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Anesthesiology > IV Drugs > Flashcards

IV Drugs Flashcards

1
Q

Describe the metabolism of NMBs

A

Succinylcholine - plasma cholinesterase
Atracurium / Cisatracurium - Hofmann elimination
Vecuronium / Rocuronium - primarily hepatic
Pancuronium - primarily renal

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2
Q

List the cardioselective B blockers

A

Block only B1 receptors

“BEAM”

Betaxolol
Bisoprolol
Esmolol
Atenolol
Acebutolol
Metoprolol
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3
Q

Which drugs are contraindicated in Parkinson’s disease?

A

Drugs which may produce extrapyramidal effects such as dopamine antagonists droperidol, promethazine; and metoclopramide (dopamine and serotonin antagonist)

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4
Q

Describe the solubility of Midazolam

A

Water-soluble drug that is converted to a lipid-soluble drug when exposed to the blood’s pH

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5
Q

Describe the effects of anticholinergics (Atropine, Glyco, Scop)

A

Decreased gastric acid secretion

Decreased salivary secretion

Decreased LES tone

Tachycardia

Mydriasis (pupil dilation)

May cause urinary retention

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6
Q

Which anticholinesterase drug can cross the BBB?

A

Physostigmine is a tertiary amine and is able to cross the BBB (useful in treating central anticholinergic syndrome)

Neostigmine, Pyridostigmine, and Edrophonium are quarternary ammonium compounds and cannot cross the BBB

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7
Q

What makes Meperidine unique?

A

Meperidine is an opioid that is structurally similar to atropine and possess mild anticholinergic properties. Instead of the usual bradycardia seen with opioids, tachycardia can be seen with Meperidine. Meperidine can also cause decreases in contractility at large doses.

Normeperidine is a metabolite of Meperidine and can lead to delirium and seizures, especially in patients with renal or hepatic impairment

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8
Q

Does Ketamine have any active metabolites?

A

Norketamine, which is about 1/3 as potent at Ketamine

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9
Q

How does Ephedrine work to increase BP?

A

Indirectly by stimulating the release of norepinephrine from sympathetic nerve fibers and to a lesser degree, by directly binding to adrenergic receptors

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10
Q

Which induction agent is most likely to cause myocardial depression? Why?

A

Thiopental

Dose dependent negative inotropic effect results from a decrease in calcium influx in the myocardium

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11
Q

What drug should be avoided in patients taking Ecothiophate for glaucoma?

A

Succinylcholine, as it’s effects can be prolonged by Ecothiophate’s inhibition of acetylcholinesterase

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12
Q

Which muscle relaxant causes slight histamine release?

A

Atracurium

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13
Q

Termination of action of norepinephrine is achieved primarily through what mechanism?

A

80% of released norepinephrine rapidly undergoes reuptake into the sympathetic nerve terminals (uptake 1) and reenters storage vesicles for future use

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14
Q

How does Metoclopramide (Reglan) work?

A

It is a dopamine antagonist that increases lower esophageal sphincter tone and stimulates gastric and upper GI tract motility

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15
Q

How much will administration of Succinylcholine raise serum [K+]?

A

0.5 mEq/L

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16
Q

What conditions or drugs can enhance neuromuscular blockade?

A

Volatile anesthetics

Aminoglycoside antibiotics (Tobra-/Genta-/Neo-/Streptomycin)

Magnesium

Local anesthetics

Furosemide

Dantrolene

Calcium channel blockers

Lithium

Hypothermia

Hypokalemia

Acidosis

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17
Q

Laudanosine is a metabolite of which drug?

A

Atracurium

Laudanosine is a tertiary amine that can cross the BBB and cause CNS stimulation at very high levels

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18
Q

Pre-treatment with a non-depolarizing muscle relaxant will have what effect on the expected side effects of Succinylcholine?

