Heart Failure: A Case Study

Heart failure is caused by the decrease cardiac output and decrease perfusion to the vital tissues of the body. Cardiac output is depended on the stroke volume and heart rate. There are three factors that influence stroke volume, which are contractility, preload and afterload. Contractility is reduced due to Ms. Boehmer’s history of acute myocardial infarction. Acute myocardial infarction causes myocyte function disruptions. Ms. Boehmer’s history of hypertension, smoking, and coronary artery disease causes myocardial workload to increase, contribute to inflammation, and neurohumoral changes. At the same time, it activates the sympathetic nervous systems (SNS) as well as renin-angiotensin-aldosterone system (RAAS), which can lead to ventricular remodeling. The myocardium dilates as the result of myocardial extracellular structure disruptions due to the remodeling. Over time, the dilation of the ventricle causes contractility reduction. Decreased contractility causes dilation of the heart and increase in preload. Under the Frank-Starling’s law of the heart, increased preload initially improves cardiac output, but eventually leads to stretching of the myocardium, thereby leading to decreased contractility. Hypertension causes peripheral vascular resistance to increase, resulting in increased afterload. In order to overcome the resistance, the ventricle has to work harder to pump blood out of the heart. Increased afterload causes myocardial hypertrophy. The angiotensin II and catecholamine are triggered with hypertrophy, which leads to increased oxygen demand by the thickened myocardium.
Ms. Boehmer has a history of AMI, CABG post AMI, symptoms such as sleeping on two pillows, feeling tired, exercise intolerance and swelling of ankles at the end of the day are all evidence of stage C