Pharmacological rationale for the use of beta blockers and nitrates in the treatment of patients with ischaemic heart disease Essay Example for Free

Pharmacological rationale for the use of beta blockers and nitrates in the discussion of forbearing roles with ischaemic heart disease EssayThe goals of treatment in subtle myocardial infection argon the restoration of blood flow to the coronary arteries and salvaging as much as possible of a running(a) myocardium. Nitrates and betablockers atomic number 18 some of the main medications used in the management of acute myocardial infarct. Nitrates atomic number 18 just due to their vasodilator effect. Nitrates are metabolized to nitric oxide in the endothelium of blood vessels (Rubenstein et al, 2006, pp261). The nitric oxide has the effect of relaxing vascular mobile muscle causing the blood vessel lumen to dilate. Vasodilation leads to a drop-off in cardiac afterload and preload.This go downd the atomic number 8 requirements of the myocardium. Vasodilation in the coronary arteries leads to an improvement in the flow of blood through the partly obstructed coronary v essels and besides through the collateral vessels. Nitrates reverse the vasoconstriction that occurs during coronary occlusion (ACC/AHA, 2006). When administered intravenously or sublingually, nitroglycerin has a rapid onset of action. Evidence for the use of nitroglycerin has shown substantive benefit in the long term geting therapy for MI.It is useful in such cases when at that place is no residual ischemia or a severe pump dys purpose (McInnes, 2008, pp255). The use of nitroglycerin is however limited by side effects such as headache, low blood pressure and tachyplaxis (Reid et al, 2006, pp62-63). The tolerance to nitrates can be overcome by providing a nitrate-free interval of eight to twelve hours or by increasing the venereal infection of nitrates.Beta blocker therapy is usually initiated within twelve hours of the start of myocardial infarction symptoms and usually continues for an noncommittal period of time. Betablockers are started intravenously and then continued orally with the dose being titrated upward until the maximum dose that can be tolerated (Mozayani and Raymond, 2004, pp220-221).Treatment using a beta blocker has the effect of lessen the point of ventricular arrhythmias, reinfarction, and recurrent ischaemia.When given early enough, the beta blockers also reduce the size of the infarct and deem overall reduce short-term mortality associated with myocardial infarction (ACC/AHA, 1999, pp). Beta blockers act by decreasing the force and rate of myocardial contraction. This decreases overall myocardial group O demand and with reduced group O supply, on that point is minimized myocardial death and injury (Roach and Ford, 2006, pp 350). Betablockers inhibit the sympathetic actions mediated by epinephrine. In blockage the sympathetic nervous system, beta blockers lead to a release of renin that in turn causes a reduction in the aldoster sensation release which causes the blood pressure to fall. They reduce the effect of physical ex ertion or inflaming on the heart rate and also reduce the force of contraction as well as dilation of blood vessels (Mozayani and Raymon, 2004, pp224).The antianginal effects of the betablockers result from i nonropic and chronotropinc effects that reduce the workload of the heart and the oxygen demand of the cardiac tissue. The negative chronotropic properties of beta blockers are responsible for the lifesaving property of control of heart rate. Betablockers excite a number of adverse effects. boldness failure is the most recognized amongst this and the most serious. Other side effects accept bronchospasm and bradycardia. The benefits in reduction of the risk for reinfarction and mortality however outweigh the side effects then in that location are no absolute contradiction to the use of beta blockers in myocardial infarction. In addition to beta blockers, statins are also given for the purpose of lipid management. High LDL cholesterol levels are likely to increase incidents of acute myocardial infarction (Bolooki, 2009).Other hypertensive drugs helpful in controlling blood pressureOther treatments that can be used in the management of acute myocardial infarction include angiotensin converting enzyme inhibitors class of drugs which postulate been shown to decrease the mortality rates of patients who have reduced left ventricular ejection fraction. ACEIs reduce myocardial afterload by causing vasodilation. ACE Inhibotros also reduce the size of myocardial infarction and improve the remodeling of the ventricles. These effects have a benefit in reducing the mortality and morbidity of patients post infarction (American Family Physician, 2001, p1). Patients who cannot tolerate the ACEIs there Angiotensin receptor blockers are used. The angiotensin receptor blockers act by causing vasodilation and reducing the secretion of vasopressin. The angiotensin II receptor blockers alsoCase Presentation Management of the patientInitial treatment for acute myocardial infarction is directed toward restoring perfusion so that the as much of the jeopardized myocardium as is possible can be salvaged. One of the ways through which this can be achieved is through thrombolytic therapy. Thrombolytic therapy is administered within twelve hours of the beginning of the symptoms (McInnes, 2008, pp255). Prehospital thrombolysis is indicated when there time of call to arrival will probably be over thirty minutes (ACC/AHA, 2006, pp240-241). The subscribe of thrombolytic therapy is to restore circulation through a blood vessel that has been occluded by a pathologic embolus or thrombus.There is however a risk for bleeding complications especially with aspirin administration (Antithrombotic Trialists (ATT) Collaboration, 2009, pp1851). The possible for haemorrhaging increases with age, thus careful consideration is outstanding in Andrews case (he is 70years old). Andrew will also have aspirin administered to him.The