Exam 7: General anesthetics Flashcards

1
Q

What are the components of the anesthetic state?

A

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

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2
Q

Define 1 MAC unit

A

minimum alveolar concentration that prevents movement in response to surgical stimulation in 50% of subjects

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3
Q

What are the strengths of MAC as a measurement?

A

alveolar concentrations can be monitored continuously, provides a direct correlate of the free concentration of anesthetic at its concentration sites in CNS, simple-to-measure end point that reflects an important clinical goal

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4
Q

What is easier to measure a MAC on: inhaled or IV anesthetics? Why?

A

IV anesthetics; lack methods to measure blood or plasma anesthetic concentration

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5
Q

What are the five primary effects of general anesthetics?

A

Amnesia, skeletal muscle relaxation, inhibition of autonomic reflexes, analgesia, unconsciousness

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6
Q

What does conscious sedation include in terms of drug classes, and what are the benefits of doing so?

A

Drug-induced alleviation of anxiety and pain + smaller doses of sedative medications; maintains a patent airway and is responsive to verbal commands

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7
Q

What benzodiazepines and IV anesthetics are useful in conscious sedation?

A

fentanyl, diazepam, midazolam, propofol

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8
Q

What is the specific receptor antagonist for both benzos and opioids?

A

Benzos: Flumazenil; Opioids: naloxone

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9
Q

What are the characteristics of deep sedation?

A

similar to light state of general anestesia; decreased consciousness, transition to general anesthesia is hard to define, often accompanied by loss of protective reflexes, inability to maintain a patent airway, lack of verbal responsiveness to surgical stimuli

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10
Q

What is the mechanism of action of deep sedation?

A

different agents produce specific components of anesthesia by actions at different molecular targets- may alter release of neurotransmitters, may change the frequency or amplitude of impulses exiting the synapse

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11
Q

Explain the enhanced inhibitory activity of deep sedation, which kinds of anesthetics do this (volatile or IV)?

A

Enhances opening of chloride channels via GABAa and glycine receptors (both volatile and IV), activates two-pore domain potassium channels (volatile)

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12
Q

Explain activation of two-pore domain potassium channels by anesthetics

A

located on both pre and post-synaptic sites, post synaptic channels are important in setting the resting membrane potential of neurons and may be the molecular locus through which these agents hyperpolarize neurons, also hyperpolarize and prevent NT release

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13
Q

Explain the inhibition of excitatory activity of anesthetics and which anesthetics do it?

A

Blocks AMPA and NMDA receptor of glutamate (ketamine, nitrous oxide), and nicotinic and muscarinic receptors of acetylcholine (inhalation anesthetics)

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14
Q

What are the volatile anesthetics?

A

halothane, enflurane, isoflurane, desflurane, sevoflurane

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15
Q

What are the gaseous anesthetics?

A

Nitrous oxide

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16
Q

What are the pharmacokinetics of inhaled anesthetics?

A

should have a rapid onset, effect should be rapidly terminated, effect site concentration in the CNS

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17
Q

What are two factors that control uptake?

A

inspired concentration and ventilation rate

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18
Q

the faster the ratio of alveolar concentration and inspired cocentration approach what number is indicative of a faster anesthesia effect?

A

1, which indicates equilibrium

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19
Q

Does increasing alveolar ventilation increase the blood rise?

A

It increases the rate of rise in the blood

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20
Q

In a ratio of blood:gas partition coefficient, which is better: 2 or 1.5? What is the trend that is better for a anesthetic?

A

1.5 is better, the greater the gas partition, the more it will diffuse into pertinent tissues

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21
Q

What is related to the clinical effect for anesthetics?

A

Undissolved drug in the blood

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22
Q

What are the three factors controlling uptake of the anesthetic?

A

1) inspired concentration and ventilation, 2) solubility, 3) alveolar-venous partial pressure difference

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23
Q

What is the threshold concentration of the partial pressure of the anesthetic in the brain determined by?

A

Potency (MAC)

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24
Q

Do anesthetics reach anesthetizing concentrations slower or faster if they are less soluble?

A

Reach it quicker

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25
Q

How can you speed the rate of induction of a volatile anesthetic?

A

Increase concentration and increase alveolar respiration rate

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26
Q

What is the recovery time (elimination) of an anesthetic dependent on?

A

rate of elimination from the brain: solubility in the brain (lower is faster), duration of exposure to the anesthetic

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27
Q

Where does immobility of the patient occur?

A

Spinal cord inhibition, and possibly inhibition of nociceptive transmission to the brain

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28
Q

Where does amnesia of the patient occur?

A

hippocampus, amygdala, prefrontal cortex and regions of the sensory and motor cortices

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29
Q

Where does inhibition of consciousness occur in the patient?

A

cerebral cortex, thalamus and reticular activating system

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30
Q

What are the cerebral effects of inhaled anesthetics?

A

Decrease metabolic activity in the brain (and decreased blood flow), but can also increase blood flow via dilation of the vessels- depends on the concentraion

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31
Q

What are the four levels of CNS depression?

A

Stage 1= analgesia, Stage 2= excitement, Stage 3= surgical anesthesia, Stage 4= medullary depression

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32
Q

Describe stage 1 of CNS depression

A

analgesia without amnesia initially, then both later in the stage

33
Q

Describe stage 2 of CNS depression

A

appears delirious, may vocalize but is completely amnesic, rapid respiration, increase HR and BP

34
Q

Describe stage 3 of CNS depression

A

slowing of respiration and HR, extends to complete cessation of spontaneous respiration (apnea)

35
Q

Describe stage 4 of CNS depression

A

deep stage of anesthesia, severe depression of CNS (vasomotor center, respiratory center)

36
Q

What are cardiovascular effects of inhaled anesthetics?

