Arrhythmias Quiz PDF

Arrhythmias **Quiz** ======== 1. What is the primary function of gap junctions in the cardiac syncytium? A) To increase the strength of contraction B\) To enable synchronized contraction of cardiac cells C\) To promote vascular smooth muscle contraction D\) To prevent electrical signals fr...

Arrhythmias **Quiz** ======== 1. What is the primary function of gap junctions in the cardiac syncytium? A) To increase the strength of contraction B\) To enable synchronized contraction of cardiac cells C\) To promote vascular smooth muscle contraction D\) To prevent electrical signals from passing between cells E\) To store calcium ions in the cytoplasm 2. In the cardiac myocyte action potential, which ion is primarily responsible for the rapid depolarisation in phase 0? A\) Potassium (K⁺) B\) Sodium (Na⁺) C\) Calcium (Ca²⁺) D\) Chloride (Cl⁻) E\) Magnesium (Mg²⁺) 3. What occurs during phase 2 (plateau) of the cardiac myocyte action potential? A\) Rapid depolarisation B\) Repolarisation via potassium channels C\) Simultaneous entry of calcium and efflux of potassium D\) Influx of sodium ions E\) Resting potential achieved 4. Which of the following is responsible for pacemaker depolarisation in the cardiac nodal action potential? A\) Sodium channels B\) Potassium channels C\) Calcium channels D\) Leak currents of sodium and potassium E\) Chloride channels 5. What is the main characteristic of an ectopic beat? A\) It originates from the sinoatrial (SA) node B\) It is initiated by myocytes outside the normal conduction pathway C\) It occurs during normal sinus rhythm D\) It leads to a regular heartbeat E\) It only occurs in the ventricles 6. Which of the following describes a common cause of tachycardia associated with after-polarisation? A\) High \[Ca²⁺\]i triggers trains of action potentials B\) Increased sodium influx during depolarisation C\) Decreased sympathetic stimulation D\) Inhibition of potassium efflux E\) Suppression of pacemaker activity 7. What is the mechanism of re-entry in arrhythmias? A\) Abnormal conduction due to high calcium concentration B\) A circulating impulse re-excites previously active tissue C\) Early afterdepolarisation due to elevated potassium D\) Spontaneous depolarisation of pacemaker cells E\) Decreased automaticity leading to prolonged refractoriness 8. Which of the following is a feature of Wolfe-Parkinson-White (WPW) syndrome? A\) Shortened PR interval due to retrograde conduction B\) Inability of the atrial cells to depolarise C\) Excessive AV node suppression D\) Ectopic beats originating from the right atrium E\) Long-term treatment with diuretics 9. What is the risk associated with early afterdepolarisation (EAD)? A\) It occurs during phase 0 and leads to prolonged depolarisation B\) It can cause ventricular arrhythmias like Torsades de Pointes C\) It results from low intracellular calcium D\) It is always associated with bradycardia E\) It causes hyperpolarisation of the cells 10. What is the Vaughan-Williams classification of Flecainide? A\) Class 1a B\) Class 1b C\) Class 1c D\) Class 2 E\) Class 3 11. What is a key characteristic of Class 1a antiarrhythmic drugs like Quinidine? A\) They block sodium channels but have minimal effect on potassium channels B\) They increase potassium efflux, promoting repolarisation C\) They have a high risk of torsades de pointes (TdP) D\) They only treat ventricular arrhythmias E\) They are used for atrial fibrillation and heart failure 12. What is the primary action of Class 1b antiarrhythmic drugs like Lidocaine? A\) They block sodium channels and slow conduction B\) They stabilize the action potential without affecting heart rate C\) They increase the refractory period in myocardial cells D\) They rapidly dissociate from sodium channels and are effective at fast heart rates E\) They act as beta-blockers for nodal arrhythmias 13. What is the main mechanism of action for Class 2 antiarrhythmic drugs (beta-blockers)? A\) Inhibition of calcium channels B\) Decrease in sympathetic activity by blocking beta receptors C\) Inhibition of sodium channel activity D\) Blockage of potassium channels E\) Increase in calcium influx into myocytes 14. What is a common adverse effect of beta-blockers used in arrhythmias? A\) Tachycardia B\) Hypotension and dizziness C\) Insomnia and anxiety D\) Hyperkalemia E\) Increased sympathetic output 15. Which Class 3 antiarrhythmic drug has some Class 1a and 2 activity and is used for both acute and chronic arrhythmias? A\) Dronedarone B\) Sotalol C\) Amiodarone D\) Flecainide E\) Procainamide 16. How do Class 3 antiarrhythmic drugs like Amiodarone work? A\) They block sodium channels to slow conduction B\) They prolong the repolarisation phase (phase 3) by blocking potassium channels C\) They inhibit calcium channels and shorten the action potential D\) They reduce sympathetic stimulation to the heart E\) They suppress automaticity by increasing sodium efflux 17. What is the risk associated with the use of Class 4 calcium channel blockers like Verapamil in arrhythmia management? A\) Increased heart rate B\) Severe bradycardia and heart block in patients with ventricular tachycardia C\) Inhibition of sodium influx D\) Prolonged depolarisation in myocytes E\) Increased contraction strength