MCQ Quiz: Pathophysiology of Arrhythmias

Cardiac arrhythmias, defined as disturbances in the normal rhythm of the heart, arise from abnormalities in electrical impulse generation, conduction, or both. These rhythm disorders can range from benign palpitations to life-threatening emergencies, significantly impacting cardiovascular health and patient outcomes. For PharmD students, a strong grasp of the underlying pathophysiological mechanisms of arrhythmias—including alterations in ion channel function, abnormal pacemaker activity, and reentrant circuits—is crucial for understanding their clinical manifestations, ECG interpretations, and the pharmacological basis of antiarrhythmic drug therapy. This MCQ quiz will test your knowledge on the fundamental pathophysiology of cardiac arrhythmias.

1. The normal pacemaker of the heart, responsible for initiating the cardiac electrical impulse, is the:

• A. Atrioventricular (AV) node
• B. Sinoatrial (SA) node
• C. Purkinje fibers
• D. Bundle of His

Answer: B. Sinoatrial (SA) node

2. Phase 0 of the fast-response action potential in atrial and ventricular myocytes is primarily due to the rapid influx of which ion?

• A. Potassium (K+)
• B. Sodium (Na+)
• C. Calcium (Ca2+)
• D. Chloride (Cl-)

Answer: B. Sodium (Na+)

3. The slow-response action potential, characteristic of SA and AV nodal cells, has a Phase 0 depolarization that is primarily mediated by the influx of:

• A. Sodium (Na+) through fast channels
• B. Calcium (Ca2+) through L-type calcium channels
• C. Potassium (K+)
• D. Chloride (Cl-)

Answer: B. Calcium (Ca2+) through L-type calcium channels

4. “Enhanced normal automaticity” as a mechanism of arrhythmia refers to:

• A. Ectopic pacemaker activity in non-pacemaker cells.
• B. The SA node or other normal pacemaker sites firing at an accelerated rate due to influences like sympathetic stimulation or hypokalemia.
• C. Conduction block within the AV node.
• D. Early afterdepolarizations.

Answer: B. The SA node or other normal pacemaker sites firing at an accelerated rate due to influences like sympathetic stimulation or hypokalemia.

5. “Abnormal automaticity” occurs when:

• A. The SA node fires too slowly.
• B. Non-pacemaker cells (e.g., atrial or ventricular myocytes) spontaneously depolarize and initiate impulses, often under pathological conditions like ischemia.
• C. There is a delay in AV nodal conduction.
• D. The QT interval is prolonged.

Answer: B. Non-pacemaker cells (e.g., atrial or ventricular myocytes) spontaneously depolarize and initiate impulses, often under pathological conditions like ischemia.

6. Early Afterdepolarizations (EADs) are abnormal depolarizations that occur during which phase(s) of the cardiac action potential, often associated with QT prolongation?

• A. Phase 0
• B. Phase 4
• C. Phase 2 or Phase 3 (repolarization phase)
• D. Only during the resting membrane potential

Answer: C. Phase 2 or Phase 3 (repolarization phase)

7. Delayed Afterdepolarizations (DADs) are abnormal depolarizations that occur after full repolarization (early Phase 4) and are typically associated with:

• A. Severe bradycardia
• B. Intracellular calcium overload
• C. Hyperkalemia
• D. Shortened QT interval

Answer: B. Intracellular calcium overload

8. Which of the following is the most common mechanism responsible for sustained tachyarrhythmias?

• A. Enhanced normal automaticity
• B. Abnormal automaticity
• C. Triggered activity (EADs or DADs)
• D. Reentry

Answer: D. Reentry

9. Three essential conditions are required for reentry to occur. These include:

• A. A single pathway of conduction, rapid conduction, and a long refractory period.
• B. An area of unidirectional block, an alternative pathway for conduction around the block, and sufficiently slowed conduction in the alternative pathway to allow re-excitation of the initially blocked area.
• C. Enhanced sympathetic tone, hypokalemia, and ischemia.
• D. A normal QT interval, rapid SA node firing, and normal AV conduction.

Answer: B. An area of unidirectional block, an alternative pathway for conduction around the block, and sufficiently slowed conduction in the alternative pathway to allow re-excitation of the initially blocked area.

10. Atrial fibrillation (AFib) is characterized pathophysiologically by:

• A. A single, stable reentrant circuit in the atria.
• B. Multiple, disorganized, and rapidly firing ectopic foci in the SA node.
• C. Complete AV block with a slow ventricular escape rhythm.
• D. Multiple, wandering reentrant wavelets in the atria leading to chaotic atrial electrical activity.

