Responsible For Pumping Sufficient Amount †Myassignmenthelp.Com

Question: Discuss About The Responsible For Pumping An Sufficient Amount? Answer: Introducation A diagnosis has been done on Mrs. Brown with acute exacerbation of heart failure (AIHF). The symptoms of AIHF are initially caused by the pulmonary oedema due to an increased filling pressure in the left ventricle (LV) (Copstead Banasik, 2013). To meet the metabolic demand of the body, the LV is responsible for pumping an sufficient amount of oxygenated rich blood to the body. The LV becomes impaired to perform this activity, which leads to increase the blood volume and blood pressure in the LV (Gallagher, 2012). This situation results to the flowing of the blood forwarded into the body, which can cause the increased blood in the LV to revert through the pulmonary veins and left atrium, resulting to an increment in the capillary pressure (Craft Gordon, 2015). The fluid more possibly becomes to penetrate into the interstitial spaces and the lungs alveoli from the capillary walls causing a lift in the capillary hydrostatic pressure leading to pulmonary oedema, as a result of increase of the pulmonary circulation hydrostatic pressure (Fenwick, 2015). The pulmonary gas exchange function can be significantly impaired due to the increased fluid and in the alveoli and airway as the interference of the gas exchange with the lungs ventilation process. Hence, severe dyspnoea would be experienced by Mrs. Browns. Due to the movement of the air that passes through the alveolar flied, sounds of the crackles are heard from the patient having pulmonary oedema (Fenwick, 2015). It is indicated from the oxygen saturation reading that Mrs. Brown is having inadequate supply of blood in her body. The situation is resulted by the incapability of the lungs for not effective oxygenation of the blood. Therefore, while leaving the pulmonary circulation, the blood gets poorly oxygenated (Gallagher, 2012). The failing heart is responsible for not delivering the adequate oxygenated blood to reach the tissue oxygen needs, resulting into the hypoxia and reduced tissue perfusion, as stated b y Fenwick (2015). AHF is connected with a remarkable reduction in the cardiac output (CO), myocardial contractility and stroke volume. Accumulated blood pressure and tachycardia has been experienced by Mrs. Brown due to the activation o compensatory mechanism responding to the reduced CO. The activation of the symoathetic nervous system is stimulated by the decreased cardiac output to discharge the no noradrenalin and adrenaline that can be the reason for increment in vasoconstriction (McCance Huether, 2014). With the activation of the vasoconstriction, the further elevation happens in the myocardial contractility, peripheral vascular constriction and the HR. A decreased blood flow to the kidneys is caused by the decreased CO, resulting to a step down in the glomerular filtration rate, additionally (McCance Huether, 2014). Chopsted and Banasik (2013) has showed in response to the above stated situation, that, to release rennin, which transforms the angiotensinogen to angiotensin I from angiotensin II the kidneys are stimulated by the rennin-angiotensin-aldosteron. A lift in the arterial blood pressure is caused by the increase of the peripheral vasoconstriction from such situation. In addition, Gordon and Craft (2015) stated that, the release of antidiuretic hormone (ADH) is stimulated by the posterior pituitary, in response to the reduction of the cerebral perfusion pressure caused by the low CO. An important role is played by the ADH in raising the reabsorption of the water of the renal tubules, which results in increased volume of blood and the water retention. If the prescribed oxygen therapy is provided to Mrs. Brown, it will relieve the symptoms of her connected with acute hypoxia and dyspnoea. The density of oxygen in airway and the alveolar space is increased and the levels of carbon dioxide are decreased by the disposal of oxygen. Therefore, this helps the gases to spread out into the capillaries of pulmonary by crossing the membrane of the alveolar capillary (Wagner Hardin-Pierce, 2014). As the result, the function of the pulmonary gas exchange improves and the symptoms of the dyspnoea decreases.the oxygen level in the blood is increased and the requirement for the tissue perfusion is improved by the oxygen therapy (Powell, Graham, OReilly Punton, 2016). Optimally, a pulse oximetry has been used for monitoring the effectiveness of oxygen therapy disposal provided to Mrs. Brown. Mrs. Brown has been placed in the high Fowler position while her feet is dangling at the bedside, which improves the gas exchange function and the ventilation by enhancing her thoracic capacity (Gallagher, 2012). Moreover, the