = Total amount of oxygen in arterial blood = reflects tissue oxygenation
202
What physical law does cerebral oximetry use?
Beer-Lambert Law
203
Does cerebral oximetry isolate pulsatile arterial blood like pulse ox?
No.
It measures mixed (arterial + venous) cerebral blood, mostly venous (~70%).
204
What is the normal range for cerebral oximetry?
60–75%
205
What change from baseline suggests cerebral ischemia?
A 20–25% decrease from baseline
206
A drop in cerebral oximetry (rSO₂) most likely reflects what imbalance?
Oxygen delivery < oxygen consumption in the brain
207
Which surgical position increases risk of cerebral desaturation?
Beach chair position
208
What type of procedures use cerebral oximetry?
Carotid endarterectomy
Cardiac surgery
Aortic surgery
Beach chair orthopedic cases
High-risk neurosurgery
209
How does hyperventilation affect cerebral oximetry?
↓ PaCO₂ → cerebral vasoconstriction → ↓ cerebral blood flow → ↓ cerebral oximetry
210
Cerebral oximetry (#17-19)
Uses Beer-Lambert law
Near-infrared spectroscopy
Measures mixed (mostly venous) cerebral blood
Normal 60–75%
20–25% drop from baseline = ischemia concern
Obtain baseline pre-induction
Drops with hypotension, anemia, hyperventilation
Beach chair = high risk
211
Why is 5-lead ECG superior to 3-lead?
5-lead allows monitoring:
Lead II (arrhythmias, inferior ischemia)
V5 (anterior/lateral ischemia)
v
3-lead cannot monitor both simultaneously.
212
Which lead is best for detecting arrhythmias?
Lead II
Why?
Because it aligns with the atrial depolarization axis.
213
Which leads are best for detecting ischemia intraoperatively?
Lead II → inferior wall
V5 → anterior & lateral wall
214
What are ALL the leads that detect inferior wall ischemia?
II, III, aVF
Associated artery =
Usually RCA
215
Which leads detect anterior/septal ischemia?
V1–V4
Associated artery:
LAD
216
Which leads detect lateral wall ischemia?
I, aVL, V5, V6
217
What does cerebral pulse oximetry estimate?
Cerebral oxygen delivery and oxygen consumption
General Principles — Liz
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