Wednesday, May 6, 2020

Congestive Hear Failure for Alcohol and Drugs - myassignmenthelp.com

Question: Discuss about theCongestive Hear Failure for Alcohol and Drugs. Answer: Congestive heart failure (CHF) is a chronic disease that is mainly caused due to the inability of the heart to pump adequate amount of blood for meeting the oxygen demand of various organs (Kemp Conte, 2012). The case study reveals the fact that Mrs. McKenzie has been suffering from diastolic cardiac failure as she has hypertension and her respiratory rate is 30 bpm. Congestive heart failure can be brought about by several causes. It can be caused by cardiomyopathy (weakening of the heart muscles), damaged valves of the heart, Ischemic cardiomyopathy, where the blood vessels supplying the coronary arteries gets blocked (Kemp Conte, 2012). Toxic exposure to alcohol and drugs can also cause this disease. Left ventricular hypertrophy (thickening of the heart muscles) that is caused due to hypertension may also act as the contributing factor. The risk factors contributing to CHF are equal to the risk of stroke, coronary heart disease. According to Kemp Conte, (2012) hypertension is the most important risk factor accounting for about CHF in 59 % of women and 39% of men (Dib, Matin, Luckert, 2012). Elevated cholesterol, diabetes and obesity are the other factors. It is evident that Mrs. Sharon McKenzie already had a past history of Myocardial infarction at the age of 65. CHF occurs in about half of the patients with MI. With CHF the stroke volume de creases but the cardiac index is maintained by an increased heart rate. The minute work and the stroke work of the left ventricles are decreased significantly further decreasing the end-diastolic pressure of the left ventricle. This complicates the myocardial infarction causing CHF. The prevention and the treatment of CHF have risen to a burgeoning public health problem. There are almost 20 million people worldwide who are affected by CHF. According to the Australian commission for health and safety, about 5.2 millions of Australians suffer from CHF, much of which is due the obesity and diabetes (Australian heart Foundation, 2018). The estimated mortality due to CHF is about 286000. It follows an exponential pattern affecting 6-10 % of the population over the age of 65. The expected cost to the disease in Australia has been recorded to be $34.8 billion (Australian heart Foundation, 2018). CHF have not only affected the physical health of Mrs. Mackenzie, but also contribute to her emotional burden. Sense of inferiority complex or discontent may come due to the inability to do daily chores. Furthermore it will also contribute to the emotional burden. CHF failure requires regular monitoring and costly medications and even hospital stay. Hence this would also affect the economic condition of the family. The patients husband may suffer from anxiety and may be perturbed about her wellbeing. Some people even face from high levels of depressive symptoms. Symptoms Underlying pathophysiology Shortness of breath Shortness of breath, which is associated to the early stage of exertion. Difficulty in breathing is related to the recumbent position due to the augmentation of the venous return to the heart (Kemp Conte, 2012). Paroxysmal nocturnal dyspnea can be caused by the pulmonary congestion with the accumulated fluid in the alveolar and the institial spaces developing pulmonary edema. Lack of appetite and nausea Fluid buildup around the liver and the gut can interfere with the process of digestion that may cause changes in the appetite (Katz Konstam, 2012). Nausea is a complex act that needs central neurologic coordination. The neurologic coordination of the components of nausea is provided by the emetic center. The onset of nausea can also be due to the changes in the hormonal levels of arginine vasopressin (Cowie Poole-Wilson, 2013). Sleeping disorders and nocturia Accumulation of the extra fluid s may increase the rate of urination at night leading to sleeping disorders (Sobotka et al., 2013). Some finds it difficult to sleep without sitting upright. Renal perfusion may increase when the patient is in a supine position as when a patient lies down the blood that has been accumulated in the extremities return back to the heart and the cardiac output increases (Sobotka et al., 2013). Compared to the daytime. The augmented cardiac output perfuses the kidney to produce more urine for decreasing the work load of the heart. Swelling of ankles Edema in congestive heart failure is due to the activation of a number of humoral and non humoral mechanisms promoting re-absorption of the sodium and