ST- Segment Elevation Myocardial Infarction


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ST Segment Elevation Myocardial Infarction

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ST- Segment Elevation Myocardial Infarction

  1. 1. <ul><li>ST-Segment Elevation Myocardial Infarction </li></ul>
  2. 2. <ul><li>650,000 - new AMI </li></ul><ul><li>450,000 - recurrent AMI each year </li></ul><ul><li>early (30-day) mortality rate - ~30% </li></ul><ul><li>1 of every 25 patients who survives the initial hospitalization dies in the first year after AMI </li></ul><ul><li>Mortality is approximately fourfold higher in elderly patients (over age 75) </li></ul>
  3. 4. <ul><li>STEMI usually occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis </li></ul><ul><li>Coronary artery thrombus develops rapidly at a site of vascular injury </li></ul><ul><ul><li>cigarette smoking </li></ul></ul><ul><ul><li>Hypertension </li></ul></ul><ul><ul><li>lipid accumulation </li></ul></ul><ul><li>STEMI occurs when the surface of an atherosclerotic plaque becomes disrupted and conditions favor thrombogenesis </li></ul><ul><ul><li>coronary plaques prone to disruption </li></ul></ul><ul><ul><ul><li>rich lipid core and a thin fibrous cap </li></ul></ul></ul>
  4. 5. platelet monolayer forms at the site of the disrupted plaque agonists promote platelet activation(collagen, ADP, epinephrine, serotonin) platelet cross-linking and aggregation thromboxane A 2 (a potent local vasoconstrictor) is released Factors VII and X are activated, ultimately leading to the conversion of prothrombin to thrombin, which then converts fibrinogen to fibrin conformational change in the glycoprotein IIb/IIIa receptor further platelet activation and potential resistance to fibrinolysis develops <ul><li>Fluid-phase and clot-bound thrombin participate in an autoamplification reaction leading to further activation of the coagulation cascade. </li></ul><ul><li>Coronary artery eventually becomes occluded by a thrombus containing platelet aggregates and fibrin strands. </li></ul>high affinity for amino acid sequences on soluble adhesive proteins (fibrinogen - can bind to two different platelets simultaneously
  5. 6. <ul><li>The amount of myocardial damage caused by coronary occlusion depends on </li></ul><ul><ul><li>(1) territory supplied by the affected vessel </li></ul></ul><ul><ul><li>(2) whether or not the vessel becomes totally occluded </li></ul></ul><ul><ul><li>(3) duration of coronary occlusion </li></ul></ul><ul><ul><li>(4) quantity of blood supplied by collateral vessels </li></ul></ul><ul><ul><li>(5) demand for oxygen of the myocardium </li></ul></ul><ul><ul><li>(6) native factors that can produce early spontaneous lysis of the occlusive thrombus </li></ul></ul><ul><ul><li>(7) adequacy of myocardial perfusion in the infarct zone </li></ul></ul>
  6. 7. Clinical Presentation
  7. 8. <ul><li>Elderly </li></ul><ul><ul><li>sudden-onset breathlessness </li></ul></ul><ul><li>Other less common presentations (with or without pain) </li></ul><ul><ul><li>sudden loss of consciousness </li></ul></ul><ul><ul><li>confusional state </li></ul></ul><ul><ul><li>sensation of profound weakness </li></ul></ul><ul><ul><li>appearance of an arrhythmia </li></ul></ul><ul><ul><li>unexplained drop in arterial pressure </li></ul></ul>