A 
Attenuates, but does not eliminate:
Cardiac dysrhythmias
Elevations in infra gastric pressure
Elevations of ICP
Myalgias

Does not eliminate hyperkalemia

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19
Q

List the order of onset of anticholinesterase drugs

A

Edrophonium (1 to 2 minutes)
Neostigmine (7 to 11 minutes)
Pyridostigmine (16 minutes)

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20
Q

List some conditions that may lead to an increased hyperkalemic response to Succinylcholine

A 
Denervation injuries
Burns
Acute upper motor neuron injuries (stroke)
Muscle trauma
Severe abdominal infections

Risk usually peaks 10 to 50 days after injury, but should be avoided if possible anytime after 24 hours from injury

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21
Q

What is the percentage of neuromuscular receptors which may be blocked and still allow a 5 second head lift?

A

50% (considered adequate recovery)

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22
Q

What is pseudocholinesterase? Where is it produced? What is its half-life?

A

Pseudocholinesterase (also known as plasma cholinesterase or butyrylcholinesterase) is an enzyme found in plasma that metabolizes acetylcholine, succinylcholine, ester-type local anesthetics, heroin, and cocaine
- Does NOT metabolize Remifentanil or Esmolol (red cell esterase for both)

It is produced by the liver

Its half-life is approximately 8 to 16 hours

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23
Q

How do NSAIDs work?

A

NSAIDs inhibit cyclooxygenase, which is necessary for prostaglandin synthesis

Prostaglandins are mediators of pain and inflammation and act at the site of injury (peripherally)

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24
Q

Why is Succinylcholine avoided in children?

A

Fear of un-diagnosed muscular dystrophy that could lead to sever hyperkalemia and cardiovascular collapse
- hyperkalemia is 2/2 rhabdomyolysis

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25
Q

Describe the onset of paralysis in central vs peripheral muscles

A

Neuromuscular blockade develops faster, lasts a shorter time, and recovers more quickly in the central muscles of the airway than in more peripheral muscle groups

Observation of the pattern of blockade of the orbicularis oculi is similar to that of the laryngeal muscles and diaphragm

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26
Q

How does Pancuronium effect the cardiovascular system?

A

Pancuronium may cause increased heart rate, MAP, and CO

Several mechanisms for this, including a vagolytic effect, norepinephrine release, and decrease reuptake of norepinephrine

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27
Q

Which opioid is resistant to reversal with naloxone?

A

Buprenorphine

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28
Q

What is Fospropofol an what are it’s advantages?

A

Fospropofol is a prodrug of Propofol

Because it is water soluble, it causes no pain on injection and carries no risk of hypertriglyceridemia, PE, or sepsis

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29
Q

Describe Clonidine

A

a2 agonist

Primarily stimulates central adrenergic receptors and decreases sympathetic response

Decreases MAC requirements
Decreases extremes in blood pressure
Has analgesic properties and decreases opioid requirements
Can decrease post-anesthetic shivering

Can be given orally, IV, epidurally, intrathecally, and in peripheral nerve blocks

When given intrathecally, has been shown to decrease persistent postsurgical pain

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30
Q

What is the dibucaine number?

A

A test to evaluate function of pseudocholinesterase

80 - normal function (up to 10 minutes of paralysis)

50 to 60 - heterozygous (up to 30 minutes of paralysis)

20 - atypical pseudocholinesterase (over 3 hours of paralysis)

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31
Q

List the a blockers

A

Phentolamine - short-acting non-selective antagonist used primarily in hypertensive emergencies from pheochromocytoma

Phenoxybenzamine - long-acting non-selective antagonist (irreversible) that is commonly used for pre-operative treatment of pheochromocytoma

Prazosin/Terazosin/Doxazosin - selective a1 antagonists used most commonly for BPH

Mirtazapine - selective a2 antagonist used in the treatment of depression

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32
Q

How does Norepinephrine work?

A

Mostly alpha stimulation

Results in increased SVR

33
Q

How does Epinephrine work?

A

Mostly beta-1 stimulation
- increased cardiac output

At high doses, alpha effects increase
- increased SVR

34
Q

How does Isoproterenol work?