water by the kidneys and the expansion of the extracellular fluid (Kemp Conte, 2012). As the right ventricle of the heart begins to fail fluid begins to collect in the feet (Kemp Conte, 2012). Fatigue Fatigue during congestive heart failure is mainly caused due to the reduced cardiac output. CHF is linked with the disruptive perfusion of the vital organs, vasoconstrictive drive and diversion of the blood flow away from the skin and muscle circulations. This diversion causes muscular fatigue. Reduced oxygen delivery can fatigue and exhaustion (Mebazaa et al., 2015). Common classes of drugs Furosemide is a diuretic drug that is normally used for eliminating the water and salt from the body (Bikdeli et al., 2013). It is used against the accumulation of the fluid in the blood. It inhibits the re-absorption of the water in the nephron by the blockage of the potassium- chloride co-transporters (NKCC22) in the Henle's loop of the nephron. This mainly occurs due to the competitive inhibition occurring in the chloride binding site of the cotransporter (Felker Mentz, 2012). It prevents the transport of the sodium from the Henle's loop in the basolateral interstitium. As a result the lumen becomes hypertonic and the interstitium becomes less hypertonic, diminishing the osmotic gradient for the absorption of the water in the nephron. The salt, water and other molecules are normally filtered out of the blood in the kidneys and the filtered fluid ultimately becomes the urine (Bikdeli et al., 2013). The sodium, chloride that has been filtered out of the blood is reabsorbed in the b lood and before the conversion of the filtered fluid in to urine. Furosemide blocks the absorption of sodium, chloride and water from the filtered fluid from the kidney leading to a profound increase of urine. Thus this medicine can be used to cure the edema in the patient with CHF and fluid retention (Felker Mentz, 2012). ACE inhibitors like lisinopril, can be used for patients having CHF, as Angiostenin converting enzymes reduce the formation of the heart damaging hormones (McMurray et al., 2013). It dilates the blood vessels to lower the blood pressure in order to lessen the heart workload. It helps in blocking the formation of angiostenin II, which narrows the blood vessels and increases the blood pressure. It works by controlling the activity of the renin- angiostenin-aldosterone system (RAAS). RAAS controls the bllod pressure fluctuations. Renin in secreted in the juxtaglomerular structure of the kidney and this then produces the angieostenin. The angiostenin is converted in to angiostenin II by the ACE which increases the fluid retention and increased blood pressure. The ACE inhibitor blocks the conversion of the angiostenin I to angeostenin II. Thus it can be considered as a suitable class of medication for Mrs Mackenzie (McMurray et al., 2013). Nursing care strategies: - At the time of admission a registered nurse should first evaluate and treat the precipitating factors that have caused the heart failure right after the admission the patient, the cardiac status of the patients should be evaluated by electrocardiogram, echocardiogram (Krim et al., 2015). The immediate drug that can be administered right after the hospital admissions are furosemide, ethacrynic acid in order to inhibit the reabsorption of the sodium , potassium and the chloride from the Henle's loop (Australian heart Foundation, 2018). Nurses should be careful regarding the dosing of the diuretics, as it is vital in maintaining the normal volume status in patients with heart failure. After the initiation of the diuretics, there should be a careful monitoring of the hemodynamics (Krim et al., 2015). Bed rest is necessary during the hospital admission for improving the diuresis, physical therapy with early ambulation is required in the first 24 hours of the admission. Foley catheter can be used if the accurate assessment of urine cannot be done due to factors such as incontinence (Krim et al., 2015). The volume status should be assessed at least once in a day, including the assessment of the peripheral edema, ascites, jugular venous pressure, hepatimegaly and body weight (Feltner et al., 2014). The symptoms should be reevaluated and focus should be given on the symptoms that triggered the hospital admission. There should be a close monitoring of the vital signs in order to see the effects of diuretics in hypotension and urine output (Bradley et al., 2013). The renal output and the balance in the electrolytes should be maintained in order to ensure the replacements of the electrolytes. At the time of the admission all the guideline directed therapies should