Which of the following is a common symptom of chronic aortic regurgitation?
Bradycardia
Abdominal pain
Exertional dyspnea
Peripheral edema
The Correct Answer is C
Rationale:
A. Chronic aortic regurgitation typically does not cause bradycardia; the heart often compensates for the increased volume load by maintaining a normal or slightly elevated heart rate to preserve cardiac output.
B. This symptom is not characteristic of aortic regurgitation. Any abdominal discomfort in cardiac patients is more likely related to comorbidities or advanced heart failure affecting liver congestion, not the valve disease itself.
C. Chronic aortic regurgitation leads to volume overload of the left ventricle, causing left ventricular dilation and eventually increased pulmonary venous pressure. This results in left-sided heart failure symptoms, such as exertional dyspnea, fatigue, and decreased exercise tolerance, which often appear gradually as the disease progresses.
D. Typically associated with right-sided heart failure, peripheral edema is not an early or primary symptom of isolated aortic regurgitation. It may appear only in advanced stages if biventricular failure develops.
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Naxlex Comprehensive Predictor Exams
Related Questions
Correct Answer is D
Explanation
Rationale:
A. Crackles are more commonly associated with left-sided heart failure, due to pulmonary congestion from fluid backing up into the lungs.
B. While a murmur can be present in some cardiac conditions, it is not a hallmark finding specific to right-sided heart failure.
C. Chest pain may occur with ischemic heart disease or myocardial infarction but is not a classic symptom of right-sided heart failure.
D. Right-sided heart failure leads to systemic venous congestion, causing fluid accumulation in dependent areas such as the legs, ankles, and feet, which is a hallmark sign of right-sided heart failure.
Correct Answer is D
Explanation
Rationale:
A. Atropine is a parasympatholytic medication used to increase heart rate in cases of bradycardia by inhibiting vagal stimulation. It has no effect on coagulation pathways and therefore does not reverse the anticoagulant effects of warfarin.
B. Epinephrine is a sympathomimetic used primarily in cardiac arrest, anaphylaxis, or severe hypotension. While it affects heart rate and vascular tone, it does not interact with the coagulation cascade or reduce an elevated INR.
C. Protamine sulfate is the specific antidote for heparin therapy. It binds to heparin to neutralize its anticoagulant effect but is ineffective against vitamin K antagonists such as warfarin. Administering protamine would not correct the patient’s supratherapeutic INR.
D. Vitamin K (phytonadione) is the antidote for warfarin. Warfarin inhibits the vitamin K–dependent synthesis of clotting factors II, VII, IX, and X. An elevated INR of 5.2 indicates that the client is at high risk for spontaneous bleeding. Administering vitamin K helps restore the synthesis of functional clotting factors, thereby reducing bleeding risk. The dose and route (oral vs. IV) depend on the severity of the INR elevation and presence of active bleeding.
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