The ‗classic‘ textbook description of acute MI is one of crushing retrosternal chest pain, with radiation of the pain to the jaw and down the left arm, associated with diaphoresis. While this presentation certainly occurs, large numbers ofinfarctions present in a more atypical fashion. Forexample, a significant
proportion of patients with MI have the following descriptions of chest pain: ―crushing, pressure, tightness, burning, indigestion, chest ache, sharp, stabbing.‖ Therefore, one must consider atypical pains as possibly being ischemic in origin.
Radiation of the chest pain is actually an insensitive, moderately specific indicator of acute MI.
Interestingly, while textbooks often describe radiation of pain to the left arm as a feature of myocardial ischemia; radiation of pain to the right arm is actually a more specific indicator of acute MI. Other
symptoms most specifically associated with acute MI are nausea/vomiting, diaphoresis, and dyspnea. The presentation of acute MI in the elderly is often non-classical. It is often without pain and
diaphoresis, but with an increased frequency of neurological symptoms such as syncope, stroke, acute confusion, and weakness as the presenting complaint. In addition, dyspnea is a more common presenting symptom than chest pain in the elderly.
Other critical diagnoses must be considered when assessing a patient with possible myocardial ischemia. Aortic dissection is characterized by a sudden ripping or tearing pain in the back. Pericarditis should be suspected if the pain has pleuritic or positional components. Pulmonary embolism produces a sudden, often pleuritic pain associated with dyspnea. The pain of myocardial infarction usually begins gradually and worsens over a short period of time. Risk factors for myocardial ischemia must be documented. The risk factors include smoking, diabetes, hypertension, family history and
All contents copyright © 2012, University of Toronto. All rights reserved hypercholesterolemia. Their presence increases the
likelihood that the pain, even if atypical, may be ischemic.
PHYSICAL EXAMINATION
The physical examination in patients with possible ischemic chest pain helps to rule out other diagnoses, establish any complications of ischemia, and provides important information to direct pharmacological and possibly mechanical intervention. In particular, attention should be directed to the appearance, vital signs (including BP in both arms), JVP, chest auscultation, cardiac exam, and peripheral pulses. Inspiratory crackles and an S3 are associated with left ventricular failure. Right-sided heart failure is characterized by an elevated JVP and peripheral edema. A new systolic murmur may indicate a ventricular septal defect or acute mitral regurgitation. An attempt should be made to determine the
hemodynamic status as follows: Killip l : well perfused, chest clear
Killip ll: some pulmonary congestion (orthopnea, crackles)
Killip lll: pulmonary edema (severe shortness of breath, crackles above scapulae)
Killip lV: poor perfusion, cardiogenic shock All patients with acute inferior MI's, in particular, should be examined for signs of right ventricular infarction. These signs include low BP, clear chest, distended JVP.
ECG
The standard 12 lead ECG remains the most definite early test to document an acute MI. It should be obtained as soon as possible in patients with any type of chest pain, epigastric pain, dyspnea, or other symptoms which may accompany an acute MI (diaphoresis, nausea, vomiting, acute confusion or stroke in the elderly). Unfortunately, the ECG may be either completely normal or may only show
nonspecific changes when the patient first presents. If the initial ECG is not diagnostic, repeat ECGs should be done in the ED, particularly during repeated episodes of pain, or if the patient describes a worsening of the pain while in the department. A 15-lead ECG is a standard 12-lead ECG with 3 additional leads - V4R, V8, and V9. The V4R lead is particularly important to diagnose right ventricular infarctions and should be done on all patients with inferior wall infarctions. The V8 and V9 leads offer a
direct look at the posterior wall of the myocardium. This allows one to diagnose a true posterior wall infarction (ST elevation) when there is ‗indirect‘ evidence on a standard 12-lead ECG (a tall R wave, ST segment depression, and an upright T wave in leads V1 and V2).
Early and subtle ECG findings in acute MI include the following:
increase in R wave voltage, usually in the precordial leads.
hyperacute T waves, usually in the precordial leads. A normal T wave is asymmetric with steeper descending than ascending limb. An abnormal T wave is symmetric and prominent (usually over 10 mm in precordial leads). Other causes of hyperacute T waves include LBBB, hyperkalemia, LVH, and subarachnoid hemorrhage.
ST segment elevation, suggesting a current of injury and acute transmural ischemia. There are other causes of ST segment elevation: pericarditis, benign early repolarization, hyperkalemia, LV aneurysm, LBBB, LVH, and hypothermia. In acute transmural MI, ST segment elevation occurs almost immediately and helps localize the area of infarction:
II, III, AVF: inferior MI V1-V3: anteroseptal 1, AVL, V4 –V6: lateral
V1-V6: anterolateral
V8,V9: posterior
In addition, the amount and distribution of ST elevation can be used to quantify the infarct. The higher the ST elevation and the more leads involved, the worse the prognosis. Greater benefits from treatment are found with extensive infarcts.
Q waves are a sign of extensive myocardial ischemia and frank necrosis. Whereas ST segment elevation occurs almost immediately in acute transmural infarction, Q waves usually require several hours to develop. Nontransmural (or subendocardial)
infarction may result in ST segment depression and T wave inversion without Q wave development. Alternatively, ST segment depression may represent ‗reciprocal‘ changes of a current of injury in another site of the heart.
Example ECGs, illustrating various myocardial infarctions can be found at the end of this chapter (see Figures 1-7).
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INVESTIGATIONS
An early Chest X-ray (CXR) is not a priority in the assessment and treatment of patients with acute MI. When aortic dissection is a possibility in a patient presenting with chest pain, a CXR should be done immediately to look for a widened mediastinum and a pleural effusion. In MI, the CXR is usually normal, but may confirm clinical evidence of congestive heart failure.
Trying to rule out myocardial ischemia by giving the patient a ‗pink lady‘ in the ED is fraught with hazard and must be avoided. A diagnostic challenge looking for relief of epigastric pain with an antacid/viscous lidocaine preparation is unreliable, insensitive, and nonspecific. Sending patients home based on their response to such a challenge is a classic medical-legal disaster.
Positive cardiac enzymes continue to be the mainstay of our ability to rule in or rule out a diagnosis of myocardial infarction when the initial ECGs are normal or non-specific. Cardiac troponin assays are widely available, but rises in troponin will not occur until at least 2 to 6 hours after the onset of symptoms; therefore, a single negative cardiac enzyme in a patient who presents with chest pain of recent duration cannot be used to rule out myocardial infarction. Serial serum troponin values, done at least 6 to 9 hours after initial presentation to the
Emergency Department, approaches 100% sensitivity in ruling out myocardial infarction (but not unstable angina) in patients without diagnostic ECG changes. Troponin levels peak in 12 to 24 hours after
infarction. The troponin testing is also limited by poor specificity. Renal failure and sepsis are examples of common conditions that can elevate troponin levels. The sensitivity of serial troponin testing is always better than obtaining a single sample.
The prime benefit of the cardiac troponins seems to be for prognostic value and for risk stratification. Patients with either unstable angina or myocardial infarction who present with higher troponin levels have higher short and long term mortality rates.