in myocardial cells 18. What is the main effect of digoxin on cardiac myocytes? A\) It inhibits the Na+/K+ ATPase pump, leading to positive inotropy B\) It increases sodium efflux from the cells C\) It blocks calcium channels to prevent arrhythmias D\) It reduces parasympathetic tone, enhancing heart rate E\) It inhibits beta receptors to reduce heart rate 19. In what scenario is adenosine most commonly used? A\) As a chronic antiarrhythmic for atrial fibrillation B\) For ventricular tachycardia management C\) As a first-line treatment for supraventricular tachycardia D\) To treat bradycardia in emergencies E\) For rate control in atrial flutter 20. Which drug is used as the first-line treatment for bradycardia? A\) Atropine B\) Dopamine C\) Amiodarone D\) Digoxin E\) Verapamil 21. What is the effect of atropine in the treatment of bradycardia? A\) It stimulates the vagus nerve B\) It blocks muscarinic receptors, reducing parasympathetic activity C\) It acts as a calcium channel blocker D\) It increases sodium influx into nodal cells E\) It inhibits beta receptors 22. What is the main therapeutic use of calcium channel blockers like Diltiazem? A\) For managing ventricular arrhythmias only B\) To control heart rate in atrial fibrillation and atrial flutter C\) To increase heart rate in cases of bradycardia D\) For treating bradyarrhythmias due to their positive inotropic effect E\) To decrease the risk of myocardial infarction in hypertensive patients 23. Which is a characteristic of atrial fibrillation treatment with rate control? A\) It restores the sinus rhythm B\) It uses antiarrhythmic drugs like amiodarone and digoxin C\) It involves drugs that slow the conduction through the AV node D\) It is ineffective for maintaining sinus rhythm long-term E\) It uses shock therapy as a first-line treatment 24. What is the primary purpose of rhythm control in atrial fibrillation? A\) To reduce the heart rate to normal levels B\) To prevent thrombus formation C\) To restore the heart\'s normal sinus rhythm D\) To reduce the frequency of ectopic beats E\) To control the symptoms of heart failure 25. Which drug is commonly used in both rate and rhythm control for atrial fibrillation? A\) Amiodarone B\) Quinidine C\) Verapamil D\) Lidocaine E\) Metoprolol **Answer guide** ---------------- **Q1: What is the primary function of gap junctions in the cardiac syncytium?** **Answer: B) To enable synchronized contraction of cardiac cells** **Explanation:** Gap junctions allow electrical signals to pass directly between cardiac cells, enabling synchronized contraction, which is crucial for effective heart function. **Q2: In the cardiac myocyte action potential, which ion is primarily responsible for the rapid depolarisation in phase 0?** **Answer: B) Sodium (Na⁺)** **Explanation:** Phase 0 of the cardiac action potential involves the rapid influx of Na⁺ ions through voltage-gated sodium channels, which causes the depolarization of the membrane. **Q3: What occurs during phase 2 (plateau) of the cardiac myocyte action potential?** **Answer: C) Simultaneous entry of calcium and efflux of potassium** **Explanation:** During phase 2 (plateau), there is a balance between calcium (Ca²⁺) influx and potassium (K⁺) efflux, which sustains the depolarization and contributes to the plateau phase of the action potential. **Q4: Which of the following is responsible for pacemaker depolarisation in the cardiac nodal action potential?** **Answer: D) Leak currents of sodium and potassium** **Explanation:** Pacemaker cells in the sinoatrial (SA) and atrioventricular (AV) nodes experience a slow depolarization due to the leak of sodium (Na⁺) and potassium (K⁺) ions, which eventually reaches the threshold to trigger an action potential. **Q5: What is the main characteristic of an ectopic beat?** **Answer: B) It is initiated by myocytes outside the normal conduction pathway** **Explanation:** Ectopic beats occur when an action potential originates outside the normal pacemaker sites (e.g., the SA node), often causing irregular heartbeats. **Q6: Which of the following describes a common cause of tachycardia associated with after-polarisation?** **Answer: A) High \[Ca²⁺\]i triggers trains of action potentials** **Explanation:** After-polarization, particularly delayed afterdepolarizations, can be triggered by high intracellular calcium (Ca²⁺) levels, leading to the initiation of additional action potentials, which can cause tachycardia. **Q7: What is the mechanism of re-entry in arrhythmias?** **Answer: B) A circulating impulse re-excites previously active tissue** **Explanation:** Re-entry arrhythmias occur when an action potential loops back and re-excites previously depolarized tissue, leading to continued abnormal electrical activity and arrhythmias. **Q8: Which of the following is a feature of Wolfe-Parkinson-White (WPW) syndrome?** **Answer: A) Shortened PR interval due to retrograde conduction** **Explanation:** WPW syndrome involves an accessory pathway that allows for rapid conduction of electrical impulses, resulting in a shortened PR interval and potential for re-entry arrhythmias. **Q9: What is the risk associated with early afterdepolarisation (EAD)?