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ACEM Primary Written > Anaesthetics: Pharmacology - General anaesthesia > Flashcards

Anaesthetics: Pharmacology - General anaesthesia Flashcards

1
Q

What are the 6 A’s of anaesthesia?

A
  1. Anaesthesia (loss of consciousness)
  2. Analgesia
  3. Amnesia
  4. Areflexia (loss of autonomic and sensory reflexes)
  5. Akinesia (skeletal muscle relaxation)
  6. Anxiolysis
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2
Q

Compare and contrast volatile vs inhaled anaesthetics in terms of vapour pressure, boiling point, and state at room temperature

A

Volatile: low vapour pressure, high boiling point, liquid at room temp
Inhaled: high vapour pressure, low boiling point, gas at room temp

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3
Q

What are the stages of anaesthesia (Guedel’s signs)?

A
  1. Analgesia: with amnesia in later part of stage 1
  2. Excitement: increased RR (also irregular), HR and BP; delirious, may vocalise but completely amnesic
  3. Surgical anaesthesia: begins with decreased RR and HR, eventuates in apnoea; four planes described based on changes in ocular movements, eye reflexes, and pupil size
  4. Medullary depression: severe CNS depression (including medullary vasomotor centre and brainstem respiratory centre)
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4
Q

What are the most reliable signs of reaching stage III of anaesthesia?

A

Loss of eyelash reflex
Establishment of regular respiratory pattern

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5
Q

Give five examples of volatile anaesthetics

A

Halothane
Enflurane
Isoflurane
Desflurane
Sevoflurane

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6
Q

Give two examples of gaseous inhaled anaesthetics

A

Nitrous oxide
Xenon

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7
Q

Describe the drugs typically used for monitor anaesthetic care

A

Midazolam for anxiolysis, amnesia and mild sedation
Followed by propofol for moderate-to-deep sedation
+/- potent opioid or ketamine for analgesia

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8
Q

Describe the principles of conscious sedation: what drugs are used, and what state is achieved?

A

Uses smaller doses of sedative medications (e.g. diazepam, midazolam, propofol)
Anxiolysis and analgesia with less alteration of consciousness
Maintains airway and responsiveness to verbal commands

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9
Q

What are the four factors influencing uptake and distribution of inhaled anaesthetics?

A
  1. Inspired concentration and ventilation
  2. Solubility
  3. Cardiac output (pulmonary blood flow)
  4. Alveolar-venous partial pressure difference
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10
Q

How does inspired drug concentration and ventilation influence uptake of inhaled anaesthetic? How can these factors be manipulated to increase uptake?

A

Higher inspired anaesthetic concentration = higher rate of transfer into blood (Fick’s law; steeper gradient between inspired and alveolar partial pressure)
Increasing partial pressure of inhaled anaesthetic increases uptake
Increasing ventilation (i.e. increased RR, TV) increases uptake

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11
Q

How does solubility of an inhaled anaesthetic agent affect its uptake?

A

Increased solubility increases the time required for F(A)/F(I) to reach equilibrium (therefore slower onset of induction)

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12
Q

How is solubility of an inhaled anaesthetic agent quantified?

A

Quantified by the blood:gas partition coefficient (measure of the relative affinity of an anaesthetic
for blood, compared to air)
Higher coefficient, higher solubility

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13
Q

What is F(A)/F(I) and what is its significance?

A

Alveolar concentration / inspired concentration
The faster it approaches 1 (i.e. inspired-to-alveolar equilibrium), the faster anaesthesia onset during inhaled induction

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14
Q

What is MAC?

A

Minimal alveolar concentration: anaesthetic concentration that produces immobility in 50% of patients exposed to a noxious stimulus

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15
Q

What is partial pressure? Give a worked example

A

Fraction of a gas mixture that a particular component comprises
E.g. mixture of 70% nitrous oxide, 29% oxygen, 1% isoflurane at barometric pressure (760mmHg) = 532mmHg nitrous oxide, 220mmHg oxygen, 7.6mmHg isoflurane

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16
Q

Give two examples of inhaled anaesthetics with low solubility and one with high solubility. What are their respective blood:gas partition coefficients?

A

Low solubility: desflurane, nitrous oxide (B:GPC < 0.5)

Higher solubility: halothane (B:GPC > 2)

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17
Q

How does cardiac output affect uptake of inhaled anaesthetic agents?

