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Background
Myocardial Infarction if the rapid development of myocardial necrosis by a critical imbalance between oxygen supply and demand to the myocardium
Classification
Acute coronary syndromes include STST-elevation MI (STEMI) Non ST-elevation MI ( NSTEMI) STUnstable Angina Cardiac markers in circulation indicates myocardial infarction and help categorize MI and is a useful adjunct to diagnosis
Classification
Anatomic or morphologic Transmural= Full thickness NonNon-transmural= Partial thickness ECG Q wave MI Non Q wave MI Does not distinguish transmural from a nonnontransmural MI as determined by pathology
Prevalence
In the US, 1.3 million cases of nonfatal MI were reported in 2006 Incidence of 600 per 100,000 people Increase in the proportion of NSTEMI compared to STEMI Approximately 500,000 to 700,000 deaths are caused by heart disease annually in the United States
History
The history is critical in making the diagnosis of MI and sometimes provide only the only clues that lead to the diagnosis in the initial phase of presentation
History
Chest Pain- anterior precordium tightness PainPain may radiate to jaw, neck and epigastrium DyspneaDyspnea- angina equivalent, poor LV function Nausea/abdominal pain with posterior MI Anxiety
History
Nausea with and without vomiting Diaphoresis or sweating Syncope or near syncope Elderly present with MS changes, fatigue, syncope or weakness As many as half of MI are clinically silent
Physical
The physical exam can often be unremarkable Hypertension Hypotension Acute valvular dysfunction may be present Rales Neck vein distention
Physical
Third heart sound may be present A fourth heart sound poor LV compliance Dysrhythmias Low grade fever
Causes
Most frequent cause is rupture of an atherosclerotic lesion within coronary wall with subsequent spasm and thrombus formation Coronary artery vasospasm Ventricular hypertrophy Hypoxia Coronary artery emboli
Causes
Cocaine Arteries Coronary anomalies Aortic dissection Pediatrics Kawasaki disease, Takayasu arteritis Increased afterload which increases myocardial demand
Differentials
Acute coronary syndrome Anxiety Aortic stenosis Asthma Cholecystitis and biliary colic Cholethiasis COPD
Differentials
Aortic Dissection Endocarditis Esophagitis Shock Myocarditis Pericarditis Pulmonary embolism
Cardiac Biomarkers
Cardiac biomarkers are protein molecules released into the blood stream from damaged heart muscle Since ECG can be inconclusive , biomarkers are frequently used to evaluate for myocardial injury These biomarkers have a characteristic rise and fall pattern
Troponin T and I
These isoforms are very specific for cardiac injury Preferred markers for detecting myocardial cell injury Rise 2-6 hours after injury 2Peak in 12-16 hours 12Stay elevated for 5-14 days 5-
Creatinine Kinase ( CK-MB) CKCreatinine Kinase is found in heart muscle (MB), skeletal muscle (MM), and brain (BB) Increased in over 90% of myocardial infraction However, it can be increased in muscle trauma, physical exertion, post-op, postconvulsions, and other conditions
Myoglobin
Damage to skeletal or cardiac muscle release myoglobin into circulation Time sequence after infarction Rises fast 2hours Peaks at 6-8 hours 6Returns to normal in 20-36 hours 20Have false positives with skeletal muscle injury and renal failure
CBC
CBC is indicated if anemia is suspected as precipitant Leukocytosis may be observed within several hours after myocardial injury and returns returns to levels within the reference range within one week
Chemistry Profile
Potassium and magnesium levels should be monitored and corrected Creatinine levels must be considered before using contrast dye for coronary angiography and percutanous revascularization
Chest X-Ray XChest radiography may provide clues to an alternative diagnosis ( aortic dissection or pneumothorax) Chest radiography also reveals complications of myocardial infarction such as heart failure
Echocardiography
Use 2-dimentional and M mode 2echocardiography when evaluating overall ventricular function and wall motion abnormalities Echocardiography can also identify complications of MI ( eg. Valvular or pericardial effusion, VSD)
Electrocardiogram
A normal ECG does not exclude ACS High probability include ST segment elevation in two contiguous leads or presence of q waves Intermediate probability ST depression T wave inversions are less specific
Localization of MI
ST elevation only Inferior wall- II, III, aVF wallLateral wall_ I, aVL, V4-V6 V4Anteroseptal- V1Anteroseptal- V1-V3 Anterolateral- V1Anterolateral- V1-V6 Right ventricular- RV4, RV5 ventricularPosteriorPosterior- R/S ratio >1 in V1 and T wave inversion
Therapy The goals of therapy in AMI are the expedient restoration of normal coronary flow and the maximum salvage of functional myocardium
Antiplatelet Agents
Aspirin at lease 160mg immediately Interferes with function of cyclooxygenase and inhibits the formation of thromboxane ASA alone has one of the greatest impact on the reduction of MI mortality. Clopidogrel, ticlopidine, have not been shown in any large scal trail to be superior to Aspirin in acute MI
Supplemental Oxygen
Because MI impairs the circulatory function of the heart, oxygen extraction by the heart and other tissues may be diminished Supplemental oxygen should be administered to patient with symptoms and or signs of pulmonary edema or pulse oximetry readings less than 90%.
Nitrates
IV nitrates to all patients with MI and congestive heart failure, persistent ischemia, hypertension, or large anterior wall MI Primary benefit vasodilator effect Metabolized to nitric oxide in the vascular endothelium, relaxes endothelium Vasodilatation reduces myocardial oxygen demand and preload and afterload
BetaBeta-blockers
Recommended within 12 hours of MI symptoms and continued indefinitely Reduces Myocardial mortality by decreasing arrythmogenic death Decrease the rate and force of myocardial contraction and decreases overall oxygen demand
Unfractionated heparin
Forms a chemical complex with antithrombin III inactivates both free thrombin and factor Xa Recommended in patients with MI who undergo PTCA or fibrinolytic therapy with alteplase
Thrombolytics
Indicated with MI and ST segment elevation greater than 0.1mV in 2 contiguous ECG leads, or new onset LBBB, who present less than 12 hours but not more than 24 hours after symptom onset The most critical variable in achieving successful fibrinolysis is time form symptom onset to drug administration
Thrombolytics
As a class the plasminogen activators have been shown to restore coronary blood flow in 5050-80% of patients Contraindication active intracranial bleeding, CVA 2months, CNS neoplasm, HTN, coagulopathy Retaplase slightly higher angiographic patency but did not translate into survival benefit Intracranial bleed risk major drawback
Surgical Revascularization
Emergent or surgical revascularization in setting of failed PTCA in patients with hemodynamic instability and coronary anatomy amendable to surgical grafting Also indicated of mechanical complications of MI including VSD, free wall rupture, or acute MR Carries a higher risk of perioperative mortality than elective CABG
Lipid Management
All post MI patients should be on AMA step II diet ( < 7% of calories from saturated fats) Post MI patients with LDL > 100 mg/dl are recommended to be on drug therapy to try to lower levels to <100 mg/dl Recent data indicate that all MI patients should be on statin therapy, regardless of lipid levels or diet
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