Answer: D. Multiple, wandering reentrant wavelets in the atria leading to chaotic atrial electrical activity.

11. Atrial flutter typically involves which pathophysiological mechanism?

• A. Enhanced automaticity of a single atrial focus
• B. A large, organized macro-reentrant circuit within the atria, often around the tricuspid annulus
• C. Triggered activity due to calcium overload
• D. Sinus node dysfunction

Answer: B. A large, organized macro-reentrant circuit within the atria, often around the tricuspid annulus

12. Atrioventricular Nodal Reentrant Tachycardia (AVNRT) is caused by a reentrant circuit located within the:

• A. Sinoatrial (SA) node
• B. Atrioventricular (AV) node, involving dual AV nodal pathways (fast and slow)
• C. Bundle of His
• D. Ventricular myocardium

Answer: B. Atrioventricular (AV) node, involving dual AV nodal pathways (fast and slow)

13. Atrioventricular Reentrant Tachycardia (AVRT) involves a reentrant circuit that includes the AV node and an:

• A. Ectopic focus in the ventricle
• B. Accessory pathway (bypass tract) connecting the atria and ventricles outside the AV node
• C. Diseased Purkinje fiber
• D. Area of myocardial scar tissue in the atria

Answer: B. Accessory pathway (bypass tract) connecting the atria and ventricles outside the AV node

14. Wolff-Parkinson-White (WPW) syndrome is characterized by the presence of an accessory pathway that can lead to pre-excitation on ECG and is a substrate for:

• A. Sinus bradycardia
• B. Atrioventricular Reentrant Tachycardia (AVRT)
• C. Atrial flutter only
• D. Ventricular fibrillation primarily

Answer: B. Atrioventricular Reentrant Tachycardia (AVRT)

15. Ventricular Tachycardia (VT) can arise from which pathophysiological mechanisms in the ventricles?

• A. Only enhanced normal automaticity of the SA node
• B. Reentry (e.g., around scar tissue from a prior MI), abnormal automaticity, or triggered activity
• C. Only AV nodal block
• D. Only sinus node dysfunction

Answer: B. Reentry (e.g., around scar tissue from a prior MI), abnormal automaticity, or triggered activity

16. Ventricular Fibrillation (VF) is a life-threatening arrhythmia characterized by:

• A. A very rapid but organized ventricular rhythm.
• B. Extremely rapid, chaotic, and uncoordinated electrical activity in the ventricles, resulting in no effective cardiac output.
• C. Complete absence of ventricular electrical activity (asystole).
• D. A slow idioventricular rhythm.

Answer: B. Extremely rapid, chaotic, and uncoordinated electrical activity in the ventricles, resulting in no effective cardiac output.

17. Torsades de Pointes (TdP) is a specific form of polymorphic ventricular tachycardia associated with:

• A. A short QT interval
• B. A prolonged QT interval and often triggered by early afterdepolarizations (EADs)
• C. AV nodal reentry
• D. Atrial flutter

Answer: B. A prolonged QT interval and often triggered by early afterdepolarizations (EADs)

18. Sick Sinus Syndrome (SSS) is a disorder of the SA node that can manifest as:

• A. Only persistent sinus tachycardia
• B. Persistent atrial fibrillation
• C. Various arrhythmias including severe sinus bradycardia, sinus arrest, SA block, or alternating bradycardia and tachycardia (tachy-brady syndrome).
• D. Ventricular tachycardia only

Answer: C. Various arrhythmias including severe sinus bradycardia, sinus arrest, SA block, or alternating bradycardia and tachycardia (tachy-brady syndrome).

19. First-degree AV block is characterized on an ECG by:

• A. Progressively lengthening PR interval until a QRS complex is dropped.
• B. A constant, prolonged PR interval (>0.20 seconds) with every P wave followed by a QRS complex.
• C. No association between P waves and QRS complexes.
• D. A normal PR interval with occasional dropped QRS complexes.

Answer: B. A constant, prolonged PR interval (>0.20 seconds) with every P wave followed by a QRS complex.

20. Second-degree AV block, Mobitz Type I (Wenckebach), is characterized by:

• A. A constant PR interval with randomly dropped QRS complexes.
• B. Progressive prolongation of the PR interval until a QRS complex is dropped.
• C. Complete dissociation of atrial and ventricular activity.
• D. ST-segment elevation.

