1DOC for brady arrhythmia
Atropine
2What is the difference between Slow conducting and fast conducting fibres
Slow conducting fibres lack Na channels whereas Fast conducting fibres have Na channels
3DOC for acute PSVT
Adenosine —>Open K+ channels
4DOC for Chronic SVT
Beta blockers
5DOC for SVT and asthma
CCB Non DHP type Verapamil and diltiazem
6DOC for SVT + Heart failure
Digoxin—>Opens K+ Channels
7Location of slow conducting and fast conducting fibres
Slow conducting fibres -SA and AV node
Fast conducting fibres - Atria muscle and ventricle muscle
8Which drugs are contraindicated in heart failure
Beta blockers and calcium channel blockers
9What is the classification of William Vaughan Singh classification
Class 1 —Sodium channel blockers
Class 2 —Beta blockers
Class 3 — Potassium channel blockers
Class 4 — Calcium channel blockers
Class 5 — ADAM
10What is the mechanism of Class I antiarrhythmics?
They block fast sodium (Na⁺) channels, decreasing phase 0 depolarization and slowing conduction velocity.
11What are the subclasses of Class I antiarrhythmics?
Class IA, IB, and IC, differing by their effect on action potential (AP) duration.
12How do Class IA antiarrhythmics affect the action potential?
They moderately block Na⁺ channels and also block K⁺ channels, increasing AP duration and effective refractory period.
13Give examples of Class IA antiarrhythmics.
Quinidine, Procainamide, and Disopyramide.
14What are the major side effects of Quinidine?
Cinchonism (tinnitus, headache, dizziness) and QT prolongation leading to torsades de pointes.
15What unique adverse effect is associated with Procainamide?
Drug-induced lupus erythematosus.
16How do Class IB antiarrhythmics act?
They mildly block Na⁺ channels, decreasing AP duration, especially in ischemic or depolarized ventricular tissue.
17Give examples of Class IB antiarrhythmics.
Lidocaine, Mexiletine, and Phenytoin.
18What is the clinical use of Lidocaine?
Treatment of acute ventricular arrhythmias, especially post-myocardial infarction.
19What are the main side effects of Lidocaine?
Central nervous system toxicity such as confusion, tremor, and seizures.
20How do Class IC antiarrhythmics act?
They strongly block Na⁺ channels, markedly slowing conduction without changing AP duration.
21Give examples of Class IC antiarrhythmics.
Flecainide and Propafenone.
22Why are Class IC antiarrhythmics contraindicated post-MI?
They are pro-arrhythmic and increase mortality after myocardial infarction.
23What is the mechanism of Class II antiarrhythmics?
They block β-adrenergic receptors, decreasing cAMP and calcium influx, reducing phase 4 depolarization in the SA and AV nodes.
24Give examples of Class II antiarrhythmics.
Metoprolol, Esmolol, Propranolol, and Atenolol.
25What is the ECG effect of beta-blockers?
Prolonged PR interval due to slowed AV conduction.
26What are the common side effects of beta-blockers?
Bradycardia, AV block, bronchospasm, and masking of hypoglycemia symptoms.
27What is the mechanism of Class III antiarrhythmics?
They block potassium (K⁺) channels, prolonging repolarization, action potential duration, and refractory period.
28Give examples of Class III antiarrhythmics.
Amiodarone, Sotalol, Ibutilide, and Dofetilide.
29What are the side effects of Amiodarone?
Pulmonary fibrosis, hepatotoxicity, thyroid dysfunction, corneal deposits, and blue-gray skin discoloration.
30Which Class III drug has multiple class actions (I, II, III, IV)?
Amiodarone.
31What is the mechanism of Class IV antiarrhythmics?
They block L-type calcium (Ca²⁺) channels, reducing conduction velocity and increasing AV nodal refractory period.
32Give examples of Class IV antiarrhythmics.
Verapamil and Diltiazem.
33What are the clinical uses of Class IV drugs?
Supraventricular tachycardias (SVT) and rate control in atrial fibrillation.
34What are the side effects of calcium channel blockers?
Constipation, flushing, edema, AV block, and bradycardia.
35What is the mechanism of Adenosine?
It increases K⁺ efflux, hyperpolarizing the AV node and causing transient AV block.
36What is the clinical use of Adenosine?
Termination and diagnosis of supraventricular tachycardia (SVT).
37What are the main side effects of Adenosine?
Flushing, chest pain, and bronchospasm.
38What is the antiarrhythmic mechanism of Digoxin?
It increases vagal tone, slowing AV nodal conduction.
39Which are the cardioselective beta blockers
Metoprolol atenolol esmolol
40Side effect of di isopyramide
Dry eyes,Mouth
Constipation
Urinary retention
41Non selective beta blockers
Propanolol Timolol Nadolol
42Anti dote for beta blocker toxicity
Glucagon hormone
43Anti dote for CCB toxicity
Calcium gluconate
44Anti dote for lignocine and amiodarone toxicity
20%Intralipid injection
45DOC for torsades de pointes
MgSO4
46DOC for ventricular tachy arrhythmia
Amiodarone
47DOC for long QT syndrome
Beta blockers
48Class 3 Anti arrhythmics are used in cases of
Flutter and fibrillation —potassium channel blockers —>Increases Action potential duration—>Imcreases QT prolongation on ECG
Side effect :Torsades de pointes