,NSG 5140 Exam 2 Advanced Pathophysiology Questions And
Answers 2026/2027 South College
Q1. A 63-year-old client develops a narrow-complex tachycardia at
190 beats/minute. Electrophysiological testing demonstrates an
atrioventricular nodal circuit involving pathways with different
conduction velocities and refractory periods. Which mechanism
most directly sustains the tachycardia?
A) Abnormal ventricular automaticity caused by ischemia
B) Unidirectional conduction block with reentry through functionally distinct
atrioventricular nodal pathways
C) Complete absence of atrioventricular conduction
D) Increased ventricular repolarization without recurrent conduction
Correct Answer: B) Unidirectional conduction block with reentry through
functionally distinct atrioventricular nodal pathways
Rationale: Atrioventricular nodal reentrant tachycardia occurs when
functionally distinct nodal pathways permit an electrical impulse to circulate
repeatedly. Differences in conduction velocity and refractoriness create
conditions for unidirectional block and reentry. The resulting circuit
repeatedly activates the atria and ventricles, producing a regular
supraventricular tachycardia.
Q2. A 29-year-old client has recurrent palpitations.
Electrocardiography during sinus rhythm reveals a short PR interval,
a delta wave, and a widened QRS complex. Which anatomical
abnormality most directly explains these findings?
A) Complete sinoatrial node destruction
B) Fibrosis of the left ventricular papillary muscles
C) A functional accessory atrioventricular conduction pathway that bypasses
normal AV nodal delay
D) Complete interruption of His-Purkinje conduction
Correct Answer: C) A functional accessory atrioventricular conduction
pathway that bypasses normal AV nodal delay
Rationale: Ventricular preexcitation occurs when an accessory pathway
conducts impulses from the atria to the ventricles without the physiological
,delay normally provided by the atrioventricular node. Early ventricular
activation produces a short PR interval and delta wave. Accessory pathways
can support reentrant tachyarrhythmias and, in some cases, dangerously
rapid ventricular activation during atrial fibrillation.
Q3. A 71-year-old client develops atrial fibrillation following
progressive left atrial enlargement caused by chronic mitral valve
disease. Which structural and electrophysiological changes promote
maintenance of the arrhythmia?
A) Atrial fibrosis, conduction heterogeneity, and shortened effective
refractory periods
B) Uniform atrial conduction without structural abnormalities
C) Complete suppression of atrial electrical activity
D) Increased sinoatrial node dominance preventing reentrant activation
Correct Answer: A) Atrial fibrosis, conduction heterogeneity, and shortened
effective refractory periods
Rationale: Atrial enlargement and fibrosis produce nonuniform electrical
conduction, while electrical remodeling may shorten atrial refractory periods.
These changes facilitate multiple reentrant wavefronts and perpetuation of
atrial fibrillation. The arrhythmia can further promote structural and electrical
remodeling, creating a self-sustaining process.
Q4. A 58-year-old client develops frequent ventricular premature
complexes after an acute myocardial infarction. The injured
myocardial border zone demonstrates delayed conduction and
regions of heterogeneous repolarization. Which mechanism
increases the risk of sustained ventricular tachycardia?
A) Complete synchronization of ventricular refractory periods
B) Increased conduction velocity throughout the infarcted myocardium
C) Elimination of all myocardial scar tissue
D) Reentrant conduction around regions of electrically inactive scar tissue
Correct Answer: D) Reentrant conduction around regions of electrically
inactive scar tissue
Rationale: Myocardial infarction can produce electrically inactive scar tissue
surrounded by surviving myocardial fibers with slow, heterogeneous
, conduction. This substrate permits unidirectional block and reentry,
supporting sustained monomorphic ventricular tachycardia. The location and
extent of scar influence arrhythmia risk.
Q5. A 46-year-old client with congenital long QT syndrome develops
recurrent episodes of polymorphic ventricular tachycardia. Which
electrophysiological abnormality most directly predisposes to
torsades de pointes?
A) Excessively rapid ventricular repolarization
B) Prolonged ventricular repolarization with early afterdepolarizations
C) Complete inhibition of calcium entry into cardiomyocytes
D) Increased conduction velocity through normal atrial tissue
Correct Answer: B) Prolonged ventricular repolarization with early
afterdepolarizations
Rationale: Long QT syndromes impair normal ventricular repolarization,
increasing the risk of early afterdepolarizations during phases 2 or 3 of the
action potential. These abnormal depolarizations may trigger torsades de
pointes, particularly when repolarization is heterogeneous across the
myocardium.
Q6. A 64-year-old client develops complete atrioventricular block
after an extensive inferior myocardial infarction.
Electrocardiography reveals atrioventricular dissociation with a slow
ventricular escape rhythm. Which mechanism explains the rhythm
disturbance?
A) Increased conduction through the atrioventricular node
B) Enhanced sinoatrial node automaticity
C) Failure of atrial impulses to conduct to the ventricles, allowing an
independent subsidiary pacemaker to control ventricular activation
D) Rapid conduction through an accessory atrioventricular pathway
Correct Answer: C) Failure of atrial impulses to conduct to the ventricles,
allowing an independent subsidiary pacemaker to control ventricular
activation
Rationale: Complete atrioventricular block occurs when atrial impulses fail to
reach the ventricles. A junctional or ventricular escape pacemaker maintains
Answers 2026/2027 South College
Q1. A 63-year-old client develops a narrow-complex tachycardia at
190 beats/minute. Electrophysiological testing demonstrates an
atrioventricular nodal circuit involving pathways with different
conduction velocities and refractory periods. Which mechanism
most directly sustains the tachycardia?
