Antiarrhythmics

Question 1

How is WPW treated?

Answer 1

acutely with a 1B antiarrhythmic agent (particularly, lidocaine); can also treat long-term with a 1A or 1C agent (es

Question 2

What are the 4 Vaughan-Williams Classes of antiarrhythmics?

Answer 2

1. Na+ channel blockers (1A, 1B, 1C)
2. Beta-blockers
3. K+ channel blockers
4. Ca2+ channel blockers

Question 3

Why is prolonged QT so dangerous?

Answer 3

It may lead to Torsades de pointe or VF.

Question 4

Na+ channel blockers affect which type of Na+ channels?

Answer 4

open or inactivated Na+ channels (NOT resting state ones)

Question 5

Which class of Na+ channel blockers causes a shorter QT?

Answer 5

1B

Question 6

Which of the Na+ channel blockers causes a prolonged QT?

Answer 6

1A

Question 7

What are the main class 1A Na+ channel blockers?

Answer 7

procainamide, quinidine

Question 8

What are the main class 1B Na+ channel blockers?

Answer 8

lidocaine

Question 9

What are the main class 1C Na+ channel blockers?

Answer 9

flecainide, propafenone

Question 10

Which of the Na+ channel blockers also has a class III (K+ blocking) effect?

Answer 10

1A (thus, prolonged APD and ERP)

Question 11

Unique adverse effect associated with procainamide?

Answer 11

lupus-like syndrome (not permanent)

Question 12

Unique adverse effect associated with quinidine?

Answer 12

tinnitus, seizure, thrombocytopenia

Question 13

What is the exclusive clinical indication for class 1B Na+ channel blockers?

Answer 13

VT during ischemia

Question 14

Which Na+ channel blocker has the weakest vs. strongest blockade effect?

Answer 14

1B < 1A < 1C

Question 15

What is the clinical indication for class 1A antiarrhythmics?

Answer 15

AFib/flutter, VT (everything…SVT and VT)

Question 16

What are the overall adverse effects of 1A antiarrhythmics?

Answer 16

prolonged QT leading to Torsades; anticholinergic effect

Question 17

How do class 1B antiarrhythmics act as local anesthetics?

Answer 17

They block Na+ channel propagation by binding depolarized Na+, thereby inhibiting the pain signal to the brain.

Question 18

Which antiarrhythmic can be used to treat digoxin arrhythmia?

Answer 18

Class 1B agents

Question 19

What are the main clinical indications for the class 1C agents?

Answer 19

refractory VT, WPW, SVT

Question 20

What is the main side effect associated with class 1C agents?

Answer 20

arrhythmias (due to delayed conduction speed)

Question 21

How do the beta blockers work?

Answer 21

They prevent epi and norepi from binding to their receptors (less cAMP=less Ca2+). They affect the NODAL action potential.

Question 22

What are the main adverse effects associated with beta blockers?

Answer 22

loss of energy (including libido) and bronchospasm (can affect beta-2 receptors as well)

Question 23

What is the physiologic effect of beta blockers?

Answer 23

They slow HR and decrease contractility. This ultimately decreases myocardial oxygen consumption.

Question 24

How is AFib treated in terms of rhythm and rate?

Answer 24

• rhythm: class 1C antiarrhythmics

- rate: beta-blockers

Question 25

What is the main side effect associated with K+ channel blockers?

Answer 25

prolonged QT and Torsades risk (EXCEPT for amiodarone)

Question 26

Which drugs belong to the K+ channel blockers?

Answer 26

amiodarone, bretylium, sotalol, ibutilide

Question 27

Which are the main 2 classes of antiarrhythmics that we worry about in terms of prolonged QT?

Answer 27

class 1A and class III

Question 28

True or false: diltiazem in combination with metoprolol is an effective treatment for AFib.

Answer 28

FALSE! Giving a calcium channel blocker AND a beta-blocker can cause cardiac collapse because both affect the nodal action potential.

Question 29

Which drugs belong to the Ca2+ channel blockers?

Answer 29

verapamil and diltiazem (cardizem)

Question 30

What are the side effects associated with Ca2+ channel blockers?

Answer 30

hypotension and flushing

Question 31

What are the adverse effects associated with amiodarone?

Answer 31

Amiodarone is RIDDLED with side effects! - Toxic to lungs (pulmonary toxicity leading to fibrosis) - Toxic to liver (hypersensitive hepatitis) - Toxic to thyroid (source of inorganic iodine leading to hypo/hyperthyroidism) - Skin changes (blue/grey deposits) - Corneal deposits - Initially acts as a beta-blocker, potentially causing bradycardia, hypotension, and heart block

Question 32

What is the drug of choice for Torsades?

Answer 32

magnesium (relatively new treatment)

Question 33

What is the treatment of choice for Torsades?

Answer 33

cardioversion

Question 34

What are the main adverse effects of Digoxin?

Answer 34

- GI (N/V/D + pain) - Hyperkalemia - Visual disturbances (yellow halos)

Question 35

What is Digoxin mainly used for clinically?

Answer 35

AFib and heart failure

Question 36

Describe the MOA of Digoxin.

Answer 36

It inhibits the Na+/K+ pump, leading to an increased driving force for Ca2+ into the cell (Na+ gets retained in the cell due to Na+/K+ pump blockade, and it is exchanged for Ca2+). Increased Ca2+ leads to increased inotropy. Digoxin also has parasympathetic effects, particularly on the SA and AV nodes, thus slowing conduction and decreasing HR.

Question 37

What is the difference between stable and unstable ventricular tachycardia?

Answer 37

- Stable: BP is okay | - Unstable: BP is too low; need to cardiovert, then administer lidocaine and amiodarone

Question 38

What does amiodarone do?

Answer 38

It slows conduction through the AV node to treat SVT. However, it can cause transient heart block at the AV node. It is better to try a vagal maneuver first.

Question 39

Torsades is considered to be which type of arrhythmia?

Answer 39

V-tach

Question 40

What is an unintended adverse event associated with AFib cardioversion?

Answer 40

stroke due to dislodgment of clot in LA

Question 41

What do Ca2+ channel blockers treat?

Answer 41

SVT and AFib (atrial side stuff)

Question 42

Which classes of antiarrhythmics affect rate vs. rhythm?

Answer 42

- rate: class II (beta-blockers) and IV (Ca2+ channel blockers) - rhythm: class I (Na+ channel blockers) and III (K+ blockers)

Question 43

What is the main physiological effect of Ca2+ channel blockers?

Answer 43

They decrease intracellular Ca2+ concentration, thereby decreasing inotropy and BP. They also decrease HR and therefore cardiac oxygen consumption.