CH 39: Dysrhythmias Flashcards

Question

A nurse notes that a patient’s ECG shows a prolonged QT interval. Which electrolyte imbalance is most likely responsible? A. Hypercalcemia B. Hypernatremia C. Hypocalcemia D. Hypokalemia

Answer 1

C. Hypocalcemia Rationale: Hypocalcemia prolongs the QT interval, increasing the risk of ventricular dysrhythmias. Hypercalcemia shortens the QT interval. Sodium imbalances do not significantly affect QT duration.

Answer 2

A. Third-degree AV block B. Ventricular fibrillation D. Asystole Rationale: * A is correct: Third-degree AV block can lead to complete loss of ventricular function. * B is correct: Ventricular fibrillation is fatal without immediate intervention. * D is correct: Asystole is the absence of electrical activity, requiring immediate resuscitation. * C is incorrect: Sinus tachycardia is not typically life-threatening unless associated with shock. * E is incorrect: Atrial flutter is abnormal but not immediately life-threatening.

Answer 3

C. Supraventricular tachycardia (SVT) Rationale: SVT is a rapid rhythm (>150 bpm) with a narrow QRS and no distinct P waves. Atrial flutter has a “sawtooth” pattern, VT has a wide QRS, and sinus tachycardia has identifiable P waves.

Answer 4

A. Vagal maneuvers B. Administering adenosine D. Synchronized cardioversion Rationale: * A is correct: Vagal maneuvers (e.g., bearing down) may terminate SVT. * B is correct: Adenosine is the drug of choice for SVT. * D is correct: If unstable, synchronized cardioversion is considered. * C and E are incorrect: Defibrillation is for pulseless VT or VF, and CPR is for cardiac arrest.

Answer 5

C. Sawtooth-shaped P waves Rationale: Atrial flutter is characterized by sawtooth-like P waves (flutter waves). Atrial fibrillation has an irregularly irregular rhythm. Wide QRS suggests VT, and a prolonged PR interval indicates AV block.

Answer 6

A. Peaked T waves B. Prolonged PR interval C. Widened QRS complex Rationale: * A is correct: Hyperkalemia causes peaked T waves. * B is correct: PR interval prolongation occurs as potassium levels rise. * C is correct: Severe hyperkalemia leads to QRS widening. * D and E are incorrect: ST depression and U waves are seen in hypokalemia.

Answer 7

D. Immediate defibrillation Rationale: Defibrillation is the first-line treatment for VF. Synchronized cardioversion is used for unstable SVT or atrial flutter, not VF. Epinephrine is given after the first shock.

Answer 8

A. A prolonged PR interval Rationale: First-degree AV block is characterized by a PR interval >0.20 sec. Widened QRS suggests bundle branch block, and more P waves than QRS complexes are seen in second- and third-degree AV blocks.

Answer 9

A. Hypokalemia B. Hypoxia D. Caffeine intake E. Myocardial ischemia Rationale: PVCs are caused by irritability in the ventricles. * Hypokalemia (A), hypoxia (B), caffeine (D), and ischemia (E) can trigger PVCs. * Hypercalcemia does not cause PVCs.

Answer 10

A. Syncope Rationale: Third-degree AV block can cause severe bradycardia and decreased cardiac output, leading to syncope (fainting).

Answer 11

A. Stroke Rationale: Atrial fibrillation increases the risk of stroke due to blood stasis and clot formation in the atria.

Answer 12

B. Amiodarone administration C. Synchronized cardioversion E. Vagal maneuvers Rationale: Stable VT is treated with vagal maneuvers, antiarrhythmic drugs (amiodarone), and cardioversion if necessary. Defibrillation and CPR are for pulseless VT.

Answer 13

B. Epinephrine and CPR Rationale: PEA is treated with CPR and epinephrine—defibrillation is not indicated.

Answer 14

C. Ventricular fibrillation Rationale: VF is a life-threatening arrhythmia requiring immediate defibrillation

Answer 15

C. Torsades de Pointes Rationale: A prolonged QT interval (>0.50 sec) increases the risk of Torsades de Pointes, a type of polymorphic VT that can deteriorate into ventricular fibrillation.

Answer 16

A. High-quality CPR Rationale: Asystole is a non-shockable rhythm. The priority is high-quality CPR and administering epinephrine. Defibrillation and cardioversion are ineffective for asystole.

Answer 17

C. Ventricular fibrillation Rationale: Ventricular fibrillation causes immediate loss of cardiac output, leading to sudden cardiac death if not treated with defibrillation.

Answer 18

D. To prevent thromboembolism Rationale: Atrial fibrillation increases the risk of stroke due to blood pooling in the atria, which can form clots. Warfarin prevents thromboembolism.

Answer 19

A. Hypomagnesemia Rationale: Low magnesium levels prolong the QT interval, increasing the risk of Torsades de Pointes.

Answer 20

C. Assess the patient for chest pain and hemodynamic stability Rationale: ST-segment depression may indicate myocardial ischemia. The nurse should first assess the patient’s symptoms, blood pressure, and oxygen saturation before notifying the provider.

Answer 21

A. A telemetry technician or nurse continuously observes ECG rhythms from a central location C. It can rapidly identify dysrhythmias, ischemia, and infarction D. The nurse must still assess the patient even if the monitor appears normal Rationale: Centralized telemetry monitoring involves continuous ECG observation from a central location. It helps detect dysrhythmias, ischemia, and infarction. However, nurses must still physically assess the patient, as some conditions may not be immediately reflected on telemetry.

Answer 22

B. Check the telemetry leads and monitor for artifact Rationale: Telemetry monitors can display false alarms due to lead misplacement, muscle activity, or electrical interference. If the patient is asymptomatic, first assess the leads and the monitor before taking further action.

Answer 23

D. It automatically stores and detects abnormal heart rhythms Rationale: Remote telemetry monitoring does not require continuous observation. It can detect and store abnormal heart rhythms, ischemia, and infarction, allowing nurses to review data as needed.

Answer 24

A. Check if the leads are properly placed and secured B. Reapply electrodes if the conductive gel has dried D. Assess the patient for excessive movement or shivering Rationale: Artifacts can result from loose leads, dry gel, and patient movement. The nurse should secure leads, replace electrodes if needed, and assess for excessive motion. Increasing alarm sensitivity is unnecessary and ignoring artifact may lead to missed true dysrhythmias.

Answer 25

A. Check the patient’s blood pressure and oxygen saturation Rationale: Frequent PVCs may reduce cardiac output, leading to dizziness and hypotension. Assessing BP and oxygenation determines hemodynamic stability before notifying the provider.

Answer 26

A. Print a rhythm strip from the ECG monitor and measure the intervals Rationale: A rhythm strip from the ECG monitor provides accurate data on heart rhythm, allowing the nurse to measure intervals and identify dysrhythmias.

Answer 27

C. Prepare for transcutaneous pacing Rationale: A ventricular rate of 35 bpm suggests a His-Purkinje system pacemaker (20-40 bpm), indicating severe bradycardia. The patient is symptomatic with hypotension and dizziness, requiring immediate pacing to restore an adequate heart rate.

Answer 28

A. The SA node normally fires at a rate of 60-100 beats per minute B. The AV node can act as a secondary pacemaker with an intrinsic rate of 40-60 beats per minute D. An ectopic focus refers to an electrical impulse originating outside the normal conduction pathway Rationale: The SA node is the primary pacemaker (60-100 bpm), and the AV node can take over at 40-60 bpm if needed. An ectopic focus is an abnormal site for impulse generation. The refractory period limits excitability, with the absolute refractory phase preventing any stimulation.

Answer 29

A. Administer IV amiodarone as prescribed Rationale: A wide-complex tachycardia in a patient with atrial fibrillation could indicate ventricular tachycardia (VT). IV amiodarone is the first-line antiarrhythmic for hemodynamically stable VT.

Answer 30

B. They occur when an impulse reenters a previously unexcitable area that has recovered Rationale: Reentrant dysrhythmias occur when an impulse travels through a unidirectional block and reactivates tissue that has recovered, leading to premature beats or rapid rhythms.

Answer 31

A. Myocardial ischemia B. Hypokalemia D. Anxiety Rationale: PVCs can result from myocardial ischemia, electrolyte imbalances (e.g., hypokalemia), and increased sympathetic activity (e.g., anxiety). Beta-blockers generally reduce ectopic beats, and hypermagnesemia is not a common cause.

Answer 32

C. Have emergency equipment readily available Rationale: Adenosine can cause transient asystole, bradycardia, or hypotension. Emergency equipment should be on hand in case resuscitation is needed.

Answer 33

B. Atrial and ventricular rhythms that are independent of each other Rationale: In complete heart block, atrial impulses do not reach the ventricles, causing the atria and ventricles to contract independently at different rates.

Answer 34

A. Hypoxia B. Electrolyte imbalances C. Fever E. Certain medications like digoxin Rationale: Triggered beats can result from hypoxia, electrolyte imbalances, fever (due to increased metabolic demand), and medications like digoxin, which increase automaticity. Vagal stimulation generally slows conduction rather than triggering ectopic beats.

Answer 35

B. “The ICD will deliver a shock if a dangerous rhythm is detected.” Rationale: ICDs monitor heart rhythms and deliver shocks to correct life-threatening dysrhythmias. Routine maintenance is not weekly, and patients can resume activities after recovery.

Answer 36

C. Second-degree AV block (Mobitz type II) Rationale: Mobitz type II AV block involves intermittent failure of QRS conduction, leading to dropped beats and bradycardia.

Answer 37

D. Defibrillate the patient immediately Rationale: VF is a life-threatening rhythm that requires immediate defibrillation to restore organized electrical activity.

Answer 38

A. It refers to the heart’s ability to generate impulses without external stimulation C. It can be increased by ischemia or electrolyte imbalances D. The SA node normally has the highest automaticity Rationale: Automaticity is the heart’s ability to generate impulses. It is highest in the SA node, and conditions like ischemia can enhance it. Beta-blockers decrease automaticity.

Answer 39

A. Perform synchronized cardioversion Rationale: Since the patient is now unstable (hypotensive, diaphoretic), immediate synchronized cardioversion is required to restore a normal rhythm. Adenosine is only used for stable patients.

Answer 40

D. “It is the phase where excitability is completely blocked.” Rationale: The absolute refractory period is when no impulses can be generated. The relative refractory period follows, during which a strong stimulus can cause an abnormal impulse, increasing the risk of dysrhythmias.

Answer 41

B) Holter monitoring Rationale: Holter monitoring continuously records the ECG while the patient is ambulatory and performing daily activities. It is useful for correlating symptoms with any dysrhythmias seen on the ECG.

Answer 42

C) Determining the rhythm by heart monitoring Rationale: In a nonmonitored setting, determining the rhythm by heart monitoring is a high priority if the patient becomes symptomatic (e.g., chest pain, syncope). This helps guide the appropriate management and treatment.

Answer 43

A) Holter monitoring B) Event monitoring C) Electrophysiologic study (EPS) Rationale: Holter monitoring, event monitoring, and EPS can assess the effectiveness of antidysrhythmic drug therapy. The signal-averaged ECG identifies late potentials and suggests the risk of developing serious ventricular dysrhythmias.

Answer 44

D) To locate accessory pathways and determine the effectiveness of antidysrhythmic drugs Rationale: An EPS study can identify the causes of heart blocks, tachydysrhythmias, bradydysrhythmias, and syncope. It also locates accessory pathways and determines the effectiveness of antidysrhythmic drugs.

Answer 45

B) The patient has exercise-induced dysrhythmias Rationale: Significant ST-segment depression during an exercise treadmill test indicates the presence of exercise-induced dysrhythmias or ischemia, which can be evaluated for treatment.

Answer 46

A) Chest pain B) Syncope D) Dizziness Rationale: Symptoms such as chest pain, syncope, and dizziness may indicate a dysrhythmia. Fever is not typically associated with dysrhythmias.

Answer 47

A) Review the Holter monitor recording for dysrhythmias during the reported event Rationale: Reviewing the Holter monitor recording for dysrhythmias during the reported event helps correlate the symptoms with the ECG findings and guides further management.

Answer 48

D) Signal-averaged ECG Rationale: The signal-averaged ECG identifies late potentials, which suggest that the patient may be at risk for developing serious ventricular dysrhythmias.

Answer 49

A) Electrolyte imbalances B) Medications C) Stress Rationale: Electrolyte imbalances, medications, and stress are common causes of dysrhythmias. High altitude is not a typical cause of dysrhythmias.

Answer 50

D) Electrophysiologic study (EPS) Rationale: An EPS study can identify the causes of syncope by evaluating the heart's electrical conduction system and locating accessory pathways.

Answer 51

A) It provides real-time ECG recordings during symptoms Rationale: Smartphone apps can obtain and save ECG recordings during symptoms, improving the evaluation of dysrhythmias in outpatients.

Answer 52

A) Activate the emergency response system (ERS) B) Determine the rhythm by heart monitoring Rationale: In a nonmonitored setting, activating the ERS and determining the rhythm by heart monitoring are high priorities for managing a patient with a symptomatic dysrhythmia. Administering oxygen and performing CPR may be necessary, but the priority is to establish the rhythm.

Answer 53

C) Keep a diary of activities and symptoms during the monitoring period Rationale: The patient should keep a diary of activities and symptoms during the Holter monitoring period to correlate events with any dysrhythmias seen on the ECG.

Answer 54

C) Electrophysiologic study (EPS) Rationale: An EPS study can locate accessory pathways and determine the effectiveness of antidysrhythmic drugs, providing valuable information for managing dysrhythmias.

Answer 55

A) Assess the heart rhythm B) Monitor changes in rhythm Rationale: Continuous ECG monitoring during hospitalization aims to assess the heart rhythm, monitor changes in rhythm, and evaluate the patient's clinical status. Providing real-time heart rate data is a benefit but not a primary goal.

Answer 56

C) The QRS complex has a normal shape and duration Rationale: Normal sinus rhythm refers to a rhythm that starts in the SA node at a rate of 60 to 100 beats/min and follows the normal conduction pathway. The P wave is normal, the PR interval is normal, and the QRS complex has a normal shape and duration.

Answer 57

all of the choices are correct Rationale: In sinus arrhythmia, the conduction pathway is the same as in sinus rhythm, but the SA node fires irregularly. The HR increases slightly during inspiration and decreases slightly during exhalation.

Answer 58

D) Normal sinus rhythm Rationale: The patient's heart rate is within the normal range (60 to 100 beats/min), and the ECG shows normal P waves, PR interval, and QRS complex. This indicates normal sinus rhythm.

Answer 59

A) Sinus arrhythmia Rationale: Sinus arrhythmia is characterized by the SA node firing irregularly, often resulting from changes in intrathoracic pressure during breathing. The heart rate increases during inspiration and decreases during exhalation.

Answer 60

A) The HR is between 60 to 100 beats/min C) The PR interval is normal Rationale: Normal sinus rhythm is characterized by a heart rate between 60 to 100 beats/min, normal P waves preceding each QRS complex, and normal PR and QRS intervals.

