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review / wrong answers > DIT review - Cardiology 4 > Flashcards

DIT review - Cardiology 4 Flashcards

1
Q

Describe what part of the action potential each class of Anti-arrhythmics works on (which electrolyte channel and which phase)

A

THINK: No Bad Boy Keeps Clean

  • Class I
    • Na+ channel blockers
    • Phase 0 of myocytes
  • Class II
    • Beta blockers
    • Phase 4 of pacemakers
  • Class III
    • K+ channel blockers
    • Phase 2 and 3 of myocytes
  • Class IV
    • Ca2+ channel blockers
    • Phase 0 of pacemakers
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2
Q

Describe the different effects on Phase 0 slope and effective refractory period of Class IA, IB, and IC antiarrhythmics

A
  • Class IA:
    • Intermediate Na+ channel binding – moderately decreased phase 0 slope
    • Also block K+ channels – prolonged refractory period
  • Class IB:
    • Weakest Na+ channel binding – minimally decreased phase 0 slope
    • Cause shortened refractory period
  • Class IC:
    • Strongest Na+ channel blocking – significantly decreased phase 0 slope
    • No effect on refractory period
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3
Q

What is the effect of Class I antiarrythmics on QRS complex

A

Widened QRS due to decreased AP conduction velocity

  • Because drug is state-dependent and effect is stronger on channels with more depolarization (rapid heart rate), QRS will be even WIDER in patients with tachycardia
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4
Q

What is the order of binding affinity for Na+ channels in the different Class I antiarrhythmics

A

IC > IA > IB

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5
Q

What are the Class IA antiarrhthmics

A
  • Quinidine
    • = dining prom queen
  • Procainamide
    • = prom king
  • Disopyramide
    • = “prom queen DISAPPEARS” headline
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6
Q

Uses of Class IA antiarrhythmics

A
  • Supraventricular and ventricular arrhythmias
    • = top and bottom of IA sign are lit up
  • Wolff-Parkinson-White (WPW) syndrome (a type of SVT)
    • = white wolf pack sign
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7
Q

Adverse effects of Quinidine

A

Cinchonism (a syndrome of tinnitus, HA, and dizziness)

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8
Q

Adverse effects of Procainamide

A

Drug-induced lupus

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9
Q

Adverse effects of Disopyramide

A

Exacerbation of heart failure (has negative inotropic effects at toxic concentrations)

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10
Q

Adverse effects of all Class IA antiarrythmics

A

QT interval prolongation (precipitates torsades) due to prolonged AP (effects on K+ channel)

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11
Q

What are the Class IB antiarrhythimcs

A
  • Lidocaine
    • = “you lied”
  • Mexiletine
    • = Mexican flag
  • Phenytoin (anti-epileptic)
    • = tow truck driver
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12
Q

What are the effects of Class IB on QT interval/torsades

A
  • No chance of prolonged QT and torsades
    • Shorten phase 2 and 3 of cardiac AP, leading to shortened refractory period (speed up AP duration)
      • = pulling curtain closed
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13
Q

Uses of Class IB antiarrhythmics

A
  • Ventricular arrhythmias (especially in ischemic tissue)
    • = illuminated cracked (ischemic) bottom of heart
    • = “you’re DEAD to me” = ischemia induced ventricular arrhythmias
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14
Q

Adverse effects of Class IB antiarrhythmics

A
  • Neuro (e.g. Parasthesias, tremor, convulsions)
    • = brain-shaped trucker hat
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15
Q

What are the Class IC anti-arrhythmics

A
  • Flecainide
    • = flakes cereal
  • Propafenone
    • = purple phone
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16
Q

Uses of Class IC antiarrhythmics

A
  • Supraventricular and ventricular arrhythmias
    • = illuminated top and bottom of heart sign
  • Atrial fibrillation (and flutter)
    • = irregularly irregular signal on TV
    • First goal is control of ventricular rate (accomplished by beta-blockers)
    • Class IC can then restore and maintain normal sinus rhythm
17
Q

Adverse effects of Class IC antiarrhythimcs

A
  • Contraindicated in patients with history of structural ischemic heart disease (due to proarrhythmic effects)
    • = “healthy heart only” cereal
18
Q

What drugs are Class II antiarrhythmics

A

Beta blockers (“-olol”)

19
Q

MOA of Class II antiarrhythmics

A
  • Do not directly modify ion channel function
  • Block sympathetic input to the SA and AV node
  • Beta blocker decrease cAMP
  • Decreased cAMP leads to closure of membrane calcium channels (needed for upstroke of nodal action potential)
  • Beta blockers lead to prolonging of phase 4 (slow depolarization) of the nodal action potential
    • In the SA node this leads to decreased sinus rate, suppressing abnormal pacemaker activity
    • In the AV node, this causes a dramatic prolongation of AV conduction time and effective refractory period
20
Q

Uses of Class II antiarrhythmics

A
  • Supraventricular arrhythmias (e.g. atrial fibrillation with RVR)
    • = top of neon heart is illuminated
  • IV beta blockers (e.g. Esmolol) can be used for acute supraventricular arrhythmias
    • = ivy
  • Atrial fibrillation (and flutter)
    • = Irregularly irregular signal on TV
    • BB can accomplish the first goal of treatment which is to control rate of the ventricles
      • = rate-controlling metronome under the TV
    • This does not fix the atrial fibrillation though (accomplished by Class IC)
21
Q

Adverse effects of beta-blockers

A
  • Heart block
    • = top of Luis Armstrong hat is a shield held up to heart
  • Heart block manifests as a prolonged PR interval on EKG
    • = Public Relations microphones
22
Q

