systemic congestion (Osborn, 2014 p1029).”
The renin-angiotensin-aldosterone system activates in response to decreased renal perfusion. A series of hormones is released in this system to increase preload, cardiac output, and blood pressure. Renin is released from the kidneys to convert angiotensin I to angiotensin II. Angiotensin II is a strong vasoconstrictor that increases afterload and stimulates the secretion of aldosterone. Aldosterone is a hormone that causes sodium and fluid retention of the kidneys to increase intravascular volume. Like the activation of the sympathetic nervous system, this system has long term effects that will lead to heart failure. These long-term effects include,” increased cardiac workload, pulmonary and systemic congestion, and chamber dilation. Abnormal cell growth manifested by myocardial hypertrophy and adverse remodeling is also triggered by angiotensin II(Osborn, 2014 p1029).” Patient’s chest radiography showed cardiomegaly as a result of abnormal cell growth due to increased workload of the heart.
In addition to decreased renal perfusion, decrease in cardiac output can affect other organs as well. Decrease cardiac output leads to ischemia because the oxygen demand from the organs is still there, however there is inadequate blood pumped by the heart to meet these demands. As a result, less oxygen is carried by red blood cells is getting to the organs.
Systolic dysfunction, also known as left ventricular systolic dysfunction(LVSD), results in volume overload and decreased contractility. It is diagnosed when the left ventricular ejection fraction (LVEF) is less than 40%. Normal LVEF is 55%-70%. Patient’s ejection fraction is 25-30% with cardiomyopathy. LVEF is the proportion of blood ejected during each ventricular contraction compared to the total ventricular filling volume. Cardiac remodeling occurs when prolonged activation of the sympathetic nervous system and renin-angiotensin-aldosterone leads to damaged and maladaptation of the myocardium. Myocytes will “revert to a fetal-type expression and ultimately changes the myocyte geometry from elliptical to spherical (Osborn, 2014 p1027).” The change in shape at the cellular level will manifest to changes in the size, shape, and function of the heart. There are three types of heart failure depending on the anatomy of the ventricles; right, left, or biventricular heart failure.
Right-sided heart failure is characterized as impairment to the pumping ability of the right side of the heart. The cause of right-sided defectiveness is left-sided dysfunction, isolated right ventricular myocardial infarction, and a process where blood cannot flow into the pulmonary vasculature in the lungs. The backup