Answer 61

B) Sinus arrhythmia Rationale: The patient's heart rate increases during inspiration and decreases during exhalation, indicating sinus arrhythmia. This condition is common in healthy adults.

Answer 62

B) It is common in healthy adults and related to breathing patterns Rationale: Sinus arrhythmia is common in healthy adults and is related to changes in intrathoracic pressure during breathing, causing the heart rate to increase during inspiration and decrease during exhalation.

Answer 63

A) The P wave precedes each QRS complex C) The QRS complex has a normal shape and duration Rationale: Normal sinus rhythm is indicated by P waves that precede each QRS complex, a heart rate of 60 to 100 beats/min, normal PR interval, and normal shape and duration of the QRS complex.

Answer 64

C) The SA node fires at a rate less than 60 beats/min Rationale: In sinus bradycardia, the conduction pathway is the same as that in sinus rhythm, but the SA node fires at a rate less than 60 beats/min.

Answer 65

C) Sinus bradycardia Rationale: The patient has a heart rate of less than 60 beats/min with symptoms of inadequate perfusion (dizziness and fatigue). The ECG shows normal P waves and QRS complexes with the SA node firing at a slower rate, indicating sinus bradycardia.

Answer 66

B) Syncope Rationale: Symptomatic bradycardia refers to a heart rate of less than 60 beats/min that causes symptoms of inadequate perfusion, such as fatigue, dizziness, chest pain, and syncope.

Answer 67

D) Inadequate cardiac output and perfusion Rationale: The primary concern with sinus bradycardia, especially when symptomatic, is inadequate cardiac output and perfusion, leading to symptoms such as chest pain and lightheadedness.

Answer 68

C) The QRS complex is normal in shape and duration Rationale: In sinus bradycardia, the conduction pathway is the same as that in sinus rhythm, so the QRS complex is normal in shape and duration. The heart rate is less than 60 beats/min, but the P wave is normal and precedes each QRS complex.

Answer 69

B) An aerobically trained athlete Rationale: Sinus bradycardia may be a normal finding in aerobically trained athletes and in some people during sleep. It can be a sign of high cardiovascular fitness in athletes.

Answer 70

D) β-blocker medication Rationale: Certain drugs, such as β-blockers, can cause sinus bradycardia by slowing the heart rate. The patient's symptoms and medication history suggest that the β-blockers are the likely cause.

Answer 71

A) Valsalva maneuver Rationale: Sinus bradycardia can occur in response to a Valsalva maneuver, which increases intrathoracic pressure and stimulates the vagus nerve, slowing the heart rate.

Answer 72

C) Increased vagal stimulation Rationale: Increased intracranial pressure can lead to increased vagal stimulation, which in turn can cause sinus bradycardia. This mechanism slows the heart rate in response to the increased pressure.

Answer 73

A) Hypothyroidism Rationale: Common disease states associated with sinus bradycardia include hypothyroidism, increased intracranial pressure, and inferior myocardial infarction (MI). Hypothyroidism slows the metabolic rate and can lead to a slower heart rate.

Answer 74

C) P wave preceding each QRS complex with a normal shape Rationale: In sinus bradycardia, the heart rate is less than 60 beats/min, and the rhythm is regular. The P wave precedes each QRS complex and has a normal shape and duration. The PR interval and QRS complex are normal.

Answer 75

C) Sinus bradycardia Rationale: The patient's heart rate is less than 60 beats/min, with a regular rhythm, normal P waves, and normal PR and QRS intervals. This describes sinus bradycardia.

Answer 76

A) Less than 60 beats/min Rationale: In sinus bradycardia, the heart rate is less than 60 beats/min. The rhythm is regular, and the ECG shows normal P waves, PR interval, and QRS complex.

Answer 77

A) The heart rate of less than 60 beats/min Rationale: The heart rate of less than 60 beats/min, combined with a regular rhythm, normal P waves, PR interval, and QRS complex, confirms the diagnosis of sinus bradycardia.

Answer 78

B) Pale, cool skin Rationale: Manifestations of symptomatic bradycardia that indicate inadequate perfusion include pale, cool skin, hypotension, weakness, angina, dizziness, confusion, and shortness of breath.

Answer 79

C) The patient is symptomatic and experiencing inadequate perfusion Rationale: The symptoms of weakness and shortness of breath in a patient with sinus bradycardia indicate symptomatic bradycardia, suggesting that the patient is experiencing inadequate perfusion.

Answer 80

B) Hypotension Rationale: Hypotension is a common manifestation of symptomatic sinus bradycardia, indicating inadequate perfusion and reduced cardiac output.

Answer 81

D) The patient may be experiencing inadequate cerebral perfusion Rationale: Dizziness and confusion in a patient with sinus bradycardia suggest inadequate cerebral perfusion, which is a significant concern and requires prompt evaluation and management.

Answer 82

B) Initiate transcutaneous pacing Rationale: If IV atropine is ineffective in treating symptomatic bradycardia, the next steps include transcutaneous pacing, or infusion of dopamine or epinephrine. These interventions help increase the heart rate and improve perfusion.

Answer 83

B) Medication-induced; hold or reduce the beta-blocker Rationale: The patient's bradycardia is likely due to the beta-blocker medication. The initial treatment approach should be to hold, stop, or reduce the beta-blocker and assess the patient's response.

Answer 84

A) IV atropine Rationale: IV atropine, an anticholinergic drug, is commonly used as a first-line treatment for symptomatic bradycardia to increase the heart rate.

Answer 85

D) Infuse dopamine or epinephrine Rationale: If symptomatic bradycardia does not respond to IV atropine or transcutaneous pacing, additional treatment options include infusing dopamine or epinephrine to increase the heart rate and improve cardiac output.

Answer 86

B) Distorted P wave Rationale: A premature atrial contraction (PAC) results in a distorted P wave due to the ectopic signal starting in the atrium and traveling across the atria by an abnormal pathway.

Answer 87

C) Premature atrial contraction (PAC) Rationale: The patient's ECG shows an early atrial contraction with a distorted P wave, which is characteristic of a PAC. This occurs when an ectopic focus in the atrium fires sooner than the next expected sinus beat.

Answer 88

B) It may be stopped, delayed, or conducted normally Rationale: At the AV node, the ectopic signal during a PAC may be stopped (non-conducted PAC), delayed (lengthened PR interval), or conducted normally through the ventricles.

Answer 89

B) The ectopic signal is delayed Rationale: A lengthened PR interval following an early atrial contraction indicates that the ectopic signal is delayed at the AV node.

Answer 90

A) An ectopic focus in the atrium Rationale: A premature atrial contraction (PAC) originates from an ectopic focus in the atrium, causing an early atrial contraction before the next expected sinus beat.

Answer 91

A) Emotional stress Rationale: In a normal heart, a PAC can result from emotional stress, fatigue, caffeine, tobacco, or alcohol use.

Answer 92

B) Premature atrial contraction (PAC) Rationale: The patient's symptoms of palpitations and a sensation of skipped heartbeats after consuming caffeine are indicative of PACs, which can result from caffeine use.

Answer 93

D) All of the above Rationale: PACs can result from hypoxia, electrolyte imbalances, hyperthyroidism, COPD, and heart disease, including CAD and valvular disease.

Answer 94

B) Premature atrial contraction (PAC) Rationale: The ECG findings of an irregular heart rhythm, a P wave hidden in the preceding T wave, and a variable PR interval are characteristic of a PAC.

Answer 95

B) QRS complex Rationale: In a PAC, the QRS complex is usually normal, although the rhythm is irregular, and the P wave may have a different shape or be hidden in the preceding T wave.

Answer 96

C) May indicate enhanced automaticity of the atria or a reentry mechanism Rationale: In a person with heart disease, frequent PACs may indicate enhanced automaticity of the atria or a reentry mechanism, and they may warn of or start more serious dysrhythmias, such as SVT.

Answer 97

C) It may be shorter or longer than the PR interval from the SA node Rationale: The PR interval during a PAC may be shorter or longer than the PR interval coming from the SA node but is within normal limits.

Answer 98

A) Hyperthyroidism Rationale: Hyperthyroidism is one of the clinical associations that can result in PACs, along with hypoxia, electrolyte imbalances, COPD, and heart disease.

Answer 99

D) The heart rate varies with the underlying rate and frequency of the PACs Rationale: The heart rate in the presence of PACs varies with the underlying rate and frequency of the PACs.

Answer 100

C) It is likely an isolated PAC with no significant clinical impact Rationale: In a person with a healthy heart, isolated PACs are not significant and may present as a sensation that the heart “skipped a beat.”

Answer 101

D) It has a different shape from a P wave originating in the SA node Rationale: In a PAC, the P wave has a different shape from that of a P wave originating in the SA node and may be hidden in the preceding T wave.

Answer 102

C) Above the bifurcation of the bundle of His Rationale: PSVT is a dysrhythmia starting in an ectopic focus anywhere above the bifurcation of the bundle of His.

Answer 103

B) Paroxysmal supraventricular tachycardia (PSVT) Rationale: The patient's symptoms and ECG findings are characteristic of PSVT, which has an abrupt onset and ending and originates above the bundle of His.

Answer 104

A) Reentrant phenomenon Rationale: PSVT occurs because of a reentrant phenomenon, which involves reexcitation of the atria when there is a one-way block.

Answer 105

D) Premature atrial contraction (PAC) Rationale: A PAC usually triggers a run of repeated premature beats, leading to PSVT.

Answer 106

B) Abrupt onset and ending Rationale: The term "paroxysmal" refers to an abrupt onset and ending of the dysrhythmia.

Answer 107

B) PSVT with AV block Rationale: A brief period of asystole may follow the termination of PSVT, and AV block can prevent some impulses from being conducted to the ventricles.

Answer 108

A) Wolff-Parkinson-White syndrome Rationale: PSVT can occur with Wolff-Parkinson-White (WPW) syndrome or “preexcitation” due to extra conduction or accessory pathways.

Answer 109

D) Paroxysmal supraventricular tachycardia Rationale: The patient's symptoms, history of WPW syndrome, and ECG findings are indicative of PSVT, which is associated with extra conduction or accessory pathways in WPW syndrome.

Answer 110

B) A dysrhythmia starting in an ectopic focus above the bifurcation of the bundle of His Rationale: PSVT is a dysrhythmia that starts in an ectopic focus anywhere above the bifurcation of the bundle of His.

Answer 111

C) Paroxysmal supraventricular tachycardia Rationale: The patient's symptoms and ECG findings are indicative of PSVT, characterized by a regular rhythm, a rapid heart rate, and P waves that may be hidden in the preceding T wave.

Answer 112

A) Premature atrial contraction Rationale: In PSVT, a PAC usually triggers a run of repeated premature beats, leading to the reentrant phenomenon.

Answer 113

C) Paroxysmal supraventricular tachycardia Rationale: PSVT is characterized by an abrupt onset and ending of the rapid heart rate, often followed by a brief period of asystole.

Answer 114

A) One-way block and reexcitation of the atria Rationale: PSVT occurs because of a reentrant phenomenon, which involves reexcitation of the atria due to a one-way block.

Answer 115

D) Paroxysmal supraventricular tachycardia Rationale: The patient's history of WPW syndrome and ECG findings are indicative of PSVT, which can occur with WPW syndrome due to extra conduction or accessory pathways.

Answer 116

A) Rheumatic heart disease Rationale: PSVT is associated with rheumatic heart disease, digitalis toxicity, CAD, and cor pulmonale.

Answer 117

B) The condition may lead to decreased cardiac output and requires intervention Rationale: A prolonged episode of PSVT with a heart rate greater than 180 beats/min can cause decreased cardiac output due to reduced stroke volume, requiring intervention.

Answer 118

C) Dyspnea Rationale: Common manifestations of PSVT include hypotension, palpitations, dyspnea, and angina.

Answer 119

B) To convert PSVT to a normal sinus rhythm Rationale: IV adenosine is the drug of choice to convert PSVT to a normal sinus rhythm. It has a short half-life and is well tolerated.

Answer 120

B) Valsalva maneuver Rationale: Common vagal maneuvers used to treat PSVT include the Valsalva maneuver and coughing.

Answer 121

C) Synchronized cardioversion Rationale: If a patient with PSVT becomes hemodynamically unstable and does not respond to vagal maneuvers, synchronized cardioversion is the next appropriate intervention.

Answer 122

D) 151 to 220 beats/min Rationale: In PSVT, the heart rate is typically between 151 to 220 beats/min.

Answer 123

A) Radiofrequency catheter ablation Rationale: Treatment of recurring PSVT and PSVT in patients with WPW syndrome includes radiofrequency catheter ablation of the accessory pathway.

Answer 124

B) Decreased stroke volume and cardiac output Rationale: A prolonged episode of PSVT with a heart rate greater than 180 beats/min can cause decreased cardiac output due to reduced stroke volume.

Answer 125

B) Sawtooth-shaped flutter waves Rationale: Atrial flutter is identified by recurring, regular, sawtooth-shaped flutter waves originating from a single ectopic focus in the atrium.

Answer 126

C) Atrial flutter Rationale: The patient's symptoms and ECG findings of sawtooth-shaped flutter waves and an atrial rate of 300 beats/min are indicative of atrial flutter.

Answer 127

A) Rheumatic fever Rationale: Atrial flutter is associated with conditions such as CAD, hypertension, mitral valve disorders, pulmonary embolus, chronic lung disease, cor pulmonale, cardiomyopathy, hyperthyroidism, and the use of certain drugs.

Answer 128

B) 2:1 Rationale: In atrial flutter, a 2:1 conduction ratio typically results in a ventricular rate of around 150 beats/min.

Answer 129

A) Variable PR interval that is not measurable Rationale: In atrial flutter, the PR interval is variable and not measurable, and the QRS complex is usually normal.

Answer 130

C) Decreased cardiac output and risk of heart failure Rationale: The high ventricular rates and loss of the atrial “kick” in atrial flutter can decrease cardiac output and cause serious problems, such as heart failure.

Answer 131

D) Formation of thrombi in the atria due to blood stasis Rationale: Patients with atrial flutter have an increased risk for stroke because thrombi can form in the atria from the stasis of blood.

Answer 132

B) To prevent stroke Rationale: The primary goal of prescribing warfarin for a patient with atrial flutter is to prevent stroke by reducing the risk of thrombus formation.

Answer 133

A) Slow ventricular response by increasing AV block Rationale: The primary goal in the treatment of atrial flutter is to slow the ventricular response by increasing AV block.

Answer 134

C) Electrical cardioversion Rationale: Electrical cardioversion may be used to convert atrial flutter to sinus rhythm in an emergency when the patient is clinically unstable.

Answer 135

C) Ibutilide Rationale: Ibutilide (Corvert) is an antidysrhythmic drug that can convert atrial flutter to sinus rhythm.

