Which of the following is a primary goal of catheter ablation in the treatment of atrial fibrillation?
To strengthen the heart muscle
To decrease the frequency of ventricular contractions
To permanently eliminate the need for anticoagulation therapy
To restore and maintain normal sinus rhythm
The Correct Answer is D
Rationale:
A. Catheter ablation does not directly improve myocardial contractility; its purpose is focused on electrical conduction rather than muscle strength.
B. While controlling ventricular response may occur with medications, ablation targets the atrial electrical pathways rather than directly controlling ventricular rate.
C. Anticoagulation decisions depend on stroke risk (e.g., CHA₂DS₂-VASc score); ablation does not automatically remove the need for anticoagulants.
D. The primary goal of catheter ablation in atrial fibrillation is to eliminate abnormal electrical pathways causing arrhythmia, thereby restoring and maintaining normal sinus rhythm and reducing symptoms.
Nursing Test Bank
Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is B
Explanation
Rationale:
A. This is not represented by the P wave. Repolarization of the ventricular conduction system is a component of the later part of the ECG, mainly within the T wave.
B. The P wave corresponds to atrial depolarization, which is the electrical activity that triggers atrial contraction. Proper identification of the P wave helps the nurse evaluate rhythm, rate, and atrial conduction.
C. Ventricular depolarization is represented by the QRS complex, not the P wave. This reflects the spread of electrical impulses through the ventricles, leading to ventricular contraction.
D. Early repolarization of the ventricles occurs at the beginning of the ST segment and is not associated with the P wave.
Correct Answer is C
Explanation
Rationale:
A. While dehydration or hypovolemia can lead to tachycardia as the body attempts to maintain cardiac output, it does not typically cause bradycardia. Bradycardia usually results from conduction abnormalities, medications, or increased vagal tone rather than low fluid volume.
B. Anxiety triggers sympathetic nervous system activation, which increases heart rate and blood pressure. Therefore, it is more likely to produce tachycardia rather than a slow heart rate.
C. Bradycardia reduces cardiac output, which lowers cerebral perfusion. This decrease in blood flow to the brain commonly manifests as dizziness, lightheadedness, fainting, or syncope. These symptoms are critical for assessing the clinical significance of bradycardia, especially in older adults or those with cardiovascular disease.
D. Fever increases metabolic demand, leading to compensatory tachycardia, not bradycardia. A slow heart rate in a febrile client would be atypical and may suggest other underlying conditions, such as conduction disorders or drug effects.
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