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The case study is about Mrs. Brown who has been admitted to hospital after the serious manifestation of acute heart failure. On physical examination, she was diagnosed with atrial fibrillation and it suggested acute exacerbation of left heart failure.
Congestive left heart failure occurs due to inefficient pumping of the heart to maintain body flow in the human body. The clinical manifestations of this disease are shortness of breath, fatigue, swelling of ankles and feet, pulmonary edema, etc. Mrs. Brown also had severe dyspnea which was evident by the high respiratory rate of 24 breaths/minute and more than normal pulse rate of 110 beats/minute. It is necessary to understand the pathogenesis of the condition causing these clinical manifestations on Mrs. Brown.
Heart failure is caused by the inefficiency of heart muscle and other conditions like myocardial infarction amyloidosis. In Patients like Mrs. Brown the normal mechanism of Frank-Starling fails and so muscle contraction becomes difficult leading to decreased cardiac output. Cardiac dysfunctions cause changes in vascular function, blood volume, and neurohumoral status. The cardiac and vascular changes accompanying left heart failure are as follows:
Decreased output is seen in patients with heart failure because of the decline in stroke volume due to systolic or diastolic dysfunction. Systolic dysfunction occurs because of loss of contractility following acute myocardial infarction. In the case of diastolic dysfunction, ventricle stiffens and impairs normal ventricular filling. Reduced ventricle filling leads to lesser ejection of blood and high ventricular end-diastolic pressure. This compensator mechanism starts by using Frank-Starling mechanism to augment stroke volume (Andrade et al., 2014).
Blood volume in left heart failure also increases due to reduced renal perfusion leading to decrease urine output and more retention of fluid. Along with this, activation of rennin-angiotensin system enhances aldosterone secretion antidiuretic hormone. The outcome is increased in the renal absorption of sodium and fluids. Although increased blood volume helps to maintain cardiac output increases venous pressure leading to pulmonary and systemic edema. Understanding of this mechanism contributes to understanding the cause of clinical manifestation in Mrs. Brown and plan treatment to reduce blood volume. Crackle sound at the base of each lung for Mrs. Brown also suggest that pulmonary edema because of which she has shortness of breath (Rosenkranz et al., 2015).
In patient’s heart like Mrs. Brown, the neurohumoral response also occurs due to heart failure. It involves activation of sympathetic nerves and release of vasopressin and atrial peptides. It leads to arterial vasoconstriction, venous constriction and increased blood volume. These are all compensatory mechanism to increase ventricular filling, but it often worsens the situation by increasing ventricular load and resulting pulmonary congestion and finally edema. Therefore knowing about the pathophysiology of heart failure is critical to find the rationale for each therapeutic intervention (Schwartzenberg et al., 2012).
Strategy to relieve dyspnoea and pulmonary edema in a patient: For management of acute breathlessness in patients, the nurse can administer diuretics to Mrs. Brown to give her relief from symptoms of dyspnoea. It will also be important for them to closely monitor renal function, urine output and fluid balance in patients. Urine output can be assessed by indwelling urinary catheter. But urinary catheter should be restricted and removes as soon possible as it leads to urinary tract infections. Several studies also have evidenced patient acquiring infection due to catheterization, and it accounts for 20% of hospital-acquired infection (McMurray et al., 2012).
Strategy to manage decreased cardiac output: As Mrs. Brown has the irregular rhythm of pulse and altered heart rate, it will be necessary to plan intervention reduces the workload of the heart and gives the patient hemodynamic stability. The nurse will first assess heart and lung sounds, monitor blood pressure and diagnostic test. They will administer cardiac glycoside agents to improve cardiac output. They will teach them to assume positions that give better chest expansion and improved pulmonary capacity (McHugh & Ma, 2013). It will be important to educate the patient about the pathophysiology of disease for proper management of disease and compliance with treatment. Several studies have shown a combination of medication leads to the risk of side-effects, so giving patients knowledge about side-effects will them cautious. The nurse can remind them to stand up slowly in case of dizziness due to certain medicines (Wakefield et al., 2013).
IV furosemide: It is a loop diuretic pill that prevents water reabsorption in the kidney by blocking potassium-chloride cotransporter. Competitive inhibition at chloride binding site on cotransporter prevents transport of sodium and diminishes osmotic gradient for water reabsorption throughout the nephron (Ali et al., 2014).