A

Increased CO increases pulmonary blood flow
Increased pulmonary blood flow increases blood volume exposed to gas and thereby slows rate of rise in F(A)/F(I), slowing induction

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18
Q

How does alveolar-venous partial pressure difference affect uptake of inhaled anaesthetic agents?

A

Partial pressure difference between alveolar and mixed venous blood is dependent on anaesthetic uptake by tissues (including nonneural)
Increased uptake by nonneural tissues increases the concentration gradient of returning venous blood
Increased concentration gradient increases amount of time to reach equilibrium with brain tissue
This is mainly influenced by highly perfused organs (brain, heart, liver, kidneys, splanchnic bed)

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19
Q

What three factors influence transfer of inhaled anaesthetic agent to various tissues?

A
  1. Solubility
  2. Concentration gradient between blood and respective tissue
  3. Tissue blood flow
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20
Q

What are the two main differences between factors affecting uptake and elimination?

A

Elimination follows some of the same principles in reverse as uptake, with two main differences:
- Transfer of anaesthetic from lungs to blood can be enhanced by increasing inspired concentration, but reverse process cannot be enhanced (concentration in lungs can’t be reduced below zero)
- Anaesthetic gas tension in different tissues may be variable depending on agent and duration of anaesthesia (whereas at induction, initial concentrations are zero)

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21
Q

How does solubility influence elimination of inhaled anaesthetic?

A

Decreased solubility increases speed of washout

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22
Q

How does duration of anaesthetic exposure influence speed of emergence?

A

Prolonged exposure causes accumulation of anaesthetic in muscle, skin and fat
Anaesthetic slowly eliminated from these tissues, so speed of emergence is slower

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23
Q

What determines time to recovery from inhaled anaesthetics?

A

Rate of elimination of anaesthetic from brain

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24
Q

What impact does ventilation have on recovery from inhaled anaesthetics?