A) Abnormal ventricular automaticity caused by ischemia
B) Unidirectional conduction block with reentry through functionally distinct
atrioventricular nodal pathways
C) Complete absence of atrioventricular conduction
D) Increased ventricular repolarization without recurrent conduction
Correct Answer: B) Unidirectional conduction block with reentry through
functionally distinct atrioventricular nodal pathways
Rationale: Atrioventricular nodal reentrant tachycardia occurs when
functionally distinct nodal pathways permit an electrical impulse to circulate
repeatedly. Differences in conduction velocity and refractoriness create
conditions for unidirectional block and reentry. The resulting circuit
repeatedly activates the atria and ventricles, producing a regular
supraventricular tachycardia.
Q2. A 29-year-old client has recurrent palpitations.
Electrocardiography during sinus rhythm reveals a short PR interval,
a delta wave, and a widened QRS complex. Which anatomical
abnormality most directly explains these findings?
A) Complete sinoatrial node destruction
B) Fibrosis of the left ventricular papillary muscles
C) A functional accessory atrioventricular conduction pathway that bypasses
normal AV nodal delay
D) Complete interruption of His-Purkinje conduction
Correct Answer: C) A functional accessory atrioventricular conduction
pathway that bypasses normal AV nodal delay
Rationale: Ventricular preexcitation occurs when an accessory pathway
conducts impulses from the atria to the ventricles without the physiological
,delay normally provided by the atrioventricular node. Early ventricular
activation produces a short PR interval and delta wave. Accessory pathways
can support reentrant tachyarrhythmias and, in some cases, dangerously
rapid ventricular activation during atrial fibrillation.
Q3. A 71-year-old client develops atrial fibrillation following
progressive left atrial enlargement caused by chronic mitral valve
disease. Which structural and electrophysiological changes promote
maintenance of the arrhythmia?
A) Atrial fibrosis, conduction heterogeneity, and shortened effective
refractory periods
B) Uniform atrial conduction without structural abnormalities
C) Complete suppression of atrial electrical activity
D) Increased sinoatrial node dominance preventing reentrant activation
Correct Answer: A) Atrial fibrosis, conduction heterogeneity, and shortened
effective refractory periods
Rationale: Atrial enlargement and fibrosis produce nonuniform electrical
conduction, while electrical remodeling may shorten atrial refractory periods.
These changes facilitate multiple reentrant wavefronts and perpetuation of
atrial fibrillation. The arrhythmia can further promote structural and electrical
remodeling, creating a self-sustaining process.
Q4. A 58-year-old client develops frequent ventricular premature
complexes after an acute myocardial infarction. The injured
myocardial border zone demonstrates delayed conduction and
regions of heterogeneous repolarization. Which mechanism
increases the risk of sustained ventricular tachycardia?
A) Complete synchronization of ventricular refractory periods
B) Increased conduction velocity throughout the infarcted myocardium
C) Elimination of all myocardial scar tissue
D) Reentrant conduction around regions of electrically inactive scar tissue
Correct Answer: D) Reentrant conduction around regions of electrically
inactive scar tissue
Rationale: Myocardial infarction can produce electrically inactive scar tissue
surrounded by surviving myocardial fibers with slow, heterogeneous
, conduction. This substrate permits unidirectional block and reentry,
supporting sustained monomorphic ventricular tachycardia. The location and
extent of scar influence arrhythmia risk.
Q5. A 46-year-old client with congenital long QT syndrome develops
recurrent episodes of polymorphic ventricular tachycardia. Which
electrophysiological abnormality most directly predisposes to
torsades de pointes?
A) Excessively rapid ventricular repolarization
B) Prolonged ventricular repolarization with early afterdepolarizations
C) Complete inhibition of calcium entry into cardiomyocytes
D) Increased conduction velocity through normal atrial tissue
Correct Answer: B) Prolonged ventricular repolarization with early
afterdepolarizations
Rationale: Long QT syndromes impair normal ventricular repolarization,
increasing the risk of early afterdepolarizations during phases 2 or 3 of the
action potential. These abnormal depolarizations may trigger torsades de
pointes, particularly when repolarization is heterogeneous across the
myocardium.
Q6. A 64-year-old client develops complete atrioventricular block
after an extensive inferior myocardial infarction.
Electrocardiography reveals atrioventricular dissociation with a slow
ventricular escape rhythm. Which mechanism explains the rhythm
disturbance?
A) Increased conduction through the atrioventricular node
B) Enhanced sinoatrial node automaticity
C) Failure of atrial impulses to conduct to the ventricles, allowing an
independent subsidiary pacemaker to control ventricular activation
D) Rapid conduction through an accessory atrioventricular pathway
Correct Answer: C) Failure of atrial impulses to conduct to the ventricles,
allowing an independent subsidiary pacemaker to control ventricular
activation
Rationale: Complete atrioventricular block occurs when atrial impulses fail to
reach the ventricles. A junctional or ventricular escape pacemaker maintains
