The initial diagnostic evaluation of the patient with acute chest discomfort centers on the recognition of life-threatening conditions, including acute coronary syndrome and pulmonary embolism.
Electrocardiography is an indispensable tool in the diagnosis and management of acute coronary syndromes (ACS). Deviation of the ST-segment is generally the earliest electrocardiographic manifestation of myocardial injury. Elevation of the ST-segment is produced over the ischemic zone when acute ischemia is transmural and may be preceded by the appearance of tall, positive, hyperacute T waves and accompanied by often prominent reciprocal STsegment depressions on leads overlying the contralateral surface of the heart. Within a period of hours to days, electrocardiographic changes evolve with T-wave inversions and Q-wave formation in the leads that demonstrated ST-segment elevations (Figures 102-1, 102-2, and 102-3).
Electrocardiogram reveals prominent anteroseptal and lateral ST-segment elevations, consistent with the thrombotic lesion visualized within the proximal left anterior descending artery and intervened upon during coronary angiography.
59-year-old gentleman presenting with chest pain and prominent inferolateral ST-segment elevations. He underwent successful deployment of bare-metal stents to the mid- and distal-right coronary artery.
Elevations of the ST-segment in the inferior leads is suggestive of a thrombotic lesion within the right coronary artery. Reciprocal changes are apparent in the lateral limb and precordial leads. ST-segment depressions in leads V1 and V2 suggest posterior involvement.
Acute Myocardial infarction
- Epicardial injury or transmural ischemia is manifested by ST-segment deviation toward the ischemic zone, manifested by ST-segment depression or elevation.
- Reciprocal ST-segment depressions in other leads support a diagnosis of ischemia rather than early repolarization.
Prior Myocardial infarction
- <1 mm ST-segment elevation in any lead and T waves upright in the leads with pathological Q waves (> 1/3 of the R-wave amplitude with duration of > 0.04 seconds).
- Suspect aneurysm or large akinetic region if wide deep Q waves across the precordial leads in a stable pattern.
Early repolarization syndrome
- Most clinically urgent problem—distinguish between early repolarization and ischemia.
- Diagnostic criteria:
- Concave ST-segment elevation <5 mm and most prominent in the precordial leads.
- Reciprocal ST depression usually seen in AVR.
- T waves usually asymmetric.
- Notching of the R wave at its junction with ST-segment (≥50% of cases).
- During exercise the ST-segment elevation of early repolarization may return to baseline.
- Depression of the PQ segment, reflecting atrial injury, early in course.
- Commonly, ST-segment elevation in all leads, except aVR, which has ST-segment depression.
- Other leads, often V1 and aVL, sometimes lead III, in which the QRS complexes are predominantly negative, may not show ST-segment elevation.
- A relatively slow sinus rate is frequent with early repolarization and infrequent with acute pericarditis.
- Almost exclusively in pericarditis:
- T wave amplitude ≤3 mm in V6.
- Ratio of height of the onset of the ST-segment to the amplitude of the T wave in V6 ≥0.25.
- Low voltage, defined as limb leads <5 mm peak to peak and precordial leads <10 mm peak to peak, is seen in less that 1% of normal people.
- Isolated low voltage in limb leads has no clinical significance.
- Low specificity of low voltage for pericardial effusion.
- Any process that reduces the mass of electrically active myocardium (eg, MI, myocardial diseases, cardiac amyloidosis).
- Interposition of air or tissue between the heart and surface electrodes.
- Lung disease—pleural effusion, pneumothorax, emphysema.
- Obesity, myxedema, as well as pericardial effusion.
- Abnormal position of heart within pericardial cavity may result in lack of normal R-wave progression in anterior leads.
- Beat-to-beat alternation of amplitude and direction of QRS (electrical alternans) seen in cardiac tamponade.
- Flattening of T waves and sinus tachycardia (large pericardial effusions with tamponade physiology).
- The slow or normal heart rate seen in myxedema is not present with other etiologies. Even though myxedema may produce large pericardial effusions, cardiac tamponade (electrical alternans) is not seen. Inflammatory changes, such as those of acute pericarditis, depend on the etiology. Idiopathic and neoplastic effusions are not associated with inflammation.
Patterns of ST-segment elevations may be useful in localizing the region of involved myocardium and may suggest the site of occlusion within the coronary arterial tree (Table 102-1).
Table 102-1 Electrocardiographic Changes and Localization of Lesions ||Download (.pdf)
Table 102-1 Electrocardiographic Changes and Localization of Lesions
|Region(s) of Myocardium Affected||Location of Culprit Stenosis or Lesion(s)||Electrocardiographic Changes|
|Anterolateral wall and septum||Proximal left anterior descending artery||ST-segment elevations in leads V1–V6 and limb leads I and aVL with reciprocal ST-segment depressions in limb leads III and aVF|
|Anterior and inferior walls||“Wrap around” left anterior descending artery that extends onto the inferior wall or multivessel disease||ST-segment elevations in leads V1–V6, accompanied by ST elevations in limbs leads II, III, and aVF|
|Inferior||Right coronary or circumflex arteries||ST-segment elevations in limb leads II, III, and aVF (and greater in lead III than lead II), along with elevation in lead V1 suggestive of occlusion of proximal or mid-right coronary artery.|
|Posterior wall||Right coronary or circumflex arteries||ST-segment depressions in leads V1 and V2 with eventual appearance of prominent R waves. Posterior leads V7–V9 (V7, posterior axillary line; V8, posterior scapular line; and V9, left border of spine) may show ST-segment elevations.|
|Right ventricle||Right coronary artery||ST-segment elevations in V1R–V6R (particularly V4R) and limb leads II, III, and aVF, along with reciprocal ST-segment depressions in limb leads I and aVL|
Pathophysiologically, ST-segment elevations do not necessarily signify atherosclerotic plaque rupture and occlusive intraluminal thrombus formation. In fact, transient ST-segment elevations may indicate vasospasm from sympathomimetic effects (Figure 102-4).