  8. 9. <ul><li>anxious and restless </li></ul><ul><ul><li>attempting unsuccessfully to relieve the pain </li></ul></ul><ul><li>Pallor, perspiration & coolness of extremities </li></ul><ul><li>substernal chest pain (>30 min) & diaphoresis </li></ul><ul><ul><li>strongly suggests STEMI </li></ul></ul><ul><li>normal PR & BP - first hour of STEMI </li></ul><ul><ul><li>one-fourth of patients with anterior infarction </li></ul></ul><ul><ul><ul><li>tachycardia and/or hypertension </li></ul></ul></ul><ul><ul><li>one-half with inferior infarction </li></ul></ul><ul><ul><ul><li>bradycardia and/or hypotension </li></ul></ul></ul>
  9. 10. <ul><li>MI progresses through the following temporal stages: </li></ul><ul><ul><li>acute - first few hours to7 days </li></ul></ul><ul><ul><li>healing – 7 to 28 days </li></ul></ul><ul><ul><li>healed - 29 days </li></ul></ul><ul><li>Laboratory tests of value in confirming the diagnosis may be divided into four groups: </li></ul><ul><ul><li>ECG </li></ul></ul><ul><ul><li>serum cardiac biomarkers </li></ul></ul><ul><ul><li>cardiac imaging </li></ul></ul><ul><ul><li>nonspecific indices of tissue </li></ul></ul><ul><ul><li>necrosis and inflammation </li></ul></ul>
  10. 11. <ul><li>Initial stage </li></ul><ul><ul><li>total occlusion of an epicardial coronary artery </li></ul></ul><ul><ul><ul><li>produces ST-segment elevation </li></ul></ul></ul><ul><ul><ul><ul><li>evolve Q waves on the ECG </li></ul></ul></ul></ul>
  11. 12. <ul><li>small proportion of patients initially presenting with ST-segment elevation will not develop Q waves </li></ul><ul><ul><li>obstructing thrombus is not totally occlusive </li></ul></ul><ul><ul><li>obstruction is transient </li></ul></ul><ul><ul><li>rich collateral network is present </li></ul></ul><ul><li>ischemic discomfort but without ST-segment elevation and serum cardiac biomarker of necrosis is detected </li></ul><ul><ul><li>NSTEMI is ultimately made </li></ul></ul>
  12. 13. <ul><li>Proteins released from necrotic </li></ul><ul><li>heart muscle after STEMI </li></ul><ul><ul><li>rate of liberation differs depending </li></ul></ul><ul><ul><li>intracellular location, molecular weight, & local blood and lymphatic flow </li></ul></ul><ul><ul><li>detectable in the peripheral blood once the capacity of the cardiac lymphatics to clear the interstitium of the infarct zone is exceeded and spillover into the venous circulation occurs </li></ul></ul>
  13. 14. <ul><li>amino acid sequences different from those of the skeletal muscle </li></ul><ul><li>increase after STEMI to levels >20 times higher than the upper reference limit </li></ul><ul><ul><li>preferred biochemical markers for MI </li></ul></ul><ul><li>Levels remain elevated for 7–10 days after STEMI </li></ul>
  14. 15. <ul><li>4–8 h (normal by 48–72 h) </li></ul><ul><li>lack of specificity for STEMI </li></ul><ul><ul><li>elevated with skeletal muscle disease or trauma (intramuscular injection) </li></ul></ul><ul><li>MB isoenzyme of CK </li></ul><ul><ul><li>advantage over total CK </li></ul></ul><ul><ul><li>not present in significant concentrations in extracardiac tissue </li></ul></ul><ul><li>ratio (relative index) of CKMB mass:CK activity 2.5 </li></ul><ul><ul><li>Suggests myocardial rather than a skeletal muscle source for the CKMB elevation </li></ul></ul>