A

Halothane, enflurane, isoflurane, desflurane and sevoflurane all depress normal cardiac contractility, decrease MAP, NO can also depress myocardial function

37
Q

In terms of cardiac effects, what do halothane and enflurane do?

A

reduce arterial pressure primarily by myocardial depression

38
Q

In terms of cardiac effects, what do isoflurane, desflurane and sevoflurane produce?

A

greater vasodilation with minimal effect on cardiac output

39
Q

Do inhaled anesthetics decrease or increase cardiac output?

A

Don’t change cardiac output

40
Q

What are the respiratory effects of inhaled anesthetics?

A

bronchodilating properties, airway irritation, decrease in tidal volume and resp. rate (except NO), respiratory depressants

41
Q

What anesthetics cause nephrotoxicity?

A

metabolism of enflurane and sevoflurane

42
Q

What is the treatment of malignant hyperthermia? What is it’s MOA?

A

Dantrolene- reduces calcium release from SR

43
Q

What anesthetic causes hepatotoxicity?

A

Halothane

44
Q

What property of IV anesthetic accounts for their rapid onset of action?

A

the fact that they are lipophilic

45
Q

In what order to IV anesthetics redistribute to different areas of the body?

A

Blood to brain and viscera, to lean tissues, to fat

46
Q

What is the most frequently administered drug for induction of anesthesia?

A

Propofol

47
Q

What is the proposed mechanism of action of propofol?

A

potentiation of the chloride current mediated through the GABAa receptor complex

48
Q

Where is propofol metabolized?

A

Liver, and also extrahepatic metabolism (probably lungs)

49
Q

What are the effects of propofol on the CNS?

A

hypnotic, not alagesic, general suppression, decrease cerebral blood flow and cerebral metabolic rate,

50
Q

What are the effects of propofol on the CV?

A

decrease in systemic BP, profound vasodilation in arterial and venous circulations,

51
Q

What are the effects of propofol on respiratory?

A

potent depressant, produces apnea

52
Q

What can occur upon injection of propofol?

A

Pain

53
Q

What are the clinical uses of propofol?

A

Facilitate induction of general anesthesia by bolus injection, often used for maintenance of anesthesia, sedation, subanesthetic doses can be used to treat postoperatvie nausea and vomiting

54
Q

What two drugs are barbituates?

A

Thiopental, methohexital

55
Q

What is the mechanism of action of barbituates (Thiopental, methohexital)?

A

enhancement of inhibitory (GABAa receptors) and inhibition of excitatory neurotransmission

56
Q

Where are barbituates (Thiopental, methohexital) metabolized?

A

in the liver

57
Q

What are the effects of barbituates (Thiopental, methohexital) on the CNS?

A

dose-dependent CNS depression (sedation–>general anesthesia), no analgesia, cerebral vasoconstriction

58
Q

What are the effects of barbituates (Thiopental, methohexital) on CV?

A

decrease systemic BP, minimal inhibition of baroreceptor reflex

59
Q

What are the effects of barbituates (Thiopental, methohexital) on respiratory?

A

depressant, transient apnea

60
Q

What are barbituates (Thiopental, methohexital) used for clinically?

A

induction of anesthesia (unconsciousness)

61
Q

What drugs are in the class of benzodiazepines?

A

Midazolam, lorazepam, diazepam

62
Q

What are the most desired effects of benzodiazepines (Midazolam, lorazepam, diazepam)

A

anxiolysis and anterograde amnesia

63
Q

What are the effects of benzodiazepines (Midazolam, lorazepam, diazepam) on the CNS?

A

decrease CMRO2 and cerebral blood flow

64
Q

What are the effects of benzodiazepines (Midazolam, lorazepam, diazepam) on CV?

A

decrease in systemic blood pressure

65
Q

what are the effects of benzodiazepines (Midazolam, lorazepam, diazepam) on respiration?

A

minimal depression of ventilation, transient apnea

66
Q

What are the clinical uses of benzodiazepines (Midazolam, lorazepam, diazepam)?

A

preoperative medication to induce sedation, suppress seizure activity, amnestic, anxiolytic and sedative

67
Q

Is Etomidate a hypnotic or analgesic?

A

only hypnotic

68
Q

What is the mechanism of action of etomidate?

A

potentiation of GABAa-mediated chloride currents,

69
Q

What are the endocrine effects of entomidate?

A

adrenocortical suppression lasting 4-8 hours after dose of drug

70
Q

What are the clinical uses of etomidate?

A

alternative to propofol and barbituates for rapid IV induction of anesthesia especially in pts with myocardial contractility issues

71
Q

What does ketamine produce that is useful?

A

significant analgesia

72
Q

What is the MOA of ketamine?

A

inhibition of the NMDA receptor complex

73
Q

Does ketamine produce as complete of amnesia as benzodiazepines?

A

No

74
Q

What are the CV effects of ketamine?

A

transient but significant increase in systemic BP, HR and CO

75
Q

what are the clinical uses of ketamine?

A

maintenance of anesthesia, profound analgesia, stimulation of SNS, bronchodilation, no resp. depression

76
Q

What class of drugs is fentanyl?

A

opioid analgesic

77
Q

What does fantanyl have to be combined with to produce general anesthesia?

A

large dose of benzodiazepines (Midazolam, lorazepam, diazepam)

78
Q

What is so effective of fentanyl with benzodiazepines (Midazolam, lorazepam, diazepam)? Negatives associated?

A

hemodynamic stability (good for patients with heart problems), artificial maintenance of respiration, chest wall can become rigid, may speed up tolerance