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A 45 year old male, smoker presented with chest pain lasting> 30 min and has a BP of 60 / 30. ECG shows widespread ST segment depression. Echo shows an EF of 20%. What should be the treatment?
A 45 year old male, smoker presented with chest pain lasting> 30 min and has a BP of 60 / 30. ECG shows widespread ST segment depression. Echo shows an EF of 20%. What should be the treatment?
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A 45 year old male, smoker presented with chest pain lasting> 30 min and has a BP of 60 / 30. ECG shows widespread ST segment depression. Echo shows an EF of 20%. What should be the treatment?
Droits d'auteur :
Attribution Non-Commercial (BY-NC)
Formats disponibles
Téléchargez comme PPT, PDF, TXT ou lisez en ligne sur Scribd
chest pain lasting> 30 min and has a BP of 60/30. ECG shows widespread ST segment depression. Echo shows an EF of 20%. • What should be the treatment? • PCI Acute coronary syndromes • Spectrum of clinical conditions ranging from unstable angina to non-ST segment elevation MI (ST segment elevation generally absent), and ST segment elevation infarction (persistent ST segment elevation) and sudden cardiac death Acute coronary syndromes • Acute myocardial ischaemic states • Chest pain is due to insufficient blood supply to the heart muscle that results from coronary artery disease • A major cause of emergency medical care and hospitalisation in the country Unstable angina • A clinical syndrome between stable angina and acute MI • Three main presentations • Angina at rest—Also prolonged, usually > 20 minutes • Angina of new onset—At least CCS class III in severity • Angina increasing—Previously diagnosed angina that has become more frequent, longer in duration, or lower in threshold (change in severity by 1 class to at least CCS class III) Unstable Angina/MI • In the absence of specific ECG changes, such as the development of new Q waves, only serial measurements of serum levels of cardiac enzymes, usually CPK and its MB isoenzyme, can differentiate unstable angina from myocardial infarction Pathophysiology • Initiation of the Cascade of Plaque Fissure and Rupture • Acute Thrombosis and Platelet Aggregation • Coronary Vasospasm • Erosion of Coronary Plaque without Rupture Disruption of an atheromatous plaque
• Clinical spectrum in patients with ischemic chest
pain at rest ranges from unstable angina, due to the partial occlusion of a coronary vessel, to acute myocardial infarction, due to complete occlusion • A coronary atherosclerotic plaque ruptures and a mural or occlusive thrombus forms, interrupting the perfusion of myocardial tissue Spectrum of acute coronary syndromes according to electrocardiographic and biochemical markers of myocardial necrosis (troponin T, troponin I, and creatine kinase MB), in patients presenting with acute cardiac chest pain Pathogenesis • Fissuring or rupture of these plaques leads to the local generation of thrombin and deposition of fibrin
• This in turn promotes platelet adhesion and
aggregation, vasoconstriction, and the formation of partially or totally occlusive intracoronary thrombus Pathophysiologic Events Culminating in the Clinical Syndrome of Unstable Angina Diagram of an unstable plaque with superimposed luminal thrombus Distal embolisation of a platelet-rich thrombus causing occlusion of intramyocardial arteriole (arrow). Such an event may result in micro-infarction and elevation of markers of myocardial Diagnosis • Unstable angina and non-ST segment elevation MI are closely related conditions • Clinical presentations may be indistinguishable • Distinction depends on whether the ischaemia is severe enough to cause myocardial damage and the release of detectable quantities of markers of myocyte necrosis Diagnosis • The initial diagnosis is made on the basis of a patient's history, ECG and the presence of elevated plasma concentrations of biochemical markers • An ECG may be normal or show minor non-specific changes • Transient ST-segment elevation of > 0.5 mm that resolves spontaneously or after nitrate is given Diagnosis • Transient or persistent ST-segment depression of > 0.5 mm • Bundle branch block • T-wave inversion of > 1 mm