- ST-segment elevation myocardial infarction (STEMI) occurs when a coronary artery becomes occluded by a thrombus, blocking blood flow and damaging heart muscle. It is a medical emergency associated with high mortality. - The electrocardiogram (ECG) is used to diagnose STEMI based on ST-segment elevation. Treatment aims to rapidly restore blood flow through fibrinolysis or percutaneous coronary intervention to limit heart muscle damage. - Aspirin, oxygen, nitroglycerin and morphine are given to relieve chest pain and reduce oxygen demand while awaiting reperfusion. Beta blockers may also be used if the blood pressure is stable enough.

1. ST-Segment Elevation Myocardial Infarction

2. 650,000 - new AMI 450,000 - recurrent AMI each year early (30-day) mortality rate - ~30% 1 of every 25 patients who survives the initial hospitalization dies in the first year after AMI Mortality is approximately fourfold higher in elderly patients (over age 75)

4. STEMI usually occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously affected by atherosclerosis Coronary artery thrombus develops rapidly at a site of vascular injury cigarette smoking Hypertension lipid accumulation STEMI occurs when the surface of an atherosclerotic plaque becomes disrupted and conditions favor thrombogenesis coronary plaques prone to disruption rich lipid core and a thin fibrous cap

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 Fluid-phase and clot-bound thrombin participate in an autoamplification reaction leading to further activation of the coagulation cascade. Coronary artery eventually becomes occluded by a thrombus containing platelet aggregates and fibrin strands. high affinity for amino acid sequences on soluble adhesive proteins (fibrinogen - can bind to two different platelets simultaneously

6. The amount of myocardial damage caused by coronary occlusion depends on (1) territory supplied by the affected vessel (2) whether or not the vessel becomes totally occluded (3) duration of coronary occlusion (4) quantity of blood supplied by collateral vessels (5) demand for oxygen of the myocardium (6) native factors that can produce early spontaneous lysis of the occlusive thrombus (7) adequacy of myocardial perfusion in the infarct zone

7. Clinical Presentation

8. Elderly sudden-onset breathlessness Other less common presentations (with or without pain) sudden loss of consciousness confusional state sensation of profound weakness appearance of an arrhythmia unexplained drop in arterial pressure

9. anxious and restless attempting unsuccessfully to relieve the pain Pallor, perspiration & coolness of extremities substernal chest pain (>30 min) & diaphoresis strongly suggests STEMI normal PR & BP - first hour of STEMI one-fourth of patients with anterior infarction tachycardia and/or hypertension one-half with inferior infarction bradycardia and/or hypotension

10. MI progresses through the following temporal stages: acute - first few hours to7 days healing – 7 to 28 days healed - 29 days Laboratory tests of value in confirming the diagnosis may be divided into four groups: ECG serum cardiac biomarkers cardiac imaging nonspecific indices of tissue necrosis and inflammation

11. Initial stage total occlusion of an epicardial coronary artery produces ST-segment elevation evolve Q waves on the ECG

12. small proportion of patients initially presenting with ST-segment elevation will not develop Q waves obstructing thrombus is not totally occlusive obstruction is transient rich collateral network is present ischemic discomfort but without ST-segment elevation and serum cardiac biomarker of necrosis is detected NSTEMI is ultimately made

13. Proteins released from necrotic heart muscle after STEMI rate of liberation differs depending intracellular location, molecular weight, & local blood and lymphatic flow 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

14. amino acid sequences different from those of the skeletal muscle increase after STEMI to levels >20 times higher than the upper reference limit preferred biochemical markers for MI Levels remain elevated for 7–10 days after STEMI

15. 4–8 h (normal by 48–72 h) lack of specificity for STEMI elevated with skeletal muscle disease or trauma (intramuscular injection) MB isoenzyme of CK advantage over total CK not present in significant concentrations in extracardiac tissue ratio (relative index) of CKMB mass:CK activity 2.5 Suggests myocardial rather than a skeletal muscle source for the CKMB elevation