be assessed and evaluated and should be adjusted depending on the patient's condition (Bradley et al., 2013). Beta blockers and ACE Inhibitors can be used to allow diuresis and perfusion of the target organs (Feltner et al., 2014). ARBs can be used in patients who cannot tolerate ACE inhibitors. The nurses should be cautious wh ile applying the Beta blockers to the patients who have taken inotropic therapy at the time of their index hospitalisation and those with newly diagnosed cardiac failure (Bradley et al., 2013). Reduced cardiac output, decreased ambulation increases the risk of thromboembolic events. In order to mitigate the risk, thromboembolism prophylaxis has to be administered to the patients (Feltner et al., 2014). Nurses should ausculate the breathe sound frequently for any crackles or wheezes, assess the bowel sounds for visceral congestion can change the intestinal function and hence any signs of anorexia should be reported. Nurses should encourage the patient to verbalize the feelings (Mebazaa et al., 2015). The abdomen should be palpated and any reports of right upper quadrant pain and tenderness should be reported (Feltner et al., 2014). The dietician should be consulted with for providing the necessary diet to the patient that meets her caloric needs within restricted sodium level. Nurses should be able to provide a holistic care approach to the patient, which involves provision of a calm and quite environment, helping the patient to manage stressful conditions, listen and respon d to their feelings (Rustad et al., 2012). References Alt, E. (2014). U.S. Patent No. 8,777,851. Washington, DC: U.S. Patent and Trademark Office. Australian Foundation, T. (2018). Heart attack treatment. The Heart Foundation. Retrieved 24 March 2018, from https://www.heartfoundation.org.au/after-my-heart-attack/heart-attack-treatment Bikdeli, B., Strait, K. M., Dharmarajan, K., Partovian, C., Coca, S. G., Kim, N., ... Krumholz, H. M. (2013). Dominance of furosemide for loop diuretic therapy in heart failure: time to revisit the alternatives?. Journal of the American College of Cardiology, 61(14), 1549-1550. Bradley, E. H., Curry, L., Horwitz, L. I., Sipsma, H., Wang, Y., Walsh, M. N., ... Krumholz, H. M. (2013). Hospital strategies associated with 30-day readmission rates for patients with heart failure. Circulation: Cardiovascular Quality and Outcomes, 6(4), 444-450. Cowie, M. R., Poole-Wilson, P. A. (2013). Pathophysiology of heart failure. In Essential cardiology (pp. 327-345). Springer, New York, NY. Dib, J. E., Matin, S. A., Luckert, A. (2012). Prehospital use of continuous positive airway pressure for acute severe congestive heart failure. Journal of Emergency Medicine, 42(5), 553-558. Felker, G. M., Mentz, R. J. (2012). Diuretics and ultrafiltration in acute decompensated heart failure. Journal of the American College of Cardiology, 59(24), 2145-2153. Feltner, C., Jones, C. D., Cen, C. W., Zheng, Z. J., Sueta, C. A., Coker-Schwimmer, E. J., ... Jonas, D. E. (2014). Transitional care interventions to prevent readmissions for persons with heart failure: a systematic review and meta-analysis. Annals of internal medicine, 160(11), 774-784. Katz, A. M., Konstam, M. A. (2012). Heart failure: pathophysiology, molecular biology, and clinical management. Lippincott Williams Wilkins. Kemp, C. D., Conte, J. V. (2012). The pathophysiology of heart failure. Cardiovascular Pathology, 21(5), 365-371. Krim, S. R., Campbell, P. T., Desai, S., Mandras, S., Patel, H., Eiswirth, C., Ventura, H. O. (2015). Management of Patients Admitted with Acute Decompensated Heart Failure. The Ochsner Journal, 15(3), 284289. McMurray, J. J., Packer, M., Desai, A. S., Gong, J., Lefkowitz, M. P., Rizkala, A. R., ... Zile, M. R. (2014). Angiotensinneprilysin inhibition versus enalapril in heart failure. New England Journal of Medicine, 371(11), 993-1004. Mebazaa, A., Yilmaz, M. B., Levy, P., Ponikowski, P., Peacock, W. F., Laribi, S., ... McDonagh, T. (2015). Recommendations on pre?hospital early hospital management of acute heart failure: a consensus paper from the Heart Failure Association of the European Society of Cardiology, the European Society of Emergency Medicine and the Society of Academic Emergency Medicine. European journal of heart failure, 17(6), 544-558. Rustad, J. K., Stern, T. A., Hebert, K. A., Musselman, D. L. (2013). Diagnosis and treatment of depression in patients with congestive heart failure: a review of the literature. The primary care companion for CNS disorders, 15(4). Sobotka, P. A., Krum, H., Bhm, M., Francis, D. P., Schlaich, M. P. (2012). 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