Symptoms
Chest pain similar to angina but more intense and persistent; not fully relieved by rest or nitroglycerin, often accompanied by nausea, sweating, apprehension. However, ~25% of MIs are clinically silent.
Physical Examination
Pallor, diaphoresis, tachycardia, S4, dyskinetic cardiac impulse may be present. If CHF exists, rales and S3 are present. Jugular venous distention is common in right ventricular infarction.
ECG
ST elevation, followed (if acute reperfusion is not achieved) by T-wave inversion, then Q-wave development over several hours.
Non-ST Elevation MI, or NSTEMI
ST depression followed by persistent ST-T-wave changes without Q-wave development. Comparison with old ECG helpful .
Cardiac Biomarkers
Cardiac-specific troponins T and I are highly specific for myocardial injury and are the preferred biochemical markers for diagnosis of acute MI. They remain elevated for 7–10 days. Creatine phosphokinase (CK) level rises within 4–8 h, peaks at 24 h, and returns to normal by 48–72 h. CK-MB isoenzyme is more specific for MI but may also be elevated with myocarditis or after electrical cardioversion. Total CK (but not CK-MB) rises (two- to threefold) after IM injection, vigorous exercise, or other skeletal muscle trauma. A ratio of CK-MB mass:CK activity ≥2.5 suggests acute MI. CK-MB peaks earlier (about 8 h) following acute reperfusion therapy (see below). Serum cardiac markers should be measured at presentation, 6–9 h later, and then at 12–24 h.
Noninvasive Imaging Techniques
Useful when diagnosis of MI is not clear. Echocardiography detects infarctassociated regional wall motion abnormalities (but cannot distinguish acute MI from a previous myocardial scar). Echo is also useful in detecting RV infarction, LV aneurysm, and LV thrombus. Myocardial perfusion imaging (thallium 201 or technetium 99m-sestamibi) is sensitive for regions of decreased perfusion, but is not specific for acute MI. MRI with delayed gadolinium enhancement accurately indicates regions of infarction, but is technically difficult to obtain in acutely ill pts.
STEMI TREATMENT
INITIAL THERAPY Initial goals are to (1) quickly identify if pt is candidate for reperfusion therapy, (2) relieve pain, and (3) prevent/treat arrhythmias and mechanical complications.
• Aspirin should be administered immediately (162–325 mg chewed at presentation, then 162–325 mg PO qd), unless pt is aspirin-intolerant.
• Perform targeted history, exam, and ECG to identify STEMI (>1 mm ST elevation in two contiguous limb leads, ≥2 mm ST elevation in two contiguous precordial leads, or new LBBB) and appropriateness of reperfusion therapy [percutaneous coronary intervention (PCI) or IV fibrinolytic agent], which reduces infarct size, LV dysfunction, and mortality.
• Primary PCI is generally more effective than fibrinolysis and is preferred at experienced centers capable of performing the procedure rapidly , especially when diagnosis is in doubt, cardiogenic shock is present, bleeding risk is increased, or symptoms have been present for >3 h.
• Proceed with IV fibrinolysis if PCI is not available or if logistics would delay PCI >1 h longer than fibrinolysis could be initiated . Door-to-needle time should be <30 min for maximum benefit. Ensure absence of contraindications before administering fibrinolytic agent. Those treated within 1–3 h benefit most; can still be useful up to 12 h if chest pain is persistent or ST remains elevated in leads that have not developed new Q waves. Complications include bleeding, reperfusion arrhythmias, and, in case of streptokinase (SK), allergic reactions. Enoxaparin or heparin [60 U/kg (maximum 4000 U), then 12 (U/kg)/h (maximum 1000 U/h)] should be initiated with fibrinolytic agents (Fig. 128-2); maintain activated partial thromboplastin time (aPTT) at 1.5–2.0 × control (~50–70 s).
