Chapter 4 CV + hematology - antiarrhythmic drugs Flashcards
Four classes
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
Quinidine
class I
- 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
Procainamide (pronestyl)
class I
- 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
Disopyramide (norpace)
class I
- 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
Lidocaine (xylocaine)
class I
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
Mexiletine (mexitil)
class I
- 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
Flecainide (tambocor)
class I
- 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
propafenone (rhythmol)
class I
- 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
Propranolol (inderal)
esmolol (kerlone)
class II
- 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)
amoidarone
class III
- 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
sotalol (betapace)
class III
- 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
Verapamil
Class IV
- 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
Digoxin (lanoxin)
unclassified
- 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
adenosine (adenocard)
- 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
