ST-Segment Elevation Myocardial Infarction



ST-Segment Elevation Myocardial Infarction


Ian J. Neeland

James A. de Lemos



I. GENERAL PRINCIPLES

A. Rapid reperfusion of the infarct-related artery (IRA), with either primary percutaneous coronary intervention (PCI) or fibrinolytic therapy, is the cornerstone of management for patients with ST-segment elevation myocardial infarction (STEMI).

B. Adjunctive therapy with aspirin, P2Y12 receptor inhibitors, β-blockers, angiotensin-converting enzyme inhibitors, and statins further reduces the risk of death and major cardiovascular events after reperfusion.

II. PATHOPHYSIOLOGY

A. Rupture of lipid-rich, inflammatory atherosclerotic plaque causes collagen exposure leading to platelet adhesion, activation, and aggregation.

B. Fibrin-platelet clot develops as thrombin converts fibrinogen to fibrin and completely occludes the IRA causing transmural myocardial injury, manifested by ST-segment elevation on the electrocardiogram (ECG).

III. DIAGNOSIS

A. Differential diagnosis: Rapidly consider/rule out pneumothorax, aortic dissection, pericarditis, tamponade, pulmonary embolism, stress cardiomyopathy with apical ballooning (takotsubo syndrome), and severe hyperkalemia.

B. History.

1. Severe, pressure-type midsternal pain, often with radiation to the left neck, arm, or jaw, occurring at rest.

2. Associated symptoms: dyspnea, nausea, vomiting, diaphoresis, or weakness.

3. Silent infarction in 25% of cases, especially in elderly and diabetic patients.

C. Physical examination.

1. Not helpful in confirming the diagnosis of STEMI.

2. Should focus on eliminating other potential diagnoses and assessing for complications of STEMI (Tables 33-1 and 33-2).

D. ECG.

1. ST elevations in regional vascular distribution with concurrent ST depression in reciprocal leads.


2. ECG mimics: pericarditis (global ST elevation with PR depression), early repolarization, old left ventricular (LV) aneurysm, and Prinzmetal angina.

3. New left bundle branch block (LBBB) may represent large anterior infarction, but has a high false-positive rate; primary PCI strongly preferred over fibrinolytic therapy for LBBB.

E. Cardiac biomarkers.

1. Biomarkers of limited use for emergency diagnosis of STEMI.

2. Cardiac troponins are the preferred biomarkers for confirmation of myocardial infarction (MI).

F. Additional evaluation.

1. Echocardiography useful when ECG is indeterminate to evaluate for focal wall motion abnormalities.

2. Risk assessment scores predict early mortality and recurrent infarction. TIMI (http://www.mdcalc.com/timi-risk-score-for-stemi). GRACE (http://www.outcomes-umassmed.org/grace/acs_risk/acs_risk_content.html).








TABLE 33-1 Electrical Complications of Acute MI























































Complication


Prognosis


Treatment


Ventricular tachycardia/fibrillation


Pulseless arrest at presentation


Variable


Defibrillation; therapeutic hypothermia if comatose


VT/VF within first 24-48 h


Good


Immediate cardioversion; lidocaine; β-blockers


VT/VF > 48 h


Poor


Immediate cardioversion; electrophysiology study/implantable defibrillator; amiodarone


Bradyarrhythmias


Sinus bradycardia


Excellent


Atropine for hypotension or symptoms


Second-degree heart block


Mobitz type I (Wenkebach)


Excellent


Atropine for hypotension or symptoms


Mobitz type II


Guarded


Temporary pacemaker


Complete heart block


Inferior MI


Good


Temporary pacemaker


Anterior MI


Poor


Temporary pacemaker followed by permanent pacemaker


Atrial tachyarrhythmias


Atrial fibrillation


Good


β-Blocker and/or amiodarone; cardioversion if unstable


VT, ventricular tachycardia; VF, ventricular fibrillation; MI, myocardial infarction.










TABLE 33-2 Mechanical Complications of Acute MI









































Complication


Timing


Pathophysiology


Exam/ECG


Intervention


Cardiogenic shock


Early


Extensive LV infarction; mechanical complications (see below)


Tachycardia, hypotension, cool and clammy extremities, altered mentation


Emergent PCI or CABG; IABPa; LVAD for refractory cases


Acute MR


Early


Necrosis of papillary muscles that tether mitral valve


Heart failure; early systolic, decrescendo, or holosystolic murmur; thrill radiating to apex ± S3


Emergent echo; right heart catheterization: large V waves. IABP; surgery


LV rupture


Acute—subacute


Necrosis of LV causing free wall rupture and flow into pericardial chamber


Usually presents as sudden death or tamponade; hypotension, muffled heart sounds, elevated JVP


IV fluids, emergent echo; pericardiocentesisb emergent surgery


RV MI


Acute


Hypokinesis or akinesis of right ventricle


Hypotension, elevated JVP; congested liver; ST elevations in V1, (±V2, V3), V3R, V4R


IV fluids; temporary pacemaker; emergent catheterization; nitrates contraindicated


LV aneurysm


Late (weeks to months)


Regional dilation and dyskinesis of LV. Risk of thrombus and arrhythmias


ECG shows persistent ST-segment elevation


Echo; oral anticoagulation


a IABP may not reduce 30-day mortality in patients with cardiogenic shock for whom an early revascularization strategy is planned.

b

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Jun 11, 2016 | Posted by in CRITICAL CARE | Comments Off on ST-Segment Elevation Myocardial Infarction

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