Answer 136

B) Ablate the ectopic foci and restore normal sinus rhythm Rationale: The goal of radiofrequency catheter ablation is to ablate (destroy) the ectopic foci in the right atrium, restoring normal sinus rhythm.

Answer 137

C) 200 to 350 beats/min Rationale: In atrial flutter, the atrial rate is typically between 200 to 350 beats/min.

Answer 138

A) β-blockers Rationale: Drugs used to control the ventricular rate in atrial flutter include β-blockers and calcium channel blockers.

Answer 139

A) Amiodarone Rationale: Amiodarone is an antidysrhythmic drug that can maintain sinus rhythm in a patient with atrial flutter.

Answer 140

D) Restoration of normal sinus rhythm Rationale: The expected outcome of radiofrequency catheter ablation is the restoration of normal sinus rhythm by destroying the ectopic foci.

Answer 141

D) Heart failure Rationale: Atrial flutter can lead to decreased cardiac output and cause serious problems such as heart failure, especially in patients with underlying heart disease.

Answer 142

C) Chaotic, fibrillatory waves replacing P waves Rationale: Atrial fibrillation is characterized by chaotic, fibrillatory waves replacing the P waves on an ECG.

Answer 143

C) Atrial fibrillation with a rapid ventricular response Rationale: The patient's symptoms and ECG findings indicate atrial fibrillation with a rapid ventricular response, characterized by chaotic, fibrillatory waves and a ventricular rate greater than 100 beats/min.

Answer 144

A) Hypertensive heart disease Rationale: Atrial fibrillation is commonly associated with conditions such as CAD, valvular heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis.

Answer 145

C) Atrial fibrillation Rationale: The patient's history of thyrotoxicosis and ECG findings of an atrial rate of 450 beats/min and fibrillatory waves are indicative of atrial fibrillation.

Answer 146

B) Decreased cardiac output Rationale: Atrial fibrillation with a rapid ventricular response can decrease cardiac output due to ineffective atrial contractions and a rapid ventricular rate.

Answer 147

D) Thrombi formation in the atria due to blood stasis Rationale: Atrial fibrillation increases the risk for stroke because thrombi can form in the atria due to blood stasis, and an embolized clot can move to the brain.

Answer 148

A) Measurable PR interval Rationale: During atrial fibrillation, the PR interval is not measurable. The QRS complex is usually normal, and the ventricular rhythm is irregular.

Answer 149

D) Controlled ventricular response Rationale: When the ventricular rate is between 60 and 100 beats/min, atrial fibrillation is described as having a controlled ventricular response.

Answer 150

D) 350 to 600 beats/min Rationale: During atrial fibrillation, the atrial rate may be as high as 350 to 600 beats/min.

Answer 151

D) Embolized clot from the atria Rationale: An embolic stroke in a patient with atrial fibrillation is most likely caused by an embolized clot that formed in the atria due to blood stasis.

Answer 152

B) Paroxysmal atrial fibrillation Rationale: Paroxysmal atrial fibrillation is characterized by episodes that begin and end spontaneously.

Answer 153

C) Palpitations and irregular heartbeats Rationale: Common clinical manifestations of atrial fibrillation include palpitations, irregular heartbeats, and a decreased cardiac output.

Answer 154

C) Elderly patients Rationale: The prevalence of atrial fibrillation increases with age, making elderly patients more susceptible to developing this dysrhythmia.

Answer 155

C) Hypertensive heart disease Rationale: Atrial fibrillation is commonly associated with underlying conditions such as hypertensive heart disease, CAD, valvular heart disease, and cardiomyopathy.

Answer 156

A) Chaotic, fibrillatory waves Rationale: During atrial fibrillation, chaotic, fibrillatory waves replace the P waves on an ECG.

Answer 157

C) Rapid ventricular response Rationale: Atrial fibrillation with a ventricular rate greater than 100 beats/min is described as atrial fibrillation with a rapid (or uncontrolled) ventricular response.

Answer 158

B) Chaotic, fibrillatory waves replacing P waves Rationale: Atrial fibrillation is characterized by chaotic, fibrillatory waves replacing the P waves on an ECG.

Answer 159

D) Atrial fibrillation with a rapid ventricular response Rationale: The patient's symptoms and ECG findings indicate atrial fibrillation with a rapid ventricular response, characterized by chaotic, fibrillatory waves and a ventricular rate greater than 100 beats/min.

Answer 160

A) Hypertensive heart disease Rationale: Atrial fibrillation is commonly associated with conditions such as CAD, valvular heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis.

Answer 161

C) Atrial fibrillation Rationale: The patient's history of thyrotoxicosis and ECG findings of an atrial rate of 450 beats/min and fibrillatory waves are indicative of atrial fibrillation.

Answer 162

B) Decreased cardiac output Rationale: Atrial fibrillation with a rapid ventricular response can decrease cardiac output due to ineffective atrial contractions and a rapid ventricular rate.

Answer 163

A) Measurable PR interval Rationale: During atrial fibrillation, the PR interval is not measurable. The QRS complex is usually normal, and the ventricular rhythm is irregular.

Answer 164

D) Controlled ventricular response Rationale: When the ventricular rate is between 60 and 100 beats/min, atrial fibrillation is described as having a controlled ventricular response.

Answer 165

C) Decrease ventricular response to less than 100 beats/min Rationale: The primary goal in the treatment of atrial fibrillation is to decrease the ventricular response to less than 100 beats/min, along with preventing stroke and converting to sinus rhythm if possible.

Answer 166

A) Calcium channel blocker (e.g., diltiazem) Rationale: Drugs used for rate control in atrial fibrillation include calcium channel blockers (e.g., diltiazem), β-blockers (e.g., metoprolol), amiodarone, and digoxin.

Answer 167

C) Amiodarone Rationale: Amiodarone is the most common antidysrhythmic drug used for conversion to and maintenance of sinus rhythm in atrial fibrillation.

Answer 168

C) 3 to 4 weeks of anticoagulation therapy with warfarin Rationale: If a patient has been in atrial fibrillation for longer than 48 hours, anticoagulation therapy with warfarin is needed for 3 to 4 weeks before attempting electrical cardioversion.

Answer 169

A) Transesophageal echocardiogram (TEE) Rationale: A transesophageal echocardiogram (TEE) may be performed to rule out clots in the atria before cardioversion in a patient with atrial fibrillation.

Answer 170

B) International normalized ratio (INR) Rationale: Patients on long-term warfarin therapy require monitoring of therapeutic levels using the international normalized ratio (INR).

Answer 171

A) Dabigatran Rationale: Alternatives to warfarin, such as dabigatran (Pradaxa), do not require routine laboratory testing for therapeutic levels.

Answer 172

B) AV nodal ablation Rationale: AV nodal ablation involves the destruction of the AV node and insertion of a permanent ventricular pacemaker for patients with atrial fibrillation refractory to drugs and electrical conversion.

Answer 173

D) Maze procedure Rationale: The Maze procedure stops atrial fibrillation by making incisions in both atria and using cryoablation to interrupt the ectopic foci causing the dysrhythmia.

Answer 174

D) Restoration of normal sinus rhythm Rationale: The expected outcome of the Maze procedure is the restoration of normal sinus rhythm by interrupting the ectopic foci causing atrial fibrillation.

Answer 175

C) Increase blood pressure Rationale: The goals of atrial fibrillation treatment are to decrease the ventricular response to less than 100 beats/min, prevent stroke, and convert to sinus rhythm, if possible.

Answer 176

A) Electrical cardioversion Rationale: Electrical cardioversion may be used to convert atrial fibrillation to normal sinus rhythm, especially in patients with reduced exercise tolerance on rate control drugs.

Answer 177

C) Diltiazem Rationale: Diltiazem is a calcium channel blocker used to control the ventricular rate in atrial fibrillation.

Answer 178

B) To prevent blood clot formation and decrease the incidence of strokes Rationale: LAA occlusion is a treatment strategy to prevent blood clot formation in patients with atrial fibrillation, thereby decreasing the incidence of strokes.

Answer 179

A) Use of a special stapler to remove the LAA Rationale: For patients who cannot use oral anticoagulants, LAA occlusion can be considered as an alternative treatment. This can be done using a special stapler to remove the LAA or an occlusion device to shut off blood flow to the LAA.

Answer 180

A) Amplatzer Amulet Occluder Rationale: The Amplatzer Amulet Occluder is a device used to occlude the LAA by preventing blood from flowing into and out of the LAA.

Answer 181

B) It prevents the formation of clots by occluding the LAA Rationale: The Amplatzer Amulet Occluder is positioned around the LAA and closed like a clamp, preventing blood from flowing into and out of the LAA, thereby preventing clot formation.

Answer 182

B) To avoid side effects of oral anticoagulants Rationale: LAA occlusion is an alternative treatment for patients with atrial fibrillation who cannot use oral anticoagulants due to contraindications or side effects.

Answer 183

A) AV junction Rationale: Junctional dysrhythmias start in the area of the AV node to the bundle of His, known as the AV junction.

Answer 184

D) Junctional dysrhythmia Rationale: The patient's ECG shows inverted P waves occurring just after the QRS complex, which is characteristic of a junctional dysrhythmia.

Answer 185

C) Failure of the SA node to fire or signal block Rationale: Junctional dysrhythmias result because the SA node does not fire, or the signal is blocked, causing the AV node to become the pacemaker of the heart and the impulse to move in a retrograde fashion.

Answer 186

B) Junctional escape rhythm Rationale: The patient's heart rate of 40 to 60 beats/min, regular rhythm, and inverted P wave hidden in the QRS complex indicate a junctional escape rhythm.

Answer 187

C) CAD Rationale: Junctional dysrhythmias are often associated with CAD, HF, cardiomyopathy, electrolyte imbalances, inferior MI, and rheumatic heart disease.

Answer 188

C) Accelerated junctional rhythm Rationale: The patient's heart rate of 61 to 100 beats/min and ECG findings of an inverted P wave before the QRS complex suggest an accelerated junctional rhythm.

Answer 189

C) 101 to 180 beats/min Rationale: In junctional tachycardia, the heart rate is typically between 101 to 180 beats/min.

Answer 190

A) Discontinuation of digoxin Rationale: If an accelerated junctional rhythm or junctional tachycardia is caused by drug toxicity (e.g., digoxin), the appropriate treatment is to stop the drug.

Answer 191

B) They serve as a safety mechanism when the SA node is not effective Rationale: Junctional escape rhythms serve as a safety mechanism when the SA node has not been effective and should not be suppressed.

Answer 192

C) Reduced cardiac output and hemodynamic instability Rationale: Junctional tachycardia indicates a more serious problem and may reduce cardiac output, causing the patient to become hemodynamically unstable (e.g., hypotensive).

Answer 193

A) Inverted P wave hidden in the QRS complex Rationale: In junctional escape rhythm, the P wave is abnormal in shape and inverted. It may be hidden in the QRS complex.

Answer 194

D) Junctional escape rhythm Rationale: The patient's heart rate of 40 to 60 beats/min, regular rhythm, and PR interval of less than 0.12 seconds suggest a junctional escape rhythm.

Answer 195

B) Atropine Rationale: If a patient has symptoms with a junctional escape rhythm, atropine can be used to increase the heart rate.

Answer 196

B) To control the ventricular rate and prevent tachycardia Rationale: In the absence of digitalis toxicity, amiodarone is used for rate control to prevent tachycardia and manage the heart rate.

Answer 197

A) To decrease sympathetic stimulation and control heart rate Rationale: β-blockers are used to decrease sympathetic stimulation and control the heart rate in patients with junctional dysrhythmias.

Answer 198

A) Rheumatic heart disease Rationale: Junctional dysrhythmias are often associated with conditions such as HF, CAD, cardiomyopathy, electrolyte imbalances, inferior MI, and rheumatic heart disease.

Answer 199

C) Less than 0.12 seconds Rationale: The PR interval is less than 0.12 seconds when the P wave precedes the QRS complex in junctional dysrhythmias.

Answer 200

A. Administer IV amiodarone Rationale: Frequent PVCs, especially in patterns like couplets and bigeminy, can progress to ventricular tachycardia (VT) or ventricular fibrillation (VF), particularly in a patient with CAD. IV amiodarone is used to stabilize the heart’s electrical activity and prevent further dysrhythmias.

Answer 201

A. Check the patient’s magnesium level Rationale: Electrolyte imbalances, particularly hypokalemia and hypomagnesemia, are major causes of PVCs. Checking the magnesium level is essential because hypomagnesemia often coexists with hypokalemia and increases the risk of ventricular arrhythmias.

Answer 202

A. Assess for possible triggers, such as electrolyte imbalances or hypoxia Rationale: PVCs in a stable patient should first be evaluated for underlying causes, such as hypoxia, electrolyte disturbances, or acid-base imbalances. Treating the underlying cause often resolves the dysrhythmia without requiring antiarrhythmic drugs.

Answer 203

C. Ventricular fibrillation Rationale: R-on-T PVCs occur during the relative refractory period, when the heart is vulnerable to chaotic electrical activity. This increases the risk of ventricular fibrillation (VF), a life-threatening dysrhythmia that leads to cardiac arrest if not treated immediately.

Answer 204

D. Continue to monitor and notify the provider if symptoms develop Rationale: Asymptomatic PVCs in a stable patient post-MI require monitoring rather than immediate intervention. The nurse should continue assessing for changes in symptoms or worsening dysrhythmias that may require treatment.

Answer 205

A. “We will check your potassium and magnesium levels to see if they are contributing to the PVCs.” Rationale: Electrolyte imbalances (especially hypokalemia and hypomagnesemia) are common causes of PVCs. Checking these levels is an essential part of the assessment to determine if replacement therapy is needed.

Answer 206

C. Administer IV potassium chloride and magnesium sulfate Rationale: Hypokalemia (K+ < 3.5) and hypomagnesemia (Mg < 1.7) increase ventricular excitability, leading to multifocal PVCs. Replacing potassium and magnesium stabilizes the myocardium and reduces the risk of life-threatening dysrhythmias.

Answer 207

C. “If I feel palpitations, I should immediately take an extra dose of my beta-blocker.” Rationale: Patients should never self-adjust their beta-blocker dosage. Taking an extra dose could cause bradycardia and hypotension, potentially worsening cardiac instability. The patient should report increased PVCs to their provider instead.

Answer 208

B. Reduce caffeine and smoking to decrease PVC frequency Rationale: Caffeine and nicotine are common triggers of PVCs because they increase myocardial excitability. Educating the patient about reducing or eliminating these stimulants is the first step in managing PVCs associated with lifestyle factors.

Answer 209

C. Advise the patient to stop consuming energy drinks Rationale: Energy drinks contain high levels of caffeine and stimulants (e.g., taurine, guarana), which can increase myocardial irritability and lead to PVCs. Eliminating these drinks can reduce ectopic activity and prevent worsening dysrhythmias.

