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Left sided Heart Failure

Question:

Discuss about the Left sided Heart Failure

Answer:

Introduction:

1. An acute exacerbation of heart failure is a sudden worsening of the clinical signs associated with heart failure. Decreased blood flow from the pulmonary blood vessels into the left atrium results in an increase in both the pulmonary blood volume and pulmonary blood pressure. The increased pressure forces fluid to flow from pulmonary capillaries into the adjacent lung tissue and alveoli (Brunner & Suddarth, 2008). This movement of fluid results in pulmonary interstitial edema which impairs gaseous exchange at the lung.

The normal respiratory rate in an adult human ranges from twelve to twenty breaths per minute (Marieb, Hoehn & Hutchinson, 2014). Respiration is controlled by breathing centers located in the medulla which determine the respiratory rate and the depth of breathing. Fluid accumulating in the pulmonary interstitium affects normal lung ventilation resulting in hypoxia. When hypoxia occurs, there is an increased level of carbon dioxide in the blood stream which is detected by chemoreceptors in the brain and the carotid and aortic bodies. Signals are therefore sent to the breathing centers in the medulla to increase the respiratory rate in an attempt to eliminate the accumulating carbon dioxide and eliminate hypoxia.

As the pulmonary edema progresses, fluid moves from the pulmonary interstitium and starts filling the alveoli. Auscultation at the base of the lungs reveals crackles which denotes presence of fluid in the alveolar space. The fluid forms a froth in the alveoli resulting in insufficient alveolar ventilation. The patient then starts experiencing a sense of suffocation which is manifested as severe dyspnea. The froth in the alveoli also further impairs O2-CO2 exchange at the lungs. This results in a further decrease in oxygen uptake at the lungs and increased carbon dioxide retention in blood and tissues. A physician performing the pulse oximetry test will therefore detect a diminished blood oxygen level (SpO2). (Brunner & Suddarth, 2008).

According to Grossman & Porth (2013), when low blood oxygen levels are registered, compensatory or adaptive responses are initiated by the body to ensure tissue perfusion is maintained to prevent cell death. The response involves stimulation of the sympathetic nervous system or the hormonal system which occurs minutes to hours after acute heart failure. Both try to maintain the heart’s pumping performance at normal levels. The sympathetic nervous system releases catecholamines into blood which speed up the heart rate and also act on the smooth muscles of blood vessels causing vasoconstriction. Alternatively, the hormonal system causes retention of sodium and water and this results in an increase in the circulatory volume. Additionally, when the cardiac output is low, the adrenal glands also release adrenaline which also stimulates an increase in the heart beat.

The vasoconstriction of the blood vessels resulting in a decreased lumen size of blood vessels combined with the increased heart rate causes an increase in the blood pressure beyond normal ranges and an elevated pulse rate as observed in Mrs. Brown.

2. The primary goal of care after acute heart failure is to eliminate congestion and lower the high blood pressure. After ensuring delivery of high concentration oxygen, administration of intravenous loop diuretics such as furosemide is initiated. The intravenous route is chosen because the diuretics will have a greater biological availability with diuresis starting 30-60 minutes later.  Loop diuretics are preferred because they lead to more excretion of sodium compared to other diuretics. The initial dose of the diuretic administered intravenously should equal a patient’s daily maintenance dose. Diuretics lead to relief of pulmonary edema hence eliminating the symptoms arising from it (Somma & Magrini, 2015).

Since Mrs. Brown showed symptoms of hypertension, the diuretic therapy is followed by administration of intravenous vasodilators. The vasodilator therapy dilates both arteries and veins decreasing both the cardiac preload and cardiac afterload resulting in a lower filling pressure of the left ventricle, increased stroke volume and improved peripheral oxygen supply. The vasodilators commonly used include nitroglycerin, nesiritide and nitroprusside. Nitroglycerin is preferred because it is short-acting and rapid. The initial dosage is 10-20µg/min which is later increased by 10-20µg increments until symptoms are eliminated. The dose should not exceed 200µg/min (Somma & Magrini, 2015).

3. (A) Furosemide works by inhibiting absorption of sodium, chloride, water and to some extent potassium by the kidney tubules. This results in decreased fluid absorption by the renal tubules and increased urine production. The fluid content of blood is therefore decreased and more fluid is absorbed from the lung interstitium and alveoli to replace the ongoing losses causing decreased pulmonary edema (Burchum & Rosenthal, 2016).

After administration, glyceryl trinitrate forms nitric oxide which is a free radical. The nitric oxide in turn activates guanylate cyclase which results in increased cyclic GMP (guanosine 3'5' monophosphate) in the smooth muscles of blood vessels. Cyclic GMP causes dephosphorylazion of myosin light chains causing relaxation of the smooth muscles resulting in vasodilation (Burchum & Rosenthal, 2016).

3 (B) Repeated or prolonged use of diuretics results in hypokalemia and hyponatremia. According to Brunner and Suddarth (2008), hypokalemia results in hypotension, ventricular dysrhythmias and general weakness while hyponatremia results in disorientation, fatigue and malaise. Once adverse effects are noticed, the diuretic therapy should be stopped. Oral potassium chloride and sodium chloride are then administered to replenish the ion levels.

Adverse effects of glyceryl trinitrate include blurred vision, nausea, headache and dry mouth. To counter the adverse effects, administration of glyceryl trinitrate should be stopped and if further vasodilator therapy is required, replacement drugs such as nesiritide and nitroprusside may be used.

3 (C) Assessing the extent of clinical symptoms helps assess the effectiveness of drugs used. Elimination of symptoms associated with pulmonary edema e.g. dyspnea and increased respiratory rate denotes the effectiveness of furosemide in eliminating the edema. A decreased cardiac silhouette, decreased alveolar and pulmonary edema and reduced pleural effusions will be seen on x-rays and CT scans.

A drop of the blood pressure and the pulse rate to a value within the normal ranges denotes that the glyceryl trinitrate medication is working. The normal blood pressure ranges from 120/80 mm Hg to 140/90 mmHg while the normal resting heart ranges from 60 to 100 beats per minutes.

References

Brunner, L.S., & Suddarth, D.S. (2010). Left-sided heart failure. Textbook of medical-surgical nursing (12th ed., pp. 346-354). Philadelphia, PA: Lippincott Williams and Wilkins.

Burchum, J. R., & Rosenthal, L. D. (2016). Lehne's pharmacology for nursing care (9th ed.). St. Louis, MO: Elsevier/Saunders.

Grossman, S.C., & Porth, C.M. (2013). Left ventricular dysfunction. Porth's pathophysiology: Concepts of altered health states (pp. 588-596). Philadelphia, PA: Lippincott Williams and Wilkins.

Marieb, E. N., Hoehn, K., & Hutchinson, M. (2014). Human anatomy & physiology (9th, Pearson new international ed.). Harlow, UK: Pearson.

Somma, S.D., & Magrini, L. (2015). Drug therapy for acute heart failure. Acute heart failure, 68(8), 706-713.


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