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Boards: Cardiovascular > SACCM 168: Antiarrhythmic Agents > Flashcards

SACCM 168: Antiarrhythmic Agents Flashcards

1
Q

What channel do Class I antiarrhythmics act and how do they generally affect the action potential (phase and shape change)?

A

fast Na-channel, decrease the slope of phase 0

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2
Q

Name 2 Class Ia antiarrhythmics

A

Procainamide
Quinidine

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3
Q

What other channels are blocked by Class Ia antiarrhythmics?

A

rectifier K current (IKr)

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4
Q

Which subclass of Na-channel blockers causes the strongest Na-channel blockage?

A

Ic - phase 0 experiences most shift

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5
Q

How do the different Na-channel blockers affect the cardiac action potential?

A

Ia - prolongs, by blocking K channels
Ib - shortens, by preventing late sustained Na release
Ic -no effect

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6
Q

What is the side effect of procainamide if given IV too fast?

A

hypotension

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7
Q

Why could procainamide IV worsen atrial tachyarrhythmias?

A

Class Ia agent

has anticholinergic effects –> increases the ventricular response rate

–> will worsen tachycardia from atrial tachyarrhythmia

give drugs that prolong the AV nodal conduction time (e.g., diltiazem)

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8
Q

What are the adverse effects of procainamide?

A

GI (vomiting, anorexia, nausea)
lupus erythematosus

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9
Q

How are Na channel blockers divided into their subcategories? (Ia, Ib, Ic)

A

according to their dissociation during the resting phase of the Na channel (i.e., during diastole Na-channel blockers should dissociate from the Na channels)

Ia: immediate dissociation
Ib: fast dissociation
Ic: slow dissociation

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10
Q

What state of the Na-channel do Class Ib antiarrhythmics primarily inhibit?

A

open and inactive state

with fast dissociation kinetics (fast onset/offset)

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11
Q

How do Class Ib antiarrhythmics shorten the action potential?

A

inhibition of the window sodium current, also called late sustained Na current

~2% of Na channels are not inactivated yet when action potential decrease –> usually prolong the action potential

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12
Q

How does the atrial action potential differ from the ventricular action potential?

A
  • more depolarized resting membrane potential (slightly less negative)
  • lack of plateau phase
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13
Q

Name 2 class Ib Na-channel blockers

A
  • Lidocaine
  • Mexiletine
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14
Q

What conditions increase lidocaine’s ability to block inward Na channels?

A
  • acidosis
  • hyperkalemia (increased extracellular potassium)
  • partially depolarized cells

–> work well in ischemic and diseased ventricles

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15
Q

What does it mean that Class I antiarrhythmics are use-dependent?

A

work best on rapidly depolarizing tissues

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16
Q

If unsure whether a tachyarrhythmia is SVT or VT why is lidocaine safer than procainamide?

A

lidocaine has little atrial tissue or AV nodal conduction effects.
lidocaine has minimal hemodynamic effects

procainamide shortens AV nodal conduction and thus increases the ventricular repsonse rate

17
Q

How is lidocaine cleared?

A

hepatic clearance –> determines serum cc –> increased toxicity risk with heart failure, hypotension, severe hepatic disease

18
Q

What are the most common adverse effects of lidocaine?

A
  • GI (vomting, nausea)
  • lethargy
  • tremors
  • seizure activity

cats prone to bradyarrhythmias and sudden death

19
Q

How is mexiletine used?

A

orally in dogs for VT and OAVRT

20
Q

What state of the Na-channels do class Ic antiarrhythmics primarily inhibit?

A

open state

21
Q

Name 2 examples of class Ic antiarrhythmics

A

propafenone (also has mild beta-blocking effects)
flecainide

22
Q

Name examples of beta-blockers

A
  • esmolol
  • atenolol
  • propranolol
  • metoprolol
23
Q

List contraindications for beta-blockers

A
  • CHF
  • pulmonary disease (bronchoconstriction)
  • patients with sinus nodal dysfunction
  • AV node conduction disturbances
24
Q

what is the effect of dromotropic agents?

A

agents that affect the conduction speed in the AV node

25
Q

What channels/currents are inhibited by beta blockers?

A
  • funny current (If)
  • inward Ca current (Ica) - indirectly by decreased tissue cyclic-AMP
26
Q

List indications for beta blockers

A
  • VT suspected to be worsened by increased sympathetic tone
  • to slow AV noda conduction in SVT
  • to slow SA node discharge rate in inappropriate sinus tachycardia (e.g., pheochromocytoma)
27
Q

Name 2 class III antiarrhythmic agents

A

Sotalol
Amiodarone

28
Q

What is the reason for proarrhythmic effects of K-channel blockers?

A

block the rapid component of the IK current (IKr) rather than the slow IK current (IKs) –> risk of early afterdepolarization

increased risk in hypokalemia, bradycardia, intact females, old age, macrolide antibiotic therapy + other drugs

29
Q

What are the mechanisms of sotalol and how does its dose affect these mechanisms?

A
  • nonselective beta-blockade (predominate at lower dosages) –> sinus and AVN depression
  • rapid K current (IKr) inhibition (at higher dosages) –> prolongation of the atrial and ventricular myocardial action potential
30
Q

What mechanisms reduces Sotalol’s negative inotropic effects?

A

negative inotropic from beta-blockade

effect is attenuated because of action potential prolongation –> leads to prolonged time for Ca reentry –> enhances contractility

31
Q

What are the antiarrhythmic mechanisms of amiodarone?

A

exhibits effects in all 4 categories (Na-channel blocker, beta-blocker, K-channel blocker, Ca-channel blocker)

32
Q

Why does the most common IV formulation of amiodarone cause significant side effects?

A

Cordarone –> polysorbate 80 and benzyl alcohol –> negative inotropic and hypotensive effects

causes life-threatening hypotension, anapyhlaxis, bradycardia, acute hepatic necrosis, death

new formulation (Nexterone) –> safer, but more expensive

33
Q

Name 2 class IV antiarrhythmic agents

A
  • Diltiazem
  • Verapamil
34
Q

what type of tachyarrhythmia is a contraindication for Ca-channel blockers?

A

wide complex tachyarrhythmias

35
Q

what are the effects of Ca-channel blockers?

A

slow the ventricular esponse rate to atrial tachyarrhythmias
prolong the AVN effective refractory period

36
Q

What is the mechanism of action of digoxin?

A

enhances central and peripheral vagal tone –> * slows the sinus nodal discharge rate
* prolongs AVN refractoriness
* shortens atrial refractoriness

37
Q

What conditions increase the risk of digoxin toxicity?

A
  • renal dysfunction
  • hypokalemia
  • advanced age
  • chronic lung disease
  • hypothyroidism
38
Q

What are the side-effects of magnesium sulfate administration?

A
  • central nervous system depression
  • weakness
  • bradycardia
  • hypotension
  • hypocalcemia
  • QT prolongation

Boards: Cardiovascular (13 decks)

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