Essay on A Short Note On Cardiovascular And Vascular Responses

Essay on A Short Note On Cardiovascular And Vascular Responses

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Definition: CHF occurs when the heart does not fill or contract with enough strength to function as a pump to meet the needs of the body. Moreover, cardiac output falls and leads to decreased tissue perfusion. Initially, the body activate inherent compensatory mechanisms to reduce cardiac output to restore tissue perfusion. After, these mechanisms exhaust, heart failure ensues, with increased morbidity and mortality. Heart failure may occur as a result of coronary heart disease, myocardial ischemia or infarct, cardiomyopathy, or myocarditis; all of which impairs myocardial contraction. In addition, valve disorders, congenital heart defects, and hypertension can damage the heart muscle as a result of excessive workload, which leads to heart failure.
The primary mechanism that activates to compensate for the impaired function and maintain cardiac output is the Frank-Starling mechanism, neuroendocrine responses which include activating the sympathetic nervous system (SNS), the renin-angiotensin-aldosterone system (RAAS), and ventricular hypertrophy. Initially, decreased output stimulates aortic baroreceptors which stimulate the SNS. This produces both cardiac and vascular responses through the release of norepinephrine, which increases heart rate and contractility by stimulating cardiac beta-receptors. Cardiac output will improve as both the heart rate and the stroke volume increases. Also, norepinephrine causes arterial and venous vasoconstriction which increases venous return to the heart. The increased venous return increases the ventricular filling and myocardial stretch, increasing the force of contraction. When over—stretching of the muscle fibers past their physiologic limits ineffective contraction occurs. Blood flow to the...

... middle of paper ...

...onstriction. The increased systemic vascular resistance causes hypertension. It is unusual that one single cause and pathologic process will be found accountable for essential hypertension. Evidence point to hypertension as a diverse group of pathophysiologic mechanism that result in common manifestation of elevated blood pressure.

Symptoms: Early stages asymptomatic, then vague symptoms such as headache, nocturia, confusion, nausea, vomiting, and visual disturbances.
Treatment: Diuretics, beta-adrenergic blockers, vasodilators, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), or calcium channel blockers.
Lab associated with the disease: U/A, Blood glucose, hematocrit, serum potassium, creatinine, and calcium, cholesterol, lipid profile, urinary albumin, and creatinine clearance.
Diagnostic test used to confirm disease: ECG

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