Management of acute M. I. With left vent. failure?

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* PROMPT ANTIHYPERTENSIVE MANAGEMENT.. WITH.. BETA BLOCKERS.. DIURETICS.. ISOSORBIDE DINITRATES .. * LMWH .. STATINS.. AND.. ANTIPLATELET .. CLOPIDOGREL .. WITH.. ASPIRIN .. * THROMBOLYSIS .. * CARDIOLOGISTS OPINION..

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Needs to control BP, diuretics, betablokers, nitrates are on priority,sos NIV. Restrict IV fluids Prefer PAMI once failure part is settled. LMWH, antiplatelets statins etc . Thrombolysis if intervention facilities are unavailable.

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In patients with heart failure and reduced ejection fraction, these pharmacologic therapies include beta-blockers, ACE inhibitors, possibly angiotensin receptor blockers, mineralocorticoid receptor antagonists (spironolactone, eplerenone), possibly isosorbide dinitrate/hydralazine, and possibly digoxin

Acute mi with lvf Iv lasix Control bp . Dispersible Disprin 4 tab Tab Clopdral 150 Tab Atorvastatin 40 mg stat. Shift the pt to higher center

Main drug to be given immediately isprbid Lasix Beta blockers Then start ecosperin Clopigral Atrovastin Use of throbolytics need special indoor.seting