A

Non-selective B-agonist

Results in increased cardiac output and decreased SVR

35
Q

How does Dobutamine work?

A

B1-receptor agonist

Increases CO with little change in SVR

36
Q

How does Dopamine work?

A 
Low doses (up to 5 nanos) stimulate DA receptors
- vasodilation
Middle doses (5-10) stimulate beta-1 receptors
- increases CO
High doses (>10) stimulate alpha receptors
- increased SVR
37
Q

Which opioid receptor responsible for increase in prolactin?

A

u1-receptor

38
Q

Which opioid receptor responsible for respiratory depression, muscle rigidity, constipation, and biliary spasm?

A

u2-receptor

39
Q

Which opioid receptor responsible for dysphoria and sedation?

A

k-receptors

40
Q

Describe the phases of depolarizing blockade

A

Phase I - occurs with depolarization of the postjunctional membrane

Phase II - occurs when the postjunctional membranes have become repolarized but do not respond normally to acetylcholine

Phase II blockade responds similarly to non-depolarizing blockade

41
Q

List the induction doses of common agents

A

Propofol: 1.5 - 2.5 mg/kg
Thiopental: 3 - 6 mg/kg
Etomidate: 0.2 - 0.5 mg/kg
Ketamine: 1 -2 mg/kg

42
Q

What is Thiopental? How does it work? What is unique about it?

A

A barbiturate

Binds to GABAa receptor, increasing duration of opening of a chloride-specific ion channel

Causes hypotension via vasodilation, with profound reflex tachycardia

Decreases ICP more than BP, thus maintaining CPP

Contraindicated in porphyria and sulfa allergy

43
Q

What is Midazolam? How does it work? What is unique about it?

A

A benzodiazepine

Binds to GABAa receptor, increasing the frequency of opening of a chloride-specific ion channel

Water-soluble, but converts to lipid-soluble drug at physiologic pH

Produces anterograde amnesia

Pts with kidney failure may accumulate high levels of metabolite a-hydroxymidazolam

44
Q

What is Ketamine? How does it work? What is unique about it?

A

Analog of phencyclidine (PCP)

Acts as an NMDA receptor antagonist, giving it some additional analgesic properties

Dissociates thalamus from limbic cortex, creating a state of dissociative anesthesia

Has an active metabolite, norketamine

Increases BP, HR, CO, PA pressures, and myocardial work

  • Indirectly via stimulation of sympathetic nerves and inhibition of norepinephrine reuptake
  • Direct myocardial depressant effects only apparent during catecholamine depletion

Bronchodilator, but also increases secretions

Increases cerebral O2 consumption, CBF, and ICP

Tolerance may develop after multiple exposures within a short period of time

Intra-operative infusions at sub-anesthetic doses have been shown to have opioid sparing effects

45
Q

What is Etomidate? How does it work? What is unique about it?

A

A carboxylated imidazole ring

Binds to subunit of GABAa receptor, increasing the receptor’s affinity for GABA

Minimal effects on the CV system compared to other induction agents

Can cause pain on injection, myoclonus, and adrenal suppression of cortisol and aldosterone synthesis via inhibition of 11-B-hydroxylase

46
Q

What is Propofol? How does it work? What is unique about it?

A

An alkylphenol

Allosterically increases the binding affinity of the GABAa receptor for GABA

Long-term infusion has been associated with Propofol Infusion Syndrome - lactic acidosis, hyperkalemia, rhabdomyolisis, lipemia, and death

Causes decreased BP via decreased SVR, decreased preload, and decreased contractility

Has antipruritic and antiemetic properties

47
Q

Describe the mechanism of depolarizing vs non-depolarizing muscle relaxants

A

Depolarizing relaxants (Succinylcholine) resemble ACh and act as receptor agonists

  • Cause continuous end-plate depolarization via the opening of peri-junctional Na+ channels
  • After initial opening and excitation, Na+ channels inactivate and cannot re-open until end-plate repolarizes

Non-depolarizing relaxants bind ACh receptors,but do not cause the necessary conformational change
- Act as competitive antagonists

48
Q

List the intubating doses of NMBs

A 
Succinylcholine: 1 - 2 mg/kg
Atracurium: 0.4 - 0.5 mg/kg
Cisatracurium: 0.1 - 0.15 mg/kg
Pancuronium: 0.1 mg/kg
Vecuronium: 0.1 mg/kg
Rocouronium: 0.6 mg/kg
49
Q

What type of drug is Succinylcholine? What is unique about it?

