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Cardio Block > Pharmacology Of Dysrhythmias > Flashcards

Pharmacology Of Dysrhythmias Flashcards

1
Q

Consequences of dysrhythmia (3)

A
  1. Compromises mechanical performance
  2. Prodysrhythmic/dysrhythmogenic: conversion of one dysrhythmia to another, v tach to v fib
  3. Thrombogenesis: atrial flutter and fibrillation contribute to increased stroke incidence
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2
Q

Causative mechanisms for dysrhythmia generation (2)

A
  1. Disorders of impulse formation (early and delayed after-depolarizations)
  2. Disorders of impulse conduction (AV nodal block, ventricular re-entry, AV nodal re-entry)
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3
Q

Class Ia Antidysrhythmic agents (3)

A
  1. Procainamide
  2. Quinidine
  3. Disopyramide
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4
Q

Class Ib Antidysrhythmic agents (2)

A
  1. Lidocaine

2. Phenytoin

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5
Q

Class Ic Antidysrhythmic agents (1)

A
  1. Flecainide
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6
Q

Class II Antidysrhythmic agents (1)

A
  1. Propranolol
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7
Q

Class III Antidysrhythmic agents (3)

A
  1. Amiodarone
  2. Sotalol
  3. Ibutilide
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8
Q

Class IV Antidysrhythmic agents (2)

A
  1. Verapamil

2. Diltiazem

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9
Q

Class V “others” Antidysrhythmic agents (3)

A
  1. Adenosine
  2. Digoxin
  3. Atropine
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10
Q

Non-nodal tissues depolarize at phase 0 when there is ______ influx.

A

Na+

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11
Q

Nodal tissues depolarize at phase 0 when there is ______ influx.

A

Ca2+

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12
Q

General Class I agent MOA (3)

A
  1. Block voltage-sensitive Na+ channels to varying degrees in conductile tissues: slows phase 0
  2. ERP/APD increased
  3. Useful in varying degrees for ventricular dysrhythmia and/or digitalis or MI-induced dysrhythmia
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13
Q

General Class Ia agent MOA (3)

A
  1. Moderate binding to Na+ channels: slows phase 0 depolarization
  2. K+ channel blockade: delays phase 3 repolarization and prolongs QRS and QT interval
  3. Ca2+ channel blocking effect at high doses: depresses phase 2 and nodal phase 0
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14
Q

General Class Ib agent MOA (2)

A
  1. Weak binding to Na+ channels: weak effect on phase 0 depolarization due to rapid “on-off” receptor kinetics
  2. Accelerated phase 3 repolarization: shortened APD and QT, good use in digitalis and MI-induced dysrhythmia
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15
Q

General Class Ic agent MOA (1)

A
  1. Strongest binding to Na+ channels: slow “on-off” kinetics with marked effects on phase 0 depolarization. Lengthened QRS and APD. QT internal unchanged. Lengthened PR interval (depressed AV nodal conduction).
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16
Q

General Class II agent MOA (4)

A
  1. Comprised of beta antagonists (beta blockers!): beta receptors are G-protein-coupled to Ca2+ channels; beta effects primarily on nodal phase 0 depolarization
  2. Depresses SA nodal automaticity (phase 4)
  3. AV nodal conduction
  4. Decreased ventricular contractility
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17
Q

General Class III agent MOA (2)

A
  1. Multiplicity of membrane effects at K+, Ca2+, Na+, and beta receptors (direct and indirect): Prolong phase 3 repolarization, increase QT interval
  2. Useful for ventricular re-entry/fibrillatory dysthythmia
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18
Q

General Class IV agent MOA (4)

A
  1. Ca2+ channel antagonists (calcium channel blockers!): similar in utility to Class II agents with primary effects on nodal phase 0 depolarization
  2. Depresses SA nodal automaticity
  3. Depresses AV nodal conduction
  4. Decreases ventricular contractility
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19
Q

Atrial fibrillation, conversion, clinically used agents (High, Moderate, Low)

A

High efficacy: Ia agents
Moderate efficacy: II, III, IV agents
Low efficacy: Ib

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20
Q

Atrial fibrillation, prophylaxis, clinically used agents (High, Moderate, Low)

