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Anesthesiology > Pharm > Flashcards

Pharm Flashcards

1
Q

Pros of IV induction agents

A

rapid induction, sedation with low doses, can be continuous infusion that is also used for maintenance.

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2
Q

Cons of IV induction agents

A

once it is in, you cannot remove it; difficulty in measuring how much anesthesia is given (no ET concentration)

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3
Q

Propofol use and mechanism

A

Used for induction and maintenance. Mechanism: facilitation of inhibitory neurotransmission at GABA receptors

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4
Q

Advantages of propofol

A

i. Rapid onset due to high lipid solubility
ii. Quick recovery with minimal residual CNS effects
iii. Specifically suppresses upper airway reflexes and bronchodilates
iv. Antiemetic

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5
Q

Disavantages of propofol

A

i. Burning pain on injection (precede with lidocaine injection)
ii. Cardiovascular depression: Drop in arterial blood pressure (20-30%) from a decrease in systemic vascular resistance, cardiac contractility, and preload
iii. Impairs baroreceptor response to hypotension
iv. Respiratory depressant: causes apnea and decreases the normal response to hypercarbia and inhibits hypoxic respiratory drive
v. Decreases cerebral blood flow
vi. Intralipid emulsion can support growth of microorganisms causing sepsis

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6
Q

How does propofol affect BP, SVR, contractility and preload?

A

Drop BP (20-30%) from decrease in SVR, contractility, and preload.

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7
Q

What are the pulm effects of propofol?

A

iv. Respiratory depressant: causes apnea and decreases the normal response to hypercarbia and inhibits hypoxic respiratory drive

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8
Q

How is propofol metabolized and excreted?

A

Intra and extra hepatic metabolism. Excreted by kidneys

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9
Q

What are some common IV induction agents?

A

propofol, thiopental, methoxexital, etomidate

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10
Q

Mechanism of thiopental?

A

mimics GABA by acting on Cl channels and increasing their duration of opening; suppresses excitatory ACh; depresses RAS (reticular activating system)

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11
Q

Uses of thiopental

A

rapid sequence induction (RSI), continuous infusion to decrease intracranial pressure; (no analgesic effects)

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12
Q

Advantages of thiopental

A

i. Rapid induction, well tolerated
ii. Cheap
iii. Less likely to cause apnea

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13
Q

Disadvantages of thiopental

A

i. Slow recovery, with CNS suppression
ii. Decrease in BP and CO and increased HR (central vagolytic)
iii. Increased CV depression (hypotension) in hypovolemic, elderly pts or those on beta-blockers of with chronic HTN (inadequate baroreceptor responses)
iv. Can cause histamine release which could lead to bronchospasm (or from cholinergic stimulation)
v. Depresses medullary ventilation center , doesn’t completely suppress airway reflexes

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14
Q

What happens to BP, CO, and HR with thiopental? Why?

A

BP decreases, CO decreases, HR increases. Because Central vagolytic

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15
Q

What patient populations should you be particularly careful with for thiopental? Why?

A

Increased hypotension in the hypovolemic, elderly, or those on beta-blockers

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16
Q

How can thiopental cause brochospasm?

A

histamine release or from cholinergic stimulation

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17
Q

For whom is thiopental contraindicated?

A

asthmatics

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18
Q

pharmokinetics

A

renal excretion of water soluble hepatic metabolites

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19
Q

Mechanism of methohexital?

A

Same as thiopental: mimics GABA by acting on Cl channels and increasing their duration of opening; suppresses excitatory ACh; depresses RAS (reticular activating system)

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20
Q

Uses of methohexital?

A

drug of choice for ECT; induction of anesthesia, (no analgesic effects)

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21
Q

Advantages of methohexital?

A

i. Minimal impact on seizure threshold
ii. Rapid recovery with minimal CNS suppression
iii. No histamine release

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22
Q

Disadvantages of methohexital

A

i. May stimulate seizure foci causeing myoclonic movement

ii. Depresses medullary ventilation center , doesn’t completely suppress airway reflexes

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23
Q

metabolism and excretion of methohexital?

