In managing a patient with SVT, what is the primary goal of therapy?

In managing a patient with SVT, what is the primary goal of therapy?

• A. Reduce heart rate to increase diastolic filling time
• B. Produce arteriolar constriction to increase perfusion pressure
• C. Dilate coronary arteries to increase myocardial O2 delivery
• D. Promote venous constriction to increase preload

Answer: (A)

The primary goal of therapy in managing a patient with supraventricular tachycardia (SVT) is to reduce the heart rate to increase diastolic filling time. When the heart beats too quickly, there is insufficient time for the ventricles to fill with blood during diastole, which can lead to reduced cardiac output and inadequate perfusion of vital organs. By slowing down the heart rate, the therapy allows more time for the ventricles to fill adequately, thereby enhancing stroke volume and improving overall hemodynamic stability. While the other options may have their merits in different clinical situations, they do not align as closely with the specific goals associated with SVT management. For instance, producing arteriolar constriction is not a desired effect in this context because it could further increase afterload and strain on the heart. Similarly, dilating coronary arteries can be beneficial in managing ischemia, but it does not directly address the immediate need to control the rapid heart rate. Promoting venous constriction to increase preload is typically relevant in the context of heart failure or shock but does not specifically address the complications or necessary interventions for SVT. Thus, focusing on heart rate control by increasing diastolic filling time is the most critical intervention in

The primary goal of therapy in managing a patient with supraventricular tachycardia (SVT) is to reduce the heart rate to increase diastolic filling time. When the heart beats too quickly, there is insufficient time for the ventricles to fill with blood during diastole, which can lead to reduced cardiac output and inadequate perfusion of vital organs. By slowing down the heart rate, the therapy allows more time for the ventricles to fill adequately, thereby enhancing stroke volume and improving overall hemodynamic stability.

While the other options may have their merits in different clinical situations, they do not align as closely with the specific goals associated with SVT management. For instance, producing arteriolar constriction is not a desired effect in this context because it could further increase afterload and strain on the heart. Similarly, dilating coronary arteries can be beneficial in managing ischemia, but it does not directly address the immediate need to control the rapid heart rate. Promoting venous constriction to increase preload is typically relevant in the context of heart failure or shock but does not specifically address the complications or necessary interventions for SVT. Thus, focusing on heart rate control by increasing diastolic filling time is the most critical intervention in