What will happen when a person is hypotensive?
Baroreceptors are less active
SNS is activated
Person will be bradycardic
SNS is suppressed
The Correct Answer is B
Choice A reason: This is not what will happen when a person is hypotensive. Baroreceptors are sensory receptors that detect changes in blood pressure. When a person is hypotensive, the baroreceptors are more active, not less, and they send signals to the brain to increase the blood pressure.
Choice B reason: This is what will happen when a person is hypotensive. SNS stands for sympathetic nervous system, which is the part of the autonomic nervous system that prepares the body for fight or flight response. When a person is hypotensive, the SNS is activated to increase the heart rate, contractility, and vasoconstriction, which all raise the blood pressure.
Choice C reason: This is not what will happen when a person is hypotensive. Person will be bradycardic means that the person will have a slow heart rate, usually below 60 beats per minute. When a person is hypotensive, the opposite will happen, as the heart rate will increase to compensate for the low blood pressure.
Choice D reason: This is not what will happen when a person is hypotensive. SNS is suppressed means that the sympathetic nervous system is inhibited or reduced in activity. When a person is hypotensive, the SNS is not suppressed, but rather stimulated, to increase the blood pressure.
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Correct Answer is D
Explanation
Choice A reason: Cardiac output has not fallen below normal levels. Cardiac output is the amount of blood pumped by the heart per minute. It is affected by the heart rate and the stroke volume. Angina pectoris does not directly affect the cardiac output, but it can reduce the stroke volume due to impaired ventricular filling.
Choice B reason: The vagus nerve is not stimulated. The vagus nerve is a cranial nerve that innervates the heart and other organs. It is part of the parasympathetic nervous system, which slows down the heart rate and lowers the blood pressure. Angina pectoris does not activate the vagus nerve, but it can trigger the sympathetic nervous system, which increases the heart rate and blood pressure.
Choice C reason: Myocardial stretch has not exceeded the upper limits. Myocardial stretch is the degree of tension or load on the cardiac muscle fibers. It is determined by the end-diastolic volume, which is the amount of blood in the ventricle at the end of relaxation. Angina pectoris does not cause excessive myocardial stretch, but it can impair the myocardial contractility due to ischemia.
Choice D reason: The myocardial oxygen supply has fallen below demand. This is the main cause of angina pectoris. It occurs when the coronary arteries, which supply blood and oxygen to the heart muscle, are narrowed or blocked by atherosclerosis or spasm. This creates an imbalance between the oxygen demand of the heart, which increases during exertion, and the oxygen supply, which is reduced by the obstruction.
Correct Answer is B
Explanation
Choice A reason: Vasodilators are not the preferred agents for the initial treatment of heart failure. They are used as adjunctive therapy to reduce the afterload and preload on the heart. However, they do not address the fluid overload that is the main cause of heart failure symptoms.
Choice B reason: Diuretics are the preferred agents for the initial treatment of heart failure. They help to reduce the fluid overload and congestion in the lungs and peripheral tissues. They also lower the blood pressure and improve the cardiac output and renal function.
Choice C reason: Calcium channel blockers are not the preferred agents for the initial treatment of heart failure. They are contraindicated in most cases of heart failure because they can worsen the cardiac function and increase the mortality. They can also cause peripheral edema and hypotension.
Choice D reason: Direct renin inhibitors are not the preferred agents for the initial treatment of heart failure. They are a newer class of drugs that block the renin-angiotensin-aldosterone system (RAAS), which is involved in the pathophysiology of heart failure. However, they have not shown any significant benefit over the existing RAAS inhibitors, such as angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs). They can also cause hyperkalemia and renal impairment.
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