A

metabolized quickly by the liver; excreted in feces

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24
Q

Mechanism of etomidate?

A

mimics inhibitory effects of GABA and depresses RAS

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25
Q

Use of etomidate

A

Rapid induction in patients with cardiovascular disease (no analgesia)

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26
Q

Advantages of etomidate

A

i. No or minimal cardiovascular effects (good for CAD, shock, valvular dz, cardiomyopathy)
ii. Rapid induction and recovery with minimal residual CNS depression
iii. Bronchodilator

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27
Q

Disadvantages of etomidate

A

i. Adrenocortical suppression of the 1-beta-hydroxylase (necessary for cholesterol  cortisol); decreases cortisol and aldosterone (increases mortality in critically ill pts)
ii. Induction dose causes resp depression
iii. Post-op nausea and vomiting
iv. Myoclonic mvt on injection (without EEG changes)
v. Can activate seizure foci

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28
Q

pharmokinetics of etomidate

A

highly protein bound, rapid onset of action (highly lipid soluble)
Hepatic metabolism to a product excreted in urine

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29
Q

Which IV induction anesthetic is used for ECT?

A

methohexital

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30
Q

Which IV induction anesthetic is best for a patient with cardiovascular disease?

A

etomidate. also very rapid induction.

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31
Q

Which IV induction anesthetic has the greatest CNS suppression?

A

thiopental

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32
Q

Which IV induction agents are barbituates?

A

thiopental, methohexital, etomidate

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33
Q

Mechanism of ketamine

A

NMDA receptor agonist, muscarinic antagonist, and opioid agonist; causes functional dissociation of the thalamus from the RAS from the limbic cortex (decreases awareness)

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34
Q

Use of ketamine

A

dissociative anesthesia (pt appears to be conscious with eyes open and nystagmus, but doesn’t respond), analgesia, and amnesia

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35
Q

Which IV induction agent is the only central cardiovascular simulant? What does this mean?

A

ketamine. It increases HR, BP, CO

36
Q

Which IV induction agents should be used for hypovolemic or cardiogenic shock?

A

ketamine, etomidate, midazolam. improves perfusion

37
Q

Advantages of ketamine

A

i. Only IV induction agent that is a central CV stimulant  increases HR, BP, CO
ii. Good for cardiogenic or hypovolemic shock (improves perfusion)
iii. Potent somatic analgesia,
iv. Minimal respiratory depression, potent bronchodilator (good in asthmatics)

38
Q

Which IV induction agent is a potent bronchodilator? what does this mean?

A

ketamine. good for asthmatics

39
Q

Disadvantages of ketamine

A

i. Respiratory depression with rapid administration
ii. Normal airway reflexes remain intact
iii. Can get excess respiratory secretions (necessitating antiChl drug-glycopyrrolate)
iv. Increased BP and HR causes increased myocardial O2 demand (not good in CAD)
v. cerebral vasodilationincreases ICP; bad with intracranial problems
vi. emergent reactions with unpleasant dreams or hallucinations or delirium

40
Q

pharmokinetics of ketamine

A

metabolized by liver, excreted renally

41
Q

Which IV induction agent is contraindicated for epileptics?

A

methohexital

42
Q

Common benzodiazepines used for IV induction

A

midazolam (Versed), diazepam, lorazepam

43
Q

Uses of benzodiazepines

A

anxiolysis and sedation

not as fast as others for induction, NO analgesia

44
Q

Mechanism of benzodiazepines

A

GABA Agonist - increase frequency of Cl opening

45
Q

Advantages of benzos

A

i. minimal CV depression (slight increase HR and decrease in BP, CO and SVR)
ii. anterograde amnesia
iii. reduce cerebral O2 use, decrease ICP, prevent seizures

46
Q

Disadvantages of benzos

A

respiratory depressant at medullary respiratory center (esp with concurrent opioids)

47
Q

pharm of benzos

A

inactive metabolites, highly lipid soluble and high VD with high hepatic metabolism and clearance (t1/2 2 hr); renal excretion

48
Q

Reversal agent of benzos

A

Flumazenil - benzo receptor antagonist. strong affinity short half life so resedation can occur after initial dose - repeat as needed

49
Q

Which drug inhibits the metabolism of midazolam? What does this cause?

