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Acute Myocardial Infarction

Acute Myocardial Infarction. Laura Kay M.D. EMS Medical Director. Worldwide Statistics. Each year: > 4 million patients are admitted with unstable angina and acute MI > 900,000 patients undergo PTCA with or without stent. Cumulative 6-month mortality from ischemic heart disease.

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Acute Myocardial Infarction

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  1. Acute Myocardial Infarction Laura Kay M.D. EMS Medical Director

  2. Worldwide Statistics Each year: • > 4 million patients are admitted with unstable angina and acute MI • > 900,000 patients undergo PTCA with or without stent

  3. Cumulative 6-month mortality from ischemic heart disease N = 21,761; 1985-1992 Diagnosis on adm to hosp 25 20 15 Deaths / 100 pts / month Acute MIUnstable anginaStable angina 10 5 0 0 1 2 3 4 5 6 Months after hospital admission Duke Cardiovascular Database

  4. It’s easy to see that most deaths occur early on. Here is where we make the difference

  5. The History of Paramedics Begins with Cardiac Care • The originalParamedic idea was based upon the need for rapid response to, identification of and emergency care for victims of: • Sudden Cardiac Death • AMI

  6. Pathophysiology

  7. Coronary Artery Without Evidence of Plaque Source: University of Utah WebPath

  8. Coronary Artery with Significant Plaque Formation In addition to reduced Lumen size, there is also a calcified portion (right side of photo) Source: University of Utah WebPath

  9. Coronary Artery with Significant Plaque Formation Source: University of Utah WebPath

  10. Plaque and Thrombus Formation Resulting in Occlusion Source: University of Utah WebPath

  11. Rupture of Plaque Results in Thrombus Formation • Rupture of “Vulnerable” plaque’s soft lipid core is the initiating event in most acute ischemic coronary events • Occlusion is dependent on clot formation and and accompanying fibrinolysis • A thrombotic occlusion that is relatively persistent (i.e., 2 to 4 hours or longer) may result in acute myocardial infarction

  12. Repeated thrombus formations may further decrease the lumen size • Intermittent non-occlusive thrombus formation results in Unstable Angina • Incomplete occlusion may also result in MI possibly due to coronary artery spasm

  13. Coronary Artery Thrombus The external anterior view of the heart shows a dark clot formation in this artery Source: University of Utah WebPath

  14. Myocardial Ischemia • Spectrum of presentation • silent ischemia • exertion-induced angina • unstable angina • acute myocardial infarction

  15. Ischemic Heart DiseaseEvaluation • Based on the patient’s • History / physical exam • Electrocardiogram during testing • Patients are categorized into 3 groups • non-cardiac chest pain • unstable angina • myocardial infarction

  16. Ischemia • Inadequate tissue blood supply • typically due to mechanical obstruction • Consequences secondary to insufficient O2 • metabolic insufficiency

  17. Mechanical Flow Obstruction • Embolism • blockage by a BOLUS of matter • Thrombus • blood clot in the lumen of a vessel • Thromboembolus • thrombus “on the move”

  18. Acute vs. Chronic Ischemia • Acute ischemia • Immediately following complete or nearly complete blockage • potentially catastrophic situation • Myocardial Infarction • Sudden Cardiac Death

  19. Acute vs. Chronic Ischemia • Chronic ischemia • long term • reduced not blocked flow • complex problems • tissue atrophy and loss of function • tissue response to ischemia

  20. Cellular injury/death in acute ischemic events • ATP demand is constant for constant workload • there is an oxygen “cushion” thanks to hemoglobin • Each hemoglobin carries 4 molecules of O2. It only loses one per stop

  21. Cellular death • No ATP production: • ion pumps cease • membrane electrical character becomes deranged • intercellular Ca++ drastically increases • cellular processes stop • DEATH

  22. After approximately 60 minutes of ischemia • Cellular explosion with return of blood flow • high [Ca++] makes cells hypertonic • water enters cell with osmotic gradient • cell swells, membrane rupture • BIG problem

  23. Under Attack

  24. Acute Coronary Syndrome HistoryPhysical Exam Ischemic DiscomfortUnstable Symptoms No ST-segmentelevation ST-segmentelevation ECG Unstable Non-Q Q-Waveangina AMI AMI AcuteReperfusion

