Chapter 4 CV + hematology - antiarrhythmic drugs

Question 1

Four classes

Answer 1

Class I drugs
* Na+ channel blockers
* slow conduction velocity and ten to prolong refractory period versus other classes (has little effect on SA node automaticity) — Class Ia
* Claas Ib agents — no clear generalizations
* Class Ic — slow conduction velocity most effectively

Class II drugs
* antaognize adrenergic receptors

Class III agents
* prolong repolarization

Class IV agents
* block slow inward (calcium driven) current

Question 2

Quinidine

class I

Answer 2

• depress automaticity of ectopic foci (Ectopic foci are abnormal pacemaker sites within the heart (outside of the SA node) that display automaticity. Their pacemaker activity, however, is normally suppressed (overdrive suppression) by the higher rate of the SA node. They can occur within the atria or ventricles.)
• slows conduction velocity in atria + His-Purkinje cells
• prolongs refractory period (heart, accessory pathways, except node)
• anticholinergic effects can enhance AV conduction in patient’s w/ rapid atrial depolarization

indication
* multifocal atrial tachy
* premature atrial depolarization
* atrial fibrillation
* premature ventricular depolarization

effects
* torsades de pointes (recurrent temporary arrhythmia)
* tachyarrhythmia
* thrombocytopenic purpura is a blood disorder characterized by an abnormal decrease in the number of platelets in the blood
* cinchonism (tinnitus, reversible hearing loss, flushing, confusion, diarrhea, and visual disturbances, including permanent blindness in some cases)
* n/v, diarrhea

prolongs QRS and QT intervals

IV causes hypotension + IM painful

interactions
* phenobarbital + phenytoin inc metabolism of this drug
* this drug can inc digoxin levels
* potentiates warfarin
* enhance hypotension

Question 3

Procainamide (pronestyl)

class I

Answer 3

• depress automaticity of ectopic foci (Ectopic foci are abnormal pacemaker sites within the heart (outside of the SA node) that display automaticity. Their pacemaker activity, however, is normally suppressed (overdrive suppression) by the higher rate of the SA node. They can occur within the atria or ventricles.)
• slows conduction velocity in atria + His-Purkinje cells
• prolongs refractory period (heart, accessory pathways, except node)
• anticholinergic effects can enhance AV conduction in patient’s w/ rapid atrial depolarization

indication
* premature atrial depolarization
* atrial afib
* atrial flutter
* wolff-parkinson-white
* v tach
* premature ventricular depolarization

effects
* cardiac toxicity (w/ fewer GI effects + anticholinergic effects than quinidine)
* Lupus like syndrome

muscle and joint pain sometimes with swelling
flu-like symptoms of fatigue and fever
serositis (inflammation around the lungs or heart that causes pain or discomfort)
certain laboratory test abnormalities

• other hypersensitivity

Prolongs QRS and QT intervals

N-acetylprocainamide (NAPA) is active and toxic — should be monitored

Interactions
* no interaction with digoxin or warfarin

Question 4

Disopyramide (norpace)

class I

Answer 4

• depress automaticity of ectopic foci (Ectopic foci are abnormal pacemaker sites within the heart (outside of the SA node) that display automaticity. Their pacemaker activity, however, is normally suppressed (overdrive suppression) by the higher rate of the SA node. They can occur within the atria or ventricles.)
• slows conduction velocity in atria + His-Purkinje cells
• prolongs refractory period (heart, accessory pathways, except node)
• anticholinergic effects can enhance AV conduction in patient’s w/ rapid atrial depolarization

indication
* premature atrial depolarization
* atrial fib
* v tach

Effects
* potent anticholinergic
* similar to quinidine (torsades, tachyarrhythmia, n/v, diarrhea, cinchonism, thrombocytopenic purpura)

Prolongs QRS and QT intervals

Must follow serum levels

Interactions
No interaction with digoxin

Question 4

Lidocaine (xylocaine)

class I

Answer 4

Depresses automaticity of foci, increases conduction velocity of AV node and His-purkinje

indication
* Wolff-parkinson-white
* v tach
* premature ventricular depolarization
* ventricular fibrillation

effects:
1) CNS
* paresthesias, restlessness
* drowsiness, confusion
* all above low doses

• High doses — seizures or disorientation
• Cardiac depression

may shorten QT interval

IV

Serum level increase when taking drugs that reduce blood flow to liver (beta blockers) and by cimetidine

