Cardiac Failure
Question One: Pathophysiology of Mr Griffin’s cardiac failure In a MI also known as a heart attack the coronary circulation becomes blocked and the cardiac muscle cells die form lack of oxygen the affected tissue then degenerates creating a nonfunctional area know as an infarct (Martini, 1998: 694). Mr Griffin who had presented with acute Anterior Myocardial Infarction four days ago to high dependency unit has subsequently developed cardiac failure. ... Tarolli (2003:3) reveal that ‘Heart failure is a complex clinical syndrome that can occur as a result of any structural or functional cardiac disorder that impairs the ability of the ventricles to fill with or eject blood’. Poor cardiac output may occur from congestion of tissues due to increased venous pressure therefore leading to increases pulmonary venous pressure causing fluid to pass from pulmonary capillaries to the alveoli therefore pulmonary edema can occur (Bare and Smeltzer, 2000:165) As cardiac output is equal to the heart rate times by the stroke volume and the stoke volume is determined by the preload, contractility and afterload then any changes in these can result in heart failure. Therefore if the heart is not working effectively then a compensatory mechanism is kicked in by the body to maintain heart rate, contractility and preload to maintain homeostasis, this is by neurohormone activation which results in water and sodium retention to increase the cardiac output and maintain blood pressure, this mechanism works short term only as it subsequently causes the heart to work harder therefore causing cardiac failure.