Antiarrhythmics

Question 1

What is procaineamide? What is its mechanism? What is unique about it?

Answer 1

Group 1A antiarrhythmic. Blocks I(Na). Used in all arrhythmias and acute MI. Can cause lupus-like toxicity. and hypotension. Adverse effects exacerbated by hyperkalemia.

Question 2

What is amiodarone? What is its mechanism? What is unique about it?

Answer 2

Group 1A/2/3 antiarrhythmic (predominantly 3). Block I(Na) and slow atrial conduction. Has greatest AP-prolonging effect due to I(K) block. Also blocks Ca channels and Beta receptors. Increases effective refractory period. Increase in QT interval.
Causes microcrystal buildupand pulmonary fibrosis.

Question 3

What is lidocaine? What is its mechanism? What is unique about it?

Answer 3

Group 1B antiarrhythmic. Most selective group of AAs (have strong effect in ischemic cells, but little effect in normal myocardium). Reduces AP duration.Useful in acute ischemic ventricular arrhythmia. (No benefit on atrial arrhythmia). Can cause local anesthesia or cardiovascular depression.

Question 4

What is flecainide? What is its mechanism? What is unique about it?

Answer 4

Group 1C antiarrhythmic. No effect on ventricular AP duration or QT interval. Powerful I(Na) blockers. Slow HR and Increase QRS duration. Effective for both atrial and ventricular arrhythmias. Has high PROarrhythmic effect chances and evidence suggests higher mortality when taking it.

Question 5

What are group 1 antiarrhythmics?

Answer 5

Na channel blockers (procainemide, amiodarone, lidocaine and flecainide)

Question 6

What are group 2 antiarrythmics?

Answer 6

Beta blockers

Question 7

What is the mechanism of group 2 antiarrhythmics?

Answer 7

Beta blockers reduce cAMP production, reducing Na and Ca currents. Prolongs PR interval

Question 8

What is sotalol? What is its mechanism? What is unique about it?

Answer 8

Group 3 antiarrhythmic. potassium blocker and beta blocker. Prolongs PR and QT intervals. Useful for ventricular arrhythmia and Afib/Vfib. Can casue torsades de pointes.

Question 9

What are group 3 antiarrhthmics?

Answer 9

Potassium channel blockers (ibutilide,

Question 10

What is ibutilide? What is its mechanism? What is unique about it?

Answer 10

Group 3 antiarrhythmic.

Question 11

What are group 4 antiarrhythmics?

Answer 11

L-type Ca blockers (verapamil, diltiazem). They increase effective refractory period and PR interval.

Question 12

What is Nifedipine’s mechanism for preventing arrhythmia?

Answer 12

Nifedipine has an extrememly short half-life and is incapable of preventing arrhythmias. It can actually promote their occurrence.

Question 13

What is verapamil? What is its mechanism? What is unique about it?

Answer 13

Verapamil is a cardio-selective L-type Ca channel blocker.

Question 14

What is diltiazem? What is its mechanism? What is unique about it?

Answer 14

Diltiazem is an intermiate-selective L-type Ca channel blocker. Have effects on both heart and vasculature.

Question 15

What is adenosine? What is its mechanism? What is unique about it?

Answer 15

AV conduction blocker. Increases potassium current to hyperpolarize cells and decreases Ca channels. Drug of choice for AV nodal arrhythmia. Can cause flushing but very low toxicity.

Question 16

What type of arrhythmia can hypokalemia cause? Hyperkalemia?

Answer 16

Hypokalemia causes increased arrhythmia risks with digitalis.
Hyperkalemia causes increased risk of reentry arrhythmias.

Question 17

What is digoxin? What is its mechanism? What is unique about it?

Answer 17

Inhibits NaK-ATPase. Slows down AV node conduction. Decreases HR. Increases contractility. Increases PR interval and decreases QT interval. Inverts T wave. ST depression. Useful for Afib, Aflutter and CHF.

Question 18

Which group 1 antiarrhythmic class has the longest rate of dissociation? Which one has the least chance of inducing arrhythmia?

Answer 18

Class IC has T > 10 sec. (flecainide). Most effective at reducing HR when it is already low.
Class IB has shortest with T1 sec. (lidocaine). Slows HR no matter what the rate.

Question 19

What is paroxysmal supraventricular tachycardia (PSVT)? How is it diagnosed with a drug?

Answer 19

Re-entry within AV node caues rapid simultaneous activation of ventricle and atria. Narrow complex QRS and no P wave before QRS. Can diagnose with by giving adenosine, which will terminate acute PSVT by blocking AV node. It will revert shortly after though because adenosine has such a short half-life.

Question 20

What is Wolff Parkinson White syndrome?

Answer 20

when there is a direct connection betwen atrium and ventricle called an accessory pathway. Allows impulses from atria to be conducted directly to the ventricle. Short PR interval and delta wave. Treat with adenosine if AV reentry suspected or treat by surgery.

Question 21

What are main toxicities of amiodarone?

Answer 21

The itis’s, the eyes, thyroid, peripheral muscle weakness

Question 22

What is sotalol?

Answer 22

class III antiarrhythmic. Prolonged QT, prolongs AP. Asthma or COPD.

Question 23

What is Ibutelide?

Answer 23

class III AA. Can cause torsades and transient asystole.

Question 24

What drugs can cause transient asystole?

Answer 24

adenosine and ibutelide

Question 25

How does digitalis work? Toxicities?

Answer 25

blocks NaK ATPase to increase intracellular Ca. Increases contractility and refractory period. Can cause eye halos and CNS problems. Amiodarone, verapamil and quinidine all increase digoxin toxicity.

Question 26

How does adenosine work?

Answer 26

blocks AV node. eliminates P waves. Used for PSVT or AV nodal reentry.

Question 27

Which statins are cyp3a4?

Answer 27

lorvastatin and atorvastatin.

Question 28

What drug can you not give with statins?

Answer 28

fibric acid derivatives like gemfibrozil.

Question 29

What drug combo should you give for chronic heart failure to save lives? (Newman question)

Answer 29

ACE inhibitors with spironolactone

Question 30

What are the major toxicities of ezetemide?

Answer 30

liver toxicity. Check AST and ALT