36.1 The principal action common to all class I antiarrhythmic drugs is:
A. Na+ channel blockade
B. K+ channel opening
C. Depression of impulse conduction
D. Prolongation of effective refractory period
36.2 The antiarrhythmic drug which decreases both rate of
depolarization (phase 0) as well as rate of repolarization
(phase 3) of myocardial fibres is:
A. Lignocaine
B. Propranolol
C. Quinidine
D. Verapamil
36.3 Quinidine has the following action on electrophysiological
properties of the heart except:
A. Decreases automaticity of Purkinje fibres
B. Abolishes after depolarizations
C. Prolongs refractory period of atrial fibres
D. Decreases membrane responsiveness of atrial and ventricular fibres
36.4 The limitations of quinidine in the treatment of cardiac
arrhythmias include the following except:
A. It has narrow spectrum antiarrhythmic activity
B. It is not tolerated by many patients
C. It can precipitate myocardial decompensation
D. It can cause marked hypotension
36.5 The following is not true of quinidine:
A. It blocks myocardial Na+ channels primarily in the open state
B. It has no effect on myocardial K+ channels
C. It produces frequency dependent blockade of myocardial Na+ channels
D. It delays recovery of myocardial Na+ channels
36.6 Quinidine can cause paradoxical tachycardia in a patient of:
A. Sick sinus syndrome
B. Atrial extrasystoles
C. Atrial fibrillation
D. Ventricular extrasystoles
36.7 Quinidine is now used primarily for:
A. Conversion of atrial fibrillation to sinus rhythm
B. Control of ventricular rate in atrial flutter
C. Termination of ventricular tachycardia
D. Prevention of recurrences of atrial fibrillation/ ventricular tachycardia
36.8 The following antiarrhythmic drug has the most prominent anticholinergic action:
A. Disopyramide
B. Quinidine
C. Procainamide
D. Lignocaine
36.9 Procainamide differs from quinidine in the following respect(s):
A. It does not cause paradoxical tachycardia
B. It has no α adrenergic blocking activity
C. It has little antivagal action
D. Both ‘B’ and ‘C’ are correct
36.10 The following is true of procainamide except:
A. It generates an active metabolite in the body
B. Its plasma half-life is longer than that of quinidine
C. On long-term use, it can cause systemic lupus erythematosus like illness
D. It is effective in many cases of ventricular extrasystoles, not responding to lignocaine
36.11 The most significant feature of the antiarrhythmic action of lignocaine is:
A. Suppression of phase-4 depolarization in ventricular ectopic foci
B. Prolongation of action potential duration
C. Prolongation of effective refractory period
D. Depression of membrane responsiveness
36.12 Myocardial Na+ channel blockade by lignocaine has the following characteristic:
A. It blocks inactivated Na+ channels more than activated channels
B. It blocks activated Na+ channels more than inactivated channels
C. It delays rate of recovery of Na+ channels
D. It produces more prominent blockade of atrial than ventricular Na+ channels
36.13 Lignocaine is the preferred antiarrhythmic for emergency control of cardiac arrhythmias following acute myocardial infarction because:
A. It has a rapidly developing and titratable antiarrhythmic action
B. It causes little myocardial depression and hypotension
C. It has broad spectrum antiarrhythmic efficacy in atrial as well as ventricular arrhythmias
D. Both ‘A’ and ‘B’ are correct
36.14 Lignocaine is effective in the following cardiac arrhythmia(s):
A. Atrial fibrillation
B. Paroxysmal supraventricular tachycardia
C. Digitalis induced ventricular extrasystoles
D. All of the above
36.15 The following is an orally active lignocaine congener used for both acute as well as chronic ventricular arrhythmias:
A. Mexiletine
B. Flecainide
C. Moricizine
D. Propafenone
36.16 Select the drug which is used by intravenous infusion for emergency control of tachycardia and sudden rise in blood pressure:
A. Amiodarone
B. Lignocaine
C. Esmolol
D. Disopyramide
36.17 The following is true of propafenone except:
A. It is a weak Na+ channel blocker
B. It markedly delays recovery of myocardial Na+ channels
C. It has additional β-adrenergic blocking property
D. It slows anterograde as well as retrograde conduction in the WPW bypass tract
36.18 Which of the following drugs depresses automaticity of SA node as well as ectopic foci, abbreviates action potential duration of Purkinje fibres, and slows atrioventricular conduction:
A. Propranolol
B. Lignocaine
C. Procainamide
D. Bretylium
36.19 The following antiarrhythmic drug accumulates in the body for a very long time:
A. Procainamide
B. Mexiletine
C. Bretylium
D. Amiodarone
36.20 Choose the antiarrhythmic drug which prolongs action potential, can aggravate atrioventricular block but not heart failure, and has broad spectrum utility in acute as well as chronic, and ventricular as well as supraventricular arrhythmias:
A. Quinidine
B. Amiodarone
C. Mexiletine
D. Diltiazem
36.21 Hypothyroidism is a possible consequence of prolonged therapy with:
A. Amiodarone
B. Mexiletine
C. Sotalol
D. Procainamide
36.22 Choose the correct statement(s) about dofetilide:
A. It is a pure class III antiarrhythmic
B. It has no adrenergic/cholinergic receptor blocking property
C. It selectively depresses the rapid component of delayed rectifier K+ current in myocardial fibres
D. All of the above
36.23 The following drug is preferred for termination as well as prophylaxis of paroxysmal supraventricular tachycardia:
A. Digoxin
B. Verapamil
C. Propranolol
D. Quinidine
36.24 The following drug terminates paroxysmal supraventricular tachycardia rapidly, but cannot be used to prevent its recurrences:
A. Verapamil
B. Adenosine
C. Propranolol
D. Digoxin
36.25 Actions of adenosine include the following except:
A. Depression of A-V node
B. Coronary vasodilatation
C. Bronchodilatation
D. Fall in BP
36.26 Use of adenosine for terminating an episode of paroxysmal supraventricular tachycardia has the following advantages except:
A. It does not produce any side effect
B. It can be given to patients with low blood pressure
C. Its action lasts less than 1 min after bolus intravenous injection
D. It is effective in patients not responding to verapamil
Ans:
36.1 A 36.2 C 36.3 B 36.4 A 36.5 B 36.6 C 36.7 D 36.8 A 36.9 D 36.10 B 36.11 A 36.12 A 36.13 D 36.14 C 36.15 A 36.16 C 36.17 A 36.18 A 36.19 D 36.20 B 36.21 A 36.22 D 36.23 B 36.24 B 36.25 C 36.26
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