A

Erythromycin. Prolongs action of midazolam

50
Q

Which drug increases diazepam concentration? How?

A

Heparin. By competing for protein binding.

51
Q

Which drug class acts synergistically with benzos to cause respiratory depression and hypotention, and decreased SVR?

A

opioids

52
Q

How do benzos affect volatile anesthetics?

A

Benzos reduce MAC up to 30%

53
Q

What is the order of recovery speed for the IV induction agents, fastest to slowest?

A

propofol > methohexital > etomidate > thiopental > midazolam > ketamine > diazepam

54
Q

Commonly used perioperative opioids

A

Morphine, fentanyl, hydromorphone (Dilaudid), remifentanil, sufentanil, alfentanil, meperidine

55
Q

Opioid mechanism

A

a. bind mu (and kappa, delta and sigma) receptors in the CNS and peripheral tissues, which inhibits the presynaptic release and postsynaptic response to excitatory neurotransmitters from sensory neurons

56
Q

Opioid use and effect on MAC

A

analgesia, some with sedation. Reduce MAC requirements

57
Q

Which opioid increases HR and decreases contractility?

A

meperidine

58
Q

Which opioids cause histamine release, causing bradycardia?

A

morphine, meperidine

59
Q

Cardiovascular effects of opioids

A

Induce bradycardia via stimulation of medullary vagal nucleus

60
Q

Respiratory effects of opioids

A

i. depresses respiratory rate; increases resting PCO2; decreases vent response to CO2 and hypoxia
ii. can induce skeletal muscle chest wall rigidity which prevents PPV (mostly fentanyl, alfentanil, and sufentanil)
iii. blunts bronchoconstrictive response to airway stimulus (intubation)

61
Q

CNS effects of opioids

A

If not hypoventilating, decreases cerebral blood flow and ICP.
Pinpoint pupils - CN III

62
Q

GI effects of opioids

A

slows gastric emptying time, can cause biliary spasm or ileus (but tolerance develops long-term); constipation, nausea and vomiting

63
Q

Endocrine effects of opioids

A

block the stress response during surgery by blocking release of catecholamines, ADH, and cortisol; good for those with ischemic heart dz

64
Q

Which opioid is most effective at decreasing post-op shivering

A

meperidine

65
Q

Shortest acting opioid

A

remifentanil

66
Q

fast onset, short acting opioids

A

fentanyl: highly lipid soluble
alfentanyl: less lipid soluble but high nonionized fraction and small Vd

67
Q

slower onset, longer acting opioid

A

morphine - low lipid solubility

68
Q

Overdose/narcotization signs

A

respiratory rate slowing/apnea; desaturation to cyanosis; bradycardia, hypotension, decreased CNS response or coma, pinpoint pupils

69
Q

Treatment of opioid overdose

A

Naloxone - competative inhibitor, side effects are tachycardia, ventricular irritability, HTN, pulm edema, vomiting. Can cause acute opioid withdrawal syndrome in opioid dependent ppl
Oxygenate/ventilate, CV support

70
Q

Depolarizing muscle relaxant

A

succinylcholine. Intraoperative paralysis- rapid onset, lasts ~5 min

71
Q

Mechanism of action of succinylcholine

A

composed of 2 ACh; binds Ach receptor and acts as agonist (generates AP) but does not dissociate off then prolonged depolarization of motor endplate and inability to generate new AP (can’t repolarize) =Phase I block; Then after prolonged infusion of sux, ionic and conformational changes at ACh receptor cause Phase II Block

72
Q

Metabolism of succinylcholine

A

must diffuse away from NMJ to get to plasma cholinesterase located in blood and liver (not AChE)