A

Increased speed of recovery with hyperventilation

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25
What impact does drug metabolism have on recovery from inhaled anaesthetics?
Elimination of modern inhaled agents is mainly by ventilation, and metabolism typically plays no significant role (but may play a role in toxicity) In older inhaled agents (e.g. halothane), hepatic metabolism may play a role (particularly with prolonged duration of anaesthesia: significant hepatic metabolism during anaesthesia results in faster-than-expected washout)
26
What is minimum alveolar concentration?
Median alveolar concentration that results in immobility in 50% of patients when exposed to a noxious stimulus (e.g. surgical incision) Measure of potency and represents ED50 on a quantal dose-response curve
27
At what MAC is immobility vs amnesia achieved?
Immobility at 1.0 MAC Amnesia at 0.2-0.4 MAC
28
Three factors that decrease MAC
1. Elderly 2. Hypothermia 2. Adjuvant agents (e.g. opioids, sympatholytics, sedative-hypnotics)
29
Two factors that increase MAC
1. Pregnancy 2. Chronic use of centrally active drugs 3. EtOH abuse
30
What is the MAC of N2O and what is the significance of this?
MAC >100% Means that even at 100% alveolar concentration, it does not produce full anaesthesia in 50% of patients and another agent must be used
31
List inhaled anaesthetic agents in order of degree of hepatic metabolism (from most to least)
HE SaID NO: Halothane Enflurane Sevoflurane Isoflurane Desflurane Nitrous oxide
32
Four CNS effects of inhaled anaesthetics
1. Decreased cerebral metabolic rate 2. Changes in cerebral blood flow: - Decreased CMR causes decreased cerebral blood flow, but some volatile anaesthetics have a direct vasodilatory effect and increase cerebral blood flow - At MAC 0.5, reduction in CMR > vasodilation, so cerebral blood flow decreases - At MAC 1.5, vasodilation > reduction in CMR, so cerebral blood flow increases - At MAC 1.0, vasodilation = reduction in CMR, so cerebral blood flow is unchanged 3. EEG changes - Activation at lower doses, slowing at 1.0-1.5 MAC, suppression at 2.0-2.5 MAC - Isolated epileptiform patterns at 1.0-2.0 MAC (frank seizure activity only seen with enflurane) 4. Sedation
33
What is the importance of changes in cerebral blood flow caused by inhaled anaesthetics?
Important to consider in patients with or at risk of raised ICP (at higher MAC, cerebral blood flow and therefore ICP is increased) Effect is smallest with N2O
34
Four CVS effects of inhaled anaesthetics (including specific effect of halothane)
1. Decreased MAP (proportional to alveolar concentration) 2. Changes in HR: - Reflex tachycardia: desflurane, isoflurane - Bradycardia (via attenuation of baroreceptor response): halothane, enflurane, sevoflurane 3. Decreased myocardial O2 demand and increased coronary blood flow 4. Halothane sensitises myocardium to circulating catecholamines
35
Which inhaled anaesthetic agents cause a decrease in MAP by decreasing CO, and which cause a decreased in MAP by reducing TPR?
Decreased CO: halothane, enflurane Decreased TPR: isoflurane, desflurane, sevoflurane
36
What is the clinical relevance of choosing an inhaled anaesthetic agent that reduces MAP by reducing TPR vs CO?
Agents that reduced MAP by reducing TPR (e.g. isoflurane, desflurane, sevoflurane) are better for patients with impaired heart function, as they preserve CO whilst decreasing preload and afterload
37
What is the effect of N2O on CO?
Reduces CO but increased sympathetic stimulation, with net effect of preservation of CO
38
What is the clinical significance of halothane's effect on myocardium?
Sensitises myocardium to circulating catecholamines, increasing the risk of ventricular arrhythmias if sympathomimetics given or in setting of increased endogenous catecholamines (e.g. stress, inadequate analgesia, phaeochromocytoma)
39
Five respiratory effects of inhaled anaesthetics
1. Bronchodilation 2. Airway irritation and bronchospasm 3. Dose-dependant reduction in TV and increase in RR (with exception of N2O): produces overall decrease in ventilation and increase in PaCO2 4. Increased apnoeic threshold and decreased response to hypoxia 5. Decreased mucociliary response: mucus plugging, atelectasis, increased risk of hypoxaemia and LRTI
40
Which two inhaled anaesthetic agents are the drug of choice in airways disease?
Halothane Sevoflurane
41
Which two inhaled anaesthetic agents have a tendency to cause airway irritation and bronchospasm?
Isoflurane Desflurane
42
Renal effects of inhaled anaesthetics
Decreased GFR and urine flow
43
Hepatic effects of inhaled anaesthetics
Concentration-dependent decreased portal vein blood flow (parallel to reduction in CO) However total blood flow may be preserved due to increase in hepatic artery flow
44
What effect do inhaled anaesthetics have on uterine smooth muscle? What is the clinical significance of this?
Halogenated anaesthetics are potent uterine smooth muscle relaxants Aid intrauterine foetal manipulation and manual extraction of placenta in third stage of labour Also increases risk of PPH
45
Four toxic effects of inhaled anaesthetics and specific agents responsible for each