  15. 16. <ul><li>Polymorphonuclear leukocytosis </li></ul><ul><ul><li>appears few hours after the onset of pain </li></ul></ul><ul><ul><li>persists for 3–7 days </li></ul></ul><ul><ul><li>WBC often reaches levels of 12,000–15,000/L </li></ul></ul><ul><li>Erythrocyte Sedimentation Rate </li></ul><ul><ul><li>rises more slowly than WBC </li></ul></ul><ul><ul><li>peaking during first week </li></ul></ul><ul><ul><li>1 or 2 weeks </li></ul></ul>
  16. 17. <ul><li>Abnormalities of wall motion on 2-D echo </li></ul><ul><ul><li>aids in management decisions </li></ul></ul><ul><ul><ul><li>patient should receive reperfusion therapy </li></ul></ul></ul><ul><ul><li>estimation of left ventricular (LV) function </li></ul></ul><ul><ul><ul><li>serves as an indication for therapy with an inhibitor of the renin-angiotensin-aldosterone system </li></ul></ul></ul><ul><li>Doppler echocardiography </li></ul><ul><ul><li>detection and quantitation of a ventricular septal defect and mitral regurgitation </li></ul></ul>
  17. 19. <ul><li>two general classes of complications: </li></ul><ul><ul><li>(1) electrical complications (arrhythmias) </li></ul></ul><ul><ul><li>(2) mechanical complications (&quot;pump failure“) </li></ul></ul><ul><li>ventricular fibrillation : MC cause of out of hospital deaths </li></ul><ul><ul><li>occur first 24 h of the onset of symptoms </li></ul></ul>
  18. 20. <ul><li>major elements of prehospital care of patients with suspected STEMI </li></ul><ul><ul><li>recognition of symptoms by the patient and prompt seeking of medical attention </li></ul></ul><ul><ul><li>rapid deployment of an emergency medical team capable of performing resuscitative maneuvers </li></ul></ul><ul><ul><li>expeditious transportation of the patient to a hospital facility </li></ul></ul><ul><ul><li>expeditious implementation of reperfusion therapy </li></ul></ul>
  19. 21. <ul><li>Goals </li></ul><ul><ul><li>control of cardiac discomfort </li></ul></ul><ul><ul><li>rapid identification of patients who are candidates for urgent reperfusion therapy </li></ul></ul><ul><ul><li>triage of lower-risk patients to the appropriate location in the hospital </li></ul></ul><ul><ul><li>avoidance of inappropriate discharge of patients with STEMI </li></ul></ul>
  20. 22. <ul><li>Aspirin </li></ul><ul><ul><li>essential in the management of patients with suspected STEMI </li></ul></ul><ul><ul><li>Rapid inhibition of cyclooxygenase-1 in platelets followed by a reduction of thromboxane A 2 levels </li></ul></ul><ul><ul><li>160–325 mg tablet </li></ul></ul><ul><ul><li>75–162 mg PO OD </li></ul></ul><ul><li>Hypoxemia </li></ul><ul><ul><li>2–4 L/min for the first 6–12 h after infarction </li></ul></ul><ul><ul><li>Reassessed </li></ul></ul>
  21. 23. <ul><li>Sublingual nitroglycerin </li></ul><ul><ul><li>0.4 mg up to three doses (5-min intervals) </li></ul></ul><ul><ul><li>diminish chest discomfort </li></ul></ul><ul><ul><li>decreasing myocardial oxygen demand (by lowering preload) </li></ul></ul><ul><ul><li>increasing myocardial oxygen supply (by dilating infarct-related coronary vessels or collateral vessels) </li></ul></ul><ul><li>intravenous nitroglycerin </li></ul><ul><ul><li>return of chest discomfort </li></ul></ul><ul><ul><li>evidence of ongoing ischemia (ST-segment or T-wave shifts) </li></ul></ul>