Answer 210

A. Potassium 2.9 mEq/L Rationale: Hypokalemia (K+ < 3.5 mEq/L) is a significant cause of PVCs because it increases cardiac excitability and the risk for life-threatening ventricular dysrhythmias, particularly in patients with heart failure. Potassium replacement is crucial to stabilize myocardial electrical activity.

Answer 211

A. Isoproterenol Rationale: Isoproterenol is a beta-adrenergic agonist that increases heart rate and myocardial excitability, making it a potential cause of PVCs. This medication should be used cautiously in patients with a history of MI to avoid inducing ventricular dysrhythmias.

Answer 212

D. Administer acetaminophen to reduce fever Rationale: Fever increases sympathetic nervous system activity, which can lead to increased myocardial excitability and PVCs. Reducing the fever with antipyretics (e.g., acetaminophen) can help decrease ectopic activity and stabilize the heart rhythm.

Answer 213

B. Premature Ventricular Contractions (PVCs) Rationale: PVCs are identified on ECG by wide and distorted QRS complexes that occur prematurely without a preceding P wave. The T wave is typically large and opposite in direction to the QRS complex due to abnormal ventricular repolarization. This distinguishes PVCs from atrial fibrillation (irregular atrial activity with fibrillatory waves), first-degree AV block (prolonged PR interval), and SVT (narrow QRS with rapid HR).

Answer 214

A. T waves are large and opposite in direction to the QRS complex Rationale: PVCs originate from an ectopic ventricular focus, causing wide and distorted QRS complexes with large, inverted T waves due to abnormal repolarization. In contrast, a normal sinus beat has a narrow QRS complex, a measurable PR interval, and a P wave preceding each QRS.

Answer 215

C. Unifocal PVCs have QRS complexes that are identical in shape, while multifocal PVCs have varying shapes Rationale: Unifocal PVCs arise from a single ectopic focus, producing PVCs with identical morphology on the ECG. Multifocal PVCs originate from multiple ectopic sites, resulting in PVCs with different shapes. Multifocal PVCs are generally more concerning because they indicate increased ventricular irritability and a higher risk for progression to ventricular tachycardia or fibrillation.

Answer 216

B. Premature ventricular contractions Rationale: PVCs may cause retrograde conduction, where the P wave appears after the QRS complex instead of preceding it. This is due to abnormal depolarization and conduction within the ventricles. PVCs are distinguished from atrial flutter (which has sawtooth flutter waves), AV blocks (which have measurable PR intervals), and idioventricular rhythm (which is a slow, regular rhythm with absent P waves).

Answer 217

B. Ventricular trigeminy Rationale: PVCs are classified based on their frequency and pattern: * Ventricular bigeminy: Every other beat is a PVC. * Ventricular trigeminy: Every third beat is a PVC. * Couplet: Two consecutive PVCs. * Ventricular tachycardia: Three or more consecutive PVCs. Since the PVCs occur every third beat, this is defined as ventricular trigeminy.

Answer 218

A. Assess the patient’s apical-radial pulse deficit Rationale: PVCs may reduce cardiac output (CO) because some contractions do not generate enough force to create a peripheral pulse. This can lead to angina, dizziness, or worsening heart failure in patients with CAD. Assessing the apical-radial pulse deficit helps determine if PVCs are compromising perfusion.

Answer 219

B. The patient is at risk for developing ventricular tachycardia (VT) or ventricular fibrillation (VF) Rationale: Multifocal PVCs indicate increased ventricular irritability, especially in the setting of acute MI. This increases the risk for ventricular tachycardia (VT) or ventricular fibrillation (VF), both of which can be life-threatening. * (A) Multifocal PVCs are not stable rhythms—they require monitoring and possible intervention. * (C) Lightheadedness can result from reduced CO due to frequent PVCs, not necessarily dehydration. * (D) PVCs are not a normal compensatory response; they reflect ventricular dysfunction and may worsen cardiac ischemia.

Answer 220

A. Assess for signs of worsening heart failure Rationale: PVCs in a patient with heart failure (HF) can further reduce cardiac output, leading to worsening symptoms like fatigue, dyspnea, and poor perfusion. The nurse should assess for signs of fluid overload, worsening pulmonary congestion, or hypotension, as PVCs can contribute to hemodynamic instability.

Answer 221

D. Hypokalemia Rationale: Hypokalemia increases ventricular irritability, making PVCs more likely, particularly in post-MI patients who are already at risk for dysrhythmias.

Answer 222

C. Obtain a 12-lead ECG Rationale: Frequent PVCs in a pattern of bigeminy in a patient with CAD and new-onset chest discomfort may indicate worsening myocardial ischemia or an impending myocardial infarction (MI). A 12-lead ECG is essential to assess for ST-segment changes and determine the need for further interventions.

Answer 223

A. Administer IV amiodarone Rationale: Frequent multifocal PVCs in a hypotensive, diaphoretic heart failure patient indicate severe ventricular irritability, increasing the risk of ventricular tachycardia (VT) or ventricular fibrillation (VF). Amiodarone is an antiarrhythmic drug used to stabilize ventricular ectopy and reduce the risk of life-threatening dysrhythmias.

Answer 224

B. Notify the provider immediately Rationale: R-on-T PVCs are dangerous because they can trigger ventricular tachycardia (VT) or ventricular fibrillation (VF). This phenomenon occurs when a PVC falls on the T wave of the preceding beat, a vulnerable period in the cardiac cycle. Immediate intervention is necessary to prevent a lethal arrhythmia.

Answer 225

A. Serum potassium of 2.9 mEq/L Rationale: Hypokalemia (K+ < 3.5 mEq/L) increases ventricular irritability, predisposing the patient to PVCs, ventricular tachycardia (VT), and ventricular fibrillation (VF). Potassium plays a crucial role in cardiac repolarization, and low levels delay repolarization, leading to ectopic ventricular beats. Immediate potassium replacement is necessary to reduce the risk of life-threatening arrhythmias.

Answer 226

B. Perform synchronized cardioversion Rationale: Synchronized cardioversion is the preferred treatment for monomorphic VT when the patient is hemodynamically unstable. It is performed to restore normal rhythm while ensuring synchronized timing to avoid inducing VF. * Amiodarone (A) may be used for VT but is not the first-line treatment in the presence of hemodynamic instability. * Lidocaine (C) is an antiarrhythmic used in VT but also not the first intervention in an unstable patient. * Atropine (D) is used for bradyarrhythmias, not tachyarrhythmias like VT.

Answer 227

A. Torsades de pointes Rationale: Torsades de pointes is a form of polymorphic VT associated with a prolonged QT interval, which causes a twisting of the points pattern on the ECG. * Hypokalemia (A) can lead to other arrhythmias but is not directly associated with torsades. * Myocardial infarction (C) typically leads to monomorphic VT, not polymorphic VT with a prolonged QT. * Atrial fibrillation (D) is a supraventricular arrhythmia, not a type of VT.

Answer 228

A. Myocardial infarction B. Prolonged QT interval C. Electrolyte imbalances E. Use of digoxin Rationale: * Myocardial infarction (A) and electrolyte imbalances (C) (such as hypokalemia or hypomagnesemia) are known triggers for VT. * Prolonged QT interval (B) predisposes patients to polymorphic VT, particularly torsades de pointes. * Digoxin (E) toxicity can lead to ventricular arrhythmias, including VT. * Bradycardia (D) is generally not a direct risk factor for VT; rather, VT is more commonly associated with tachycardia or other conditions such as ischemia or structural heart disease.

Answer 229

D. Administer 100% oxygen and obtain an ECG Rationale: For a nonsustained VT episode that causes symptoms, the first action should be to administer oxygen to improve oxygenation and obtain an ECG to evaluate the rhythm. This helps assess the severity and decide on further interventions. * Amiodarone (B) may be appropriate later but is not the first step without further assessment. * Synchronized cardioversion (C) is needed for sustained VT causing hemodynamic instability, but nonsustained VT requires more monitoring and assessment. * Monitoring and documenting (A) is important, but the symptoms of lightheadedness and drop in BP suggest a need for further intervention.

Answer 230

D. Wide QRS complexes that are consistent in size, shape, and direction Rationale: Monomorphic VT is characterized by wide, uniform QRS complexes that are consistent in shape, size, and direction. * Polymorphic VT (A) is associated with gradual changes in the QRS shape and direction. * Frequent P waves (C) are not seen in VT because it originates in the ventricles, not the atria. * A short QT interval (D) is not a defining characteristic of VT; instead, a prolonged QT can be associated with torsades de pointes.

Answer 231

B. Prepare for synchronized cardioversion Rationale: In a patient with sustained VT and hemodynamic instability (hypotension), synchronized cardioversion is the most immediate intervention to restore normal rhythm and improve the patient’s hemodynamics. * Fluid boluses (A) are useful for hypotension but are not the first-line treatment for VT. * Atropine (C) is used for bradycardia, not for tachyarrhythmias like VT. * Vagal maneuvers (D) are used for supraventricular tachycardias, not for ventricular arrhythmias like VT.

Answer 232

A. Chest pain B. Palpitations C. Shortness of breath D. Loss of consciousness Rationale: * Chest pain (A), palpitations (B), shortness of breath (C), and loss of consciousness (D) are common symptoms associated with sustained VT, which can cause reduced cardiac output. * Bradycardia (E) is typically not seen in VT, as it is a tachyarrhythmia, not a bradyarrhythmia.

Answer 233

C. Avoid medications that prolong the QT interval Rationale: Long QT syndrome increases the risk of developing torsades de pointes or other forms of polymorphic VT. The most effective way to manage this risk is to avoid QT-prolonging medications. * Administering IV potassium (A) may be appropriate for some arrhythmias but does not directly address the underlying long QT syndrome. * Lidocaine infusion (B) is used to treat VT but is not the first-line treatment in a patient with long QT syndrome. * Immediate defibrillation (D) is indicated for ventricular fibrillation (VF), not for treating VT without signs of hemodynamic instability.

Answer 234

C. Central nervous system disorder Rationale: Central nervous system disorders, such as head trauma, can trigger ventricular arrhythmias, including VT, even in the absence of heart disease. The sympathetic nervous system can become overstimulated due to brain injury, leading to arrhythmias. * Electrolyte imbalances (A) and drug toxicity (B) are common causes of VT but are not the most likely causes in this scenario based on the history of head injury. * Coronary artery disease (D) is not indicated in a patient with no heart disease.

Answer 235

D. Cardiomyopathy Rationale: Cardiomyopathy is strongly associated with ventricular tachycardia (VT) due to structural heart changes that can lead to electrical disturbances in the ventricles. * MI and CAD (A) may also cause VT but are not as directly related to cardiomyopathy as the primary cause. * Electrolyte imbalances (B) and long QT syndrome (C) are potential causes of VT but are not the main association with cardiomyopathy.

Answer 236

C. Ventricular tachycardia with AV dissociation Rationale: In ventricular tachycardia (VT), AV dissociation occurs when the atria and ventricles beat independently. The P waves may be buried in the QRS complex, and the PR interval is not measurable. This indicates that the atria and ventricles are not synchronized, which is characteristic of VT. * Complete AV block with retrograde conduction (A) is a possible cause of AV dissociation, but the wide QRS and regular rhythm more strongly indicate VT. * Sinus tachycardia with a bundle branch block (B) would not have the characteristic AV dissociation seen in VT. * Atrial fibrillation with ventricular response (D) typically shows irregular rhythms and no clear P waves, unlike VT.

Answer 237

A. Ventricular depolarization occurring asynchronously Rationale: A wide QRS complex greater than 0.12 seconds is a hallmark of ventricular tachycardia (VT), where the ventricles depolarize asynchronously. This results in a distorted and wide QRS that is characteristic of VT. * Impulse originating from the AV node (A) would not cause a wide QRS complex as seen in VT. * A premature atrial contraction (C) would not cause a wide QRS complex; it typically produces a normal QRS. * A prolonged PR interval (D) would affect the P wave to QRS relationship but not the QRS width.

Answer 238

C. Electrical discordance in VT Rationale: In ventricular tachycardia (VT), the T waves are typically in the opposite direction of the QRS complex, which is indicative of electrical discordance. This is a common finding in VT due to the asynchronous depolarization of the ventricles. * Left bundle branch block (A) would cause specific changes to the QRS morphology but not the T wave direction. * Myocardial ischemia (B) can cause changes in ST segments but does not typically cause the opposite T wave direction seen in VT. * Hyperkalemia (D) causes peaked T waves, not the opposite T wave direction seen in VT.

Answer 239

A. The patient is at risk for developing ventricular fibrillation Rationale: Ventricular tachycardia (VT) with wide QRS complexes, buried P waves, and an unstable rhythm places the patient at high risk for progressing to ventricular fibrillation (VF), which is a life-threatening arrhythmia. * Stable VT (A) would typically be characterized by a regular rhythm and no immediate risk for VF. * Atrial arrhythmias (C) would show a different pattern, typically with irregular rhythms and P waves not buried in the QRS. * Sinus tachycardia (D) would present with normal P waves and narrow QRS complexes, not the characteristics of VT.

Answer 240

A. There is a lack of communication between the atria and ventricles Rationale: The lack of a measurable PR interval and P waves occurring independently of the QRS complexes indicate AV dissociation, which is characteristic of ventricular tachycardia (VT). This means that the atria and ventricles are not synchronized, and each is firing independently. * Atrial and ventricular rhythms synchronized (A) would not show AV dissociation or buried P waves. * Heart rate within normal limits (C) does not apply in VT, where the rate is typically 150-250 beats per minute. * QRS originating from the SA node (D) would not result in the findings seen in VT, where the QRS is wide and distorted.

Answer 241

A. Immediate defibrillation Rationale: In ventricular tachycardia (VT), especially with ventricular rates exceeding 200 beats per minute, there is a high risk of progressing to ventricular fibrillation (VF). Immediate defibrillation is the priority intervention to prevent VF and restore a normal rhythm. * IV amiodarone (B) may be used to manage VT in certain situations but is not the first-line intervention when VT is life-threatening. * Supplemental oxygen (C) can be supportive but does not directly address the emergency of VT. * Monitoring for bradycardia (D) is not applicable to VT, as this rhythm is tachycardic.

Answer 242

A. Decreased ventricular diastolic filling times and loss of atrial contraction Rationale: In sustained VT, the rapid heart rate reduces the ventricular diastolic filling time and causes a loss of atrial contraction, resulting in severe decreases in cardiac output (CO). This leads to hypotension, pulmonary edema, and decreased cerebral blood flow. * Increased sympathetic nervous system activation (B) may occur in response to hypotension, but it is not the primary cause of the symptoms. * Increased preload and afterload (C) are not the causes of the symptoms seen in sustained VT. * Enhanced myocardial oxygen supply (D) is not related to the pathophysiology of sustained VT.

Answer 243

B. Antiarrhythmic medications such as amiodarone Rationale: For stable VT with a pulse and symptoms such as hypotension, the initial treatment is typically antiarrhythmic medications such as amiodarone to control the rhythm. * Immediate defibrillation (A) is used for pulseless VT or ventricular fibrillation (VF), not for stable VT with a pulse. * Administering oxygen and fluids (C) can be supportive but is not the primary treatment for managing VT. * Inserting a temporary pacemaker (D) is typically not the first-line intervention for stable VT with a pulse.