aspirin can be chewed or dispersible. Asp irin has antiplatelet activity which interferes with platelet cohesion and alliance an effect which benefits all patients with coronary syndromes (Mozayani and Raymond, 2004, pp338-339). Clopidogrel can be combined with low dose aspirin in cases of myocardial infarction with ST-segment elevation (Reid et al, 2006, pp61).The patient should also be put on supplemental oxygen to ensure that the red blood cells are fully saturated to the maximum carrying capacity. This consideration is important because myocardial infarction impairs the function of the heart in circulation which could lead to decreased oxygen uptake.To determine what treatment is subdue it is important to view MI as part of a wide spectrum of coronary syndromes (ACC/AHA, 2006, pp238). This spectrum includes ST elevated myocardial infarction non ST elevated myocardial infarction and unstable angina. Those patients who persistently have an elevated ST are considered for reperfusion therapy (ACC/AHA, 2006. pp238-239). An drew is one of these hence thrombolyis is a very significant factor in his treatment process. For those who there is no ST elevation, this indicates that there may be no myocardial injury. Thus such a patient may not require immediate thrombolysis but can receive anti-ischemic therapy. The initial focus of the ECG is to determine whether there is an ST elevation or not. Once identified, then thrombolysis should be started.Because the pain from MI is intense, it requires adequate and prompt analgesia. The broker of choice for pain management is morphine sulfate. The morphine sulfate will be given at five to fifteen minute intervals. Precaution should be taken administering morphine as it has the likelihood of do hypotension worse which Andrew has.Additionally it also has the side effect of nausea which can lead to an increase in nausea. Since morophine increases the incidence of nausea, it should be administered with an anti-emetic. When myocardial ischaemia is reduced, the patient s pain is also reduced, thus nitrates, oxygen therapy and betablocker agents all serve to complement the effect of morphine. trinitroglycerin should also be administered as it helps to relax the smooth muscles of vessels causing their dilation. It can be administered intravenously or sublingually. These modes provide a rapid onset of action. Nitroglycerin has its serum concentrations increased by aspirin thus dose adjustment may be unavoidable when giving both nitroglycerin and aspirin.Specific prehospital care will thus include, obtaining intravenous access, providing supplemental oxygen and providing pulse oximetry to monitor oxygen saturation levels.Immediate administration of aspirin will then follow coupled with administration of nitroglycerin to reduce the chest pain. Additionally, telemetry and a prehospital ECG will be provided for monitor of the patients cardiac activity. Blood will also be taken for renal function tests, electrolytes, clotting screen, cardiac enzymes, C reactive protein, glucose, lipids and full blood count. Precaution however needs to be taken in administering nitroglycerin as Andrew already has a low systolic blood pressure. The patient is in hypotension with a blood pressure of 90/60 mmHg.Questions to ask the wife and patient virtually of the questions that Andrew or his wife may be asked relate to compliance with the treatment that has been prescribed for him. Other questions include any life style habits that he may have. There is a possibility for difficulty in compliance with treatment due to the long term nature of the medication such aspirin and the beta blockers. Andrew will thus be asked about his compliance to the medication to find out whether he has been fetching the medication as prescribed. It is also important to find out what effects the medication have when the patient takes them that is does he feel relieved, does he have symptoms of nausea, haemorrhaging and unawareness of hypoglycaemia. These are important to identify as they are some of the side effects of the drugs that could have a negative impact on his adherence to treatment.It is important for Andrew to maintain his lipid levels at a low point so other questions will wind around the patients lifestyle such as whether he has modified his diet to decrease the intake of foods high in cholesterol, whether he is taking the statins to reduce cholesterol levels and whether he smokes or not and whether he has been participating in exercise.ReferencesACC/AHA, 1999, ACC/AHA Guidelines for the Management of Patients with Acute myocardial Infarction, 1999, A report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee on Management of Acute myocardial Infarction). J Am Coll Cardiol. 34 1999 890-911.American Family Physician, 2001, Use of ACE Inhibitors in Treating Acute MI, available at http//www.aafp.org/afp/20000501/tips/4.htmlACC/AHA, 2006, ACC/AHA clinical performance measures for a dults with ST-elevation and non-ST-elevation myocardial infarction a report of the American College of Cardiology/American Heart Association Task Force on Performance Measures (Writing Committee to Develop Performance Measures on ST-Elevation and Non-ST-Elevation Myocardial Infarction). J Am Coll Cardiol. 47 2006 236-265Antithrombotic Trialists (ATT) Collaboration, 2009, Aspirin in the primary and secondary prevention of vascular disease collaborative meta-analysis of individual participant data from randomised trials, Lancet.May 302009 373(9678) pp1849-1860McInnes G, 2008, Clinical Pharmacology and therapeutics of hypertension, Elsevier Health, ISBN-13 978-0-444-51757-9Mozayani A and Raymon LP, 2004, Handbook of drug interactions a clinical and forensic guide, Humana PressReid JL, Rubin PC and Walters RM, 2006, Lecture notes clinical materia medica and therapeutics, Wiley-BlackwellRoach SS and Ford SM, 2006, Introductory Clinical Pharmacology, Lippincott Williams and WilkinsRubens tein D, Wayne D and Bradley, 2003, Lecture notes on clinical medicine, Wiley-Blackwell