Question 5

Mexiletine (mexitil)

class I

Answer 5

• Decreases automaticity of AV node + ectopic foci
• Prolongs refractory period of HIs-purkinje, ventricle, and accessory pathway

indication
* premature ventricular depolarization
* ventriclar tachycardia

effects
* worsen arrhythmias
* hepatotoxicity

Maintain dose < 1.2 g/day to reduce CNS toxicity

p450 inducing drugs (rifampin + phenytoin) reduce half life of this drug

Question 6

Flecainide (tambocor)

class I

Answer 6

• reduces automaticity of SA node and ectopic foci
• dec conduction velocity throughout
• prolongs refractory period in his-purkinje, ventricle, accessory pathways

indication
* chronic therapy for a fib

effects
* worsen arrhythmias
* rarely induce AV block

prolongs PR, QRS, QT

interactions
* cimetidine inc half life of encainide

Question 7

propafenone (rhythmol)

class I

Answer 7

• slows conduction throughout
• prolongs atrial and ventricular refractory period
• weak beta adrenergic and calcium entry blocking effects

indication
* chronic or actue therapy for atrial fib

effects
* nausea
* dizziness
* constipation
* altered taste sensation
* worsen HF or arrhythmia

prolongs PR, QRS, QT

titrates dose carefully

interactions
* propaferone inc plas levels of propranolol, digoxin, warfarin
* cimetidine can increase this drug’s levels

Question 8

Propranolol (inderal)
esmolol (kerlone)

class II

Answer 8

• beta adrenergic receptor antagonist
• derease HT, contractility, and automaticity
• Prolongs AV conduction time + refractory period
• B1 adrenergic receptor preferring antagonist – esmolol but similar to propranolol

indication
* sinus tach
* atrial flutter
* atrial fib
* AV reentry
* wolff parkinson white

effects
* HF
* depressed AV conduction
* bronchospasm (less esmolol)
* hypotension

ECG
slow HR — prolong PR and QT interval

interactions
* propranolol — AV block when combined with digitalis
* no significant interactions with digoxin (esmolol)

Question 9

amoidarone

class III

Answer 9

• reduce K+ efflux
• reduce automaticity - SA node + ectopic foci
• reduce conduction velocity
• inc refraction

indication
* ventricular fibrillation
* v tach
* wolff-parkinson-white
* atrial fibrillation

effects
* pulmonary fibrosis
* photosensitivity
* hyper or hypo thyroidism
* corneal deposits (reversible)

prolong PR, QRS, QT

Maximal response may take weeks

interactions
* inc serum levels of digoxin, warfarin, flecainide

Question 10

sotalol (betapace)

class III

Answer 10

• beta adrenergic blocker that slows refractory period of purkinje fibers + heart muscles

indication
* v tach

effects
* arrhythmias

interaction
* increased risk of arrhythmias with other antiarrhythmics

Question 11

Verapamil

Class IV

Answer 11

• reduce Ca++ entry into myocardial cells
• reduce automaticity SA node + ectopic foci
• reduce conduction and inc refractory period of AV node

indication
* multifocal atrial tachycardia
* atrial flutter

effects
* sinus brady
* AV block
* hypotension
* left ventricular failure (if infused rapidly in elderly)
* GI upset/constipation

Half life inc up to fourfold in cirrhotic patients

interactions
* inc serum digoxin levels
* enhance AV node suppression of digoxin or propranolol => AV block

CONTRAINDICATED with wolff-parkinson-white may induce lethal arrhythmia

Question 12

Digoxin (lanoxin)

unclassified

Answer 12

• only drug - inc automaticity of ectopic pacemakers
• slows conduction velocity THROUGHOUT
• inc parasympathetic tone

indication
* a fib
* a flutter
* paroxysmal atrial tachycardia (common with wolff-parkinson-white)
* A narrow complex rhythm which is fast, usually over 160 and sometimes even over 200 beats per minute. Generally P waves are buried in T waves or QRS complexes and can’t be seen. Typically, the rhythm starts and stops abruptly.

effect
* digitalis intoxication (confusion, loss of appetite, nausea, vomiting, diarrhea, or vision problems. Other signs of overdose are changes in the rate or rhythm of the heartbeat (becoming irregular or slow), palpitations (feeling of pounding in the chest), or fainting) + hyperkalemia
* arrhythmias
* complete heart block and accelerated junctional rhythm

slows rate, prlongs PR interval, short QT, diminish T wave

Question 13

adenosine (adenocard)

Answer 13

• decrease conduction velocity
• prolong refractory period
• decrease automaticity in AV nod

indication
* paroxysmal supraventricular tachyarrhythmias
* A narrow complex rhythm which is fast, usually over 160 and sometimes even over 200 beats per minute. Generally P waves are buried in T waves or QRS complexes and can’t be seen. Typically, the rhythm starts and stops abruptly.

effects
* dypsnea
* flushing
* chest pain
* arrhythmias

IV - deanimated to inosine

Theophylline and other methyxanthines antagonize adenosine