73
Q

Side effects of succinylcholine

A
  1. fasciculations
  2. profound bradycardia with multiple doses or in kids
  3. malignant hyperthermia
  4. hyperkalemia (dangerous for pts with burns, trauma, stroke, imobilized, myopathies, GBS…)
  5. CV: low does is neg. chronotropic and inotropic; high dose is opposite
    NO dry mouth
74
Q

Reversal of succinylcholine

A

by diffusion away from NM junction over time; can’t use ACHE inhibitors (they increase duration of depolarizing blockade by preventing sux metabolism)

75
Q

Contraindications for succinylcholine

A

Kids: due to risk of hyperkalemia, rhabdomyolysis, and cardiac arrest in kids with undiagnosed myopathies
Pts with burns, trauma, stroke, imobilized, myopathies, GBS…

76
Q

Nondepolarizing muscle relaxants and use

A

Rocuronium, Cisatracurium, vecuronium

Use: intraoperative paralysis

77
Q

Mechanism of nondeplarizing muscle relaxants

A

bind ACh receptors as competitive antagonists; cannot cause conf change necessary for ion channel opening so they prevent AP; only needs one alpha subunit bound to produce NM blockade

78
Q

Speed of onset and duration of action of nondepolarizing m. relaxants

A

i. Speed of onset: roc 1.5 min, cisatra and vec 2-3 min

ii. Duration of action: roc 35-75 min

79
Q

What potentiates block for nondepolarizing m. relaxants?

A

i. Hypothermia prolongs block by decreasing metabolism and excretion
ii. Hypokalemia, hypoCa, and hyperMg potentiates block
iii. Volatile inhalation anesthetics potentiate block

80
Q

Reversal of nondepolarizing m. relaxants?

A

i. Neostigmine: acetylcholinesterase inhibitors can cause increased ACh in the NM junction and compete away the NDMR
ii. Anticholinergic agents (glycopyrrolate, atropine) must be given with the cholinesterase inhibitor to prevent increased ACh at muscarinic receptors (bradycardia, increased secretions)

81
Q

Metabolism of nondepolarizing m. relaxants?

A

i. Rocuronium: no metabolism, elim mostly by liver, slightly by kidneys;
ii. Cisatracurium: degradation in plasma at physiologic pH and temp by Hofmann elimination (good in liver or renal failure)
iii. Vecuronium: metabolized by liver, biliary excretion (primarily with 25% renal); prolonged action in renal failure

82
Q

Risks of neuromuscular blockade

A

a. Difficult airway: must ensure adequate mask ventilation after induction of general anesthetic and before giving muscle relaxant; otherwise may need to emergently establish airway by LMA or trach
b. Post-extubation residual NM blockade so cannot breathe; must mask or use LMA

83
Q

Perioperative hemodynamic support drugs

A

Ephedrine

Phenylephrine

84
Q

How does ephedrine work?

A

Indirect and direct Adrenergic Agonist (noncatecholamine): alpha 1, beta1, beta2. Increases BP, HR, contractility, CO. Bronchodilates.

85
Q

How does phenylephrine work?

A

Direct noncatecholamine Adrenergic Agonist - alpha1 . Increases SVR which increases BP, decreases HR and CO.

86
Q

Anti-emetic drugs

A
  1. Odansetron (Zofran) 5HT3 (seratonin) antag in brain and abdominal vagal afferents. can cause headache and prolonged QTc
  2. Metoclopramide - ACh agonist peripherally and DA antag centrally (CTZ region)
  3. Droperidol - DA antag in CTZ
  4. Diphenhydramine - H1 antag
  5. Scopalamine - antimuscarinic - dryness and mystriasis
87
Q

Sedative drug

A

Dexmeditomidate: selective alpha2 agonist that causes sedation/hypnosis (easy to arouse), anxiolysis, amnesia, mild analgesia, and sympatholytic (decreases HR and BP)

i. No respiratory depression
ii. Bradycardia and hypotension if given too rapidly or in hypovolemic pt

Anesthesiology (9 decks)

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