  25. Acute Coronary Syndrome • The spectrum of clinical conditions ranging from: • unstable angina • NSTEMI • STEMI • characterized by the common pathophysiology of a disrupted atheroslerotic plaque

  26. Unstable Angina - Definition • angina at rest (> 20 minutes) • new-onset (< 2 months) exertional angina (at least CCSC III in severity) • recent (< 2 months) acceleration of angina (increase in severity of at least one CCSC class to at least CCSC class III) Canadian Cardiovascular Society Classification Agency for Health Care Policy Research - 1994

  27. Unstable AnginaLikelihood of CAD • Previous history of CAD • presence of risk factors • older age • ST-T wave ischemic ECG changes

  28. Unstable Anginaprecipitating factors • Inappropriate tachycardia • anemia, fever, hypoxia, tachyarrhythmias, • High afterload • aortic valve stenosis, LVH • High preload • high cardiac output, chamber dilatation • Inotropic state • sympathomimetic drugs, cocaine intoxication

  29. Unstable Anginapathogenesis • Vasoconstriction • the culprit lesion in response to deep arterial damage or plaque disruption • area of dysfunctional endothelium near the culprit lesion • platelet-dependent and thrombin-dependent vasoconstriction, mediated by serotonin and thromboxane A2

  30. Acute Coronary Syndrome • Process of resolution • spontaneous thrombolysis • vasoconstriction resolution • presence of collateral circulation • Delayed or absence of resolution may lead to NSTEMI or STEMI myocardial infarction

  31. NSTEMIclues to diagnosis • Prolonged chest pain • Associated symptoms from the autonomic nervous system • nausea, vomiting, diaphoresis • Persistent ST-segment depression after resolution of chest pain

  32. Coronary Ischemia/Angina • Duration of pain 1-10 minutes • Substernal location • Pain increases with exertion/ decreases with rest • Radiation of pain to left arm or jaw • Pressure/heaviness/squeezing • dyspnea

  33. Myocardial Infarction • Duration of pain > 15 minutes • Substernal location • Pressure/heaviness/squeezing • Dyspnea • Radiation of pain to left arm or jaw • Diaphoresis • Pain increases with exertion • Nausea

  34. Ischemic and injured tissue have reduced blood flow but may be salvaged. The area of the Penumbra may be viable for several hours after onset of occlusion. Source: Emergency Cardiovascular Care Library (CD-ROM), American Heart Association, Dallas, 1997

  35. Prompt recognition • Immediate Intervention critical • Clinical Presentation • most occur at rest or moderate activity • 59% during sleep

  36. Injury • Causes ST segment to appear to be displaced off the baseline in some leads. • Location of ischemic region can be determined by plotting ST segment vector shift.

  37. Location of MI • The damage can be located by noting which leads indicative changes. • Leads I II III • show the inferior or diaphragmatic area of the heart • The precordial or chest leads reflect changes on the anterior surface

  38. Only 15% • Of all infarcts show no changes on the initial tracing. • The EKG changes evolve later, hours to days as tissue damage changes electrical conduction pathways. • Most of the dangerous arrhythmias happen in the first two hours following initial symptoms.

  39. The first findings • During Impending MI • Elevation of the ST segment. Acute problem, returns to baseline Ischemia • Followed by T wave inversion, ischemia • Then Q wave pronouncement (greater than 1/3 the height of the QRS complex, or 1 sm. box, 0.04 sec. wide) • As the infarcts heals, the Q wave may remain as the only sign of an old infarction.

  40. Treatment

  41. Treatment Considerations • “MONA” greets all patients • Morphine • Oxygen • Nitrates • Aspirin • Not in that order though

  42. Treatment Considerations • Consider Rapid Transport • Consider appropriateness of destination facility • Frequently reassess for changing status (progression) and Treat accordingly • Obtain additional history

  43. General Management“MONA” greets all patients • Oxygen therapy - FIRST! • Decrease myocardial work • May decrease size of infarct. • Titrate to SaO2 95% or better • ECG Monitoring • high incidence of life-threatening arrhythmias such as ST changes, PVC, V. Tach, V. FIB • IV access

  44. Nitrates • Must have baseline ECG (look for right side involvement) • Do not use if systolic BP< 100mm/Hg • Question use of sexual performance enhancing drugs. Withhold nitrates if used in past 48 hours • Must have IV in place

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