A

High efficacy: Ia agents
Moderate efficacy: II and IV agents
Low efficacy: Ib and III agents

21
Q

Atrial fibrillation, rate control, clinically used agents (High, Low)

A

High efficacy: II, III, and IV

Low efficacy: Ia and Ib

22
Q

PSVT clinically used agents (High, Moderate, Low)

A

High efficacy: II and IV agents
Moderate efficacy: Ia agents
Low efficacy: Ib

23
Q

Atrial premature depolarizations (PACs) clinically used agents (High, Moderate)

A

High efficacy: Ia, II, and IV agents

Moderate efficacy: Ib agents

24
Q

Ventricular premature depolarizations (PVCs) clinically used agents (High, Moderate, Low)

A

High efficacy: Ia agents
Moderate efficacy: Ib and II agents
Low efficacy: IV agents

25
Q

Tachycardia, unsustained, clinically used agents (High, Moderate, Moderate-low, Low)

A

High efficacy: Ia agents
Moderate efficacy: Ib agents
Moderate-low efficacy: II agents
Low efficacy: IV agents

26
Q

Tachycardia, sustained, clinically used agents (High, Moderate, Moderate-low, Low)

A

High efficacy: Ia agents
Moderate efficacy: Ib, Ic, and III agents
Moderate-low efficacy: II agents
Low efficacy: IV agents

27
Q

Atrial tachycardia with block (digitalis-induced) clinically used agents (High, Moderate, Low)

A

High efficacy: Ib agents
Moderate efficacy: II agents
Low efficacy: Ia agents

28
Q

Nonparoxysmal AV junctional tachycardia (digitalis-induced) clinically used agents (High, Moderate, Low)

A

High efficacy: Ib agents
Moderate efficacy: II agents
Low efficacy: Ia agents

29
Q

Ventricular dysrhythmia (digitalis-induced) clinically used agents (High, Moderate, Low)

A

High efficacy: Ib agents
Moderate efficacy: II agents
Low efficacy: Ia agents

30
Q

Quinidine, Ia (general, uses, and pharmokinetics)

A

Cinchona bark alkaloid.
Used for atrial flutter, atrial fibrillation, PAT, and PSVT, and ventricular tachycardia.
Decreases nodal automaticity and increases QRS and QT in non-nodal tissues.
Dose adjustment required in renal dysfunction and elderly with reduced renal function.

31
Q

Quinidine, Ia, ADRs (4)

A
  1. Nausea, vomiting, diarrhea
  2. Cinchonism (tinnitus, hearing loss, blurred vision)
  3. Hypotension due to alpha blocking effect
  4. TdP due to drug-induced increases in QT interval
32
Q

TdP (twisted points) are usually treated with what agent?

A

MgSO4 (magnesium!) at 6-8mEq in D5W

33
Q

Procainamide, Ia (general, uses, and pharmokinetics)

A

Similar pharmacology to quinidine.
Used for atrial flutter, atrial fibrillation, PAT, PSVT, and ventricular tachycardia.
Metabolism depends on hepatic N-acetyltransferase activity and renal function; 70% of procainamide is excreted in urine unchanged, rapid acetylators half life = 2.5-3 hrs, slow acetylators half life = greater than 5 hours (30-40% of patients)

34
Q

Procainamide, Ia, ADRs (4)

A
  1. *Slow acetylators develop lupus-like syndrome upon chronic use: arthralgia, pericarditis, fever, weakness, skin lesions, lymphadenopathy, anemia, and hepatomegaly
  2. Nausea/vomiting
  3. Decreased renal function
  4. Mental confucion and *TdP
35
Q

Lidocaine, Ib (general, uses, and pharmokinetics)

A

Also used as a local anesthetic.
Inhibits reentry mechanisms in ventricular tissue and suppresses spontaneous ventricular depolarizations.
Preferential action on ischemia tissue.
Excellent use in post-MI or digoxin-induced tachycardia.
IV administration only.

36
Q

Flecainide, Ic (general, uses, and pharmokinetics)

A

Potent Na+ channel blockade.
Marked depression of cardiac conduction.
Not considered a first-line agent due to prominent prodysrhythmic effects.
Use only in treatment of refractory life-threatening ectopic ventricular dysrhythmia; prolongs phase 0 and widens QRS.

