Antidysrhythmic Drugs Flashcards
class I:
sodium channel blockers
class II:
beta blockers
class III:
potassium channel blockers
class IV:
calcium channel blockers (some are better for high bp, some are better for dysrhythmia
dysrhythmia definition
an abnormality in the rhythm of the heart
two basic types of dysrhythmias
tachydysrhythmia and bradydysrhythmia
tachydysrhythmia
heart rate is increased
bradydysrhythmia
heart rate is slowed
dysrhythmia are also known as
arrhythmias
what is the pacemaker of the heart
sinoatrial node - fires 60-100 per min
impulse conduction
pathways and timing
AV node
fires 40-60 times/min; has pacemaker abilities if SA node fails
His- purkinje system
fires less 4o times/min; so used if SA and AV node both shut down
cardiac action potentials
occur in fibers of the His-Purkinje system and in atrial and ventricular muscle
phases of cardiac action potentials
0 - depolarization; 1 - (partial repolarization; 2 - plateau; 3 - repolarization; 4 - stable potential
always have electrical event followed by a **
mechanical effect
fundamental causes of dysrhythmias
disturbances of automaticity; disturbances of conduction
disturbances of automaticity
SA or AV node will not fire
disturbances of conduction
atriventricular block, reentry (recirculating activation) (not conducting through normal pathway of the heart)
supravantricular dysrhythmias
impulse arises above the ventricle, atrial flutter, atrial fibrillation, sustain supraventricular tachycardia (SVT)
atrial fibrillation
Firing of electrical current in several different places in the atria; clotting prblem with a fib so put pt on anticoagulent; amiodanone diltiazem (cardezan); decreased cardiac output and potential for clots**
supraventricular **
any impulse that arrives above ventazole
supraventricular tachycardia (SVT)
atria doesn’t dump blood down into ventricles (not as much)
ventricular dysrhythmias
sustained ventricular tachycardia; ventricular fibrillation; digoxin-induced ventricular dysrhythmias
ventricular dysrhythmias are
life threatening, won’t have cardiac output so no pulse ready for death, rapid firing in the ventricles
ventricular premature beats
every now and then, too much caffeine or too much stress
no pulse and no blood pressure
call 911 and start CPR 1. defiberate; DOC after 2. CPR 3. epinephrine 4. amiodarone 5. potassium or magnesium
sodium channel blockers treat
atrial and ventricular dysrhythmias; DOC lidocaine
lidociane (xylocaine) effects on the heart and ECG **
blocks cardiac sodium channels - slows conduction in the atria, ventricles and his purkinje system; reduces automaticity in the ventricles and his-purkinje fibers
class II:beta blockers - **
propranolol (Inderal), carvedilol (Coreg)
carvedilol (Coreg)
specifically for rapid heartbeats
class II:beta blockers effects on the heart and ECG **
decreased automaticity of the SA node; decreased velocity of conduction through the AV node; decreased myocardial contractility - negative inotropic effect
class II:beta blockers therapeutic effects
dysrhythmias caused by excessive sympathetic stimulation; SA tachydysrhythmias
SA tachydysrhythmia
suppression of excessive discharge; slowing of the heart rate
class II:beta blockers adverse effects
heart block, heart failure, AV block, sinus arrest, hypotension, bronchospasm (in asthma pts)
other class II:beta blockers
acebutolol (sectral), exmolol (brevibloc)
class III: potassium channel blockers have both **
atrial and ventricular fibrillation
class III: potassium channel blockers
amiodarone
class III: potassium channel blockers therapeutic uses
long term therapy for life threatening ventricular dysrhythmias and converting a fib to normal sinus rhythm; recurrent ventricular fibrillation; recurrent hemodynamically unstable ventricular tachycardia
amiodarone effects on heart
reduces automaticity in the SA node, reduced contractility, reduced conduction velocity, QRS widening, prolongation of the PR and QT intervals
amiodarone adverse effects
- pulmoary toxicity; cardiotoxicty; toxicity in pregnancy and breast feeding; corneal microdeposits; optic neuropathy (last two high doses)
pulmoary toxicity
damage to lung tissue
cardiotoxicity
toxic to heart muscle
potassium channel blockers have lots of
drug interactions: quidine, diogoxin, procainamide, diliazem, phenytoin, warfarin
class IV: calcium channel blockers
verapamil and diltiazem
verapamil and diltiazem
reduces SA nodal automaticity; delays AV nodal conduction; reduces myocardial contractility
class IV: calcium channel blockers therapeutic uses
slows hr (a fib or atrial flutter); terminate SVT cause by an AV nodal reentrant circuit (slowing of HR and decrease in BP)
verapamil and diltiazem adverse effects
bradycardia; hypotension; AV block; heart failure; peripheral edema; constipation
adenosine
decreases automaticity in the SA node; slows conduction through the AV node; prolongation of PR interval
therapeutic uses of adenosine
termination of paroxysmal SVT
paroxysmal
sudden rapid HR
adenosine adverse effects
sinus bradycardia, possible assystole; dyspnea; hypotension; facial flushing
adenosine drug interactions
methylzanthines, dipyridamole