Answer: B. Progressive prolongation of the PR interval until a QRS complex is dropped.

21. Third-degree (complete) AV block is characterized by:

• A. A 1:1 conduction of P waves to QRS complexes.
• B. A fixed ratio of P waves to QRS complexes (e.g., 2:1, 3:1).
• C. Complete absence of P waves.
• D. Complete dissociation between atrial (P waves) and ventricular (QRS complexes) activity, with atria and ventricles beating independently.

Answer: D. Complete dissociation between atrial (P waves) and ventricular (QRS complexes) activity, with atria and ventricles beating independently.

22. Myocardial ischemia and infarction can predispose to arrhythmias by causing:

• A. Enhanced vagal tone only.
• B. Alterations in ion channel function, cell-to-cell coupling (gap junctions), development of scar tissue (creating reentrant circuits), and abnormal automaticity.
• C. Uniformly rapid conduction throughout the myocardium.
• D. Decreased sympathetic activity.

Answer: B. Alterations in ion channel function, cell-to-cell coupling (gap junctions), development of scar tissue (creating reentrant circuits), and abnormal automaticity.

23. Electrolyte abnormalities that can significantly contribute to cardiac arrhythmias include:

• A. Only hyponatremia
• B. Hypokalemia, hyperkalemia, hypomagnesemia, and calcium imbalances
• C. Only hyperchloremia
• D. Elevated bicarbonate levels

Answer: B. Hypokalemia, hyperkalemia, hypomagnesemia, and calcium imbalances

24. “Channelopathies” are a group of genetic disorders that cause arrhythmias by affecting the structure or function of:

• A. Myocardial contractile proteins
• B. Cardiac ion channels (e.g., sodium, potassium, calcium channels)
• C. Mitochondrial enzymes
• D. Endothelial cell receptors

Answer: B. Cardiac ion channels (e.g., sodium, potassium, calcium channels)

25. Long QT Syndrome (LQTS) is characterized by a prolonged QT interval on the ECG, which predisposes individuals to:

• A. Atrial fibrillation
• B. Sinus bradycardia
• C. Torsades de Pointes (TdP) and sudden cardiac death
• D. AV nodal block

Answer: C. Torsades de Pointes (TdP) and sudden cardiac death

26. Brugada Syndrome is an inherited channelopathy often associated with mutations in the SCN5A gene (cardiac sodium channel) and is characterized by specific ECG patterns and an increased risk of:

• A. Atrial flutter
• B. Ventricular fibrillation and sudden cardiac death, particularly during sleep or rest
• C. Severe bradycardia
• D. AVNRT

Answer: B. Ventricular fibrillation and sudden cardiac death, particularly during sleep or rest

27. How does increased sympathetic tone affect cardiac electrophysiology to promote tachyarrhythmias?

• A. It decreases SA node firing rate and slows AV conduction.
• B. It increases SA node firing rate, enhances AV conduction, increases automaticity of latent pacemakers, and can promote DADs.
• C. It primarily prolongs the refractory period of myocardial cells.
• D. It causes uniform hyperpolarization of cardiac cells.

Answer: B. It increases SA node firing rate, enhances AV conduction, increases automaticity of latent pacemakers, and can promote DADs.

28. Vagal stimulation (parasympathetic) primarily affects which parts of the heart’s conduction system, generally leading to bradyarrhythmias?

• A. Ventricular myocardium and Purkinje fibers
• B. Sinoatrial (SA) node and Atrioventricular (AV) node
• C. Bundle branches
• D. Accessory pathways

Answer: B. Sinoatrial (SA) node and Atrioventricular (AV) node

29. Atrial remodeling (structural and electrical changes in the atria) in chronic atrial fibrillation can lead to:

• A. Spontaneous conversion to sinus rhythm.
• B. Perpetuation of AFib by creating more stable reentrant circuits and promoting fibrosis.
• C. A decrease in stroke risk.
• D. Improved response to antiarrhythmic drugs.

Answer: B. Perpetuation of AFib by creating more stable reentrant circuits and promoting fibrosis.

30. The “wavelength” of a reentrant circuit is determined by the product of conduction velocity and refractory period. For reentry to be sustained, the wavelength must be:

• A. Longer than the path length of the circuit.
• B. Shorter than the path length of the circuit.
• C. Equal to the path length of the circuit.
• D. Unrelated to the path length of the circuit.

Answer: B. Shorter than the path length of the circuit.