** **Answer: B) It can cause ventricular arrhythmias like Torsades de Pointes** **Explanation:** Early afterdepolarizations (EADs) are associated with prolonged repolarization and can lead to abnormal action potentials that trigger dangerous arrhythmias such as Torsades de Pointes. **Q10: What is the Vaughan-Williams classification of Flecainide?** **Answer: C) Class 1c** **Explanation:** Flecainide is classified as a Class 1c antiarrhythmic, which blocks sodium channels and is used for treating atrial arrhythmias. **Q11: What is a key characteristic of Class 1a antiarrhythmic drugs like Quinidine?** **Answer: C) They have a high risk of torsades de pointes (TdP)** **Explanation:** Class 1a antiarrhythmic drugs, such as Quinidine, prolong the action potential and have a risk of causing torsades de pointes, a type of arrhythmia. **Q12: What is the primary action of Class 1b antiarrhythmic drugs like Lidocaine?** **Answer: D) They rapidly dissociate from sodium channels and are effective at fast heart rates** **Explanation:** Class 1b drugs like Lidocaine block sodium channels, but they dissociate rapidly, making them particularly effective at controlling arrhythmias at fast heart rates. **Q13: What is the main mechanism of action for Class 2 antiarrhythmic drugs (beta-blockers)?** **Answer: B) Decrease in sympathetic activity by blocking beta receptors** **Explanation:** Class 2 drugs (beta-blockers) block beta-adrenergic receptors, reducing sympathetic stimulation, which slows the heart rate and reduces arrhythmia. **Q14: What is a common adverse effect of beta-blockers used in arrhythmias?** **Answer: B) Hypotension and dizziness** **Explanation:** Beta-blockers can lower blood pressure by reducing heart rate and myocardial contractility, leading to side effects such as hypotension and dizziness. **Q15: Which Class 3 antiarrhythmic drug has some Class 1a and 2 activity and is used for both acute and chronic arrhythmias?** **Answer: C) Amiodarone** **Explanation:** Amiodarone is a Class 3 antiarrhythmic drug with some Class 1a and Class 2 effects, and it is used for both acute and chronic arrhythmias due to its broad spectrum of action. **Q16: How do Class 3 antiarrhythmic drugs like Amiodarone work?** **Answer: B) They prolong the repolarisation phase (phase 3) by blocking potassium channels** **Explanation:** Class 3 antiarrhythmic drugs like Amiodarone block potassium channels, prolonging the repolarization phase and thus preventing arrhythmias. **Q17: What is the risk associated with the use of Class 4 calcium channel blockers like Verapamil in arrhythmia management?** **Answer: B) Severe bradycardia and heart block in patients with ventricular tachycardia** **Explanation:** Class 4 drugs like Verapamil block calcium channels, which can slow down the heart rate significantly. In patients with ventricular tachycardia, this can lead to severe bradycardia or heart block. **Q18: What is the main effect of digoxin on cardiac myocytes?** **Answer: A) It inhibits the Na+/K+ ATPase pump, leading to positive inotropy** **Explanation:** Digoxin inhibits the Na+/K+ ATPase pump, leading to an increase in intracellular calcium and improved myocardial contractility (positive inotropic effect). **Q19: In what scenario is adenosine most commonly used?** **Answer: C) As a first-line treatment for supraventricular tachycardia** **Explanation:** Adenosine is used as a first-line treatment for supraventricular tachycardia, as it slows conduction through the AV node and can terminate reentrant arrhythmias. **Q20: Which drug is used as the first-line treatment for bradycardia?** **Answer: A) Atropine** **Explanation:** Atropine is the first-line treatment for acute bradycardia, as it blocks parasympathetic effects and increases heart rate by inhibiting muscarinic receptors. **Q21: What is the effect of atropine in the treatment of bradycardia?** **Answer: B) It blocks muscarinic receptors, reducing parasympathetic activity** **Explanation:** Atropine blocks muscarinic receptors, reducing parasympathetic influence on the heart, which increases heart rate in cases of bradycardia. **Q22: What is the main therapeutic use of calcium channel blockers like Diltiazem?** **Answer: B) To control heart rate in atrial fibrillation and atrial flutter** **Explanation:** Calcium channel blockers like Diltiazem are used to control the heart rate in atrial fibrillation and atrial flutter by slowing conduction through the AV node. **Q23: Which is a characteristic of atrial fibrillation treatment with rate control?** **Answer: C) It involves drugs that slow the conduction through the AV node** **Explanation:** Rate control in atrial fibrillation involves drugs like beta-blockers or calcium channel blockers, which slow AV node conduction and reduce the ventricular rate. **Q24: What is the primary purpose of rhythm control in atrial fibrillation?** **Answer: C) To restore the heart\'s normal sinus rhythm** **Explanation:** Rhythm control aims to restore normal sinus rhythm in atrial fibrillation, often through pharmacologic or electrical cardioversion. **Q25: Which drug is commonly used in both rate and rhythm control for atrial fibrillation?** **Answer: A) Amiodarone** **Explanation:** Amiodarone is commonly used for both rate and rhythm control in atrial fibrillation due to its broad spectrum of antiarrhythmic effects.