1. Nephrotoxicity: enflurane and sevoflurane both produce nephrotoxic metabolites but only enflurane has been seen to cause significant renal injury 2. Haematotoxicity: megaloblastic anaemia (N2O due to decreased methionine synthase activity), CO poisoning (especially desflurane) 3. Malignant hyperthermia 4. Hepatotoxicity: rare fulminant hepatic failure after exposure to halothane
46
Pharmacokinetic properties of IV anaesthetics
Distribution: lipophilic, preferentially partition into highly perfused lipophilic tissues (brain, spinal cord) -> rapid onset of action Metabolism/elimination: termination of effect is determined by redistribution of drug into less perfused and inactive tissues (therefore single bolus of different anaesthetic agents share similar duration of action despite different rates of metabolism)
47
Which anaesthetic agent is contraindicated in the setting of egg allergy and why?
Propofol, as it contains lecithin (major component of egg yolk phosphatide fraction)
48
How is propofol formulated?
Poorly soluble in water, formulated as emulsion (10% soybean oil, 2.25% glycerol, 1.2% lecithin)
49
pH of propofol
7
50
What is the mechanism of action of propofol?
Presumed to act through potentiation of chloride current mediated by GABA(A) receptors
51
Describe the pharmacokinetics of propofol
Absorption: IV only Distribution: short distribution half-life (2-8mins), high Vd (97% protein-bound) Metabolism: rapidly metabolised in liver, also extrahepatic metabolism (likely in lungs, responsible for up to 30% of elimination) Elimination: in urine as inactive metabolites (glucuronide and sulfate conjugates), <1% unchanged, elimination half-life 30-60mins
52
What is context-sensitive half-time?
Elimination half-life of a drug after cessation of continuous infusion, expressed as function of infusion duration
53
What is propofol's context-sensitive half-time and what is the clinical relevance of this?
Short context-sensitive half-time, even after prolonged infusion Prompt recovery from anaesethesia
54
Three CNS effects of propofol
1. Hypnotic (not analgesic) 2. Decreased ICP and IOP due to decreased cerebral blood flow and CMR 3. Burst suppression in EEG
55
Two CVS effects of propofol
1. Decreased TPR due to profound vasodilation, decreased MAP 2. Inhibition of baroreceptor reflex: small increase in HR, bradycardia or asystole
56
What three factors exaggerate propofol's hypotensive effects?
1. Increased age 2. Hypovolaemia 3. Rapid injection
57
Four respiratory effects of propofol
1. Apnoea with induction dose 2. Decreased minute ventilation with maintenance dose (due to decreased TV and RR) 3. Decreased ventilatory response to hypoxia and hypercapnoea 4. Greater reduction in upper airway reflexes compared with thiopentol
58
GIT effect of propofol
Antiemetic
59
What are the clinical features of propofol-related infusion syndrome?
Acute refractory bradycardia leading to asystole, with 1 or more of: - Metabolic acidosis - Rhabdomyolysis - Hyperlipidaemia - Enlarged or fatty liver
60
What is the main advantage of fospropofol over propofol?
Less injection pain
61
What dose of propofol is used for: - Induction - Maintenance - Sedation - Nausea and vomiting
- Induction: 1-2.5mg/kg IV - Maintenance: plasma concentration 3-8mcg/ml, infusion rate 100-200mcg/kg/min - Sedation: plasma concentration 1-2mcg/ml, infusion rate 25-75mcg/kg/ml - Nausea and vomiting: 10-20mg IV bolus or 10mcg/kg/min infusion
62
In what settings should induction dose of propofol be reduced? In what settings should the induction dose be increased?
Reduced: increased age, decreased CV reserve, premedication with e.g. opioids Increased: children
63
How does fospropofol compare with propofol in terms of time to onset and offset?
Fospropofol has more complex pharmacokinetics as relies on metabolism to propofol More prolonged onset and offset
64
What is one the major adverse effects of fospropofol?
Paraesthesias (especially perianal)
65
Two examples of barbiturates used in general anaesthesia
Thiopental Methohexital
66
Describe the pharmacokinetics of thiopental
Absorption: IV only Distribution: highly lipid soluble, crosses BBB, produces LOC in one circulation time; rapidly redistributed to muscle, fast, and eventually all body tissues -> short duration of action Metabolism: slow hepatic metabolism mostly by oxidation, long elimination t1/2 (9hrs) Elimination: <1% excreted unchanged by kidney
67
Four CNS effects of thiopental
1. Dose-dependent CNS depression 2. May cause hyperalgesia 3. Reduced ICP: potent cerebral vasoconstrictor, decreased cerebral blood flow, decreased CMR 4. Anticonvulsant (decreased electrical activity on EEG)
68
Two CVS effects of thiopental
1. Transiently decreased MAP (less so than propofol) 2. Negative inotropy
69
Four respiratory effects of thiopental
1. Transient apnoea at induction 2. Decreased minute ventilation (decreased TV and RR) with maintenance 3. Decreased ventilatory response to hypoxia and hypercapnia 4. Limited suppression of upper airway reflexes (risk of laryngospasm)
70
What are three other adverse effects of thiopental?