Answer 244

A. Initiate prophylactic antiarrhythmic therapy Rationale: To reduce the risk of recurrent episodes of VT, prophylactic antiarrhythmic therapy is recommended. This treatment helps prevent the recurrence of VT and ventricular fibrillation (VF). * Increasing physical activity (B) could potentially exacerbate the arrhythmia and increase the risk of further episodes. * Monitoring for bradycardia (C) is not appropriate, as VT is a tachycardic arrhythmia. * Increasing fluid intake (D) may help with hypotension, but it does not directly address the need for antiarrhythmic therapy to prevent recurrent VT.

Answer 245

B. Start chest compressions and prepare for defibrillation Rationale: For a pulseless VT patient, the first action is to start chest compressions and prepare for defibrillation. This is the priority intervention to attempt to restore a normal rhythm and prevent cardiopulmonary arrest. * Administering intravenous amiodarone (A) is appropriate for stable VT, but in the case of pulseless VT, defibrillation is the first line of treatment. * Synchronized cardioversion (C) is used for unstable rhythms such as atrial fibrillation or SVT, but defibrillation is needed for pulseless VT. * Inserting a temporary pacemaker (D) is not the initial treatment for pulseless VT, as defibrillation is the most critical intervention.

Answer 246

A. IV procainamide Rationale: For monomorphic VT in a clinically stable patient with a pulse and preserved left ventricular function, IV procainamide is an appropriate treatment. * IV magnesium (B) is used for polymorphic VT with a prolonged QT interval, not for monomorphic VT. * IV isoproterenol (C) is used for polymorphic VT with a prolonged QT interval, not for monomorphic VT. * IV amiodarone (D) can also be used for monomorphic VT, but procainamide is the preferred option for this specific case.

Answer 247

D. IV magnesium Rationale: For polymorphic VT with a prolonged baseline QT interval, the recommended treatment is IV magnesium. * IV procainamide (A) and IV lidocaine (C) are used for monomorphic VT, not for polymorphic VT with a prolonged QT interval. * IV amiodarone (D) may be used for VT but is not specifically recommended for polymorphic VT with a prolonged QT interval.

Answer 248

C. IV procainamide Rationale: For polymorphic VT with a normal baseline QT interval, IV procainamide is an appropriate treatment. * IV magnesium (A) is used for polymorphic VT with a prolonged QT interval, not for those with a normal QT interval. * IV isoproterenol (C) and antitachycardia pacing (D) are used for polymorphic VT with a prolonged QT interval, not for those with a normal QT interval.

Answer 249

B. Administer vasopressors such as epinephrine Rationale: For pulseless VT, after defibrillation fails, the next step is to administer vasopressors such as epinephrine. This helps to improve circulation during CPR. * IV lidocaine (A) and IV procainamide (C) are used for VT with a pulse, not for pulseless VT. * Synchronized cardioversion (D) is used for unstable rhythms with a pulse, not for pulseless VT.

Answer 250

D. Initiate CPR and prepare for defibrillation Rationale: For a pulseless VT patient, the priority intervention is to initiate CPR and prepare for defibrillation, which is the first line of treatment. * Administering antidysrhythmics (A) and starting IV fluids (C) are appropriate after defibrillation if necessary, but defibrillation comes first. * Synchronized cardioversion (D) is used for unstable rhythms with a pulse, not for pulseless VT.

Answer 251

A. Administer the medication as ordered, as it is effective for VT Rationale: IV lidocaine is appropriate for treating VT with a normal baseline QT interval and can be safely administered as ordered. * Monitoring for signs of QT prolongation (B) is not necessary in this case, as lidocaine does not cause QT prolongation. * Verifying the physician’s order (C) is unnecessary, as lidocaine is a standard treatment for VT. * Monitoring for signs of bradycardia (D) is not the primary concern for lidocaine, as it typically causes tachycardia, not bradycardia

Answer 252

B. Administering IV magnesium Rationale: For polymorphic VT with a prolonged baseline QT interval, the treatment of choice is IV magnesium, which helps stabilize the rhythm. * IV procainamide (A) and lidocaine (D) are not appropriate for polymorphic VT with a prolonged QT interval. * Synchronized cardioversion (C) may be used for unstable rhythms, but the first-line treatment for polymorphic VT with a prolonged QT is IV magnesium.

Answer 253

C. Administer epinephrine and continue CPR Rationale: For a pulseless VT patient who is unresponsive to defibrillation, the next step is to administer epinephrine and continue CPR to improve circulation and prepare for the next defibrillation attempt. * IV atropine (A) is used for bradycardia, not pulseless VT. * IV amiodarone (B) may be used for VT with a pulse, but it is not the immediate next step for pulseless VT. * Synchronized cardioversion (D) is used for unstable rhythms with a pulse, not for pulseless VT.

Answer 254

B. No effective contraction of the ventricles Rationale: In ventricular fibrillation (VF), the ventricles quiver with no effective contraction, leading to the absence of cardiac output (CO). * Decreased ventricular diastolic filling (A) may occur in other dysrhythmias but is not the primary cause in VF. * Increased CO (C) does not occur in VF; CO is essentially absent. * Normal electrical conduction (D) is disrupted in VF, as it is characterized by irregular, erratic electrical activity.

Answer 255

C. Initiate CPR and prepare for defibrillation Rationale: The immediate intervention for VF is to initiate CPR and prepare for defibrillation, as it is a life-threatening arrhythmia. * Administering vasopressors (A) is part of the treatment after defibrillation, not the first step. * Synchronized cardioversion (B) is used for rhythms with a pulse, not for pulseless VF. * Antidysrhythmics (D) are not the first-line treatment for VF; defibrillation is.

Answer 256

C. Rapid defibrillation Rationale: The priority in the management of VF is rapid defibrillation to restore a normal rhythm. * Administering oxygen (A) is important but should not delay defibrillation. * Monitoring for QT interval prolongation (B) is not a primary focus in VF; the priority is defibrillation. * Administering IV magnesium (D) is used for certain dysrhythmias like polymorphic VT with prolonged QT, but not for VF.

Answer 257

B. Irregular waveforms of varying shapes and amplitudes Rationale: Ventricular fibrillation (VF) is characterized by irregular waveforms of varying shapes and amplitudes, which represent chaotic electrical activity. * Regular, evenly spaced QRS complexes (A) are not seen in VF. * P waves and QRS complexes occurring at a fixed interval (C) would indicate a regular rhythm, not VF. * A narrow, uniform QRS complex (D) is typical of normal rhythms, not VF.

Answer 258

B. VF is a lethal dysrhythmia that requires immediate treatment Rationale: Ventricular fibrillation (VF) is a lethal dysrhythmia that requires immediate treatment to prevent death. * Medications alone (A) are not sufficient to treat VF; defibrillation is the first-line treatment. * VF is not benign (C) and will not resolve without treatment. * Electrolyte imbalances (D) can contribute to VF, but the primary cause is typically electrical instability in the ventricles, not always an imbalance.

Answer 259

D. Hyperkalemia Rationale: Hyperkalemia is a recognized risk factor for ventricular fibrillation (VF) due to its effects on the electrical conductivity of the heart. * Normal cardiac conduction (A) would not lead to VF. * While decreased oxygen supply (C) to the heart can contribute to ischemia and arrhythmias, hyperkalemia (B) directly affects the electrical system and increases VF risk. * Increased blood pressure (D) is not a typical direct cause of VF.

Answer 260

A. Impaired ventricular function leading to electrical instability Rationale: Impaired ventricular function in heart failure (HF) leads to electrical instability, increasing the risk of ventricular fibrillation (VF). * Increased blood flow to the myocardium (B) is generally beneficial and does not contribute to VF. * Low serum potassium (C) can increase the risk of arrhythmias, but it is not the primary factor for VF in HF. * Effective cardiac pacing (D) helps to regulate the heart rhythm, reducing the risk of VF.

Answer 261

A. Stimulation of the ventricle by the catheter Rationale: During cardiac catheterization, stimulation of the ventricle by the catheter is a known cause of ventricular fibrillation (VF). * Improved myocardial oxygenation (B) would reduce the likelihood of arrhythmias, not increase it. * Administration of anticoagulants (C) can increase bleeding risk but is not a primary cause of VF. * Increased sympathetic nervous system activity (D) can contribute to arrhythmias but is less directly linked to VF in this context.

Answer 262

A. The reperfusion of coronary arteries Rationale: Reperfusion of coronary arteries after thrombolytic therapy can lead to ventricular fibrillation (VF) due to the sudden changes in myocardial electrical stability. * Decreased myocardial oxygen demand (B) typically occurs as a result of successful reperfusion, but it does not directly cause VF. * Reduction in ventricular filling time (C) is related to ventricular dysfunction but not directly linked to VF. * Increased heart rate (D) can be a side effect of certain medications but is not a primary cause of VF in this scenario.

Answer 263

B. Ventricular fibrillation Rationale: The described ECG findings are characteristic of ventricular fibrillation (VF), which is marked by an irregular and chaotic rhythm, with no measurable P wave, PR interval, or QRS interval. * Atrial fibrillation (A) has a chaotic rhythm but still has visible P waves, though they are not clearly defined. * Sinus arrest (C) involves a pause in the normal rhythm, but it does not present with the chaotic rhythm described here. * Normal sinus rhythm (D) would have a regular rhythm with measurable P waves, PR intervals, and QRS intervals.

Answer 264

C. Begin chest compressions Rationale: For ventricular fibrillation (VF), immediate chest compressions are the priority, as they help maintain circulation and provide some perfusion to vital organs until defibrillation can be performed. * Administering IV amiodarone (A) and oxygen therapy (C) are important but come after chest compressions in the emergency treatment sequence. * Synchronized cardioversion (D) is used for certain arrhythmias but is not the initial treatment for VF.

Answer 265

A. To restore the heart’s electrical activity to normal sinus rhythm Rationale: Defibrillation aims to deliver an electric shock to the heart to restore normal electrical activity and stop the chaotic rhythm seen in ventricular fibrillation (VF). * Defibrillation (B) does not temporarily stop the heart; it is intended to reset the electrical activity, not just halt it. * Stimulating the atria (C) is not the goal in VF treatment, as the ventricular rhythm must be corrected. * Increasing heart rate (D) applies to conditions of bradycardia, not VF.

Answer 266

D. Absence of a pulse, unresponsiveness, and apnea Rationale: Ventricular fibrillation (VF) leads to complete loss of effective cardiac output, resulting in no pulse, unresponsiveness, and apnea. * Regular pulse and normal blood pressure (A) are not consistent with VF, which causes cardiac arrest. * Slow and irregular pulse (C) is seen in arrhythmias like bradycardia or heart block, but VF leads to pulselessness. * Bounding pulse (D) would indicate good circulation, which is not present in VF.

Answer 267

C. To promote vasoconstriction and improve coronary perfusion Rationale: Epinephrine is administered in ventricular fibrillation (VF) to promote vasoconstriction, which helps improve coronary perfusion during CPR, increasing the chances of successful defibrillation. * Increasing heart rate (A) is not the primary effect of epinephrine; its role is improving perfusion. * Stimulating pacemaker cells (B) is not the purpose of epinephrine in VF. * Correcting electrolyte imbalances (D) is not the primary action of epinephrine.

Answer 268

B. Performing chest compressions while awaiting defibrillation Rationale: Chest compressions are the first and most important step in ventricular fibrillation (VF) treatment to maintain circulation and perfusion until defibrillation can be performed. * Administering fluids (A) may be helpful in other cases but is not a priority in VF treatment. * Giving aspirin (C) is not a priority in VF, as the immediate goal is to restore the heart’s rhythm. * Checking blood pressure (D) is unnecessary when the patient is pulseless.

Answer 269

B. Rapid, irregular ventricular rate with no identifiable P waves Rationale: During ventricular fibrillation (VF), the ECG shows a rapid, irregular ventricular rate with no identifiable P waves, PR interval, or QRS complex. * Wide, regular QRS complexes (A) are seen in other arrhythmias but not in VF. * Slow, regular rhythm (C) is not typical of VF, which is chaotic and irregular. * Normal sinus rhythm (D) is a healthy rhythm, not associated with VF.

Answer 270

D. Begin CPR with chest compressions Rationale: The first step in the ACLS protocol for ventricular fibrillation (VF) is to begin CPR with chest compressions, which helps maintain circulation until defibrillation can be performed. * Defibrillation (A) is performed after CPR has been initiated. * Epinephrine (B) is given after chest compressions, not immediately. * Assessing the airway (D) is important but should be done simultaneously with chest compressions.

Answer 271

D. Asystole Rationale: The description of no ventricular electrical activity with occasional P waves and the absence of ventricular contraction is characteristic of asystole. In this condition, there is no electrical activity in the ventricles, and the patient is unresponsive, pulseless, and apneic. * Ventricular fibrillation (A) presents with chaotic, irregular electrical activity in the ventricles, not as a flatline with P waves. * Atrial fibrillation (C) shows irregularly irregular rhythms and rapid atrial activity, but not a flatline pattern. * Sinus bradycardia (D) involves a slow, regular rhythm, which would not lead to a flatline appearance.

Answer 272

B. Start chest compressions immediately Rationale: In the case of asystole, chest compressions should be started immediately as part of the ACLS protocol to provide circulation until other interventions can be initiated. * Defibrillation (A) is not indicated in asystole, as there is no electrical activity to reset. * High-dose epinephrine (C) is an appropriate treatment after chest compressions have been initiated, but it is not the first step. * Synchronized cardioversion (D) is used for certain arrhythmias but not for asystole.

Answer 273

A. Assess the rhythm in multiple leads Rationale: Before diagnosing asystole, the nurse should assess the rhythm in more than one lead, as ventricular fibrillation (VF) can occasionally masquerade as asystole in a single lead. * Administering amiodarone (B) is appropriate for treating ventricular arrhythmias, not asystole. * Monitoring (C) for 5 minutes is too long to wait in an emergency situation like this. Immediate action is needed. * Synchronized cardioversion (D) is used for certain arrhythmias but not for asystole.

Answer 274

B. A flatline with occasional P waves Rationale: Asystole is characterized by a flatline on the ECG, with occasional P waves sometimes seen, but there is no ventricular electrical activity or contraction. * Chaotic and irregular rhythm (A) describes ventricular fibrillation, not asystole. * Regular, slow rhythm (C) is seen in sinus bradycardia, not asystole. * Rapid, irregular rhythm with wide QRS complexes (D) is characteristic of ventricular tachycardia, not asystole.