  22. 24. <ul><li>Contraindication </li></ul><ul><ul><li>low systolic arterial pressure (<90 mmHg) </li></ul></ul><ul><ul><li>clinical suspicion of right ventricular infarction </li></ul></ul><ul><ul><ul><li>inferior infarction on ECG </li></ul></ul></ul><ul><ul><ul><li>elevated jugular venous pressure </li></ul></ul></ul><ul><ul><ul><li>clear lungs </li></ul></ul></ul><ul><ul><ul><li>hypotension </li></ul></ul></ul><ul><ul><li>patients taking phosphodiesterase-5 inhibitor sildenafil within the preceding 24 h </li></ul></ul><ul><li>idiosyncratic reaction to nitrates - sudden marked hypotension </li></ul><ul><ul><li>IV atropine </li></ul></ul>
  23. 25. <ul><li>Morphine </li></ul><ul><li>2–4 mg repetitive (every 5 min) IV </li></ul><ul><li>effective analgesic for the pain associated with STEMI </li></ul><ul><li>reduce sympathetically mediated arteriolar and venous constriction </li></ul><ul><ul><li>reduce cardiac output and arterial pressure </li></ul></ul><ul><ul><li>elevation of the legs </li></ul></ul><ul><ul><li>volume expansion with IV saline </li></ul></ul><ul><li>vagotonic effect </li></ul><ul><ul><li>bradycardia or advanced degrees of heart block </li></ul></ul><ul><ul><li>IV atropine 0.5 mg </li></ul></ul>Control of Discomfort
  24. 26. <ul><li>Intravenous beta blockers </li></ul><ul><li>control pain effectively in some patients </li></ul><ul><ul><li>diminishing myocardial O 2 demand (ischemia) </li></ul></ul><ul><li>reduce the risks of reinfarction and ventricular fibrillation </li></ul><ul><li>Metoprolol </li></ul><ul><ul><li>5 mg every 2–5 min (3 doses) </li></ul></ul><ul><ul><ul><li>heart rate >60 bpm </li></ul></ul></ul><ul><ul><ul><li>systolic pressure >100 mmHg </li></ul></ul></ul><ul><ul><ul><li>PR interval <0.24 s </li></ul></ul></ul><ul><ul><ul><li>rales that are no higher than 10 cm up from the diaphragm </li></ul></ul></ul><ul><ul><li>50 mg every 6 h for 48 h PO </li></ul></ul><ul><ul><ul><li>followed by 100 mg every 12 h </li></ul></ul></ul><ul><ul><ul><li>Fifteen minutes after the last intravenous dose </li></ul></ul></ul>Control of Discomfort
  25. 27. <ul><li>Primary tool for screening patients </li></ul><ul><ul><li>initial 12-lead ECG </li></ul></ul><ul><ul><li>ST-segment elevation of at least 2 mm in two contiguous precordial leads and 1 mm in two adjacent limb leads </li></ul></ul><ul><ul><ul><li>candidate for reperfusion therapy </li></ul></ul></ul><ul><ul><li>absence of ST-segment elevation </li></ul></ul><ul><ul><ul><li>fibrinolysis is not helpful </li></ul></ul></ul>
  26. 28. <ul><li>Primary Percutaneous Coronary Intervention </li></ul><ul><li>angioplasty and/or stenting without preceding fibrinolysis </li></ul><ul><li>effective in restoring perfusion in STEMI in first few hours of MI </li></ul><ul><li>Advantages </li></ul><ul><ul><li>applicable to patients with contraindications to fibrinolytic therapy </li></ul></ul><ul><ul><li>more effective than fibrinolysis in opening occluded coronary arteries </li></ul></ul><ul><li>generally preferred over fibrinolysis when </li></ul><ul><ul><li>diagnosis is in doubt </li></ul></ul><ul><ul><li>presence of cardiogenic shock </li></ul></ul><ul><ul><li>bleeding risk </li></ul></ul><ul><ul><li>symptoms for at least 2–3 h when the clot is more mature and less easily lysed by fibrinolytic drugs </li></ul></ul>
