Chapter 21 Marini Acute Coronary Syndromes

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SECTION II • Medical and Surgical Crises

discomfort, which has been described as burn- ing, squeezing, or pressure-like sensation lasting for more than 30 minutes. The discomfort may radiate to the arms, neck, back, or jaw. It must be emphasized that the pain description may be highly atypical (burning, stabbing, sharp) or may be localized only to the arm, neck, or epi- gastrium. Autonomic symptoms (nausea, vom- iting, sweating) are more common than in UA, especially when the MI is inferior. Up to 20% of MIs are painless (more likely in diabetics and the elderly). Young age, paucity of classic risk factors, and atypical chest pain character are more com- mon in patients with cocaine-induced infarction. 2. Atypical Presentation: Symptoms may mimic gastroesophageal reflux, cholecystitis, or an acute abdomen. Acute onset of shortness of breath, heart failure, dizziness, syncope, and weakness are occasionally encountered as atyp- ical manifestations of an AMI. 3. SilentMI: Clinically silent infarcts are detected incidentally on an ECG, echocardiogram, or nuclear scan. Silent MI is usually experienced by diabetics with autonomic dysfunction. Physical Examination Blood pressure and pulse rate usually are mildly increased. (Tachycardia is more common in anterior or lateral MI than in inferior or posterior MIs, in which bradycardia is more likely.) Fever may accom- pany uncomplicated MI but rarely exceeds 101°F or persists beyond 1 week. An S4 gallop is very common, whereas an S3 suggests congestive fail- ure, especially if accompanied by pulmonary rales. A paradoxically split S2 indicates increased LV ejection time or left bundle-branch block (LBBB). A systolic murmur should raise the suspicion of acute papillary muscle dysfunction, especially if the patient has presented late (typically, a few days after onset of symptoms). A pericardial friction rub com- monly appears in the first 48 hours after a transmu- ral MI and may be easily confused with a murmur. Although also possible in a classic MI, findings of a hyperadrenergic state (mydriasis, agitation, hyper- tension, diaphoresis, and/or tachycardia) should raise suspicion of cocaine-induced infarction. Electrocardiogram 1. ST Segment Deflection: ST elevation greater than or equal to 1 mm in two or more contigu- ous leads is highly suggestive of STEMI. ST

elevation has high localizing value (Table 21-1). The typical ST elevation seen with STEMI has an outward convexity. The ST segment eleva- tions usually return to baseline with myocardial reperfusion and can be used to monitor rep- erfusion therapies. The differential diagnosis includes hyperkalemia, acute central nervous system (CNS) injury, acute myocarditis, acute pericarditis, left ventricular hypertrophy, api- cal cardiomyopathy, Wolff–Parkinson–White syndrome, early repolarization abnormalities, and LV aneurysm. Some of these may mimic an AMI and hence have been termed “pseudo- infarct” patterns. 2. Evolution of ECG Changes: A series of repolarization changes are seen on ECG after complete coronary artery occlusion. The first transient abnormalities seen are the hypera- cute T waves (tall, peaked, and symmetrical T waves). Hyperacute T waves are usually gone by the time of initial presentation for emer- gency care. This is followed by convex, upward ST elevation, which is a sign of transmural myocardial ischemic injury. The number of leads showing the abnormality has a bearing on the size of the infarction and prognosis. T wave inversions are seen with persistent transmural ischemia. By this time, the ST elevations have begun to subside. Q waves are a sign of com- pletion of the infarction and may take hours to days to develop. Persistent ST elevation beyond 3 to 4 weeks is a sign of an LV aneurysm. 3. Posterior MI: This manifests as ST depres- sion (>2 mm) in leads V 1 to V 3 . It is usually seen in conjunction with an inferior wall MI, Table 21-1.  Anatomic Patterns of Myocardial Injury Location of Injury Affected Leads Inferior II, III, F Anterior/septal V 2 –V 4 Anterolateral V 3 –V 6 Lateral I, AVL, occasionally V 6 Apical II, III, F, V 5 , V 6 Posterior a V 1 and V 2 and V 3 R, V 4 R a ST segment depression with R waves; T wave is inverted initially and then becomes upright.