within 12 hours before or after chest pain, or • Raised serum concentration of CK-MB • Cardiac troponins are the preferred markers • More specific and reliable than CK or CKMB Right coronary artery angiogram in patient with non-ST segment elevation myocardial infarction (top left), showing hazy appearance of intraluminal thrombus overlying a severe stenosis (arrow). Abciximab was given before direct stenting (top right), with good angiographic outcome (bottom) Diagnosis • Physical examination may exclude important differential diagnoses • Pleuritis, pericarditis, or pneumothorax, as well as revealing evidence of ventricular failure and haemodynamic instability • Look for risk factors Management • All patients suspected of having ACS should be managed as medical emergencies and monitored in the CCU and assessed by a cardiologist on the day of presentation • Baseline tests must include 12 lead ECG, CXR, and haemoglobin and markers of myocardial damage, preferably cardiac troponin T or I Medical treatment • Medical treatment includes bed rest, oxygen, opiate analgesics to relieve pain, anti-ischaemic and anti-thrombotic drugs • Should be started at once on admission and continued in those with probable or confirmed unstable angina or non-ST segment elevation myocardial infarction Management • Medical Therapy • Antiplatelet Therapy • Aspirin • Clopidogrel • Ticlopidine • Platelet Glycoprotein IIb/IIIa Receptor Antagonists Antithrombin Therapy • Heparin- Unfractionated, Low- Molecular-Weight Heparins • Direct Thrombin inhibitors • Conventional Antianginal Therapy • Beta-Blockers • Nitrates • Calcium-Channel Blockers • Coronary Revascularization Revascularization/reperfusion • Cardiogenic shock • Overt heart failure/severe LV dysfunction • Recurrent/persistent angina despite intensive medical therapy • Hemodynamic instability due to mechanical complications (VSD,Acute MR) • Unstable arrhythmias (AF, sustained V arrhythmias) Treatment for angina • Aspirin 300 mg followed by a low dose of 75-150 mg daily • Clopidogrel 600 mg followed by 75 mg per day (aspirin intolerance) • Anti-ischemic • Intravenous nitroglycerin • Beta Blockers should also be given Treatment for angina
• Rate limiting calcium antagonists can be
used if beta blockers are contraindicated or are already being used • Antithrombotic drugs • Aspirin, clopidogrel, I/V unfractionated heparin or LMWH and glycoprotein IIb/IIIa inhibitors Antithrombotic treatment • Ideally, patients should be given LMWH (enoxaparin) according to their weight • If LMWH is unavailable, unfractionated heparin may be used • Intravenous heparin is given as a bolus dose of 5000 U, followed by an infusion at a rate of 1250U per hour, with the APTT maintained in the range of 50 to 70 seconds Antithrombotic treatment • LMWH should be given for at least two days, and for up to eight days or longer in cases of • Recurrent ischaemia or • Where myocardial revascularisation is delayed or contraindicated Anti platelet agents • Ticlopidine and clopidogrel, are antiplatelet agents that inhibit the platelet aggregation induced by adenosine diphosphate, thereby reducing ischemic events • Aspirin blocks the thromboxane-mediated pathway Subsequent management • Patients should be observed over the next eight to 12 hours • When patients have been free from symptoms and ischaemic ECG changes for >48 hours, and any intravenous treatments and heparin have been stopped for >24 hours, risk assessment with stress testing should be performed unless contraindicated Subsequent management • Long term treatment with aspirin, clopidogrel (especially after stenting),Beta blockers, ACE inhibitors • Aggressive modification of risk factors • Smoking should be strongly discouraged Statins should be used to lower blood lipid levels • Antihypertensive & antidiabetic drugs Summary • The diagnosis of unstable angina or non-ST segment elevation myocardial infarction demands urgent hospital admission and coronary monitoring. A clinical history and examination, 12 lead electrocardiography, and measurement of troponin concentration are the essential diagnostic tools. Bed rest, aspirin, clopidogrel, heparin, antianginal drugs, and opiate analgesics are the mainstay of initial treatment.