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In this case study, Mrs. Brown, a 78 years old female was admitted to the emergency department at 6am. She had a history of heart failure, 2 years ago. The patient showed severe dyspnoea, during the time of admission. Her respiratory rate was 24/minute. Oxygen saturation at room air was 85%. She showed the sign of hypertension with blood pressure 170/95 mmHg. Her pulse rate was also very fast, i.e. 110 beats/minute. On auscultation, crackles at the base of each lung have been shown. An ECG monitor showed atrial fibrillation, indicating acute exacerbation of heart failure. Her vital signs and clinical manifestation signs are indicating the left heart failure of the patient. Now, it is important to understand the pathophysiology causing Mrs. Brown’s condition.
Heart failure is state o body, when the heart is not able to pump enough blood to meet the metabolic needs of body. In the case of left heart failure, the function of left side of the heart, including left ventricle and auricle becomes impaired. The left heart failure compromises aortic flow to the boy and brain. Because of faulty blood circulation by the left part of the heart, the entire body fails to receive sufficient amount blood, leading to the oxygen-deficiency of heart tissues (McMurray et al., 2012). These events lead to fatigue and pulmonary edema. There are several factors having significant contribution in the pathogenesis of left heart failure. One of the significant factors in case of Mrs. Brown’s case study was her high blood pressure. According to her vital signs during the admission, she had 170/95 mmHg blood pressure. This high blood pressure had a significant contribution in left heart failure. Left heart failure or left ventricular failure is considered as a life-threatening disease. In case of Mrs. Brown, she experienced the left ventricular heart failure. Her medical history shown that she started to feel breathlessness after waking up in the morning.
The left ventricle of heart receives blood, rich in oxygen from the lungs and pumps it to left auricle, from where the blood is being pumped to the other parts f the body. As the ability of heart to pump blood forward from the left side has been decreased, the remainder of the body does not receive sufficient oxygen, which results in fatigue. Systolic and diastolic dysfunctions are the key reasons behind left heart failure. When the myocardial contractility takes place in the left ventricle, reduction in myocardial contractility promotes decreased left ventricular ejection fraction. Reduced contractility is caused as a result of ventricle overload, as the ventricle is filled with blood, heart muscle contraction efficiency becomes low. It is caused because of inability or decreased capability of heart muscle to establish cross-link between “actin and myosin filaments” in overstretched heart muscle. The cardiac output is based on the contractility and stroke volume (Hosenpud & Greenberg, 2015). These factors are interrelated. Increase in contractility enhances stroke volume, thereby decreasing the cardiac output, which in turn leads to left heart failure. On the other hand, decreased diastolic volume results from impaired ventricular filling, which is occurred due to lowered compliance of ventricle. Terminally differentiated heart muscle fibers causes increased size of myocardium or hypertrophy, which is a way of improving contractility. It can contribute to increased stiffness and reduced ability to relax during diastole. It results in reduced cardiac output and enhanced strain on heart, thereby enhancing the chance of heart failure (Guazzi & Borlaug, 2012).
In the case of Mrs. Brown, impaired contractility and increased metabolic rate might caused the condition. She has a history of heart failure, however, she failed to maintain her blood pressure low or inadequate intake of diuretics might contributed in enhanced circulatory volume, leading to left heart failure.
Mrs. Brown was admitted to the emergency department with vital signs of acute congestive heart failure. Therefore, the first priority of the nurse would be to assess the patient’s physical and mental stability through a thorough assessment. After her admission, the nurse would assess all her vital signs including BP, BGL, mental status, consciousness, pain or angina, respiratory rate, oxygen saturation and previous medication. The nurse would also have to assess her heart sounds, presence of abnormal heart sounds, fluid overload and arrange the environment in such a way that can promote rest and emotional strengthening (Katz, 2013).
The next intervention would be the management of dyspnea. The nurse would assist Mrs. Brown to decrease dyspnea. Administration of oxygen will be done after consulting with the cardiologist. The nurse can elevate her head to promote comfort and continuously monitor and report the signs of dyspnea. After consulting with the cardiologist, appropriate dose of diuretics can be administered along with the assessment of side effects. Mrs. Brown would be encouraged to intake adequate fluid as ordered by the physician and monitored for fluid overload (Rahko, 2013).
Glyceryl trinitrate is a vasodilating agent, which is used for relaxation of vascular smooth muscle. The dilation of arterial bed would lead to reduced blood pressure, respiratory rate as well as decreased pulse rate (Uil & Brugts, 2015). While assessing Mrs. Brown’s vital signs, it was revealed that these factors were elevated in case of Mrs. Brown, thus, the medication would help to reduce the worsening of the health issue.
b) According to the pharmacology of furosamide, the drug has adverse effect like nausea, vomiting, stomach pain, weight loss and enhanced heart rate. Monitoring her vital signs regularly, the adverse effects can be measured.
On the other hand, Glyceryl trinitrate’s adverse effects include headache, elevated heart beat, loss of consciousness temporarily and diarrhea. Monitoring heart beat regularly; the adverse effects can be monitored (Uzu et al., 2011).
c) As Mrs. Brown represented the vital signs related to pulmonary edema, thus water retention is important for enhancing her cardiac output and reducing edema. The effect of the medication can be evaluated by assessing the relief of the elevated blood pressure, thereby reducing the signs of dyspnea and respiratory rate. On the other hand, glyceryl trinitrate is important for dilating the blood vessels and thereby lowering the blood pressure and pulse rate (Peacock, 2012).
Guazzi, M., & Borlaug, B. A. (2012). Pulmonary hypertension due to left heart disease. Circulation, 126(8), 975-990.
Hosenpud, J., & Greenberg, Barry H. (2015). Congestive Heart Failure (3rd ed.). Philadelphia: Wolters Kluwer Health.
Katz, S. (2013). Heart failure : A practical guide for diagnosis and management(Oxford American cardiology library).
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.
Peacock, W. (2012). Short Stay Management of Acute Heart Failure (2nd ed., Contemporary Cardiology). Totowa: Springer.
Rahko, P.(2013). Heart Failure A Case-Based Approach. New York: Demos Medical Publishing.
Uil, C., & Brugts, A. (2015). Impact of Intravenous Nitroglycerin in the Management of Acute Decompensated Heart Failure. Current Heart Failure Reports, 12(1), 87-93.
Uzu, T., Araki, S., Isshiki, K., & Maegawa, H. (2011). Furosemide-associated nephrocalcinosis and renal cysts. Kidney International, 80(5), 556.
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