Answer 275

C. Very poor, with minimal chance of recovery Rationale: The prognosis for a patient in asystole is generally very poor, as it is a lethal dysrhythmia with minimal chances of recovery if not treated immediately and effectively. * Excellent prognosis (A) is unlikely in asystole, especially without rapid intervention. * Defibrillation (C) is not effective in asystole, as there is no electrical activity to reset. * Moderate prognosis (D) may apply to other conditions but not to asystole, where the prognosis is extremely poor.

Answer 276

B. End-stage heart failure Rationale: Asystole is often a result of advanced heart disease, severe conduction system issues, or end-stage heart failure (HF). This patient’s history of heart disease makes end-stage HF a likely cause. * Myocardial infarction (A) can lead to arrhythmias, but asystole is more commonly associated with end-stage heart disease or prolonged arrest. * Atrial fibrillation (C) and ventricular tachycardia (D) are distinct arrhythmias that would not typically lead directly to asystole.

Answer 277

B. Epinephrine Rationale: For asystole, epinephrine is the first-line drug used during CPR and ACLS measures to stimulate cardiac activity. * Defibrillation (A) is not indicated in asystole because there is no electrical activity to reset. * Amiodarone (C) and Lidocaine (D) are used for arrhythmias like ventricular fibrillation or ventricular tachycardia, not asystole.

Answer 278

C. Chest compressions with CPR Rationale: For asystole, chest compressions with CPR should be started immediately to maintain circulation. This is the most crucial first step. * Intubation (A) may be necessary later, but chest compressions are the priority. * Synchronized cardioversion (B) is used for certain arrhythmias, not asystole. * Defibrillation (D) is ineffective in asystole since there is no electrical activity to reset.

Answer 279

A. Hyperkalemia Rationale: Hyperkalemia is a known cause of asystole and should be ruled out as part of the underlying cause. * Hypertension (B), atrial fibrillation (C), and left-sided heart failure (D) are not direct causes of asystole, though they can contribute to heart failure or other conditions that increase the risk of asystole.

Answer 280

D. Continue chest compressions and assess for a pulse Rationale: The most important action is to continue chest compressions and assess for a pulse regularly. This provides the necessary circulation and ensures proper perfusion during the resuscitation effort. * Synchronized cardioversion (A) is not used for asystole. * Sodium bicarbonate (B) is not typically used in the initial treatment of asystole. * Assessing the rhythm in more than one lead (C) should have been done early in the process to confirm the diagnosis of asystole.

Answer 281

C. Correcting the underlying cause Rationale: The most critical step in managing PEA is identifying and correcting the underlying cause. This can significantly impact prognosis. * Immediate defibrillation (A) is not effective in PEA since there is organized electrical activity, not a shockable rhythm. * Sodium bicarbonate (B) is not indicated unless acidosis is present. * Inserting a temporary pacemaker (D) is not a first-line treatment for PEA.

Answer 282

C. Hyperkalemia Rationale: Hyperkalemia is a common cause of PEA. Other causes include hypovolemia, hypoxia, metabolic acidosis, and more. * Atrial fibrillation (A) and ventricular fibrillation (D) are not causes of PEA but are other types of dysrhythmias. * Coronary artery disease (B) can lead to PEA if it results in conditions like myocardial infarction (thrombosis).

Answer 283

D. Epinephrine Rationale: The first-line drug for PEA is epinephrine, which should be administered as part of CPR to stimulate cardiac activity and improve prognosis. * Lidocaine (A) and amiodarone (C) are used for other arrhythmias, but not for PEA. * Magnesium sulfate (D) is used for certain arrhythmias, such as torsades de pointes, but not for PEA.

Answer 284

B. Administration of fluid resuscitation Rationale: In hypovolemia-induced PEA, the priority treatment is fluid resuscitation to restore circulating blood volume. * Immediate defibrillation (A) is not effective in PEA. * Magnesium sulfate (C) is not the first treatment for hypovolemia. * Antitachycardia pacing (D) is not used for PEA.

Answer 285

A. Drug therapy and intubation Rationale: For PEA caused by drug overdose, drug therapy (e.g., epinephrine) and intubation are necessary to manage the patient. * Rapid defibrillation (A) is not appropriate for PEA, as it is not a shockable rhythm. * Pacemaker insertion (C) is not indicated for PEA. * Correcting electrolyte imbalances (D) is important but is part of managing the underlying cause.

Answer 286

C. Restoring mechanical cardiac function Rationale: The primary goal in PEA is to restore mechanical cardiac function, as there is electrical activity but no effective cardiac contraction. * Restoring electrical activity (A) is not the main goal; mechanical function must be restored for effective circulation. * Preventing further arrhythmias (B) and correcting the cause (D) are important but secondary to restoring cardiac output.

Answer 287

C. Insertion of a chest tube Rationale: For a tension pneumothorax, the priority intervention is to insert a chest tube to relieve the pressure and restore normal circulation. * Intubation (A) and mechanical ventilation may be needed but are secondary to treating the tension pneumothorax. * Sodium bicarbonate (C) and defibrillation (D) are not indicated for tension pneumothorax.

Answer 288

A. Hyperkalemia Rationale: Hyperkalemia is one of the common causes of PEA, and it must be identified and corrected to improve the prognosis. * Hypertension (B), atrial fibrillation (C), and coronary artery disease (D) may predispose to other arrhythmias but are not the most common causes of PEA.

Answer 289

B. Obtain baseline ECG and vital signs Rationale: Before administering any antidysrhythmic medication, the nurse must obtain a baseline ECG to assess for preexisting conduction abnormalities and monitor for changes after administration. Vital signs, especially heart rate and blood pressure, are essential to evaluate the patient’s stability and response to treatment. Amiodarone has significant effects on cardiac conduction, so baseline data are crucial.

Answer 290

B. “I will check my pulse daily and report any irregularities to my healthcare provider.” C. “I need to avoid drinking grapefruit juice while taking this medication.” D. “If I develop a dry cough or shortness of breath, I should notify my provider immediately.” Rationale: * B: Patients taking antidysrhythmic medications should monitor their pulse daily, as these drugs can alter heart rate and rhythm. * C: Grapefruit juice can interfere with the metabolism of certain antidysrhythmics, such as amiodarone, leading to toxicity. * D: Antidysrhythmic drugs, particularly amiodarone, can cause pulmonary toxicity, which may present as a dry cough or shortness of breath. This requires immediate medical attention. * A and E are incorrect because most antidysrhythmic drugs are better tolerated with food to prevent GI upset, and smoking can exacerbate cardiac dysrhythmias.

Answer 291

A. Stop the infusion and notify the provider Rationale: Lidocaine toxicity can present as confusion, slurred speech, dizziness, and even seizures. The nurse should immediately stop the infusion and notify the provider to prevent further complications. Continuing the infusion or delaying intervention could worsen neurotoxicity and cardiac effects.

Answer 292

B. Thyroid dysfunction Rationale: Amiodarone contains iodine and can cause hypo- or hyperthyroidism. Symptoms such as fatigue, weight gain, and cold intolerance suggest hypothyroidism, a common adverse effect. The nurse should notify the provider and expect thyroid function tests.

Answer 293

A. Monitor the ECG for asystole and bradycardia B. Have emergency equipment readily available D. Assess for flushing, dizziness, or chest discomfort Rationale: * A: Adenosine causes a brief period of asystole before converting the rhythm. This is expected but should be closely monitored. * B: Emergency equipment should always be available in case the patient does not recover from the brief asystole. * D: Side effects of adenosine include flushing, dizziness, and chest discomfort, which should be assessed and documented. * C is incorrect because adenosine should be administered as a rapid IV push followed by a saline flush. * E is incorrect because repeated doses should be given only if ordered and with a proper time interval.

Answer 294

A. Pharmacist, to evaluate drug interactions Rationale: Diltiazem, a calcium channel blocker, can interact with other medications like beta-blockers and digoxin, increasing the risk of bradycardia and hypotension. The pharmacist plays a crucial role in assessing drug interactions. While other team members may be involved in the patient’s care, the pharmacist is most relevant in managing antidysrhythmic therapy.

Answer 295

B. Administer potassium replacement Rationale: Hypokalemia increases the risk of life-threatening dysrhythmias, especially in patients on sotalol, a beta-blocker with class III antidysrhythmic properties. Correcting potassium is crucial to preventing arrhythmias like torsades de pointes.

Answer 296

D. Check the patient’s potassium and magnesium levels Rationale: A prolonged QT interval increases the risk of torsades de pointes. Low potassium or magnesium levels can contribute to QT prolongation, so checking electrolytes is the priority. If abnormalities are present, they should be corrected to prevent life-threatening arrhythmias.

Answer 297

C. Deliver a defibrillation shock as soon as the defibrillator is available Rationale: Defibrillation is the priority intervention for VF or pulseless VT. It is most effective when performed within 2 minutes of cardiac arrest. CPR should be initiated while the defibrillator is being retrieved, but once it is available, immediate defibrillation takes precedence. Epinephrine is given after the first shock and CPR cycle.

Answer 298

A. “Defibrillation is the treatment of choice for pulseless ventricular tachycardia.” B. “CPR should be paused while the defibrillator is charging.” C. “The defibrillator should deliver an initial 360-joule shock when using a monophasic defibrillator.” E. “After the first shock, I should immediately resume CPR, starting with chest compressions.” Rationale: * A: Defibrillation is the first-line treatment for pulseless VT and VF. * B: CPR should be paused briefly while the defibrillator is charging to minimize interruptions. * C: Monophasic defibrillators deliver an initial shock of 360 joules. * E: After defibrillation, CPR should be resumed immediately to maintain circulation. * D is incorrect because biphasic defibrillators require lower energy shocks (120-200 joules), leading to fewer post-shock dysrhythmias.

Answer 299

B. Confirm the absence of a pulse and initiate CPR Rationale: Before defibrillating, the nurse must confirm that the patient is truly pulseless. Once pulseless VT or VF is confirmed, CPR should begin immediately while preparing for defibrillation. Defibrillation should never be delayed for medication administration. Synchronized mode is used for cardioversion, not for pulseless rhythms.

Answer 300

A. Ensure the patient’s chest is dry before placing the AED pads C. Confirm that no one is touching the patient before delivering a shock E. Allow the AED to analyze the rhythm before delivering a shock Rationale: * A: The chest should be dry to ensure proper conduction of electrical energy. * C: No one should touch the patient when the shock is delivered to prevent accidental injury. * E: The AED automatically analyzes the rhythm before instructing the user to deliver a shock. * B is incorrect because medication patches should be removed before placing AED pads. * D is incorrect because pediatric pads should not be used on adults; if only pediatric pads are available, manual CPR should be performed until proper equipment is obtained.

Answer 301

B. The respiratory therapist Rationale: During cardiac resuscitation, the respiratory therapist is responsible for managing the airway, including providing oxygenation and ventilations. The nurse focuses on defibrillation, medication administration, and CPR coordination.

Answer 302

B. Resume CPR immediately and prepare to administer epinephrine Rationale: If the first defibrillation attempt is unsuccessful, CPR should be resumed immediately to maintain circulation. Epinephrine is then given per ACLS protocol to increase the likelihood of successful defibrillation. A pulse check should not be performed until after CPR and rhythm assessment. Cardioversion is used for tachyarrhythmias with a pulse.

Answer 303

B. 300 mg IV push Rationale: According to ACLS guidelines, the first dose of amiodarone in cardiac arrest due to VF or pulseless VT is 300 mg IV push. A second dose of 150 mg may be given if needed.

Answer 304

A. Ensure the “all clear” command is given before delivering a shock D. Position the defibrillator pads at least 1 inch away from pacemaker sites E. Confirm that the defibrillator is set to the appropriate energy level Rationale: * A: The “all clear” command ensures no one is in contact with the patient. * D: Pads should be placed at least 1 inch from pacemakers to prevent device malfunction. * E: Proper energy selection is crucial for effective defibrillation. * B is incorrect because conductive gel pads should not be placed over ECG electrodes. * C is incorrect because synchronized mode is used for cardioversion, not defibrillation.

Answer 305

C. “I should check for a pulse after the AED advises a shock.” Rationale: The AED automatically assesses the heart rhythm. Rescuers should not delay CPR to check for a pulse after a shock. Instead, CPR should be resumed immediately as per AED instructions.

Answer 306

A. Administration of IV adenosine before considering cardioversion Rationale: In a stable patient with SVT, the first-line treatment is vagal maneuvers followed by IV adenosine to terminate the rhythm. If the rhythm persists, synchronized cardioversion may be required. Defibrillation is only used for pulseless rhythms or ventricular fibrillation (VF). Transcutaneous pacing is used for bradycardia, not tachyarrhythmias.

Answer 307

A. Ensure the synchronizer switch is turned on before delivering the shock B. Start with an initial energy level of 50 to 100 joules with a biphasic defibrillator C. Sedate the patient with IV fentanyl if hemodynamically stable E. Be prepared to switch to defibrillation mode if the patient becomes pulseless Rationale: * A: The synchronizer switch must be turned on to ensure the shock is delivered on the R wave. * B: The initial energy for cardioversion in atrial flutter or SVT is 50 to 100 joules (biphasic). * C: If the patient is stable, sedation is administered before cardioversion. * E: If the patient deteriorates into a pulseless rhythm (e.g., VF), the synchronizer must be turned off, and defibrillation should be performed. * D is incorrect because defibrillator pads should not be placed over ECG electrodes.

Answer 308

C. 120-200 joules Rationale: Atrial fibrillation requires a higher energy level for cardioversion than SVT or atrial flutter. The recommended starting energy for synchronized cardioversion of atrial fibrillation using a biphasic defibrillator is 120-200 joules.

Answer 309

D. Prepare for synchronized cardioversion at 100 joules Rationale: The patient has VT with a pulse but is hemodynamically unstable (hypotension, diaphoresis). In this case, synchronized cardioversion should be performed as quickly as possible. If the patient were stable, IV antiarrhythmic drugs like amiodarone would be considered first. Defibrillation is used only if the patient becomes pulseless.

Answer 310

A. Ensure the synchronizer mode is activated before delivering the shock B. Confirm that all personnel are clear of the patient before delivering the shock D. Continuously monitor the patient’s airway and oxygenation E. If the patient becomes pulseless, turn off the synchronizer and defibrillate Rationale: * A: The synchronizer switch must be turned on to prevent an R-on-T phenomenon, which can cause VF. * B: Ensuring that no one is touching the patient prevents accidental electrical injury. * D: Airway monitoring is critical, especially if sedation is used. * E: If the patient loses a pulse or the rhythm changes to VF, defibrillation is required. * C is incorrect because initial energy settings depend on the rhythm (50-100 joules for SVT/VT with a pulse, higher for AFib).

Answer 311

D. Initiate CPR and prepare to administer epinephrine Rationale: Asystole following cardioversion indicates that the heart is not generating electrical activity. The immediate priority is to initiate CPR and administer epinephrine as per ACLS protocols. Additional shocks are not indicated for asystole.

Answer 312

D. Airway patency and respiratory status Rationale: Sedation with midazolam or fentanyl can cause respiratory depression. Maintaining a patent airway and monitoring respiratory status is the highest priority during cardioversion.

