Chapter 52: Antidysrhythmic Drugs Flashcards
what is an dysrhythmia
- abnormality in the rhythm of the heartbeat
- arises from electrical impulse formation disturbances
pathway of conduction of electrical impulses in a heathy hear
SA –> atria –> AV –> ventricles
sinoatrial (SA) node
pacemarker of the heart
Atrioventricular (AV) node
- slow enough to allow ventricles to fill with blood
His-Purkinje system
rapid ejection of blood
fast potentials occur
in fibers of the His-Purkinje and the atrial and ventricular muscle
what are the 5 phases of fast potentials
phase 0: depolarization
phase 1: (partial) depolarization
phase 2: plateau
phase 3: repolarization
phase 4: stable potential
slow potentials occur
in the SA and AV node
Phases of slow potentials
Phase 0: slow depolarization (mediated by calcium influx)
Phase 1: absent
phase 2 and 3: not significant
phase 4: depolarization
P wave
depolarization in the atria
QRS complex
depolarization of the ventricles
T wave
repolarization of the ventricles
what are the 2 fundamental causes of dysrhythmias
- disturbances of automaticity
- disturbances of conductions (AV block, reentry)
what are antidysrhythmic drugs classified by
Vaughan Williams classification
Class I
sodium channel blockers
- slow impulse conduction
Class II
beta blockers
- depress depolarization
Class III
Potassium channel blockers
- delay repolarization
Class IV
Calcium channel blockers
- similar to beta blockers
Antidysrhythmic drugs should be used only when
dysrhythmias are symptomatically significant and only when the potential benefits clearly outweigh the risks
Prodysrhythmic effects of antidysrhythmic drugs
- prolongation of the QT interval
- Torsades de pointes
Supraventricular dysrhythmias
Impulse arises above the ventricle
- atrial fibrilation
- atrial flutter
- sustained supraventricular tachycardia (SVT)
Ventricular dysrhythmias
- sustained ventricular tachycardia
- ventricular fibrilation
- premature ventricular complexxes
- digoxin induced ventricular dysrhythmias
- torsades de pointes
example of class IA agents
Quinidine
- Procainamide (procan)
- Disopyramide (Norpace)
Quinidine effects on the heart
- blocks sodium channel blockers
- slows impulse conduction
- delays repolarization
- blocks vagal input to the heart
Quinidine effects on ECG
- widens the QRS complex
- prolongs QT interval
Quinidine therapeutic uses
- used for supraventricular and ventricular dysrhythmias
Quinidine side effects
- diarrhea, hypersensitivity, carditoxicity
Class IB agents examples
Lidocaine [Xylocaine]
- mexiletine
- phenytoin
Lidocaine [Xylocaine] effects on the heart
- blocks sodium channels (slows conduction)
- reduces automaticity in the ventricles and His-Purkinje system (accelerates repolarization)
Lidocaine [Xylocaine] is used for
ventricular dysrhythmias
Lidocaine [Xylocaine] side/adverse effects
- drowsiness
- confusion
- paresthesia
- toxic doses produce seizures and respiratory arrest
Lidocaine [Xylocaine] administration
IV use only
- rapid hepatic metabolism
Class IC agents
- block cardiaac sodium channels
- delay ventricular repolarization
all class IC agents negative effects
- exacerbate existing dysrhythmias and create new ones
what are the two class IC agents
- Flecainide [Tambocor]
- Propafenone [Rhythmol]
what are the main beta blockers used to treat dysrhythmias
- propranolol [inderal]
- Acebutolol [Sectral]
- Sotalol [Sotacor]
- Bidoprolol [Monocor]
Propranolol [Inderal] effects on the heart
- decreased automacity of the SA node
- decreased velocity of conduction through AV node
- decreased myocardial contracility
Propranolol therapeutic use
- dysrhythmias caused by excessive sympathetic stimulation
- supra ventricular tachydysrhythmias (suppression of excessive discharge, slowing of ventricular rate)
Amiodarone [Cordarone] therapeutic uses
life threatening ventricular dysrhythmias only
Amiodarone [Cordarone] effects on the heart
- reduced automaticity in the SA node; contracilirty; reduced conduction velocity
- QRS widening; prolongation of PR and QT intervals
Amiodarone [Cordarone] toxicity
- protracted half life (25-110 days)
- pulmonary toxicity
- cardiotoxicity
- toxicity in pregnancy and breat feeding
- corneal microdeposits
- optic neuropathy
- liver toxicity
Amiodarone [Cordarone] adverse effects
- photosensitivity
- skin discoloration
- GI upset
- thyroid toxicity
Amiodarone [Cordarone] loading dose
6 weels
Amiodarone [Cordarone] drug interactions
- Quinidine
- Diltiazem
‘- cyclosporine - digoxin
- procainamide
- diltiazem
- phenytoin
- warfarin
- Lovastatin, simvastatin, atorcastatin
Amiodarone levels can be increased by
grapefruit juice and inhibirots of CTP3A4
Amiodarone levels can be reduced by
Cholestyramine
(potassium channel blockers) the risk of severe dysrhythmias is increased by
diuretics
combining amiodarone with a beta blocker, verapamil, or diltiazem can lead to
excessive slowing of the heart
Calcium channel blockers examples
- Verapamil [Isoptin]
- Diltiazem [Cardizem]
calcium channel blockers effects
- reduce Sa modal automaticity
- delay AV nodal conduction
- reduce myocardial contractility
calcium channel blockers therapeutic uses
- slow ventricular rate (atrial fibrillation or atrial flutter)
- terminate SVT caused by an AV nodal reentrant circuit
Adenosine [Adenocard] effects on the heart
- decreases automaticity in the SA node
- slows conduction through AV node
- Prolongs PR interval
Adenosine [Adenocard] therapeutic use
termination of paroxysmal SVT
Adenosine [Adenocard] adverse effects
- sinus bradycardia
- dyspnea
- hypotension
- facial flushing
- chest discomfort
Digoxin is primarily used in
heart failure
Digoxin is used in
- heart failure
- treat supraventricular dysrhythmias
Digoxin [Lanoxin] adverse effects
Cardiotoxicity
- risk increased by hypokalemia