31. Which phase of the SA nodal action potential is responsible for its automaticity (pacemaker potential)?

• A. Phase 0 (upstroke)
• B. Phase 2 (plateau)
• C. Phase 3 (repolarization)
• D. Phase 4 (spontaneous diastolic depolarization)

Answer: D. Phase 4 (spontaneous diastolic depolarization)

32. The “funny current” (If) in SA nodal cells, mediated by HCN channels, contributes to pacemaker activity by allowing an inward current of primarily which ions during Phase 4?

• A. Calcium ions
• B. Sodium and Potassium ions
• C. Chloride ions
• D. Magnesium ions

Answer: B. Sodium and Potassium ions (predominantly Na+ influx).

33. Drugs that prolong the QT interval increase the risk of Torsades de Pointes by:

• A. Shortening the duration of the ventricular action potential.
• B. Delaying ventricular repolarization (Phase 3), which can promote early afterdepolarizations (EADs).
• C. Increasing the heart rate significantly.
• D. Blocking sodium channels during depolarization.

Answer: B. Delaying ventricular repolarization (Phase 3), which can promote early afterdepolarizations (EADs).

34. Hypokalemia can predispose to arrhythmias by:

• A. Increasing the resting membrane potential (making it less negative) and accelerating repolarization.
• B. Decreasing the resting membrane potential (making it more negative/hyperpolarizing), slowing conduction, and promoting EADs/DADs.
• C. Directly activating beta-adrenergic receptors.
• D. Causing AV nodal block exclusively.

Answer: B. Decreasing the resting membrane potential (making it more negative/hyperpolarizing), slowing conduction, and promoting EADs/DADs.

35. In the context of ischemia-induced arrhythmias, accumulation of extracellular potassium can:

• A. Hyperpolarize the resting membrane potential, making cells less excitable.
• B. Depolarize the resting membrane potential, potentially inactivating fast sodium channels and slowing conduction, which can promote reentry.
• C. Have no effect on cardiac electrophysiology.
• D. Enhance AV nodal conduction.

Answer: B. Depolarize the resting membrane potential, potentially inactivating fast sodium channels and slowing conduction, which can promote reentry.

36. The “vulnerable period” for inducing ventricular fibrillation occurs during which part of the cardiac cycle, if a premature stimulus falls there?

• A. Mid-diastole
• B. The peak of the T wave on the ECG (relative refractory period of repolarization)
• C. During the QRS complex
• D. During the P wave

Answer: B. The peak of the T wave on the ECG (relative refractory period of repolarization) (R-on-T phenomenon).

37. Cardiac fibrosis, often seen in conditions like chronic heart failure or post-MI, can create an anatomical substrate for which type of arrhythmia mechanism?

• A. Enhanced normal automaticity
• B. Abnormal automaticity due to healthy cells
• C. Reentry, by creating areas of slow conduction and block
• D. Only bradyarrhythmias

Answer: C. Reentry, by creating areas of slow conduction and block

38. Which of these is a direct arrhythmogenic consequence of increased intracellular calcium concentration (calcium overload) in cardiomyocytes?

• A. Shortening of the action potential duration
• B. Decreased automaticity
• C. Development of Delayed Afterdepolarizations (DADs)
• C. Hyperpolarization of the resting membrane potential

Answer: C. Development of Delayed Afterdepolarizations (DADs)

39. The normal orderly spread of electrical activation from atria to ventricles is ensured by the insulating nature of the __________ and the sole conducting pathway through the __________.

• A. Pericardium; SA node
• B. Fibrous cardiac skeleton; AV node/His-Purkinje system
• C. Epicardium; coronary arteries
• D. Myocardium itself; bundle branches

Answer: B. Fibrous cardiac skeleton; AV node/His-Purkinje system

40. Decremental conduction, a property of the AV node, means that:

• A. Conduction velocity increases with higher heart rates.
• B. Conduction velocity decreases with higher rates of atrial stimulation, which helps protect the ventricles from excessively rapid atrial rhythms.
• C. The AV node cannot conduct impulses at all.
• D. The AV node has a very short refractory period.

Answer: B. Conduction velocity decreases with higher rates of atrial stimulation, which helps protect the ventricles from excessively rapid atrial rhythms.

41. In Wolff-Parkinson-White (WPW) syndrome, the ECG typically shows a short PR interval and a delta wave. The delta wave represents:

• A. Delayed ventricular repolarization.
• B. Early ventricular depolarization (pre-excitation) via the accessory pathway.
• C. Atrial hypertrophy.
• D. A conduction block in the AV node.