Answer 313

C. “The shock may feel like a sudden jolt, but it is brief and lifesaving.” Rationale: Patients with ICDs often fear the sensation of the shock. It is important to reassure them that the shock, while potentially startling, is brief and intended to restore a normal heart rhythm. The ICD does not shock for bradycardia, and patients do not need to seek immediate medical attention unless they experience multiple shocks or symptoms.

Answer 314

A. “Avoid lifting your arm above your shoulder on the side of the ICD placement for at least 6 weeks.” B. “You should notify your healthcare provider if you receive more than one shock within a short period.” D. “Avoid standing near strong electromagnetic fields, such as airport security scanners.” E. “You should wear a medical alert bracelet indicating you have an ICD.” Rationale: * A: Patients should avoid excessive arm movement on the ICD side to prevent lead displacement. * B: Multiple shocks in a short time could indicate an issue that requires medical evaluation. * D: Strong electromagnetic fields can interfere with ICD function. * E: A medical alert bracelet helps emergency responders identify the ICD. * C is incorrect because most ICDs are not MRI-compatible unless specifically designed for MRI use.

Answer 315

B. Call for emergency help and begin CPR immediately. Rationale: If the ICD fails to restore a normal rhythm, CPR should be initiated immediately while awaiting emergency response. ICDs are programmed and maintained by specialists; nurses cannot adjust shock thresholds or reprogram the device.

Answer 316

A. A 55-year-old who survived sudden cardiac death due to ventricular fibrillation C. A 60-year-old with spontaneous sustained ventricular tachycardia D. A 45-year-old with hypertrophic cardiomyopathy at high risk for ventricular dysrhythmias Rationale: * A: ICDs are indicated for patients who have survived sudden cardiac death due to VF. * C: ICDs are recommended for sustained VT to prevent life-threatening arrhythmias. * D: ICDs are used for high-risk patients with conditions like hypertrophic cardiomyopathy. * B and E are incorrect because bradycardia is treated with pacemakers, and atrial fibrillation is usually managed with medications, cardioversion, or ablation.

Answer 317

B. “Check your pulse, and if it is normal and you feel fine, continue monitoring for additional symptoms.” Rationale: A single shock without ongoing symptoms may indicate the ICD appropriately treated a transient arrhythmia. However, multiple shocks or associated symptoms should prompt medical evaluation.

Answer 318

C. “I need to avoid microwave ovens at home.” Rationale: Modern microwave ovens do not interfere with ICDs. However, patients should still avoid strong electromagnetic fields, such as MRI machines and industrial magnets.

Answer 319

B. “If you receive more than one shock in a short period, seek medical attention immediately.” C. “If you feel unwell after a shock, call 911.” Rationale: * B: Multiple shocks could indicate an ongoing life-threatening arrhythmia requiring immediate medical evaluation. * C: If a patient feels unwell after a shock, emergency services should be contacted. * A, D, and E are incorrect because resting alone is not sufficient, and ICDs cannot be manually reset by patients.

Answer 320

A. Ensure the ICD is turned off before surgery. Rationale: Electrocautery used during surgery can interfere with the ICD. The device should be temporarily turned off by a cardiology specialist to prevent inappropriate shocks.

Answer 321

C. Swelling and redness around the incision site with a temperature of 101°F (38.3°C) Rationale: Signs of infection, such as redness, swelling, and fever, require immediate intervention to prevent complications, including sepsis or device-related infections. Mild discomfort is expected, and body image concerns should be addressed with support and education.

Answer 322

A. “Carry a medical alert ID indicating you have an ICD.” B. “Inform airport security that you have an ICD before passing through metal detectors.” C. “Avoid placing your cell phone in a pocket near the ICD.” E. “When traveling, bring a copy of your ICD identification card and your healthcare provider’s contact information.” Rationale: * A & E: Carrying identification and healthcare provider information ensures appropriate care if an emergency arises. * B: Airport security scanners contain electromagnetic fields that may interfere with ICDs; patients should notify security personnel. * C: Cell phones should be kept at least 6 inches away from the ICD to avoid interference. * D is incorrect because air travel is safe for patients with ICDs.

Answer 323

C. “You may gradually return to normal activities, but avoid contact sports and heavy lifting for now.” Rationale: Patients can resume normal activities but should avoid activities that could displace leads (such as heavy lifting) or cause direct trauma to the ICD (such as contact sports).

Answer 324

D. Ask the patient if they experienced symptoms such as dizziness, chest pain, or syncope. Rationale: The presence of symptoms can indicate that the shocks were appropriate for life-threatening dysrhythmias. If symptoms are present, urgent evaluation is needed. While notifying the provider is important, gathering more data first helps guide clinical decision-making.

Answer 325

A. Reassessing ICD settings and lead placement B. Checking for electrolyte imbalances such as hypokalemia E. Evaluating for triggers such as strong electromagnetic interference Rationale: * A: Improper lead placement or incorrect device programming may cause inappropriate shocks. * B: Electrolyte imbalances can cause arrhythmias that trigger unnecessary ICD shocks. * E: Environmental factors, such as electromagnetic interference, may falsely trigger the ICD. * C is incorrect because while anxiety management is important, it does not address the cause of inappropriate shocks. * D is incorrect because patients should never turn off their ICD on their own.

Answer 326

A. Place the patient on continuous ECG monitoring. Rationale: Continuous ECG monitoring allows for assessment of the underlying rhythm and determines if the ICD shocks were appropriate. While resting, glucose monitoring, and anxiety management may be beneficial, they are not the priority.

Answer 327

B. “I can place my cell phone in my chest pocket next to the ICD for easy access.” Rationale: Cell phones should be kept at least 6 inches away from the ICD to prevent electromagnetic interference. The other statements reflect appropriate post-procedure care.

Answer 328

C. The patient’s heart rate is 40 beats per minute despite the pacemaker being set at 60 beats per minute. Rationale: A heart rate significantly below the pacemaker’s set rate indicates pacemaker malfunction, such as failure to capture or failure to pace. This requires immediate intervention to assess the device and prevent hemodynamic instability. Mild discomfort at the incision site is expected, occasional dizziness may be related to orthostatic hypotension, and paced beats with capture indicate normal pacemaker function.

Answer 329

A. “I will carry a pacemaker identification card with me at all times.” B. “I should avoid MRI scans unless my pacemaker is MRI-compatible.” C. “I can safely use my microwave at home.” D. “I will avoid lifting my affected arm above my shoulder until cleared by my doctor.” Rationale: * A & B: Patients should carry identification in case of emergencies and avoid MRI if the pacemaker is not MRI-compatible. * C: Modern pacemakers are shielded, making microwaves safe to use. * D: Raising the affected arm above the shoulder too soon can dislodge leads. * E is incorrect because cell phones should be kept at least 6 inches away from the pacemaker to avoid electromagnetic interference.

Answer 330

A. Check the pacemaker battery function. Rationale: Dizziness in a pacemaker-dependent patient with no paced beats suggests pacemaker malfunction, possibly due to battery depletion or lead displacement. Checking battery function is a priority to ensure proper pacing. Increasing fluids or lying down does not address the underlying issue, and dizziness is not a normal or expected symptom of a functioning pacemaker.

Answer 331

A. Increase the pacemaker’s milliamperage output. Rationale: Pacing spikes without QRS complexes indicate failure to capture, meaning the pacemaker’s impulse is not strong enough to depolarize the myocardium. Increasing the milliamperage enhances electrical stimulation to promote capture. Atropine is used for bradycardia but does not address pacemaker failure. Trendelenburg positioning and arm repositioning are not appropriate interventions for pacemaker capture failure.

Answer 332

A. The patient’s ECG shows pacing spikes but no QRS complexes. B. The patient reports feeling lightheaded and fatigued. D. The ECG shows random pacing spikes not followed by a heartbeat. Rationale: * A & D: Pacing spikes without associated QRS complexes suggest failure to capture, a sign of pacemaker malfunction. * B: Lightheadedness and fatigue may indicate inadequate cardiac output due to pacemaker failure. * C is incorrect because the pacemaker only functions when the HR drops below its set threshold. * E is incorrect because occasional palpitations without abnormal ECG findings do not necessarily indicate pacemaker malfunction.

Answer 333

C. The ECG shows loss of sensing and erratic pacemaker firing. Rationale: Electromagnetic interference (EMI) from power tools can disrupt pacemaker function, causing inappropriate pacing. Loss of sensing and erratic pacing indicate pacemaker malfunction, which requires immediate evaluation. A stable HR, mild soreness, and temporary memory loss are not as concerning as potential pacemaker dysfunction.

Answer 334

C. The patient states, “I feel like something is pounding in my chest.” Rationale: A sensation of pounding in the chest could indicate pacemaker lead dislodgement or malfunction. This requires immediate evaluation. Restraining the affected arm is inappropriate, as gentle movement is encouraged to prevent stiffness. A clean incision site and consistent pacemaker function are expected findings.

Answer 335

D. “You can resume most normal activities, but avoid contact sports and heavy lifting until cleared by your doctor.” Rationale: Patients with pacemakers can return to regular activities, but contact sports and heavy lifting can displace leads or damage the device. Avoiding all activity is unnecessary, and unrestricted strenuous activity without clearance is unsafe.

Answer 336

B. Teach the patient to avoid lifting the affected arm above the shoulder. Rationale: Lifting the affected arm above the shoulder too soon after pacemaker implantation can dislodge the pacing leads. The patient should avoid excessive movement of the arm for several weeks. Range-of-motion exercises should be limited initially, and sleeping on the pacemaker side may cause discomfort and increase the risk of lead dislodgment. Immediate resumption of normal activities is not recommended.

Answer 337

C. “I can have an MRI whenever needed.” D. “I should avoid standing near strong magnets, such as in airport security.” Rationale: * C: Not all pacemakers are MRI-compatible. The patient must check with their provider before undergoing an MRI. * D: Strong electromagnetic fields, such as those in airport security, can interfere with pacemaker function. The patient should inform security personnel about their device. * A, B, and E are correct statements and demonstrate proper understanding of post-pacemaker care.

Answer 338

C. Prepare to initiate transcutaneous pacing. Rationale: A heart rate of 30 bpm without pacemaker spikes suggests pacemaker failure (failure to pace). Transcutaneous pacing is the priority intervention to maintain cardiac output while awaiting further evaluation. Atropine may be considered but is not the first-line treatment for pacemaker failure. Trendelenburg positioning does not address the underlying issue, and increasing the pacemaker’s sensitivity setting is not within the nurse’s scope of practice.

Answer 339

A. “A leadless pacemaker eliminates the risk of lead-related complications.” Rationale: Leadless pacemakers do not require transvenous leads, reducing complications such as lead dislodgment, fracture, or infection. They are typically smaller but have a similar battery lifespan to traditional pacemakers. Most leadless pacemakers remain in the heart after the battery depletes, with a new device implanted as needed. Leadless pacemakers are primarily used for single-chamber pacing, not dual-chamber pacing.

Answer 340

A. Sudden dizziness or fainting. B. Persistent hiccups. C. Heart rate consistently below the programmed rate. E. Frequent palpitations. Rationale: * A, B, C, and E: Dizziness, fainting, persistent hiccups (which may indicate diaphragmatic pacing), a low heart rate, and frequent palpitations could indicate pacemaker malfunction and require prompt evaluation. * D is incorrect because mild discomfort is expected postoperatively, but worsening pain or signs of infection should be reported.

Answer 341

D. Notify the surgical team so they can place a magnet over the pacemaker to switch it to asynchronous mode if needed. Rationale: During surgery, electrocautery can interfere with pacemaker function. Placing a magnet over the device switches it to asynchronous mode, ensuring consistent pacing. Lead-lined rooms are unnecessary, and patients should never turn off their own pacemaker. Adjusting the pacing rate is a decision made by the cardiologist, not the nurse.

Answer 342

D. “CRT will improve ventricular contraction and overall heart function.” Rationale: CRT improves ventricular synchrony, enhancing systolic function and cardiac output. It does not eliminate the need for medications, cure heart failure, or prevent all dysrhythmias, though it may reduce their occurrence when combined with an ICD.

Answer 343

A. Increased exercise tolerance C. Reduced symptoms of heart failure, such as dyspnea D. Improved cardiac output Rationale: * A, C, and D: CRT improves cardiac function, leading to increased exercise tolerance, reduced heart failure symptoms, and enhanced cardiac output. * B is incorrect because CRT aims to improve, not decrease, ejection fraction. * E is incorrect because CRT reduces, not increases, ventricular dyssynchrony.

Answer 344

C. Assess the patient for signs of worsening heart failure or dysrhythmias. Rationale: Multiple ICD shocks indicate recurrent dysrhythmias or worsening heart failure, requiring immediate assessment. The nurse should evaluate the patient’s condition and notify the provider. Magnets are used to deactivate ICD shocks temporarily in emergency situations but should not be applied without medical direction.

Answer 345

C. Implantable cardioverter-defibrillator (ICD) Rationale: Patients with severe left ventricular dysfunction are at high risk for life-threatening ventricular arrhythmias, so CRT is often combined with an ICD to provide both resynchronization and defibrillation if needed. An external pacemaker is not a long-term solution, an AED is for external use, and an LVAD is typically reserved for end-stage heart failure or transplant candidates.

Answer 346

A. Administer pain medication and sedation as prescribed. Rationale: Transvenous pacemaker insertion can be uncomfortable, so sedation and analgesia should be provided when appropriate. The device is temporary, not permanent (B is incorrect). Defibrillator pads are not routinely required for pacemaker placement (C is incorrect). A transvenous pacemaker requires an external power source (D is incorrect).

Answer 347

A. Closely monitor for signs of infection at the insertion site. B. Secure and insulate the pacemaker wires to prevent accidental dislodgment. D. Avoid manipulating or pulling on the pacing leads. Rationale: * A, B, and D: Infection risk, wire security, and avoiding lead displacement are critical for epicardial pacemaker care. * C is incorrect: If wires are dislodged, CPR is not the immediate action unless cardiac arrest occurs. * E is incorrect: Epicardial pacemakers are temporary, typically used postoperatively.

Answer 348

B. “The discomfort is temporary, and we will provide pain relief and sedation as needed.” Rationale: Transcutaneous pacing often causes muscle contractions, which can be uncomfortable. The nurse should reassure the patient while also providing pain management. Pain is expected, so stating that there is no way to reduce discomfort (A) or that the patient will not feel any pain (C) is inaccurate. Discontinuing pacing immediately is not an option if the patient requires it for life-saving purposes (D).

Answer 349

B. Administer prescribed analgesics or sedatives to improve comfort. Rationale: Transcutaneous pacing is often painful, so pain management is crucial. Increasing the pacing current (A) would worsen discomfort. Turning off the pacemaker (C) may compromise the patient’s cardiac output. Repositioning pads (D) may not help and could interfere with pacing effectiveness.

