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NR 507 Week 3: Discussion Part Two

NR 507 Week 3: Discussion Part Two

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.

  1. What is the etiology of congestive heart failure?
  2. Describe in detail the pathophysiological process of congestive heart failure.
  3. Identify hallmark signs identified from the physical exam, diagnostic lab work and symptoms.
  4. Describe the pathophysiology of complications of congestive heart failure
  5. 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.

 

What is the etiology of congestive heart failure?

Heart failure is a chronic disease where the left ventricle, the right ventricle, or both, are unable to squeeze effectively, be it from enlarged ventricles or myocardial hypertrophy or compromised cardiac output. If the left ventricle is unable to pump blood through the aorta to the body efficiently, a decrease in oxygenated blood to the body is present and blood back up into the lungs. If the right ventricle is not pumping efficiently, a decrease in blood to the lungs is present and there is a backup of blood into the right atrium and body. Risk factors for heart failure include any disease process that can reduce heart contracture or alter ventricle filling, such as hypertension, coronary heart disease, diabetes mellitus, stenosis, regurgitation, cardiomyopathies, and arrhythmias (Rogers & Bush, 2015). Even though this is a disease that can be caught early and managed well, its prevalence is a serious public health concern and accounts for countless hospitalizations each year (Marques de Sousa, dos Santos Oliveira, Oliveira Soares, Amorim de Araújo, & dos Santos Oliveira, 2017).

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 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,

NR 507 Week 3 Discussion Part Two
NR 507 Week 3 Discussion Part Two

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.

Identify hallmark signs identified from the physical exam, diagnostic lab work, and symptoms.

57-year-old with dyspnea on exertion, fatigue, frequent dyspepsia, nausea, occasional epigastric pain, trouble breathing at night especially while lying on back, vital signs of 180/110 blood pressure. After a thorough assessment, to diagnosis heart failure and rule out other disease processes, such as valvular dysfunctions, a chest x-ray, and echocardiogram (Echo) would be ordered. A chest x-ray will reveal if the heart is enlarged and if there is any fluid in the lungs. An echo will measure the heart’s ability to pump, therefore conveying the EF. A serum BNP should be obtained to assess the severity of the disease (McCance et al., 2013). BNP is secreted via the ventricles when pressures within the ventricles change, the higher the serum level, the more severe the disease progression (McCance et al., 2013).

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Describe the pathophysiology of complications of congestive heart failure.

When heart failure occurs, they heart may not be strong enough to pump out as much blood as the body needs. As it tries to move more blood, the heart gets larger. It also pumps faster, and the blood vessels narrow to get more blood out to the body. As the heart works harder, it becomes weaker, and the damage increases. The body gets less oxygen, and the symptoms such as shortness of breath, swelling in the legs, and fluid buildup are present. In a normal heart, the upper chambers (called the atria) and lower chambers (the ventricles) squeeze and relax in turn to move blood through the body. If the ticker is weak, these chambers might not squeeze at the right time. The heart might beat too slowly, too quickly, or in an irregular pattern. When the rhythm is off, the heart can’t pump enough blood out to one body. Atrial fibrillation (AFib) is one type of abnormal heart rhythm that heart failure can cause. It causes the heart to quiver and skips instead of beating. An irregular heartbeat can lead to clots and cause a stroke. Also as the heart damage gets worse, the heart has to work harder to pump out blood, and it gets bigger and can damage the valves. Just like your other organs, they need a steady supply of blood to work as they should. Without the amount of blood, they need, they won’t be able to remove enough wastes from your blood. This is called kidney failure. Damaged kidneys can’t remove as much water from the blood as healthy ones. Consequently, the body will start to hold onto fluid, cause high blood pressure and make the heart work even harder.

What teaching would you provide this patient to avoid heart failure symptoms?

To help prevent recurrence of heart failure symptoms in patients I would stress the importance of home control and monitoring of daily weight. Patients must be instructed to check their weight in the morning after urinating and before breakfast, wearing light clothes and using the same scale. An increase of 1.3 kg or more in body weight in two days, or of 1.3 – 2.2 kg in one week may be an indication of fluid retention (Roger & Bush, 2015). I would also educate on the use of their medication and diet. It is import to teach patients that they must always take their medication, even when they feel well in order to obtain efficient treatment. Also, fluid restrictions and managing salt intake would be highlighted. Most importantly, self-care education, including the control of non-pharmacological measures, would be part of the daily management, reinforcement, improvement, and evaluation of self-care abilities.

References:

Marques de Sousa, M., dos Santos Oliveira, J., Oliveira Soares, M.G., Amorim de Araújo, A., & dos Santos Oliveira, S.H. (2017). Quality of life of patients with heart failure: Integrative review. Journal of Nursing UFPE/Revista De Enfermagem UFPE, 11(3), 1289-1287. doi: 10.5205/reuol.10544-93905-1-RV.1103201720

McCance, K. L., Huether, S. E., Brashers, V. L., & Rote, N. S. (2013). Pathophysiology: The biologic basis for disease in adults and children (7th ed.). St. Louis, MO: Mosby.

McMurray, J. J., Gerstein, H. C., Holman, R. R., & Pfeffer, M. A. (2013). Heart failure: a cardiovascular outcome in diabetes that can no longer be ignored. The Lancet Diabetes & Endocrinology2(10), 843-851.

Rogers, C. & Bush, N. (2015). Heart failure: Pathophysiology, diagnosis, medical treatment guidelines, and nursing management. Nursing Clinics of North America, 50(4), 787-799.