cardiac preload caused by the ineffective systematic circulation is decreased by this particular position. During diastole, the blood amount returning to the left ventricle gets less overfilled, as a result of the decreased return of venous (Wagner Hardin-Pierce, 2014). Consequently, this improves the LV performance. Furosemide is one of the loop diuretic drugs. The reabsorption of the chloride and the sodium ions into the interstitial fluid from the loops inhibited by the direct working of the ascending loops medullary part of Henle, which result into a hypotonic interstitial fluid environment (Bullock Manias, 2013). The reduction of the pulmonary venous pressure is helped by the Furosemide, by circulating the oedemous fluid, which can be responsible for resulting to the optimal exchange of gas. The intravascular volume is decreased by this which can lead to a reduction of return of venous to the preload and LV. This can benefit the improvement of the cardiac output by allowing the overfilled LV to constrict more effectively by the reduced venous return (Gallagher, 2012). The electrolyte imbalances and the dehydration are affected by the common adverse. The main affected electrolyte is the potassium ions and imbalances in the potassium level can lead to cardiac dysrhythmias, hypokalaemia and co nfusions in aged patients (Riley, 2013). Thus, the nurses are suggested to monitor and document the fluid and electrolyte status of the patient, prior to begin the therapy of intravenous (IV) furosemide. The IV furosemide usage on an aged patient needs to be as low dose as possible, and generally not more than 4mg per minute not to cause ototoxicity. The patient needs to be monitored frequently for dizziness, headache, dry mouth and loss of skin turgor as the signs of dehydration. For further advice, these symptoms are needed to be documented and reported to the doctors (Bullock Manias, 2013). Glyceryl trinitrate is one of the peripheral vasodilator drugs, which is absorbed by the endothelial cells of the wall of the blood vessel and transformed into nitric oxide (NO) in the vascular muscle. The activation of the second manager system depended on calcium is stimulated by the NO for releasing cyclic guanosine monophosphate thatalerts the myosins activity resulted into the dilating of the blood vessels (Gallagher, 2012). The NO levels in the vascular smooth muscle, which is responsible for the activation of the vasodilatation, is increased by the glyceryl trinitrate. This results into the systematic vascular response (SVR) and reduction of venous return that further results into decreased cardiac preload and cardiac after load. Dilating the pulmonary vasculature is acted by this which is responsible for the result of the increase in venous capacitance (Gallagher, 2012). The facial flushing, hypotension and the headache is caused by the common adverse. The blood pressure that is resulted from the reduced SVR is decreased by glyceryl trinitrate. Thus, is considered to be important to observe the blood pressure of the patient frequently, every 5 to 10 minutes for avoiding the systematic hypotension. The nurses are required to document and report to the doctors immediately, if a large reduction in the systolic blood pressure can be seen in the patient (Riley, 2013). Reference: Bullock, S., Manias, E. (2013). Fundamental of Pharmacology (7th ed.). Pearson Australia. Copstead, L., Banasik, J. (2013). Pathophysiology (5th ed.). Elsevier Astralia. Craft, J., Gordon, C. (2015). Understanding Pathophysiology (2nd ed.). Chatswood, Australia: Elsevier Australia. Fenwick, R. (2015). Mnagaement of acute heart failure in the emergency department. Emergency Nurse. 23(8), 26-35. Retrieved from https://search.proquest.com/docview/1784630412/fulltextPDF/A56CA91C5E14460PQ/1?accountid=36155 Gallagher, R. (2012). Problems of oxygenation: perfusion. In Brown, D., Edwards, H. (3rd edition.). Lewiss medical-surgical nursing: assessment and management of clinical problems. (pp. 883-898). Chatswood, NSW: Elsevier Australia. McCance, K., Huether, S. (2014). Pathophysiology: the biologic basis for disease in adults and children (7th edi.). Elsevier Australia. Powell, J., Graham, D., oReilly, S., Punton, G. (2016). Acute pulmonary oedema. Nursing Standard. 30(23),51. Retrieved from https://search.proquest.comezproxy.uws.edu.au/docview/1784938311.fulltext/71A552B44E73PQ/1?accountid=36155 Riley, J. (2013). Acute decompensate heart failure: diagnosis and management. British Journal of Nursing. 22(22), 1290-1295. Retrieved from https://web.b.ebscohost.com.ezproxy.uws.edu.au/ehost/pdfviewer?sid=c609c3a5-1919-41fc-8ff8-eac9facfea9f%40sessionmgr4009vid=5hid=4201 Wagner, K., Hardin-Pierce, M. (2014). High-acuity nursing (6th ed.). Upper saddle river, New Jersey: Pearson.