Acute myocardial infarction:

Acute myocardial infarction: PowerPoint PPT Presentation


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Acute myocardial infarction:

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1. Acute myocardial infarction: Cardiac muscle necrosis secondary to protracted lack of coronary perfusion Usual etiology: Thrombus at site of vascular injury

3. Other Etiologies of Acute Myocardial Infarction Coronary embolus Coronary spasm Coronary anomoly Primary in situ thrombosis Vasculitis Hypotension

4. Determinants of Extent of Damage: Territory supplied Duration of occlusion Existence of collaterals Oxygen demand at time of occlusion Vasospasm

5. Presenting Symptoms of Acute MI Pain- *typical-crushing substernal chest pain *atypical - jaw, neck, shoulder, back pain, indigestion *painless - “silent” Dyspnea- systolic and/or diastolic dysfunction Dizziness-hypotension, arrhythmia Nausea, vomiting Elderly patients: Failure to thrive Anxiety, restlessness, “sense of impending doom”

6. Presenting Signs in Acute MI Appearance: Pallor, diaphoretic, anxious Vital Signs: Normal or abnormal BP and P Hypertension and tachycardia: SNS Hypotension and tachycardia: Cardiogenic shock Myocardial rupture Tachyarrhythmia Hypotension and bradycardia vagal stimulation Bradyarhythmia

7. Presenting Signs in Acute MI (Cont.) Lungs: Rales - CHF Heart: Displaced LV impulse S3 S4 Murmur of mitral regurgitation Murmur of ventricular septal rupture Pericardial rub

10. Natural History of Acute Myocardial Infarction Death- Arrhythmia: VT/VF Asystole Myocardial rupture Cardiogenic shock Chronic Heart Disease - LV dysfunction - remodeling Papillary muscle dysfunction: MR RV dysfunction

11. Natural History of Acute Myocardial Infarction, (Cont.) Stabilization ?compensated LV dysfunction Post-infarction angina/ischemia (spontaneous or induced) Recurrent MI Post-infarction ventricular tachycardia

12. Treatment of Acute Myocardial Infarction: Acute Phase Prevent/resuscitate from sudden death: monitor, admit to CCU Re-establish coronary flow Thrombolytic therapy Primary infarct angioplasty/stent

15. Major Contraindications To the Use of Thrombolytic Therapy Any previous history of hemorrhagic stroke History of stroke, dementia, or central nervous system damage within 1 year Head trauma or brain surgery within 6 months Known intracranial neoplasm Suspected aortic dissection Internal bleeding within 6 weeks Active bleeding or known bleeding disorder Major surgery, trauma, or bleeding within 6 weeks Traumatic cardiopulmonary resuscitation within 3 weeks

16. Treatment of acute MI: acute phase (cont.) Decrease myocardial oxygen demand Pain relief/anxiolytics (Morphine sulfate) Slow HR, control BP (beta blockers) Increase myocardial oxygen supply Oxygen Prevent platelet aggregation/coronary thrombus (aspirin, IIbIIIa inhibitors, clopidigrel/heparin) Prevent spasm (nitrates) Augment collateral flow (nitrates)

17. Treatment of Acute Myocardial Infarction: Acute Phase (Cont.) Stabilize plaques, restore endothelial function ? HMG CoA reductase inhibitors (“statins”) Prevent ventricular remodeling ACE inhibitors Prevent mural thrombus/embolization Heparin Coumadin for patients at high risk for thrombus (anterior wall akinesis).

18. Treatment of Acute Myocardial Infarction - Intermediate Phase Monitor/treat arrhythmias Monitor/treat heart failure: systolic, diastolic, MR Monitor/treat recurrent ischemia/infarction Watch for pericarditis, Dressler’s Syndrome Monitor for myocardial rupture (free wall, VSD, MR) Monitor for stroke

19. Determinants or Prognosis after Acute MI LV function (ejection fraction) Inducible ischemia/coronary anatomy Arrhythmia potential

20. Treatment of acute myocardial infarction: Pre-discharge Risk assessment Is there LV systolic dysfunction? Is there inducible ischemia? Is there “high risk” coronary anatomy? Is there VT/VF risk?

21. Tests for LV function Echocardiogram Radionuclide ventriculogram (MUGA) Contrast left ventriculogram (cath)

22. Echocardiogram in Acute Myocardial Infarction Wall motion abnormalities Ejection fraction Thrombus Right ventricular MI Papillary muscle dysfunction- mitral regurgitation Free wall rupture/ventricular septal defect/papillary muscle rupture

23. Test for Inducible ischemia: Stress Test 1. Positive: Ischemic ST segment depression - ?1mm horizontal or downsloping ST depression 2. Negative: Patient reaches 85% maximum predicted heart rate (MPHR) without #1 3. Nondiagnostic: No ischemia but patient fails to reach 85% MPHR

27. Test to Define Coronary Anatomy: Coronary Angiogram Controversy: Should all patients undergo coronary angiogram after an MI? Definite indications for coronary angiogram after MI: Recurrent chest pain Positive stress test High risk features: CHF, low EF, prior MI

28. Risks of Coronary Angiography: (all are rare) Stroke Myocardial infarction Arrhythmia Renal failure Allergic reaction to contrast agent

29. Tests to Determine Arrhythmia Risk: Monitoring throughout hospitalization Stress test Electrophysiologic testing Controversy: Who should undergo EP study after MI? Sustained VT Nonsustained VT with depressed ejection fraction

30. Treatment of Acute Myocardial Infarction Late Phase (Post-Hospital) Risk factor reduction: Smoking Hypertension Diabetes Dyslipidemia Obesity/sedentary life style Hyperhomocysteinemia Stress/depression Monitor for recurrent ischemia Monitor for LV remodeling/CHF

31. ABCs of Treatment and Secondary Prevention of AMI Aspirin-prophylactic Rx for recurrent ischemic events; give for at least 3 mo. after AMI, probably indefinitely Beta blockers-prophylactic, for reduction of cardiac mortality; Rx for 2 yr-indefinitely Converting enzyme inhibitors-all pts with LV dysfunction to reduce risk of progressive heart failure and death. Diet and lipid lowering Rx-statins have been shown to reduce risk of subsequent MI, need for revascularization and mortality (4S, Care) Exercise and rehabilitation-essential in restoration of confidence and improvement in quality of life

34. Creatine Phosphokinase (CK) Rises within 4-8 hours, rapidly cleared by 24-24 hours Other Sources: Skeletal Hypothyroidism Renal failure Stroke Isoenzymes MM skeletal muscle BB brain MB cardiac CKMB? 4% suggests acute myocardial infarction+++

35. Cardiac Specific Troponins (cTnT, cTnI) Rise within 4-8 hours, remain elevated 7-14 days (T>I) 30% of patients with UAP show ? levels cTnT or I, indicating increased risk of adverse outcome

36. Relative Contraindications To the Use of Thrombolytic Therapy Oral anticoagulant therapy Acute pancreatitis Pregnancy or within 1 week postpartum Active peptic ulceration Transient ischemic attack within 6 months Dementia Infective endocarditis Active cavitating pulmonary tuberculosis Advanced liver disease Intracardiac thrombi Uncontrolled hypertension (systolic blood Pressure >180 mm Hg, diastolic blood pressure > 110 mm Hg Puncture of noncompressible blood vessel within 2 weeks Previous streptokinase therapy

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