37
Q

Propanolol, II (general, uses, and pharmokinetics)

A

Competitive beta-receptor antagonist.
Decreases HR and CO.
Decreases atrial, AV node, and ventricular conduction velocity.
Decreases SA and AV nodal automaticity.
Excellent use in atrial flutter, atrial fibrillation, PAT, and digoxin-induced dysrhythmia.
Taken PO.

38
Q

Propanolol, II, ADRs (4)

A
  1. Hypotension
  2. Asystole
  3. Bronchospasm with non-selective antagonists
  4. Rebound withdrawal effect due to receptor up-regulation
39
Q

Amiodarone, III (general, uses, and pharmokinetics)

A 
Alters K+ flux during phase 3.
Increases ERP and APD.
Used in refractory ventricular dysrhythmia.
Purported less prodysrhythmic potential.
Taken PO or IV.
40
Q

Amiodarone, III, ADRs (5)

A

75% incidence rate in chronic oral administration.

  1. Nausea/vomiting
  2. Pulmonary toxicity (10-17% pneumonitis/ARDS)
  3. May elevate liver enzymes
  4. Photosensitivity (micro-deposition)
  5. Thyroid disorders/tumors
41
Q

Ibutilide, dofetilide, etc., III (general, uses, and pharmokinetics)

A

Only agents clinically indicated for rapid conversion of atrial fibrillation/flutter to NSR.
MOA different from other class III - promotes Na+ influx through slow inward Na+ channels, thus prolonging APD.
Administered IV.

42
Q

Verapamil, IV (general, uses, and pharmokinetics)

A

Calcium channel blocker.
Affects nodal tissues mainly.
Decreases HR, SA node automaticity, and AV node conduction.
Increases PR interval.
Causes cardiac depression (lower CO from decreased SV and HR).
Useful in treatment of SVT (diltiazem may also be used).
Can also treat angina and HTN at higher dose.
Ventricular dysrhythmias are unaffected.
Administered IV for rapid SVT conversion.
Taken PO for maintenance of recurrent SVT.
Highly lipophilic. Hemodialysis ineffective.

43
Q

Verapamil, IV, ADRs (5)

A
  1. Constipation
  2. Hypotension
  3. Exacerbate CHF
  4. AV heart block in combination with beta blockers
  5. Male sexual dysfunction
44
Q

Adenosine (general, uses, and pharmokinetics)

A

Purine nucleoside useful for conversion of re-entrant SVT (PAT, PSVT, WPW) to NSR.
AV nodal hyperpolarization due to adenosine-stimulated opening of membrane K+ channels.
Produces complete AV nodal block.
Less toxic than verapamil due to shorter half-life (10-15s).
Susceptibility to acid degradation and rapid plasma metabolism relegates IV use.
Rapid bolus at 6-12mg proximal to heart.

45
Q

Adenosine ADRs (5)

A
  1. Hypotension
  2. Flushing
  3. Complete heart block
  4. CNS effects
  5. Dyspnea
46
Q

Digoxin (general, uses, and pharmokinetics)

A

Cardiac glycoside.
Useful in treatment of CHF and control of ventricular rate in chronic atrial fibrillation (CCBs are more preferred).
Slows ventricular rate by decreasing the number of P wave depolarizations that reach the ventricles (sympathetic stimulation may override this effect).
Inhibits Na+/K+ ATPase.
Vagal stimulation effect resulting in a negative dromotropic effect at the AV node resulting in prolonged refraction.
Taken PO.

47
Q

Digoxin ADRs (1)

A
  1. Highly dysrhythmogenic (prodysrhythmic) due to effects on plasma potassium (hypokalemia): requires magnesium therapy to facilitate potassium distribution, class Ib and II agents also appear effective in treating some digoxin-induced ventricular dysrhythmias.
48
Q

Agents for management of bradycardia (3)

A
  1. Atropine: produces vagal block to increase HR
  2. Isoproterenol: B1-stimulated increase in HR
  3. Pacemaker: morphologic AV nodal block
49
Q

Management of sinus tachycardia (1)

A
  1. Vagal stimulation through carotid sinus massage or Valsalva maneuver

Cardio Block (9 decks)

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