Antiarrhythmics

Question 1

What 4 ways can you change the rate of pacemaker cells?

Answer 1

1) maximum diastolic potential
2) slope of phase 4 depolarization
3) threshold potential
4) duration of action potential

Question 2

What are the two goals of antiarrhythmics?

Answer 2

1) Reduce ectopic pacemaker activity

2) Modify conduction or refractoriness to disable reentry

Question 3

What are the 4 mechanisms to treat arrhythmias?

Answer 3

1) Sodium channel blockade
2) Blockade of sympathetic effects
3) Prolongation of the effective refractory period
4) Calcium channel blockade (slows repolarization)

Question 4

What is the major mechanism of disturbance of impulse conduction?

Answer 4

reentry mechanism

Question 5

What are class 1 antiarrhythmics?

Answer 5

Sodium channel blockers

Question 6

What are the mechanisms of class 1a drugs? What drugs are they?

Answer 6

blocks open or activated Na+ channels to lengthen the duration of the action potential (increase ERP); quinidine, procainamide

Question 7

What is the MOA of class 1c drugs? What drugs are they?

Answer 7

binds to all sodium channels, no effect on the duration of action potential (no change in ERP); flecainide

Question 8

What is the MOA of class 1b drugs? What drugs are they?

Answer 8

blocks inactivated sodium channels to shorten the duration of the AP (decrease ERP); lidocaine

Question 9

What drugs are in class II? What is their main property?

Answer 9

Beta blockers, reduce adrenergic activity on the heart

Question 10

What drugs are in class III? What is their main property?

Answer 10

K+ channel blockers to increase ERP; amiodorone and sotalol

Question 11

What drugs are in class IV? What is their main property?

Answer 11

CCBs to decrease HR and contractility; verapamil and diltiazem

Question 12

What are the drugs in the misc category of antiarrhythmics? What is their route of administration?

Answer 12

adenosine, magnesium, potassium, digoxin; all IV only

Question 13

What drug is used for acute and chronic treatment of SVT and ventricular arrhythmias?

Answer 13

Quinidine (cardioquin)

Question 14

What 3 actions does quinidine have?

Answer 14

decreases automaticity, decreases membrane response, increases diastolic threshold (the threshold needed to reach relaxation phase)

Question 15

What does the muscarinic receptor blockade of quinidine cause?

Answer 15

increased HR and AV node conduction

Question 16

What are some adverse effects of quinidine?

Answer 16

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

Question 17

What other drug, when give with quinidine, increases chance for quinidine syncope?

Answer 17

digitalis

Question 18

What is a benefit to procainamide over quinidine use?

Answer 18

Less prominent antimuscarinic effects, potential to cause LUPUS, other adverse effects similar to quinidine

Question 19

What is the MOA for lidocaine?

Answer 19

rapidly blocks inactivated Na+ channels, shortens APD

Question 20

What is the DOC for ventricular arrhythmias? How is it administered?

Answer 20

lidocaine; IV

Question 21

What are two common adverse effects of lidocaine?

Answer 21

High contractility, CONVULSIONS

Question 22

What is the last ditch effort drug binds to all sodium channels?

Answer 22

Flecainide

Question 23

What is the non-specific BBlocker for arrhythmias?

Answer 23

Propranolol

Question 24

What is the B1-blocker with a normal half-life for arrhythmias?

Answer 24

acebutolol

Question 25

What is the B1-blocker with a short half-life? What is it used for?

Answer 25

Esmolol; Chronic treatment of PVST

Question 26

What is the MOA of amiodarone?

Answer 26

Blocks K+ channels (hence class III), binds to inactivated Na+ channels, and binds to some calcium channels, thereby INCREASING APD SIGNIFICANTLY!

Question 27

What is the overall effect of amiodarone?

Answer 27

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.

Question 28

What drug has a half-life of 13-103 days and an extra long loading period?

Answer 28

Amiodarone

Question 29

What fact about amiodorone makes it the DOC for ventricular arrhythmias for ACLS? What else is it effective against?

Answer 29

It does not cause torsade de points; supraventricular and ventricular arrhythmias; oral

Question 30

What are two major side effects of amiodarone, one of which is cause for removal?

Answer 30

Pulmonary fibrosis in 5-15%, thyroid dysfunction

Question 31

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?

Answer 31

Sotalol; same indications as amiodarone; Torsade de pointes

Question 32

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?

Answer 32

Verapamil (cardio specific); beta blockers

Question 33

What drug inhibits calcium influx in both myocardial and vascular smooth muscle cells, causing vasodilation?

Answer 33

Diltiazem

Question 34

What are some indications for diltiazem use?

Answer 34

to decrease heart rate, PSVT and to control ventricular rate in a fib

Question 35

What is the order of drug usage for PSVT?

Answer 35

Acute: Adenosine (IV) then Esmolol then Diltiazem (IV)

Question 36

Which drug enhances K+ conductance and inhibits cAMP-induced calcium influx?

Answer 36

Adenosine (hyperpolarizes everything and "resets" the heart, so it literally stops the heart for a matter of seconds)

Question 37

What is adenosine used to treat?

Answer 37

PSVT and WPW, has a very short half life

Question 38

What is the DOC for torsade de pointes?

Answer 38

Magnesium

Question 39

What is useful for the management of seizures and/or hypertension in eclampsia?

Answer 39

Magnesium

Question 40

What is useful for treating digitalis induced arrhymias?

Answer 40

Magnesium

Question 41

What is the MOA of potassium?

Answer 41

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