A.O. is an 89-year-old woman with a long history of systolic heart failure secondary to a large left ventricular infarct when she was in her 70s. She had poor activity tolerance and required assistance with activities of daily living. Even minimal activity was associated with moderately severe dyspnea and exertional chest pain, which was relieved by rest. A.O. also exhibited marked pedal edema bilaterally. She is being treated with digitalis, furosemide (Lasix), KCl, and sublingual nitroglycerin.
What compensatory mechanisms are likely to be operative in A.O. to enhance cardiac output?
A. Prolonged stretch on the myocardium results in myocardial atrophy.
B. Baroreceptors detect low blood pressure and cardiac output and activate the parasympathetic system resulting in increased heart rate.
C. Renin-angiotensin system activation causes decreased glomerular filtration rate and fluid retention, which results in increased preload.
D. Baroreceptors detect low blood pressure and cardiac output and activate the sympathetic system resulting in decreased heart rate.

Question

01-05-2021
Biology

contestada

A.O. is an 89-year-old woman with a long history of systolic heart failure secondary to a large left ventricular infarct when she was in her 70s. She had poor activity tolerance and required assistance with activities of daily living. Even minimal activity was associated with moderately severe dyspnea and exertional chest pain, which was relieved by rest. A.O. also exhibited marked pedal edema bilaterally. She is being treated with digitalis, furosemide (Lasix), KCl, and sublingual nitroglycerin.
What compensatory mechanisms are likely to be operative in A.O. to enhance cardiac output?
A. Prolonged stretch on the myocardium results in myocardial atrophy.
B. Baroreceptors detect low blood pressure and cardiac output and activate the parasympathetic system resulting in increased heart rate.
C. Renin-angiotensin system activation causes decreased glomerular filtration rate and fluid retention, which results in increased preload.
D. Baroreceptors detect low blood pressure and cardiac output and activate the sympathetic system resulting in decreased heart rate.

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Answer:

The correct answer is ''C. Renin-angiotensin system activation causes decreased glomerular filtration rate and fluid retention, which results in increased preload.''

Explanation:

In states of low cardiac output, the renin-angiotensin-aldosterone pathway is activated as a compensatory mechanism, whose objective is to fundamentally modify the peripheral circulation, which operates in conjunction with the activation of the medullary neuro-adrenal system, to maintain blood pressure. These two mechanisms, which are totally different, are closely linked; thus, stimulation of beta-1 adrenoreceptors in the juxtaglomerular apparatus, as a consequence of a high adrenergic output, causes renin output in heart failure. On the other hand, the activation of baroreceptors in the renal vascular bed caused by a reduction in renal blood flow, is also responsible for the release of renin, it occurs in patients with severe heart failure managed with diuretics and salt restriction.