Answer 350

A. “It provides immediate electrical stimulation to the heart until more definitive therapy is available.” Rationale: A TCP is a temporary, emergency measure to sustain heart function until a transvenous or permanent pacemaker is placed. It does not permanently correct arrhythmias (B), is not ideal for long-term use due to discomfort (C), and does not directly reduce MI risk (D).

Answer 351

A. “This pacemaker requires an external power source to function.” B. “The leads of the pacemaker are inserted through a vein and into the heart.” D. “You may experience mild discomfort at the insertion site.” Rationale: * A and B: A transvenous pacemaker has leads inserted into the heart and relies on an external power source. * D: Some discomfort at the insertion site is expected. * C is incorrect: This pacemaker is temporary. * E is incorrect: It may support the heart but does not necessarily mean complete dependence.

Answer 352

A. Increase the pacing output (mA) to improve capture. Rationale: Increasing the pacing output can improve capture. Waiting for instructions (B) could delay necessary intervention. Turning off the pacemaker (C) could lead to hemodynamic instability. Trendelenburg position (D) is not indicated.

Answer 353

C. Insulate the pacemaker wires and notify the healthcare provider. Rationale: Epicardial wires must be secured and insulated to prevent electrical disturbances. Removing leads (A) is not within the nurse’s scope. Disconnecting the pacemaker (B) may cause bradycardia or asystole. Increasing the pacing rate (D) does not address the underlying problem.

Answer 354

D. Failure to capture Rationale: Failure to capture occurs when the pacemaker generates an electrical stimulus, but the myocardium does not respond with a contraction, leading to pacemaker spikes without QRS complexes. Common causes include battery failure, dislodged leads, or insufficient electrical charge.

Answer 355

A. Pacemaker spikes occurring randomly throughout the ECG strip B. Pacemaker firing during the refractory period, increasing the risk of ventricular tachycardia D. Pacemaker activity not adjusting in response to the patient’s intrinsic heart rhythm Rationale: * A & B: Failure to sense occurs when the pacemaker does not detect the heart’s intrinsic activity and fires inappropriately. * D: The pacemaker should adjust based on intrinsic activity, and failure to sense prevents this. * C is incorrect: Consistent pacing before QRS complexes suggests appropriate function. * E is incorrect: Continuous asystole suggests failure to pace, not failure to sense.

Answer 356

A. Check the pacemaker battery and replace it if necessary Rationale: Failure to pace occurs when the pacemaker does not deliver an electrical impulse. Common causes include battery failure, wire fractures, or lead displacement. The priority is to assess and replace the battery if needed before considering other interventions.

Answer 357

D. “I can use my microwave, but I should avoid standing too close while it’s on.” Rationale: Modern pacemakers are shielded against microwave interference, so there is no need to avoid standing near a microwave. The other statements are correct regarding activity restrictions, pulse monitoring, and MRI safety.

Answer 358

A. Monitor the patient’s ECG rhythm for pacemaker malfunction C. Assess the insertion site for signs of infection or hematoma D. Educate the patient to avoid vigorous arm and shoulder activity on the operative side Rationale: * A: ECG monitoring helps detect pacemaker malfunctions. * C & D: Monitoring for infection and limiting shoulder movement prevents complications. * B is incorrect: Arm and shoulder activity should be limited initially to avoid lead dislodgement. * E is incorrect: Prophylactic antibiotics are given before and after pacemaker insertion to prevent infection.

Answer 359

C. Notify the provider immediately and assess for signs of infection Rationale: Increasing pain and swelling at the insertion site may indicate infection or hematoma formation. Immediate assessment and possible intervention are needed to prevent complications.

Answer 360

B. Failure to capture Rationale: Lead displacement can prevent the pacemaker from delivering an effective electrical stimulus, resulting in failure to capture. Pneumothorax (A) is a potential complication but is not directly caused by lead displacement.

Answer 361

A. Reposition the patient to improve lead contact Rationale: A change in position may help restore contact between the pacemaker lead and the myocardium. Increasing the threshold (B) or replacing the battery (C) should be done if repositioning fails. External pacing (D) is a last resort.

Answer 362

B. “You should avoid lifting your arm above your shoulder for at least 4 to 6 weeks.” Rationale: Lifting the arm above the shoulder too soon increases the risk of lead displacement.

Answer 363

C. Persistent hiccups Rationale: Persistent hiccups may indicate lead displacement stimulating the diaphragm. This requires immediate intervention.

Answer 364

B. “I should avoid standing in antitheft devices at store entrances.” Rationale: Cell phones and Wi-Fi do not interfere with modern pacemakers, but patients should avoid placing a cell phone directly over the pacemaker.

Answer 365

D. “Routine follow-up visits will detect when the battery is near the end of its life.” Rationale: Pacemaker batteries are monitored regularly, and elective replacement is scheduled before failure occurs.

Answer 366

B. Burn or ablate areas of the heart’s conduction system causing dysrhythmias Rationale: Radiofrequency catheter ablation therapy uses electrical energy to destroy abnormal conduction pathways responsible for tachydysrhythmias. It is a definitive treatment for certain atrial dysrhythmias, including atrial fibrillation and AV nodal reentrant tachycardia.

Answer 367

A. Obtain informed consent before the procedure C. Hold anticoagulant medications as prescribed before the procedure D. Instruct the patient that they may feel a burning sensation during the ablation E. Monitor the patient for signs of bleeding or hematoma formation at the catheter insertion site Rationale: * A: Informed consent is required for invasive procedures. * C: Anticoagulants are often held before ablation to reduce bleeding risk. * D: Patients may feel a burning sensation during the ablation as heat energy is applied. * E: Bleeding or hematoma formation is a potential complication at the catheter insertion site.

Answer 368

c. Observe for symptoms of hypotension and angina.

Answer 369

b. Administer IV amiodarone.

Answer 370

b. Chest pain and palpitations

Answer 371

d. Cardioversion is painful for an awake patient.

Answer 372

b. Take and record a daily pulse rate. c. Obtain and wear a Medic Alert ID device at all times. d. Avoid lifting arm on the side of the pacemaker above shoulder.

Answer 373

c. The procedure will destroy areas of the conduction system that are causing rapid heart rhythms.

Answer 374

d. QRS complex Rationale: The QRS complex represents ventricular depolarization. The P wave represents the depolarization of the atria. The PR interval represents depolarization of the atria, atrioventricular node, bundle of His, bundle branches, and the Purkinje fibers. The Q wave is the first negative deflection following the P wave and would be narrow and short.

Answer 375

b. Print a 1-minute electrocardiogram (ECG) strip and count the number of QRS complexes. Rationale: The accurate way to measure the heart rate from an EKG of a patient with an irregular rhythm is to count the number of QRS complexes in 1 minute. The other methods are accurate for regular heart rhythms.

Answer 376

c. 40 to 60 Rationale: If the sinoatrial (SA) node does not discharge, the atrioventricular (AV) node will automatically discharge at the normal rate of 40 to 60 beats/min. The slower rates are typical of the bundle of His and Purkinje system and may be seen with failure of both the SA and AV node to discharge. The normal SA node rate is 60 to 100 beats/min.

Answer 377

d. Ventricular tachycardia Rationale: The absence of P waves, wide QRS, rate greater than 150 beats/min, and the regularity of the rhythm indicate ventricular tachycardia. Atrial flutter is usually regular, has a narrow QRS configuration, and has flutter waves present representing atrial activity. Sinus tachycardia has P waves. Ventricular fibrillation is irregular and does not have a consistent QRS duration.

Answer 378

b. Ventricular bigeminy Rationale: Ventricular bigeminy describes a rhythm in which every other QRS complex is wide and bizarre looking. Pairs of wide QRS complexes are described as ventricular couplets. There is no indication that the premature ventricular contractions are multifocal or that the R-on-T phenomenon is occurring.

Answer 379

b. Document the finding and monitor the patient. Rationale: First-degree atrioventricular block is asymptomatic and usually not serious. There is no treatment for first-degree AV block; treatment of associated conditions may be considered. Monitor patients for changes in heart rhythm (e.g., more serious AV block). The rate is normal, so there is no indication that atropine is needed. Immediate notification of the health care provider about an asymptomatic rhythm is not necessary.

Answer 380

d. Prepare to give IV amiodarone per agency dysrhythmia protocol. Rationale: The burst of sustained ventricular tachycardia indicates that the patient has significant ventricular irritability, and antidysrhythmic medication administration is needed to prevent further episodes. The nurse should notify the health care provider after the medication is started. Cardioversion is not indicated given that the patient has returned to a sinus rhythm. Documentation and continued monitoring are not adequate responses to this situation.

Answer 381

a. Increase in the patient‘s heart rate Rationale: Atropine will increase the heart rate and conduction through the AV node. Because the drug increases electrical conduction, not cardiac contractility, the quality of the peripheral pulses is not used to evaluate the drug effectiveness. Premature atrial or ventricular contractions are not a feature of second degree AV block.

Answer 382

a. Anticoagulant therapy Rationale: Atrial fibrillation therapy that has persisted for more than 48 hours requires anticoagulant treatment for 3 weeks before attempting cardioversion. This is done to prevent embolization of clots from the atria. Cardioversion may be done after several weeks of anticoagulation therapy. Adenosine is not used to treat atrial fibrillation. Pacemakers are routinely used for patients with bradydysrhythmias. Information does not indicate that the patient has a slow heart rate.

Answer 383

c. The procedure uses electrical energy to destroy areas of the conduction system. Rationale: Radiofrequency catheter ablation therapy uses electrical energy to “burn” or ablate areas of the conduction system as definitive treatment of atrial flutter (i.e., restore normal sinus rhythm) and tachydysrhythmias. All other statements about the procedure are incorrect.

Answer 384

d. “I won‘t lift the arm on the incision side until I see the health care provider.” Rationale: The patient is instructed to avoid lifting the arm on the pacemaker side above the shoulder to avoid displacing the pacemaker leads. The patient should notify airport security about the presence of a pacemaker before going through the metal detector, but there is no need to notify the airlines when making a reservation. Microwave oven use does not affect the pacemaker. The insertion procedure involves minor surgery that will have a short recovery period.

Answer 385

c. The nurse encourages the patient to do active range-of-motion exercises for all extremities. Rationale: The patient should avoid moving the arm on the ICD insertion site until healing has occurred to prevent displacement of the ICD leads. The other actions by the nurse are appropriate for this patient.

Answer 386

b. Give a sedative before cardioversion is implemented. Rationale: When a patient has a nonemergency cardioversion, sedation is used just before the procedure. The synchronizer switch is turned “on” for cardioversion. The initial level of joules for cardioversion is low (e.g., 50). Assisted ventilations are not indicated for this alert patient.

Answer 387

a. Approve the student to participate on the soccer team. Rationale: In an aerobically trained individual, sinus bradycardia is normal. The student‘s normal BP and negative health history indicate that there is no need for a cardiology referral or for more detailed information about the family‘s health history. Dyspnea during an aerobic activity such as soccer is normal.

Answer 388

d. QRS interval of 0.14 second Rationale: Because the normal QRS interval is less than 0.12 seconds, the patient‘s QRS interval of 0.14 seconds indicates that the conduction through the ventricular conduction system is prolonged. The PR interval and QT interval are within normal range and ST segment should be isoelectric (flat).

Answer 389

d. Serum potassium of 2.9 mEq/L Rationale: Hypokalemia increases the risk for ventricular dysrhythmias such as PVCs, ventricular tachycardia, and ventricular fibrillation. The health care provider will need to prescribe a potassium infusion to correct this abnormality. Although the other laboratory values are also abnormal, they are not likely to be the cause of the patient‘s PVCs and do not require immediate correction.

Answer 390

b. Perform immediate defibrillation. Rationale: The patient‘s rhythm and assessment indicate ventricular fibrillation and cardiac arrest; the initial action should be to defibrillate. If a defibrillator is not immediately available or is unsuccessful in converting the patient to a better rhythm, begin chest compressions. The other actions may also be appropriate but should not be done first.

Answer 391

c. Hold the scheduled metoprolol (Lopressor) and call the health care provider. Rationale: The patient has progressive first-degree atrioventricular (AV) block, and the -blocker should be held until discussing the drug with the health care provider. Documentation is appropriate later. The patient with first-degree AV block usually is asymptomatic; if the patient became symptomatic, a pacemaker or atropine may be used.

Answer 392

d. Apply the transcutaneous pacemaker (TCP) pads. Rationale: The patient is experiencing symptomatic bradycardia and treatment with TCP is appropriate. Calcium channel blockers will further decrease the heart rate and the diltiazem should be held. The Valsalva maneuver will further decrease the rate. Repositioning on the left side may decrease cardiac output and blood pressure further.

Answer 393

c. Ask the patient about current stress level and caffeine use. Rationale: In a patient with a normal heart, occasional PVCs are a benign finding. The timing of the PVCs suggests stress or caffeine as possible etiologic factors. The patient is hemodynamically stable, so there is no indication that the patient needs supplemental O 2 , an IV, or to be seen in the ED.

Answer 394

d. A patient whose implantable cardioverter-defibrillator (ICD) fired twice today and has a dose of amiodarone due Rationale: The frequent firing of the ICD indicates that the patient‘s ventricles are very irritable. The priority is to assess the patient and give the amiodarone. The other patients can be seen after the amiodarone is given.

Answer 395

c. Give supplemental O 2 at 2 to 3 L/min via nasal cannula. Rationale: Because this patient has dyspnea and chest pain in association with the new rhythm, the nurse‘s initial actions should be to address the patient‘s airway, breathing, and circulation (ABC) by starting with O 2 administration. The other actions are also important and should be implemented rapidly.

Answer 396

a. Start cardiopulmonary resuscitation (CPR). Rationale: The patient‘s manifestations indicate pulseless electrical activity, and the nurse would immediately start CPR. The other actions would not benefit this patient.

Answer 397

b. Instruct the patient to call for help before getting out of bed. Rationale: A patient with fainting episodes is at risk for falls. The nurse will plan to minimize the risk by having assistance whenever the patient is up. The other actions may be needed if dysrhythmias are found to be the cause of the patient‘s syncope but are not appropriate for syncope of unknown origin.

Answer 398

b. Injects IV adenosine over 2 seconds for a patient with supraventricular tachycardia. Rationale: Adenosine must be given over 1 to 2 seconds to be effective. The other actions indicate a need for more teaching about treatment of heart dysrhythmias. The RN should hold the diltiazem until discussing it with the health care provider. The treatment for asystole is immediate CPR. The synchronizer switch should be “off” when defibrillating.

Answer 399

atria contracts depolarization

Answer 400

ventricles contract depolarization

Answer 401

ventricles relax, get filled with blood

Answer 402

Movement of electrical activity from the atria to the ventricles

Answer 403

Time between ventricular depolarization and repolarization (ventricular contraction)

Answer 404

Time taken from ventricles to depolarize, contract, and repolarize

Answer 405

contract, squeeze electric

Answer 406

false DO NOT SHOCK ASYSTOLE