  27. 29. <ul><li>Fibrinolysis </li></ul><ul><li>ideally initiated within 30 min of presentation (door-to-needle time 30 min) </li></ul><ul><li>principal goal : </li></ul><ul><ul><li>prompt restoration of full coronary arterial patency </li></ul></ul><ul><ul><li>Promotes conversion of plasminogen to plasmin then lyses fibrin thrombi </li></ul></ul>
  28. 30. <ul><li>fibrinolytic agents </li></ul><ul><ul><li>tissue plasminogen activator (tPA) </li></ul></ul><ul><ul><ul><li>15 mg bolus followed by 50 mg intravenously over the first 30 min </li></ul></ul></ul><ul><ul><ul><li>followed by 35 mg over the next 60 min </li></ul></ul></ul><ul><ul><li>Streptokinase </li></ul></ul><ul><ul><ul><li>1.5 million units (MU) intravenously over 1 h </li></ul></ul></ul><ul><ul><li>tenecteplase (TNK) </li></ul></ul><ul><ul><ul><li>single weight-based intravenous bolus of 0.53 mg/kg over 10 s </li></ul></ul></ul><ul><ul><li>reteplase (rPA) </li></ul></ul><ul><ul><ul><li>double-bolus regimen consisting of a 10-MU bolus given over 2–3 min, followed by a second 10-MU bolus 30 min later </li></ul></ul></ul>
  29. 32. <ul><li>Clear contraindications </li></ul><ul><li>history of cerebrovascular hemorrhage at any time </li></ul><ul><li>nonhemorrhagic stroke or other cerebrovascular event within the past year </li></ul><ul><li>marked hypertension at any time during the acute presentation </li></ul><ul><ul><li>systolic arterial pressure >180 mmHg </li></ul></ul><ul><ul><li>diastolic pressure >110 mmHg </li></ul></ul><ul><li>suspicion of aortic dissection </li></ul><ul><li>active internal bleeding (excluding menses) </li></ul>
  30. 33. <ul><li>Relative contraindications </li></ul><ul><li>current use of anticoagulants </li></ul><ul><li>recent (<2 weeks) invasive or surgical procedure or prolonged (>10 min) cardiopulmonary resuscitation </li></ul><ul><li>known bleeding diathesis </li></ul><ul><li>Pregnancy </li></ul><ul><li>hemorrhagic ophthalmic condition </li></ul><ul><li>active peptic ulcer disease </li></ul><ul><li>history of severe hypertension that is currently adequately controlled </li></ul>
  31. 34. <ul><li>Streptokinase </li></ul><ul><ul><li>Allergic reactions </li></ul></ul><ul><ul><ul><li>~2% of patients </li></ul></ul></ul><ul><ul><ul><li>should not receive streptokinase within preceding 5 days - 2 yrs </li></ul></ul></ul><ul><ul><ul><li>Hypotension </li></ul></ul></ul><ul><ul><ul><ul><li>4–10% </li></ul></ul></ul></ul><ul><li>Hemorrhage </li></ul><ul><li>Hemorrhagic stroke </li></ul><ul><ul><li>most serious complication </li></ul></ul><ul><ul><li>~0.5–0.9% </li></ul></ul><ul><ul><li>increases with advancing age </li></ul></ul>
  32. 35. <ul><li>Coronary Care Units </li></ul><ul><ul><li>permits continuous monitoring </li></ul></ul><ul><li>Activity </li></ul><ul><ul><li>bed rest for the first 12 h </li></ul></ul><ul><ul><li>absence of complications </li></ul></ul><ul><ul><ul><li>Encouraged an upright posture by dangling their feet over the side of the bed and sitting in a chair within the first 24 h </li></ul></ul></ul><ul><ul><li>absence of hypotension and other complications </li></ul></ul><ul><ul><ul><li>2nd or 3rd day patients – ambulate with increasing duration and frequency </li></ul></ul></ul><ul><ul><li>day 3 after infarction </li></ul></ul><ul><ul><ul><li>ambulate to a goal of 185 m (600 ft) at least three times a day </li></ul></ul></ul>
