Contractility is reduced by diseases that disrupt myocyte activity Myocardial

Contractility is reduced by diseases that disrupt

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afterload. Contractility is reduced by diseases that disrupt myocyte activity. Myocardial infarction is the most common cause of decreased contractility; other causes include myocarditis and cardiomyopathies. These diseases contribute to inflammatory, immune, and neurohumoral changes (activation of the SNS and RAAS) that mediate a process called ventricular remodeling. Ventricular remodeling results in disruption of the normal myocardial extracellular structure withresultant dilation of the myocardium and causes progressive myocyte contractile dysfunction over time. When contractility is decreased, stroke volume falls, and left ventricular end-diastolic volume (LVEDV) increases. This causes dilation of the heart and an increase in preload. Preload,or LVEDV, increases with decreased contractility or when there is an excess of plasma volume 19
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(intravenous fluid administration, renal failure, mitral valvular disease). Increases in LVEDV canactually improve cardiac output up to a certain point, but as preload continues to rise, it causes a stretching of the myocardium that eventually can lead to dysfunction of the sarcomeres and decreased contractility. This relationship is described by the Frank-Starling law of the heart. Increased afterload is most commonly a result of increased peripheral vascular resistance (PVR), such as that seen with hypertension. Although much less common, it also can be the result of aortic valvular disease. With increased PVR, there is resistance to ventricular emptying and moreworkload for the left ventricle, which responds with hypertrophy of the myocardium. This process differs from the physiologic myocyte response to increased workload (exercise) in whichthe workload is intermittent rather than sustained, resulting in an increase in muscle mass but no distortion of the cardiac architecture. Sustained afterload leads to pathologic hypertrophy which is characterized by myocyte death, fibrosis, inflammation, and alterations in cardiac energetics and is mediated by ang II, catecholamines, and changes in intracellular signaling within the myocytes. This pathologic increase in muscle mass results in an increase in oxygen and energy demand. When demand for energy is greater than the ability of these systems to supply the necessary ATP, contractility of the myocardium is compromised. An energy-starved state develops that further contributes to changes in the myocytes themselves and ventricular remodeling that significantly impairs contractility and therefore ventricular function. Remodelingalso results in the deposition of collagen between the myocytes, which can disrupt the integrity of the muscle, decrease contractility, and make the ventricle more likely to dilate and fail. Weakness of the cardiac muscle due to hypertension induced hypertrophy is called hypertensive hypertrophic cardiomyopathy. As cardiac output falls, renal perfusion diminishes with activation of the RAAS, which acts to increase PVR and plasma volume, thus increasing afterload and preload further. In addition, baroreceptors in the central circulation detect the decrease in
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  • Spring '17
  • keisha lovence

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