1. Acute porphyria (increases production of porphyrins) 2. Ischaemic injury with inadvertent intra-arterial injection (causes severe vasoconstriction) 3. Garlic or onion taste with administration
71
Three benzodiazepines commonly used in the perioperative period
1. Midazolam 2. Lorazepam 3. Diazepam (less frequently)
72
What effects relevant to anaesthesia do benzodiazepines have?
Anterograde amnesia Anxiolysis
73
What is the reversal agent for benzodiazepines?
Flumazenil
74
Describe the pharmacokinetics of benzodiazepines (specifically in relation to distribution)
Lipophilic, rapidly enters CNS (rapid onset - although still slower than thiopental, propofol, etomidate) Slow effect-site equilibration than propofol and thiopental (doses should be spaced to allow peak effect to be reached before repeat dosing)
75
Two CNS effects of benzodiazepines
1. Decreased CMR and cerebral blood flow (less than propofol and barbiturates) 2. Anticonvulsant
76
CVS effect of benzodiazepines
Decreased MAP (likely due to decreased TPR)
77
Three respiratory effects of benzodiazepines
1. Minimal depression of ventilation (may see transient apnoea with rapid IV administration) 2. Airway obstruction due to hypnotic effects 3. Decreased ventilatory response to hypercapnia (not usually significant if administered alone)
78
What is the dose of midazolam used for preoperative medication?
1-2mg IV 0.5mg/kg PO
79
What are the anaesthetic effects of etomidate?
Hypnotic NOT analgesic
80
What is the benefit of etomidate over other anaesthetic agents?
Minimal haemodynamic effects
81
Describe the pharmacokinetics of etomidate
Absorption: rapid onset Distribution: highly protein-bound Metabolism: via ester hydrolysis to inactive metabolites Elimination: excreted in urine (<3% unchanged) and bile
82
Three CNS effects of etomidate
1. Potent cerebral vasoconstrictor (similar to thiopental) 2. May activate seizure foci 3. Myoclonus
83
CVS effect of etomidate
Modest or absent decrease in BP (due to decreased TPR)
84
Respiratory effect of etomidate
Less pronounced than barbiturates, occasional apnoea
85
Endocrine effect of etomidate
Adrenocortical suppression due to dose-dependent 11B-hydroxylase inhibition Lasts for 4-8hrs post induction dose and limits use of etomidate for continuous infusion
86
GIT effect of etomidate
Increased incidence of post-operative nausea and vomiting
87
Which IV anaesthetic agent may cause adrenocortical suppression?
Etomidate
88
What two characteristics distinguish ketamine from other IV anaesthetic agents?
Has analgesia properties Low protein-binding
89
What is the chemical structure of ketamine?
Arylcyclohexylamine, structurally similar to phencyclidine (PCP)
90
What state is produced by an induction dose of ketamine?
"Dissociative amnesia": eyes open with slow nystagmic gaze (cataleptic state)
91
Mechanism of action of ketamine
Likely related to glutamate blockade via NMDA inhibition
92
Describe the pharmacokinetics of ketamine
Absorption: highly lipophilic, rapid onset of action Distribution: low protein binding Metabolism: primarily hepatic via CYP450, with production of active metabolite norketamine (1/3 to 1/5 as potent) Elimination: norketamine subsequently hydroxylated to water-soluble conjugates and excreted in urine
93
Three CNS effects of ketamine
1. Raised ICP via cerebral vasodilatory effect and increase in CMR (may be attenuated by maintaining normocapnia) 2. Anticonvulsant 3. Emergence phenomenon
94
How can the risk of emergence phenomenon with ketamine be reduced?
Co-administration of benzodiazepine
95
CVS effect of ketamine
Transient but significant increase in HR, BP, CO (likely due to centrally mediated sympathetic stimulation)
96
Three respiratory effects of ketamine
1. Transient hypoventilation or apnoea with large rapid IV dose on induction (otherwise not thought to cause respiratory depression) 2. Risk of laryngospasm due to increased salivation (especially in children) 3. Bronchial smooth muscle relaxation (good in reactive airways disease)
97
Mechanism of action of dexmedetomidine
Highly selective a2-adrenergic agonist
98
How is dexmedetomidine metabolised and excreted?
Rapidly metabolised by liver Excreted in urine and bile
99
Four CNS effects of dexmedetomidine
1. Hypnosis and sedation due to a2 adrenoceptor stimulation in locus coeruleus (resembles physiologic sleep state) 2. Analgesia (effect originates at level of spinal cord) 3. Decreased cerebral blood flow (no change in CMR or ICP) 4. Tolerance, dependence
100
Two CVS effects of dexmedetomidine
1. Decreased BP (due to decreased TPR) and HR with infusion (transient increased BP and profoundly decreased HR with bolus dose) 2. Heart block, severe bradycardia, asystole (due to unopposed vagal stimulation; responds to anticholinergics)
101
Two respiratory effects of dexmedetomidine
1. Small to moderate decreased TV (RR unchanged) 2. May cause upper airway obstruction due to sedation
102
What detrimental effects may be seen with high doses of benzodiazepines in anaesthesia?
Increased chest wall and laryngeal rigidity -> may impair ventilation Also complicates postoperative pain management

ACEM Primary Written (150 decks)

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