  33. 36. <ul><li>Diet </li></ul><ul><li>NPO or clear liquids by mouth - first 4–12 h </li></ul><ul><li>30% of total calories as fat and have a cholesterol content of 300 mg/d </li></ul><ul><li>Complex carbohydrates should make up 50–55% of total calories </li></ul><ul><li>Bowels </li></ul><ul><li>stool softener such as dioctyl sodium sulfosuccinate (200 mg/d) </li></ul><ul><li>laxative </li></ul><ul><li>Sedation </li></ul><ul><li>require sedation to withstand the period of enforced inactivity with tranquillity </li></ul><ul><ul><li>Diazepam (5 mg) </li></ul></ul><ul><ul><li>Oxazepam (15–30 mg) </li></ul></ul><ul><ul><li>Lorazepam (0.5–2 mg) </li></ul></ul><ul><ul><li>three or four times daily </li></ul></ul>
  34. 38. <ul><li>Aspirin </li></ul><ul><ul><li>standard antiplatelet agent </li></ul></ul><ul><li>Aspirin + Clopidogrel </li></ul><ul><ul><li>reduces the risk of clinical events </li></ul></ul><ul><ul><ul><li>death </li></ul></ul></ul><ul><ul><ul><li>reinfarction </li></ul></ul></ul><ul><ul><ul><li>stroke </li></ul></ul></ul>
  35. 39. <ul><li>unfractionated heparin (UFH) </li></ul><ul><ul><li>standard antithrombin agent </li></ul></ul><ul><ul><li>helps to maintain patency of the infarct-related artery when added to aspirin and fibrinolytic agents </li></ul></ul><ul><ul><li>recommended dose </li></ul></ul><ul><ul><ul><li>initial bolus of 60 U/kg (maximum 4000 U) </li></ul></ul></ul><ul><ul><ul><li>followed by an initial infusion of 12 U/kg per hour (maximum 1000 U/h) </li></ul></ul></ul>
  36. 40. <ul><li>low-molecular-weight heparin (LMWH): </li></ul><ul><ul><li>alternative to UFH </li></ul></ul><ul><ul><li>Advantages: </li></ul></ul><ul><ul><ul><li>high bioavailability permitting administration subcutaneously </li></ul></ul></ul><ul><ul><ul><li>reliable anticoagulation without monitoring </li></ul></ul></ul><ul><ul><ul><li>greater antiXa:IIa activity </li></ul></ul></ul><ul><ul><li>Enoxaparin </li></ul></ul>
  37. 41. <ul><li>Benefits </li></ul><ul><ul><li>Acute intravenous beta blockade </li></ul></ul><ul><ul><ul><li>improves the myocardial O 2 supply-demand relationship </li></ul></ul></ul><ul><ul><ul><li>decreases pain </li></ul></ul></ul><ul><ul><ul><li>reduces infarct size </li></ul></ul></ul><ul><ul><ul><li>decreases the incidence of serious ventricular arrhythmias </li></ul></ul></ul><ul><ul><li>Given for secondary prevention after an infarction </li></ul></ul><ul><ul><ul><li>reduction in mortality rate is seen with beta blockers </li></ul></ul></ul>
  38. 42. <ul><li>reduce the mortality rate after STEMI </li></ul><ul><ul><li>additive to those achieved with aspirin and beta blockers </li></ul></ul><ul><li>mechanism </li></ul><ul><ul><li>reduction in ventricular remodeling after infarction with a subsequent reduction in the risk of congestive heart failure (CHF) </li></ul></ul>
  39. 43. <ul><li>patients who are intolerant of ACE inhibitors </li></ul><ul><li>who have either clinical or radiological signs of heart failure </li></ul><ul><li>Long-term aldosterone blockade should be prescribed for STEMI patients without significant renal dysfunction </li></ul><ul><ul><li>creatinine 2.5 mg/dL in men and 2.0 mg/dL in women </li></ul></ul><ul><ul><li>hyperkalemia (potassium 5.0 mEq/L) </li></ul></ul><ul><ul><li>LV ejection fraction 40 percent </li></ul></ul><ul><ul><li>symptomatic heart failure or diabetes mellitus </li></ul></ul>
  40. 44. <ul><li> </li></ul>