Antiarrhythmics Flashcards
What 4 ways can you change the rate of pacemaker cells?
1) maximum diastolic potential
2) slope of phase 4 depolarization
3) threshold potential
4) duration of action potential
What are the two goals of antiarrhythmics?
1) Reduce ectopic pacemaker activity
2) Modify conduction or refractoriness to disable reentry
What are the 4 mechanisms to treat arrhythmias?
1) Sodium channel blockade
2) Blockade of sympathetic effects
3) Prolongation of the effective refractory period
4) Calcium channel blockade (slows repolarization)
What is the major mechanism of disturbance of impulse conduction?
reentry mechanism
What are class 1 antiarrhythmics?
Sodium channel blockers
What are the mechanisms of class 1a drugs? What drugs are they?
blocks open or activated Na+ channels to lengthen the duration of the action potential (increase ERP); quinidine, procainamide
What is the MOA of class 1c drugs? What drugs are they?
binds to all sodium channels, no effect on the duration of action potential (no change in ERP); flecainide
What is the MOA of class 1b drugs? What drugs are they?
blocks inactivated sodium channels to shorten the duration of the AP (decrease ERP); lidocaine
What drugs are in class II? What is their main property?
Beta blockers, reduce adrenergic activity on the heart
What drugs are in class III? What is their main property?
K+ channel blockers to increase ERP; amiodorone and sotalol
What drugs are in class IV? What is their main property?
CCBs to decrease HR and contractility; verapamil and diltiazem
What are the drugs in the misc category of antiarrhythmics? What is their route of administration?
adenosine, magnesium, potassium, digoxin; all IV only
What drug is used for acute and chronic treatment of SVT and ventricular arrhythmias?
Quinidine (cardioquin)
What 3 actions does quinidine have?
decreases automaticity, decreases membrane response, increases diastolic threshold (the threshold needed to reach relaxation phase)
What does the muscarinic receptor blockade of quinidine cause?
increased HR and AV node conduction
What are some adverse effects of quinidine?
Low therapeutic index, cardiac toxicity, SA/AV block, ventricular arrhythmia and severe hypotension at toxic doses
WIDENING OF QRS AND QT INTERVAL, causes QUINIDINE SYNCOPE, TORSADE DE POINTES
DIARRHEA
CINCHONISM
What other drug, when give with quinidine, increases chance for quinidine syncope?
digitalis
What is a benefit to procainamide over quinidine use?
Less prominent antimuscarinic effects, potential to cause LUPUS, other adverse effects similar to quinidine
What is the MOA for lidocaine?
rapidly blocks inactivated Na+ channels, shortens APD
What is the DOC for ventricular arrhythmias? How is it administered?
lidocaine; IV
What are two common adverse effects of lidocaine?
High contractility, CONVULSIONS
What is the last ditch effort drug binds to all sodium channels?
Flecainide
What is the non-specific BBlocker for arrhythmias?
Propranolol
What is the B1-blocker with a normal half-life for arrhythmias?
acebutolol
What is the B1-blocker with a short half-life? What is it used for?
Esmolol; Chronic treatment of PVST
What is the MOA of amiodarone?
Blocks K+ channels (hence class III), binds to inactivated Na+ channels, and binds to some calcium channels, thereby INCREASING APD SIGNIFICANTLY!
What is the overall effect of amiodarone?
Slows sinus rate, conduction, and prolongs QT and QRS (like a beta blocker). It has a much longer APD and MUCH LONGER ERP, which makes it the jack of all antiarrhymics.
What drug has a half-life of 13-103 days and an extra long loading period?
Amiodarone
What fact about amiodorone makes it the DOC for ventricular arrhythmias for ACLS? What else is it effective against?
It does not cause torsade de points; supraventricular and ventricular arrhythmias; oral
What are two major side effects of amiodarone, one of which is cause for removal?
Pulmonary fibrosis in 5-15%, thyroid dysfunction
Which drug is a non-selective BB that is a class III antiarrhymic? What is it used for? What is one potential adverse side effect?
Sotalol; same indications as amiodarone; Torsade de pointes
What drug blocks slow L-type cardiac Ca2+ channels, has indication for atrial and supraventricular tachycardias due to marked effect on the SA and AV nodes? What drugs should you not combine it with?
Verapamil (cardio specific); beta blockers
What drug inhibits calcium influx in both myocardial and vascular smooth muscle cells, causing vasodilation?
Diltiazem
What are some indications for diltiazem use?
to decrease heart rate, PSVT and to control ventricular rate in a fib
What is the order of drug usage for PSVT?
Acute: Adenosine (IV) then Esmolol then Diltiazem (IV)
Which drug enhances K+ conductance and inhibits cAMP-induced calcium influx?
Adenosine (hyperpolarizes everything and “resets” the heart, so it literally stops the heart for a matter of seconds)
What is adenosine used to treat?
PSVT and WPW, has a very short half life
What is the DOC for torsade de pointes?
Magnesium
What is useful for the management of seizures and/or hypertension in eclampsia?
Magnesium
What is useful for treating digitalis induced arrhymias?
Magnesium
What is the MOA of potassium?
increased serum K+ can both depolarize and hyperpolarize the membrane, but it has the tendency to hyperpolarize so it decreases the APD, conduction, pacemaker rate, and pacemaker arrhythmogenesis
