Chapter 171 - Antiarrhythmic agents

Question 1

2 reasons for initiating antiarrhythmic therapy

Answer 1

1. alleviate significant clinical signs (weakness, syncope, precipitation of CHF)
2. prolong survival (owner euth for CSx rather than decreased chance of sudden death)

Question 2

Alternate antiarrhythmic classification system to Vaughan-Williams and reason it isn’t used much

Answer 2

Sicilian Gambit, too unwieldy

Question 3

T/F: Procainamide is more effective than lidocaine for acutely terminating ventricular tachyarrhythmia in human patients.

Answer 3

True

Question 4

What are the things that can enhance the lidocaine’s ability to block fast sodium current?

Answer 4

the presence of acidosis, increased extracellular potassium concentrations, partially depolarized cells.

Question 5

What condition can result in decreased lidocaine metabolism and predispose the patient to lidocaine toxicity?

Answer 5

Lidocaine is flow limited drug and its clearance determines its serum concentration. Heart failure,
hypotension, and severe hepatic disease

Question 6

Contraindication of beta blockers?

Answer 6

sinus nodal dysfunction, AV nodal conduction disturbances, pulmonary disease (particularly true for non-selective beta blockers or high dose beta-1 selective blockers), or overt congestive heart failure

Question 7

T/F: esmolol, atenolol, metoprolol, sotalol, and propranolol are non-selective beta agents

Answer 7

beta-1: esmolol, atenolol, metoprolol / non-selective: propranolol, sotalol

Question 8

What is the effect of class 3 antiarrhythmic agents?

Answer 8

block the repolarizing Ik, which results in prolongation of action potential duration and effective refractory period.

Question 9

Which one is known for the least reported proarrhythmic activity of class 3 agents?

Answer 9

amiodarone

Question 10

What is the mechanism of action of sotalol?

Answer 10

non-selective beta blocker (low dose), potassium channel blocker (high dose)

Question 11

How can amiodarone (specifically Cordarone) IV formulation can cause hypotension?

Answer 11

solvents (polysorbate 80 and benzyl alcohol) exhibit negative inotropic and hypotensive effect

Question 12

What is the first line antiarrhythmic treatment for Torsade des pointes

Answer 12

Magnesium

Question 13

Mechanism of action of digoxin

Answer 13

Digoxin’s primary mechanism of action involves inhibition of the sodium potassium adenosine triphosphatase (Na+/K+ ATPase), mainly in the myocardium. This inhibition causes an increase in intracellular sodium levels, resulting in decreased activity of the sodium-calcium exchanger, which normally imports three extracellular sodium ions into the cell and transports one intracellular calcium ion out of the cell. The reversal of this exchanger causes an increase in the intracellular calcium concentration that is available to the contractile proteins. Increased intracellular calcium lengthens phase 4 and phase 0 of the cardiac action potential, which leads to a decrease in heart rate.[24] Increased amounts of Ca2+ also leads to increased storage of calcium in the sarcoplasmic reticulum, causing a corresponding increase in the release of calcium during each action potential. This leads to increased contractility (the force of contraction) of the heart without increasing heart energy expenditure.