16. Polymorphonuclear leukocytosis appears few hours after the onset of pain persists for 3–7 days WBC often reaches levels of 12,000–15,000/L Erythrocyte Sedimentation Rate rises more slowly than WBC peaking during first week 1 or 2 weeks

17. Abnormalities of wall motion on 2-D echo aids in management decisions patient should receive reperfusion therapy estimation of left ventricular (LV) function serves as an indication for therapy with an inhibitor of the renin-angiotensin-aldosterone system Doppler echocardiography detection and quantitation of a ventricular septal defect and mitral regurgitation

19. two general classes of complications: (1) electrical complications (arrhythmias) (2) mechanical complications ("pump failure“) ventricular fibrillation : MC cause of out of hospital deaths occur first 24 h of the onset of symptoms

20. major elements of prehospital care of patients with suspected STEMI recognition of symptoms by the patient and prompt seeking of medical attention rapid deployment of an emergency medical team capable of performing resuscitative maneuvers expeditious transportation of the patient to a hospital facility expeditious implementation of reperfusion therapy

21. Goals control of cardiac discomfort rapid identification of patients who are candidates for urgent reperfusion therapy triage of lower-risk patients to the appropriate location in the hospital avoidance of inappropriate discharge of patients with STEMI

22. Aspirin essential in the management of patients with suspected STEMI Rapid inhibition of cyclooxygenase-1 in platelets followed by a reduction of thromboxane A 2 levels 160–325 mg tablet 75–162 mg PO OD Hypoxemia 2–4 L/min for the first 6–12 h after infarction Reassessed

23. Sublingual nitroglycerin 0.4 mg up to three doses (5-min intervals) diminish chest discomfort decreasing myocardial oxygen demand (by lowering preload) increasing myocardial oxygen supply (by dilating infarct-related coronary vessels or collateral vessels) intravenous nitroglycerin return of chest discomfort evidence of ongoing ischemia (ST-segment or T-wave shifts)

24. Contraindication low systolic arterial pressure (<90 mmHg) clinical suspicion of right ventricular infarction inferior infarction on ECG elevated jugular venous pressure clear lungs hypotension patients taking phosphodiesterase-5 inhibitor sildenafil within the preceding 24 h idiosyncratic reaction to nitrates - sudden marked hypotension IV atropine

25. Morphine 2–4 mg repetitive (every 5 min) IV effective analgesic for the pain associated with STEMI reduce sympathetically mediated arteriolar and venous constriction reduce cardiac output and arterial pressure elevation of the legs volume expansion with IV saline vagotonic effect bradycardia or advanced degrees of heart block IV atropine 0.5 mg Control of Discomfort

26. Intravenous beta blockers control pain effectively in some patients diminishing myocardial O 2 demand (ischemia) reduce the risks of reinfarction and ventricular fibrillation Metoprolol 5 mg every 2–5 min (3 doses) heart rate >60 bpm systolic pressure >100 mmHg PR interval <0.24 s rales that are no higher than 10 cm up from the diaphragm 50 mg every 6 h for 48 h PO followed by 100 mg every 12 h Fifteen minutes after the last intravenous dose Control of Discomfort

27. Primary tool for screening patients initial 12-lead ECG ST-segment elevation of at least 2 mm in two contiguous precordial leads and 1 mm in two adjacent limb leads candidate for reperfusion therapy absence of ST-segment elevation fibrinolysis is not helpful

28. Primary Percutaneous Coronary Intervention angioplasty and/or stenting without preceding fibrinolysis effective in restoring perfusion in STEMI in first few hours of MI Advantages applicable to patients with contraindications to fibrinolytic therapy more effective than fibrinolysis in opening occluded coronary arteries generally preferred over fibrinolysis when diagnosis is in doubt presence of cardiogenic shock bleeding risk symptoms for at least 2–3 h when the clot is more mature and less easily lysed by fibrinolytic drugs