MOA of Class III antiarrhythmics

A
  • Class III anti-arrhythmics block K+ channels of the myocardium, prolonging phase 2 and phase 3, and allowing myocardium to be depolarized for longer (prolonged refractory period)
23
Q

What drugs are Class III anti-arrhythmics

A
  • Amiodarone
    • = Amigos
  • “-tilide” suffix (e.g. Dofetilide and Ibutilide)
    • = “til I die” note
  • Sotalol
    • = soda
    • Is also a beta blocker (-lol suffix)
      • Muted bugle
24
Q

MOA of Amiodarone

A
  • Shares properties of class I, II, III, and IV anti-arrhythmics
    • = uno, dos, tres, quatro
  • Blocks inactivated Na+ channels (class I), weak beta-adrenergic effects (class II), blocks K+ channels (class III), and weak Ca2+ blocking effects (class IV)
25
Q

Uses of Class III antiarrhythmics

A
  • Both supraventricular and ventricular arrthmias
    • = Heart illuminated on top and bottom
  • Atrial fibrillation
    • = irregularly irregular signal on TV
    • Useful for restoring and maintaining normal sinus rhythm (along with Class IC)
26
Q

Adverse effects of Amiodarone

A
  • Neuro side effects (e.g. tremor, ataxia, peripheral neuropathy, sleep disturbances)
    • = skull brains on amigos hats
  • Gray corneal micro deposits (usually asymptomatic)
    • = gray sunglasses
  • Hyper- or hypothyroidism
    • = big and small bowties on amigos
  • Pulmonary fibrosis (restrictive lung disease)
    • = fibrotic lung embroidery
    • = tight button = restrictive
  • Heart block (due to Class II and IV depressing conduction through AV node
    • = hat shield held against chest
  • Heart failure
    • = trampled failing heart balloon
  • Hypersensitivity hepatitis
    • = liver spot on cow
  • Gray-blue skin discoloration
    • = gray-blue outfits
  • Photodermatitis
    • = flash photo
  • Is an inhibitor of CYP450
    • = broken chrome bumper
  • Widening of QT interval (can induce torsades) – caused by Sotalol, Dofetilide,** and **Ibutilide
    • = twisted streamer near soda and “til I die” note
27
Q

What drugs are Class IV antiarrhythmics

A

Non-dihydropyridine calcium channel blockers:

  • Verapamil = very vanilla
  • Diltiazem = Delicious dark chocolate
28
Q

Uses of Class IV antiarrhythmics

A
  • Supraventricular arrhythmias (e.g. atrial fibrillation with RVR)
    • = illuminated top of heart neon sign
  • Atrial fibrillation
    • = irregularly irregular signal on TV
    • CCB will control ventricular rate, preventing rapid ventricular response (“rate control”)
      • = metronome
    • This does not fix the atrial fibrillation though
29
Q

Adverse effects of Class IV antiarrhythmics

A
  • Prolonged PR interval on EKG because conduction from atrial P-wave to ventricular QRS is delayed
  • Heart block
30
Q

Describe Digoxin’s MOA as an anti-arrhythic

A
  • Exerts direct parasympathomimetic effects via direct stimulation of the vagus nerve, leading to AV inhibition
  • Similar effect of beta-blockers (Class II) and Ca2+ blockers (Class IV)
31
Q

Uses of Digoxin as an anti-arrhythmic

A
  • Atrial arrhythmias, including A-fib
    • = irregularly irregular signal on light board behind DJ
    • Controls ventricular rate, preventing rapid ventricular response
      • = metronome with Vegas sign on top
32
Q

Uses of Magnesium as an anti-arrhythmic

A
  • Useful for the treatment of certain arrhythmias (e.g. torsades)
33
Q

Describe the effects of hyper- and hypo-kalemia on EKG

A
  • Both hyper- and hypokalemia can induce arrhythmias
    • = male banana dancer pointing up and female banana dancer pointing down
  • Hyperkalemia can cause peaked T waves with shorted QT interval
    • = peaked streamer above hyperkalemia banana dancer
  • Hypokalemia can cause U waves at the end of the T wave
    • = streamer that hypokalemia banana dancer is pointing to
34
Q

Describe the MOA of Adenosine as an anti-arrhythmic

A
  • Adenosine is a purine nucleotide
    • = purine shaped gate
  • Activates inhibitor A1 receptors on the myocardium and at the SA and AV nodes
    • = A1 written on gate
  • Activation of A1 receptors increases potassium outward conduction and suppresses calcium inward current
    • = banana flying out of cup
    • = falling calci-yum ice cream
  • This causes membrane potential to remain negative for a longer period and calcium-dependent action potentials (at nodes) are suppressed
    • = note-shaped dance floor
  • This decreases AV conduction, leading to prolonged AV refractory period
    • = disconnected bottom of neon heart
35
Q

Uses of Adenosine as an anti-arrhythmic

A
  • First line agent for acute treatment of supraventricular arrhythmias
    • = illuminated top of neon heart with #1 ribbon
  • Coronary dilation (mediated by A2 receptors)
    • = dilated coronary crown
36
Q

Adverse effects of Adenosine

A
  • High-grade AV block
    • = hat blocking heart of swing dancer
  • Shortness of breath, chest pain, major flushing, and sense of impending doom
    • = flushed dancer clutching chest
  • Hypotension (due to vasodilation) and HA
    • = fainting dancer
37
Q

What substances inhibit the action of Adenosine

A

Caffeine and Theophylline

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