Pathogenesis of Fluid Volume Excess in an Acute Exacerbation Chronic Heart Failure Patient Essay

Heart failure is a clinical syndrome of decreased tolerance and fluid retention callable to geomorphological means disease. Despite much advancement in discourse of the treatment of nubble failure, there still exists a high annual mortality.In rule situations, an append in total channel volume results in an increase in renal levels of sodium and wet excretion. These renal excretions are due to reflexes that help maintain normal body volume in increase of atrial pressure. Thus any atrial pressure increase results to a decreased release of antidiuretic horm adept, an increased release of atrial natriuretic peptide and a decreased renal sympathetic tone.In contrast, when a patient has an acute exacerbation of inveterate midsection failure, the total blood volume does not affect renal excretion of sodium and water. Rather, due to either decreased or increased cardiac output, underfilling of the arterial circulation and general arterial vasodilation occurs. To compensate the c hange, total blood volume is increased by the expansion of blood volume in the venous circulation and the increased after-load (systemic vascular resistance). This results in an acute increase in left ventricular end-diastolic pressure.pulmonary venous pressure and the acute increase in left ventricular end-diastolic leads to increased alveoli pressure which results to pulmonary congestion when the alveoli cells are overwhelmed.Further, the stimulated normal reflexes, as a result of increased atrial pressure, are alter by reflexes initiated in the high pressure arterial circulation. For example, renin-angiotensin-aldosterone system is activated by increased arterial pressure to release angiotensin II. angiotensin II acts to help in reabsorption of sodium in the proximal tubules. Glomerular filtration rate and excretion of water and sodium is also increased. This, however, is alter in acute heart failure by renal vasoconstriction and a re lineion of sodium delivery to the distal n ephron. Resulting in the release of arginine vasopressin, as a result of arterial undefilling, which increases plasma and urine osmolalities and leading to fringy arterial vasoconstriction and water reabsorption in the cells of the distal tubule and collecting duct in the kidney, promoting hyponatremia.The Nitroglycerin and angiotensin II receptor blockers strategies as care for strategies apply to manage pulmonary oedema.Pulmonary oedema is the accumulation of exorbitance watery fluids in the air sacs of the lungs and a common result of heart failure.The main objective in managing pulmonary oedema is to improve oxygenation and trim down pulmonary congestion. Two of the several managing strategies are use of Nitroglycerin (NTG) and Angiotensin II receptor blockers.NitroglycerinNitroglycerin (NTG) is an effective, predictable and rapidly-acting medication utilise for preload reduction. According to Sovari 2012, several studies have demonstrated the efficacy, safety and faster deed onset of NTG than of furosemide or morphine sulfate.NTG can be sublingual, local or intravenous. Sublingual is associated with preload reduction within 5 minutes and with round afterload reduction.Topical NTG, although as effective as sublingual NTG, should be avoided in patients with severe left ventricular failure because of poor skin perfusion then poor absorption.Intravenous NTG is an excellent monotherapy for patients with severe cardiogenic pulmonary oedema. It can be started with 10mcg/min and then rapidly uptitrated to more than100mcg/min. It can be given up as 3 mg boluses every 5 minutes (Sovari, 2012).The on the spur of the moment half-life of nitrates justifies the high dosage for cardiogenic pulmonary oedema, especially with patients presenting a hyperadrenergic advance and moderately elevated blood pressure. Nitrates, however, should be avoided in hypotensive patients and used with caution in cases of aortic stenosis and pulmonary hypertension.Angiotensin II Receptor BlockersAngiotensin II receptor blockers (ARBs) have comparable salutary effects in heart failure. Studies have proposed a role for ARBs in preventing structural and electrical remodeling of the heart which reduced incidence of arrhuthmias.The Valsartan Heart nonstarter Trial showed that valsartan reduces the incidence of atrial fibrillation by 37% (Sovari, 2012).The Mechanism of furosemideFurosemide is a potent diuretic (water pill) that is used to eliminate water and salt from the body.Implications of administering Furosemide to a patient with an acute exacerbation of chronic heartFurosemide is often given in conjunction with a super acid supplement or a potassium-sparing diuretic to counteract potassium loss. The medication has a rapid onset of effect of about one hour when taken orally and five minutes by injection. duration of action is about six hours so it is possible to use a twice daily dose if necessary.ReferencesAdams, K. F., Jr Fonarow,G.C.,Emerman,C.L. (20 05). ADHERE Scientific Advisory charge and Investigators. 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DIABETES CARE, 27(1).Packer, M., Coats,A.J.,Fowler,M.B.,. (2001). for the Carvedilol Prospective Randomized Cumulative Survival carry Group. Effect of carvedilol on survival in severe chronic heart failure. N Engl J Med, 344, 1651-1658.Sovari, A. (2012, February 1). Cardiogenic Pulmonary EdemaTreatment & Management. Retrieved September 17, 2014, from http//emedicine.medscape.com/ bind/157452-treatmentaw2aab6b6b3WHO. (October 2013). Model List of EssentialMedicines. World Health Organization.Source document