Msn hearts6/17/2023 The end result is additional deterioration in cardiac performance and increased neurohormonal activation. As myocytes stretch, local norepinephrine activity and angiotensin and endothelin release are increased. The myocardium undergoes remodeling (molecular, cellular and interstitial changes) which manifests as change in size, shape and function of the heart muscle. Initially this is a good compensatory response, but if prolonged it will result in the loss of myocytes and extracellular matrix (Figueroa & Peters, 2006). This leads to increased vasoconstriction and increased afterload (impedance of blood flow from the left ventricle ), and adds to contractility. When the renin-angiotensin system is activated, preload (volume of blood entering the left ventricle) is increased by retention of sodium and water. Smith presents with fatigue and dyspnea on exertion, she is probably retaining excess fluid related to decreased cardiac output which is affecting perfusion to her muscles, especially the legs and respiratory accessory muscles (Figueroa & Peters, 2006).ĬHF involves both the inability of the heart muscle to maintain adequate oxygen delivery to the body (structural abnormality), and a cardiovascular (systemic) response that is attempting to compensate for poor perfusion by activation of the renin-angiotensin system. The Chest X-ray would most likely show cardiomegaly, cephalization of blood vessels, increased interstitial markings and pleural effusion. Smith is probably presenting with acute or sub acute left sided mild to moderate congestive heart failure (CHF) ( American Heart Association, 2016 ). Can other factors come into play with the development of heart failure? Based on the information presented, what do you think the Chest X-ray would show and why? Describe the pathophysiological changes in the heart that occur as a result of heart failure.
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