29. Fibrinolysis ideally initiated within 30 min of presentation (door-to-needle time 30 min) principal goal : prompt restoration of full coronary arterial patency Promotes conversion of plasminogen to plasmin then lyses fibrin thrombi

30. fibrinolytic agents tissue plasminogen activator (tPA) 15 mg bolus followed by 50 mg intravenously over the first 30 min followed by 35 mg over the next 60 min Streptokinase 1.5 million units (MU) intravenously over 1 h tenecteplase (TNK) single weight-based intravenous bolus of 0.53 mg/kg over 10 s reteplase (rPA) double-bolus regimen consisting of a 10-MU bolus given over 2–3 min, followed by a second 10-MU bolus 30 min later

32. Clear contraindications history of cerebrovascular hemorrhage at any time nonhemorrhagic stroke or other cerebrovascular event within the past year marked hypertension at any time during the acute presentation systolic arterial pressure >180 mmHg diastolic pressure >110 mmHg suspicion of aortic dissection active internal bleeding (excluding menses)

33. Relative contraindications current use of anticoagulants recent (<2 weeks) invasive or surgical procedure or prolonged (>10 min) cardiopulmonary resuscitation known bleeding diathesis Pregnancy hemorrhagic ophthalmic condition active peptic ulcer disease history of severe hypertension that is currently adequately controlled

34. Streptokinase Allergic reactions ~2% of patients should not receive streptokinase within preceding 5 days - 2 yrs Hypotension 4–10% Hemorrhage Hemorrhagic stroke most serious complication ~0.5–0.9% increases with advancing age

35. Coronary Care Units permits continuous monitoring Activity bed rest for the first 12 h absence of complications Encouraged an upright posture by dangling their feet over the side of the bed and sitting in a chair within the first 24 h absence of hypotension and other complications 2nd or 3rd day patients – ambulate with increasing duration and frequency day 3 after infarction ambulate to a goal of 185 m (600 ft) at least three times a day

36. Diet NPO or clear liquids by mouth - first 4–12 h 30% of total calories as fat and have a cholesterol content of 300 mg/d Complex carbohydrates should make up 50–55% of total calories Bowels stool softener such as dioctyl sodium sulfosuccinate (200 mg/d) laxative Sedation require sedation to withstand the period of enforced inactivity with tranquillity Diazepam (5 mg) Oxazepam (15–30 mg) Lorazepam (0.5–2 mg) three or four times daily

38. Aspirin standard antiplatelet agent Aspirin + Clopidogrel reduces the risk of clinical events death reinfarction stroke

39. unfractionated heparin (UFH) standard antithrombin agent helps to maintain patency of the infarct-related artery when added to aspirin and fibrinolytic agents recommended dose initial bolus of 60 U/kg (maximum 4000 U) followed by an initial infusion of 12 U/kg per hour (maximum 1000 U/h)

40. low-molecular-weight heparin (LMWH): alternative to UFH Advantages: high bioavailability permitting administration subcutaneously reliable anticoagulation without monitoring greater antiXa:IIa activity Enoxaparin

41. Benefits Acute intravenous beta blockade improves the myocardial O 2 supply-demand relationship decreases pain reduces infarct size decreases the incidence of serious ventricular arrhythmias Given for secondary prevention after an infarction reduction in mortality rate is seen with beta blockers

42. reduce the mortality rate after STEMI additive to those achieved with aspirin and beta blockers mechanism reduction in ventricular remodeling after infarction with a subsequent reduction in the risk of congestive heart failure (CHF)

43. patients who are intolerant of ACE inhibitors who have either clinical or radiological signs of heart failure Long-term aldosterone blockade should be prescribed for STEMI patients without significant renal dysfunction creatinine 2.5 mg/dL in men and 2.0 mg/dL in women hyperkalemia (potassium 5.0 mEq/L) LV ejection fraction 40 percent symptomatic heart failure or diabetes mellitus

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