The first 24 hours:- Once hospitalized, the patient with acute MI should be continuously monitored by electrocardiography and the diagnosis of acute MI confirmed by serial ECGs and measurements of serum cardiac markers of myocyte necrosis, such as creatine kinase isoenzymes or cardiac specific troponin T or I. The patient should be monitored closely for adverse electrical or mechanical events because reinfarction and death occur most frequently within the first 24 hours. The patient's physical activities should be limited for at least 12 hours, and pain and/or anxiety should be minimized with appropriate analgesics. Although the use of prophylactic antiarrhythmic agents in the first 24 hours of hospitalization is not recommended, atropine, lidocaine, transcutaneous pacing patches or a transvenous pacemaker, a defibrillator, and epinephrine should be immediately available. Patients who survive a large anterior MI or who have a LV mural thrombus seen on echocardiography are at high risk of having an embolic stroke. Some data suggest that this risk is reduced by early administration of intravenous heparin. For the patient without a large anterior MI or LV mural thrombus who did not receive reperfusion therapy, there are few data on the benefit of heparin beyond that of aspirin, β-adrenoceptor blocking agents, nitrates, and angiotensin converting enzyme (ACE) inhibitors. For the patient given thrombolytic therapy, the recommendations for subsequent heparin administration are based more on current practice than on evidence and depend on the specific thrombolytic agent. There is only limited evidence that heparin (given intravenously or subcutaneously) is beneficial in the patient who receives a nonspecific fibrinolytic agent such as streptokinase, anisoylated plasminogen streptokinase activator complex (APSAC), or urokinase. When TPA (alteplase) is administered, intravenous heparin increases the likelihood of patency in the infarct-related artery (assessed angiographically), but this may not necessarily lead to improved clinical outcome. Considering the superior performance of accelerated TPA plus intravenous heparin in the Global Utilization of Streptokinase and TPA for Occluded Arteries (GUSTO) trial, it seems judicious to give heparin intravenously for at least 48 hours after alteplase is given. When primary PTCA is performed, high-dose intravenous heparin is recommended. Aspirin, 160 to 325 mg daily, initially given in the ED, should be continued indefinitely. Despite the absence of definitive outcome data, it is reasonable to treat the patient with acute MI and without hypotension, bradycardia, or excessive tachycardia with intravenous nitroglycerin for 24 to 48 hours after hospitalization. Concern exists about oral nitrate preparations in the patient with acute MI because of inability to titrate the dose to effect in an acutely evolving hemodynamic situation, whereas intravenous infusion of nitroglycerin can be titrated successfully with frequent measurement of heart rate and cuff blood pressure. Nitroglycerin should not be used as a substitute for narcotic analgesics that are often required in the patient with acute MI. The patient with evolving acute MI should receive early intravenous β-adrenergic blocker therapy, followed by oral therapy, provided that there is no contraindication. β-Adrenoceptor blocker therapy should be initiated regardless of whether reperfusion therapy was given, because several studies in the prethrombolytic as well as the thrombolytic era showed that β-adrenoceptor blockers diminish morbidity and mortality. Calcium channel blockers have not been shown to reduce mortality in patients with acute MI, and in certain persons with cardiovascular disease they appear to be harmful. In the patient without ST-segment elevation or LBBB in whom pulmonary congestion is absent, diltiazem may reduce the incidence of recurrent ischemic events, but its benefit beyond that of β-adrenoceptor blockers and aspirin is unclear. Immediate-release dihydropyridines (eg, nifedipine) are contraindicated in the patient with acute MI. In the patient with evolving acute MI with ST-segment elevation or LBBB, an ACE inhibitor should be initiated within hours of hospitalization, provided that the patient does not have hypotension or a contraindication. Subsequently, the ACE inhibitor should be continued indefinitely in the patient with impaired LV systolic function (ejection fraction less than 40%) or clinical congestive heart failure (CHF). In patients without complications and no evidence of symptomatic or asymptomatic LV dysfunction by 6 weeks, ACE inhibitors can be stopped. On admission to the hospital, a lipid profile and serum electrolyte concentration (including magnesium) should be measured in all patients. After the first 24 hours:- After the first day in the hospital, the patient with acute MI should continue to receive aspirin 160 to 325 mg/d indefinitely with a β-adrenergic blocker; an ACE inhibitor should be administered for at least 6 weeks. Nitroglycerin should be infused intravenously for 24 to 48 hours, and magnesium sulfate should be given as needed to replete magnesium deficits for 24 hours. For the patient receiving alteplase, it is current practice to give intravenous heparin for an additional 48 hours. Patients with myocardial ischemia that is spontaneous or provoked in the days to weeks after acute MI, irrespective of whether they received thrombolytic therapy, ordinarily should undergo elective angiographic evaluation, with subsequent consideration of percutaneous or surgical revascularization. There is considerable variability in the use of coronary angiography and catheter interventions among survivors of uncomplicated acute MI with preserved LV systolic function. Although some practitioners routinely perform angiography and PTCA during the days after acute MI in virtually all patients, the available data suggest that such a management strategy does not salvage myocardium nor reduce the incidence of reinfarction or death. Accordingly, coronary angiography and subsequent revascularization should be reserved for survivors of acute MI who have preserved LV systolic function and spontaneous or provoked ischemia. During hospitalization the patient with acute MI should be closely observed for prompt recognition and management of complications. The patient with recurrent chest pain believed due to pericarditis should receive high-dose aspirin (650 mg every 4 to 6 hours). Recurrent chest discomfort thought to be caused by myocardial ischemia should be treated with intravenous nitroglycerin, analgesics, and antithrombotic medications (aspirin, heparin). Coronary angiography with subsequent revascularization therapy should be considered. The patient with heart failure should receive a diuretic (usually intravenous furosemide) and an afterload-reducing agent. For the patient in cardiogenic shock, consideration should be given to insertion of an intra-aortic balloon pump and emergency coronary angiography, followed by PTCA or CABG. The patient with right ventricular infarction and dysfunction should be treated vigorously with intravascular volume expansion (using normal saline) and inotropic agents if hypotension persists. In the patient with acute MI, the appearance of atrial fibrillation is often a manifestation of extensive LV systolic dysfunction. If its occurrence causes hemodynamic compromise or ongoing ischemia, direct-current cardioversion should be performed. In the absence of these, β-adrenoceptor blocking agents or digitalis should be given to slow the ventricular response. Episodes of ventricular fibrillation should be treated with immediate direct-current countershock; the same is true for episodes of monomorphic ventricular tachycardia associated with angina, pulmonary congestion, or hypotension. If monomorphic ventricular tachycardia is not accompanied by chest pain, pulmonary congestion, or hypotension, it should be treated with intravenous lidocaine, procainamide, or amiodarone. The patient with acute MI and symptomatic sinus bradycardia or atrioventricular block should receive atropine. Temporary pacing should be performed in the patient with (1) sinus bradycardia unresponsive to drug therapy, (2) Mobitz type II second-degree atrioventricular block, (3) third-degree heart block, (4) bilateral bundle branch block (BBB), (5) newly acquired BBB, and (6) right or left BBB in conjunction with first-degree atrioventricular block. Immediate surgical intervention is often required for the patient with (1) failed PTCA with persistent chest pain or hemodynamic instability; (2) persistent or recurrent ischemia refractory to medical therapy who is not a candidate for catheter intervention; (3) cardiogenic shock and coronary anatomy not amenable to PTCA; or (4) a mechanical abnormality leading to severe pulmonary congestion or hypotension, such as papillary muscle rupture (with resultant mitral regurgitation) or ventricular septal defect (VSD).

ACUTE MI +LVF NEED NITROGLYCERIN CONTROL BP - BETA BLOCKERS ATORVASTATIN +ASPIRIN THROMBOLYTIC- STREPTOKINASE FUROSEMIDE (LVF) LOAD DECREASE

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