A

The only depolarizing NMB currently in use

Consists of 2 joined ACh molecules

Is rapidly metabolized by plasma pseudocholinesterase

Many side effects

  • Cardiac arrhythmias, especially bradycardia
  • Fasciculations and subsequent myalgias
  • Increased intra-gastric, intra-ocular, and intra-cerebral pressures
  • Hyperkalemia
  • Possible trigger of MH
50
Q

Describe the types of non-depolarizing NMBs

A

Benzylisoquinolones

  • Atracurium
  • Cisatracurium

Aminosteroids

  • Pancuronium
  • Vecuronium
  • Rocuronium
51
Q

What type of drug is Atracurium? What is unique about it?

A

An intermediate-acting benzylisoquinolone

Metabolized by both nonspecific ester hydrolysis and by Hofmann elimination
- Unaffected by renal or hepatic function

Triggers dose-dependent histamine release, resulting in hypotension and tachycardia (bronchospasm in asthmatics)

Toxic metabolite called laudanosine that can accumulate in individuals with renal failure

52
Q

What type of drug is Cisatracurium? What is unique about it?

A

An intermediate-acting benzylisoquinolone

Metabolized by Hofmann elimination

Does not cause histamine release

53
Q

What type of drug is Pancuronium? What is unique about it?

A

A long-acting aminosteroid

Mostly renal metabolism

Causes vagal blockade and sympathetic stimulation, leading to hypertension and tachycardia

54
Q

What type of drug is Vecuronium? What is unique about it?

A

An intermediate-acting aminosteroid

Mostly hepatic metabolism

Has an active metabolite

55
Q

What type of drug is Rocuronium? What is unique about it?

A

An intermediate-acting aminosteroid

Mostly hepatic metabolism

Can be given “double-dose” with onset of action that almost approaches that of Succinylcholine

56
Q

What are the side effects of cholinesterase inhibitors (ie. Neostigmine, Edrophonium, Pyridostigmine)?

A

Bradycardia
Bronchospasm and increased respiratory secretions
Increased GI activity (nausea/vomiting/incontinence)

57
Q

Define half-life. What are the 2 types?

A

Half-life (t1/2) is the time it takes for blood levels of drug to decrease to half of what it was at equilibrium

Alpha (distribution) half-life is due to distribution to tissue reservoirs

Beta (elimination) half-life is due to the drug being metabolized and excreted

58
Q

What is the equation for volume of distribution (Vd)?

A

(amount of drug in the body) / (concentration of drug in plasma)

59
Q

What does the volume of distribution (Vd) tell us about the amount of drug in plasma vs tissue?

A

Small Vd - drug stays mainly in plasma, with little in tissues

Medium Vd - similar concentration of drug in plasma and tissue

Large Vd - drug mostly in tissues, with little staying in the plasma

60
Q

What is the equation for half-life?

A

t1/2 = 0.69 x (volume of distribution/clearance)

61
Q

What is the mechanism of Acetazolamide?

A

Inhibits carbonic anhydrase

Results in decreases H+ secretion and increased loss of Na, HCO3-, and water

62
Q

What is Amiloride? Any side effects?

A

A K+ sparing diuretic that inhibits the epithelial Na channel (ENaC), reducing Na reabsorption

Can result in hyperkalemia

63
Q

What is Amiodarone? How does it work? Any side effects?

