Jesse is a 57-year-old male who presents with gradual onset of dyspnea on exertion and fatigue

Jesse is a 57-year-old male who presents with gradual onset of dyspnea on exertion and fatigue

Jesse is a 57-year-old male who presents with gradual onset of dyspnea on exertion and fatigue. He also complains of frequent dyspepsia with nausea and occasional epigastric pain. He states that at night he has trouble breathing especially while lying on his back. This is relieved by him sitting up. His vitals are 180/110, P = 88, T = 98.0 F, R = 20. After a thorough work-up, he is diagnosed with congestive heart failure.

What is the etiology of congestive heart failure?
Describe in detail the pathophysiological process of congestive heart failure.
Identify hallmark signs identified from the physical exam, diagnostic lab work and symptoms.
Describe the pathophysiology of complications of congestive heart failure
What teaching would you provide this patient to avoid heart failure symptoms?
In addition to the textbook, utilize at least one peer-reviewed, evidence-based resource to develop your post.

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Describe in detail the pathophysiological process of congestive heart failure.
In general, the pathophysiologic mechanisms of CHF in infants and children are very similar to those in adults. The same compensatory mechanisms are activated in the face of inadequate cardiac output. An acute decrease in blood pressure stimulates

Jesse is a 57-year-old male who presents with gradual onset of dyspnea on exertion and fatigue
Jesse is a 57-year-old male who presents with gradual onset of dyspnea on exertion and fatigue

stretch receptors and baroreceptors in the aorta and carotid arteries, which in turn stimulate the sympathetic nervous system. With the release of catecholamines and the stimulation of β receptors, heart rate and the force of myocardial contraction increase (McCance et al., 2013). Venous smooth muscle tone also increases, which increases the return of venous blood to the heart. Sympathetic stimulation also decreases blood flow to the kidneys, skin, spleen, and extremities so that maximum flow to the brain, heart, and lungs can be maintained. Decreased blood flow to the kidneys causes the release of renin, angiotensin, and aldosterone. If chronic, this cycle results in retention of sodium and fluid by the kidneys, which in turn increases volume in the circulatory system (McCance et al., 2013). These neurohumoral and hemodynamic changes create abnormal ventricular wall stress and cause the myocardium to hypertrophy. The myocardial fibers also stretch to accommodate the increased volume. Hypertrophy and fiber stretch temporarily increase contractility and hence the force of ventricular contraction. These mechanisms eventually fail to maintain cardiac output as CHF progresses.