Answer: B. Early ventricular depolarization (pre-excitation) via the accessory pathway.

42. The effective refractory period (ERP) of cardiac tissue is the interval during which:

• A. A normal stimulus can elicit a propagated action potential.
• B. A supranormal stimulus is required to elicit an action potential.
• C. The cell cannot be re-excited by any stimulus, regardless of strength, to produce a propagated action potential.
• D. The cell is spontaneously depolarizing.

Answer: C. The cell cannot be re-excited by any stimulus, regardless of strength, to produce a propagated action potential.

43. How does myocardial hypertrophy (e.g., due to chronic hypertension) contribute to the pathophysiology of arrhythmias?

• A. It always improves electrical stability.
• B. It can lead to altered ion channel expression, changes in cell coupling, fibrosis, and increased dispersion of refractoriness, creating a substrate for arrhythmias.
• C. It primarily causes bradycardia.
• D. It shortens the QT interval.

Answer: B. It can lead to altered ion channel expression, changes in cell coupling, fibrosis, and increased dispersion of refractoriness, creating a substrate for arrhythmias.

44. The primary mechanism by which ischemia causes ST-segment depression on an ECG is often related to:

• A. Transmural ischemia leading to epicardial injury currents.
• B. Subendocardial ischemia causing an injury current that appears as ST depression from the perspective of overlying leads.
• C. Delayed ventricular repolarization only.
• D. Accelerated AV nodal conduction.

Answer: B. Subendocardial ischemia causing an injury current that appears as ST depression from the perspective of overlying leads.

45. In contrast to ST depression, ST-segment elevation in acute myocardial infarction typically signifies:

• A. Only atrial ischemia
• B. Subendocardial injury
• C. Transmural myocardial injury/ischemia
• D. A well-perfused myocardium

Answer: C. Transmural myocardial injury/ischemia

46. The “dispersion of repolarization” across the ventricular myocardium refers to:

• A. Uniform repolarization times throughout the ventricles.
• B. Differences in the timing of repolarization (action potential duration) between different regions of the ventricles, which can create a substrate for reentry.
• C. The rate at which the SA node fires.
• D. The speed of conduction through the AV node.

Answer: B. Differences in the timing of repolarization (action potential duration) between different regions of the ventricles, which can create a substrate for reentry.

47. Catecholaminergic Polymorphic Ventricular Tachycardia (CPVT) is a genetic arrhythmia syndrome triggered by adrenergic stress, often due to mutations affecting:

• A. Potassium channels responsible for repolarization.
• B. Intracellular calcium handling proteins, particularly the ryanodine receptor (RyR2) or calsequestrin.
• C. Sodium channels responsible for depolarization.
• D. The SA node pacemaker current.

Answer: B. Intracellular calcium handling proteins, particularly the ryanodine receptor (RyR2) or calsequestrin.

48. The underlying pathophysiology of most drug-induced Torsades de Pointes involves:

• A. Enhanced activity of outward potassium currents (e.g., IKs).
• B. Blockade of the rapid component of the delayed rectifier potassium current (IKr), leading to QT prolongation and EADs.
• C. Increased activity of the sodium-potassium pump.
• D. Shortening of the ventricular action potential duration.

Answer: B. Blockade of the rapid component of the delayed rectifier potassium current (IKr), leading to QT prolongation and EADs.

49. “Concealed conduction” in the AV node refers to:

• A. An atrial impulse that conducts normally through the AV node to the ventricles.
• B. An atrial impulse that penetrates the AV node but fails to conduct through to the ventricles, yet makes the AV node refractory to subsequent impulses.
• C. An impulse originating in the ventricles that conducts retrogradely to the atria.
• D. Normal conduction that is not visible on the surface ECG.

Answer: B. An atrial impulse that penetrates the AV node but fails to conduct through to the ventricles, yet makes the AV node refractory to subsequent impulses.

50. The development of scar tissue after a myocardial infarction can create a fixed anatomical obstacle. How does this contribute to reentrant ventricular tachycardia?

• A. The scar tissue itself becomes an ectopic pacemaker.
• B. The scar tissue provides pathways of slow conduction and block around which a reentrant wavefront can circulate, often involving surviving but diseased tissue within or at the border of the scar.
• C. The scar tissue enhances sympathetic innervation.
• D. The scar tissue secretes pro-arrhythmic cytokines only.

Answer: B. The scar tissue provides pathways of slow conduction and block around which a reentrant wavefront can circulate, often involving surviving but diseased tissue within or at the border of the scar.