Glyceryl trinitrate: This drug activates guanylate cyclase enzyme and stimulates the release of cyclic guanosine 3',5'-monophosphate. It leads to protein kinase dependent phosphorylation in the smooth muscle cells and causes dephosphorylation of myosin chain of smooth muscle. Calcium ion is then released resulting relaxation of smooth muscle cells and vasodilation (Bath et al., 2016).
After giving Furosemide drugs to the patient, the nurse will check the patient for signs of allergic reaction to the drugs like swelling of the face, drowsiness, nausea, jaundice and kidney problem. As Furosemide is used to prevent the body from absorbing too much salt, it may also lead to electrolyte imbalance. So nurse should check for signs of dry mouth, muscle cramp, thirst or no urination (Ricci et al., 2015).
Glyceryl trinitrate is used to treat angina and heart failure. The nurse should check for allergies to nitrates in patients and precaution should be taken before giving it to patients with low blood pressure, heart patients, anaemia, and glaucoma. The nurse should monitors side-effect of the drug in patients with vomiting, dizziness, rapid heartbeat, swelling and rashes (Münzel & Gori, 2013).
Therapeutic effect of the drug will be evaluated by checking if symptoms of breathlessness and swelling have decreased or not. It will minimize the chance of heart attack (Ali, 2014).
Glyceryl nitrate is a nitrate vasodilator, and the therapeutic effects of the drug will be judged by checking if symptoms of heart failure have been relieved on patients (Münzel & Gori, 2013).
Ali, Y., Parekh, A. M., Rao, R. K., & Baig, M. R. (2014). Furosemide Induced Electrolyte Imbalance: A Real Danger of Overdiuresis in Patients with Heart Failure. Journal of International Translational Medicine, 2(4), 482-484.
Andrade, J., Khairy, P., Dobrev, D., & Nattel, S. (2014). The clinical profile and pathophysiology of atrial fibrillation relationships among clinical features, epidemiology, and mechanisms. Circulation research, 114(9), 1453-1468.
Bath, P. M., Woodhouse, L., Krishnan, K., Anderson, C., Berge, E., Ford, G. A., ... & in Acute Stroke Collaboration. (2016). Effect of Treatment Delay, Stroke Type, and Thrombolysis on the Effect of Glyceryl Trinitrate, a Nitric Oxide Donor, on Outcome after Acute Stroke: A Systematic Review and Meta-Analysis of Individual Patient from Randomised Trials. Stroke research and treatment, 2016.
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McMurray, J. J., Adamopoulos, S., Anker, S. D., Auricchio, A., Böhm, M., Dickstein, K., ... & Jaarsma, T. (2012). ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2012. European journal of heart failure, 14(8), 803-869.
Münzel, T., & Gori, T. (2013). Nitrate therapy and nitrate tolerance in patients with coronary artery disease. Current opinion in pharmacology, 13(2), 251-259.
Ricci, Z., Haiberger, R., Pezzella, C., Garisto, C., Favia, I., & Cogo, P. (2015). Furosemide versus ethacrynic acid in pediatric patients undergoing cardiac surgery: a randomized controlled trial. Critical Care, 19(1), 1.
Rosenkranz, S., Gibbs, J. S. R., Wachter, R., De Marco, T., Vonk-Noordegraaf, A., & Vachiéry, J. L. (2015). Left ventricular heart failure and pulmonary hypertension. European heart journal, ehv512.
Schwartzenberg, S., Redfield, M. M., From, A. M., Sorajja, P., Nishimura, R. A., & Borlaug, B. A. (2012). Effects of vasodilation in heart failure with preserved or reduced ejection fraction: implications of distinct pathophysiologies on response to therapy. Journal of the American College of Cardiology, 59(5), 442-451.
Tanai, E., & Frantz, S. (2014). Pathophysiology of heart failure.Comprehensive Physiology.
Wakefield, B. J., Boren, S. A., Groves, P. S., & Conn, V. S. (2013). Heart failure care management programs: a review of study interventions and meta-analysis of outcomes. Journal of Cardiovascular Nursing, 28(1), 8-19.
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