• If chest pain or ST elevation persists >90 min after fibrinolysis, consider referral for rescue PCI. Coronary angiography after fibrinolysis should also be considered for pts with recurrent angina or high-risk features (Fig. 128-2) including extensive ST elevation, signs of heart failure (rales, S3, jugular venous distension, LVEF ≤35%), or systolic BP <100 mmHg. The initial management of NSTEMI (non-Q MI) is different (Chap. 129). In particular, fibrinolytic therapy should not be administered.
ADDITIONAL STANDARD TREATMENT (Whether or not reperfusion therapy is undertaken):
• Hospitalize in CCU with continuous ECG monitoring.
• IV line for emergency arrhythmia treatment.
• Pain control: (1) Morphine sulfate 2–4 mg IV q5–10 min until pain is relieved or side effects develop [nausea, vomiting, respiratory depression (treat with naloxone 0.4–1.2 mg IV), hypotension (if bradycardic, treat with atropine 0.5 mg IV; otherwise use careful volume infusion)]; (2) nitroglycerin 0.3 mg SL if systolic bp >100 mmHg; for refractory pain: IV nitroglycerin (begin at 10 μg/min, titrate upward to maximum of 200 μg/min, monitoring bp closely); do not administer nitrates within 24 h of sildenafil or within 48 h of tadalafil (used for erectile dysfunction); (3) β-adrenergic antagonists (see below).
• Oxygen: 2–4 L/min by nasal cannula (if needed to maintain O2 saturation >90%).
• Mild sedation (e.g., diazepam 5 mg, oxazepam 15–30 mg, or lorazepam 0.5–2 mg PO three to four times daily).
• Soft diet and stool softeners (e.g., docusate sodium 100–200 mg/d).
• β-Adrenergic blockers (Chap. 126) reduce myocardial O2 consumption, limit infarct size, and reduce mortality. Especially useful in pts with hypertension, tachycardia, or persistent ischemic pain; contraindications include active CHF, systolic bp <95 mmHg, heart rate <50 beats/min, AV block, or history of bronchospasm. Consider IV (e.g., metoprolol 5 mg q2–5min to total dose of 15 mg) if pt is hypertensive. Otherwise, begin PO regimen (e.g., metoprolol tartrate 25–50 mg four times daily).
• Anticoagulation/antiplatelet agents: Pts who receive fibrinolytic therapy are begun on heparin and aspirin as indicated above. In absence of fibrinolytic therapy, administer aspirin, 160–325 mg qd, and low-dose heparin (5000 U SC q12h) or low-molecular-weight heparin (LMWH, e.g., enoxaparin 40 mg SC daily) for DVT prevention. Full-dose IV heparin (PTT 1.5-2 × control) or LMWH (e.g., enoxaparin 1 mg/kg SC q12h) followed by oral anticoagulants is recommended for pts with severe CHF, presence of ventricular thrombus by echocardiogram, or large dyskinetic region in acute anterior MI. If used, oral anticoagulants are continued for 3–6 months, then replaced by aspirin. The addition of a P2Y12 platelet receptor antagonist after STEMI (e.g., clopidogrel 75 mg daily) reduces future adverse cardiac events whether or not fibrinolysis or PCI are undertaken.
• ACE inhibitors reduce mortality in pts following acute MI and should be prescribed within 24 h of hospitalization for pts with STEMI—e.g., captopril (6.25 mg PO test dose advanced to 50 mg PO tid). ACE inhibitors should be continued indefinitely after discharge in pts with CHF or those with asymptomatic LV dysfunction (ejection fraction ≤40%); if pt is ACE inhibitor intolerant, use ARB (e.g., valsartan or candesartan).
• Aldosterone antagonists (spironolactone or eplerenone 25–50 mg daily) further reduce mortality in pts with LVEF ≤40% and either symptomatic heart failure or diabetes; do not use in pts with advanced renal insufficiency (e.g., creatinine ≥2.5 mg/dL) or hyperkalemia.
• Serum magnesium level should be measured and repleted if necessary to reduce risk of arrhythmias.
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