A

An anti-arrhythmic that blocks myocardial K and Ca channels, slowing conduction speed in SA node causing prolongation of the refractory period

Can cause hypotension and bradycardia

Associated with abnormal TFTs, PFTs, and LFTs

64
Q

Describe anti-platelet drug mechanisms

A

ASA/NSAIDs:
Inhibit COX, decreasing TXA2

Clopidogrel/Prasugrel/Ticlopidine:
Block ADP receptor, decreasing activation of platelets

Abciximab/Eptifibatide/Tirofiban:
Inhibit glycoprotein IIb/IIIa, decreasing platelet aggregation

65
Q

What type if drugs are Hydrochlorthiazide and Metolazone? Any side effects?

A

Thiazides diuretics that inhibit the Na-Cl cotransporters of the renal tubules

Results in decreases reabsorption of Na and Cl

Can cause hypercalcemia and hyperglycemia

66
Q

What type of drug is Furosemide? Any side effects?

A

A loop diuretic that inhibits the Na-K-2Cl cotransporter

Results in decreased Na and H2O reabsorption

Can cause metabolic alkalosis due to increased Cl excretion

67
Q

How do burns effect NMB?

A

More sensitive to succinylcholine

More resistant to non-depolarizing NMBs

68
Q

How does Phenytoin effect NMB?

A

Acute administration potentiates the effects of NMBs

Chronic administration results in decreased effect of NMBs

69
Q

What is unique about Alfentanil?

A

Rapid onset due to very low pKa

Very short duration of action due to very low volume of distribution

70
Q

How does renal failure effect Neostigmine

A

Neostigmine is almost completely eliminated by the kidneys

Renal failure prolongs the duration of action of Neostigmine
- dosage must be reduced around 50 to 75%

71
Q

Why is fentanyl a “short-acting” opioid when it has the same elimination half-life of Morphine and Dilaudid?

A

Fentanyl is much more lipophilic so it has a much shorter alpha-half-life (distribution)

72
Q

Why is it okay to use Succinylcholine in pregnant women?

A

An insignificant amount of Succinylcholine crosses the placenta due to its high ionization and low lips solubility

73
Q

List the drugs that should be dosed based on ideal body weight (IBW)

A

Propofol (infusion)
Vecuronium
Rocuronium
Remifentanil

74
Q

If you use succinylcholine to re-intubate a patient after reversal with neostigmine, how is the duration of action of succinylcholine affected and why?

A

Prolonged duration of action due to Phase 1 Block augmentation

75
Q

Which pressor increases cerebral oxygenation in addition to increasing CPP?

A

Vasopressin

76
Q

Why is sodium bicarbonate given? What are its effects?

A

Sodium bicarbonate is often given peri-operatively to correct an acidosis

Associated with a transient increase in paCO2, EtCO2, and intracranial pressure

Can cause hypotension due to hypocalcemia, ventricular depressant effects, and redistribution of blood volume from pulmonary vasculature

77
Q

Describe sodium nitroprusside toxicity

A

Sodium nitroprusside administration has potential for causing toxicity due to accumulation of its metabolic byproducts: cyanide and thiocyanate

Cyanide toxicity:

  • elevated mixed venous oxygen
  • tachyphylaxis to SNP
  • metabolic acidosis
  • flushing

Thyiocyanate toxicity:

  • hypoxia
  • nausea
  • tinnitus
  • muscle spasm
78
Q

What are the pharmacologic implications of major burns?

A

Severe burns lead to hypoalbuminemia, which can increase the free fraction of anesthetic drugs

  • lower doses of benzos required
  • higher doses of opioid required due to tolerance, despite higher free fraction

Increased catecholamine and corticosteroid levels
- insulin resistance, usually requiring larger doses

Proliferation of extrajunctional Ach receptors

  • exagerated response to succinylcholine
  • resistance to non-depolarizing NMBs
79
Q

What is the correct de-fasciculating dose for non-depolarizing NMBs prior to giving succinylcholine?

A

10% of ED95 dose

- NOT 10% of intubating dose

Anesthesiology (12 decks)

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