General Anesthetics Flashcards

1
Q

components of anesthetic state

A

amnesia, immobility in response to noxious stimulation, attenuation of autonomic responses to noxious stimuli, analgesia, unconsciousness

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2
Q

measurement of inhalational anesthetics

A

MAC units
minimum alveolar concentration= prevents movements in response to surgical stimulation in 50% of subjects (use about 1.3-1.5 MACs)

can be monitored continuously (end-tidal anesthetic concentration) and correspond with free concentration in blood

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3
Q

modern anesthesiology relies on

A

combinations of iv and inhaled drugs to balance properties

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4
Q

minor superficial surgery or invasive diagnostic procedures

A

general anesthesia not necessary
local anesthesia, analgesia or sedation
retention of patients ability to maintain airway, respond to verbal commands

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5
Q

extensive surgical procedures

A

begin with preoperative benzodiazepines
induced with an intravenous agent (eg, thiopental or propofol)
maintained with a combination of inhaled (eg, volatile agents, nitrous oxide) and/or IV drugs (eg, propofol, opioid analgesics)

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6
Q

How do GA enhance inhibitory activity

A
Chloride channels (volatile and IV)
Activation of two-pore domain K channels (volitile)
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7
Q

How do GA inhibit excitatory activity

A

AMPA, NMDA (glutamate) - ketamine, nitrous oxide

Nicotinic and muscarinic receptors (Ach)

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8
Q

Volatile anesthetics

A

Halothane, enflurane, isoflurane, desflurane, sevoflurane
Low vapor pressures, high boiling points
Liquids at room temperature (20°C)
Administered using vaporizers

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9
Q

Gaseous anesthetics

A

Nitrous oxide
High vapor pressure, low boiling point
Gas at room temperature

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10
Q

factors controlling uptake of inhaled anesthetics

A

inspired concentration and ventilation
Solubility
Alveolar-venous partial pressure difference

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11
Q

alveolar venous partial pressure difference

A

Dependent mainly on uptake of the anesthetic by the tissues, including nonneural tissues

Influenced by tissue:blood partition coefficients, rates of blood flow to the tissues, and concentration gradients.

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12
Q

4 stages of CNS depression

A
analgesia (some amnesia)
excitement (delirious, rapid respiration, hr and bp inc)
surgical anesthesia (slowing of respiration and hr)
medullary depression (require circulatory and respiratory support)
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13
Q

barbiturates examples

A

thiopental, methohexital

largely replaced as induction agents by propofol

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14
Q

barbiturates MOA

A

Combination of enhancement of inhibitory and inhibition of excitatory neurotransmission
Inhibitory transmission: activation of the GABAA receptor complex
Effects on excitatory transmission are less well understood

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15
Q

barbs PK

A

Pharmacokinetics
Hepatic metabolism
Thiopental is metabolized more slowly, long elimination half-time
Recovery after single bolus is comparable for thiopental and methohexital - depends on redistribution to inactive tissue sites rather than on metabolism

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16
Q

barbs effects

A

CNS - sedation to GA
no analgesia, may reduce pain threshold
CD - decrease BP d/t vasodilation
Respiratory depressants

17
Q

benzodiazepines examples

A

midazolam, lorazepam, diazepam

18
Q

desired effects benzos

A

Most desired effects are anxiolysis and anterograde amnesia

19
Q

action of benzos terminated by

A

selective antagonist, flumazenil

20
Q

pk benzos

A

Highly lipid-soluble, rapidly enter the CNS, rapid onset of action
Followed by redistribution to inactive tissue sites and termination of effect
Midazolam has the shortest context-sensitive half-time
Only benzodiazepine drugs suitable for continuous infusion

21
Q

benzos act through

A

GABA receptors

22
Q

etomidate desired effects

A

hypnotic but not analgesix

23
Q

etomidate mechanism

A

Likely acts through potentiation of GABAA-mediated chloride currents, like most other intravenous anesthetics.

24
Q

etomidate pk

A

Induction dose of etomidate produces rapid onset of anesthesia
Recovery depends on redistribution to inactive tissue sites
Larger doses, repeated boluses, or continuous infusions can safely be administered
Because (1) minimal effects on hemodynamics and (2) short context-sensitive half-time

25
Q

etomidate effects

A

cerebral vasoconstrictor
cv stability
some resp depression
adrenocortical suppression

26
Q

Hghly lipid-soluble phencyclidine (PCP) derivative producing significant analgesia

A

Ketamine

27
Q

kind of anesthesia ketamine does

A

“dissociative anesthesia,”

patient’s eyes remain open with a slow nystagmic gaze (cataleptic state)

28
Q

moa ketamine

A

inhibition of nmda receptor complex

29
Q

pharmacokinetics ketamine

A

High lipid solubility of ketamine ensures a rapid onset of its effect
Metabolism occurs primarily in the liver
Effect of a single bolus injection terminated by redistribution to inactive tissue sites

30
Q

ketamine effects

A

amnesia (not as complete as benzodiazepines)
cerebral vasodilator
unpleasant emergence reactions
transient but significant inc bp, hr, co
no resp depression, bronchodilation

31
Q

opioid analgesics distinct how

A

Recall not reliably prevented unless hypnotic agents such as benzodiazepines are also used

Postoperative analgesia and intraoperatively as part of a balanced anesthesia

32
Q

fentanyl is a

A

opioid analgesic

33
Q

___ + ____ = GA state

A

Large dose opioids + large dose benzodiazepines

34
Q

AE opioid analgesics

A

Hemodynamic stability - good for patients with compromised myocardial function
Respiration must be maintained artificially and may be depressed into the postoperative period
Can induce chest wall (and laryngeal) rigidity, acutely impairing mechanical ventilation
May speed up tolerance, complicate postoperative pain management

35
Q

how do inhaled anesthetics affect cardiovascular

A

Halothane, enflurane, isoflurane, desflurane, and sevoflurane all depress normal cardiac contractility (at some level)
Tend to decrease mean arterial pressure in direct proportion to alveolar concentration
Halothane and enflurane → myocardial depression (reduced CO) (little change in vascular resistance)
Isoflurane, desflurane, and sevoflurane produce greater vasodilation with minimal effect on CO (preferred for patients with impaired myocardial function)
Nitrous oxide also depressed myocardial function in a concentration-dependent manner (may be offset by activation of SNS → preservation of CO)