55-year-old gentleman with nonobstructive coronary artery disease. Electrocardiogram reveals prominent inferolateral ST-segment elevations, attributed to coronary vasospasm and successfully treated with nitrates and calcium-channel blockade.
When ischemia is primarily subendocardial, ST-segment depressions appear in the overlying leads (Figure 102-5).
When ischemia is subendocardial, ST-segment depressions with or without T-wave inversions may appear, as in this electrocardiogram of a 44-year-old gentleman with obstructive stenoses within the left anterior descending and left circumflex arteries on coronary angiography.
Although hyperacute T waves may precede or accompany ST-segment elevations, inversion of the T wave or pseudonormalization of previously inverted T waves may also indicate ischemia. Deep and symmetrically inverted T waves in the anterior precordial leads, in particular, may indicate high-grade stenosis in the proximal left anterior descending artery, an exception to the rule that leads in which T-wave inversions are present do not correlate with the location of coronary stenoses (in contrast to localization allowed by ST-segment elevations or pathologic Q waves) (Figure 102-6).
Prominent and new T-wave inversions in the anterior precordial leads (a.k.a. Wellen sign) may indicate a high-grade proximal stenosis within the left anterior descending artery. This 70-year-old gentleman had a 90–95% thrombotic and ulcerated obstructive lesion within the left anterior descending artery.
Symmetric giant T waves (amplitude > 10 mm in two or more leads) may be associated with pericarditis, pheochromocytoma, severe aortic insufficiency, myocarditis, and cerebrovascular disease. Commonly inverted in all precordial leads at birth, T waves may remain inverted in the right precordial leads in normal persons in a persistent juvenile pattern. Inversion of the T waves may also be normal in leads III, aVR, and V1.
While a normal ECG throughout the course of an acute infarct is uncommon, the ECG has limited sensitivity and specificity in the diagnosis of acute coronary syndromes. Clinicians should recognize that changes in the ST-segment and T wave are not specific for myocardial ischemia and/or infarction and should, in particular, distinguish the changes associated with acute pericarditis and the normal variant of early repolarization from those seen with myocardial ischemia and infarction. In contrast to the regional ST-segment elevations created by myocardial infarction, acute pericarditis creates diffuse ST-segment elevations, often in the presence of PR segment elevation in aVR and reciprocal PR segment depressions in the other leads (Figure 102-7).
Acute pericarditis creates diffuse ST-segment elevations, often in the presence of PR-segment elevation in aVR and reciprocal PR-segment depressions in the other leads.
Also in contrast to the appearance of T-wave inversions while the ST-segments remain elevated, T-wave inversions in acute pericarditis generally do not develop until the ST-segments have returned to isoelectric baseline. The electrocardiographic signature of early repolarization is ST-segment elevation, especially in the midprecordial leads and more commonly at slow heart rates and among young adult men (Figure 102-8).
The ST-segment elevation of early repolarization may mimic acute ischemia. In contrast to the convexity seen in ST-segment elevations associated with myocardial ischemia, ST-elevations seen with early repolarization are generally concave in form and associated with notching of the R wave at its junction with the QRS complex, as in this tracing from a healthy 23-year-old gentleman. During exercise, the ST-segment elevations of early repolarization may return to baseline.
In contrast to the convexity seen in ST-segment elevations associated with myocardial ischemia, those seen with early repolarization are generally concave in form and associated with notching of the R wave at its junction with the QRS complex. Biphasic T-wave inversions may also accompany the ST-segment elevations seen with early repolarization.
Among patients with acute coronary syndrome, the electrocardiogram also offers utility in the recognition of ischemia-related benign and malignant arrhythmias and postinfarct complications. Accelerated idioventricular rhythm (AIVR) is a regular wide-complex ventricular rhythm, generally at a rate of 50–100.
Ventricular aneurysm may be suggested by ST-segment elevations that persist despite reperfusion.
New left bundle branch block (LBBB) in the setting of symptoms consistent with acute MI may indicate a large, anterior wall acute MI (Figure 102-9).
New left bundle branch block, as shown in this electrocardiogram, may indicate a large, anterior wall acute MI in the appropriate clinical setting.
With preexisting LBBB, the diagnosis of acute STEMI may be obscured, but the presence of the following may be suggestive of acute ischemia: ST-segment elevation ≥1 mm concordant with the QRS complex; ST-segment depression ≥mm in lead V1, V2, or V3; or ST-segment elevation ≥5 mm discordant with the QRS. Right bundle branch block (RBBB) may obscure the diagnosis of an acute anterior MI by interfering with the interpretation of ST-segment elevations in leads V1-3, but the pseudonormalization of the normally discordant T waves (ie, normally opposite the terminal deflection of the QRS complex) may suggest acute ischemia. Because RBBB itself may produce a large R wave in V1, it is generally difficult to diagnose a posterior infarct in the presence of a RBBB.
ECG in pulmonary embolism is clinically helpful mainly in patients with no history of heart or lung disease.
- Sinus tachycardia
- S1Q3T3 pattern
- Right atrial abnormality, right axis deviation, complete or incomplete RBBB
- Left axis deviation, indeterminate axis, S1S2S3, late precordial transition, low-voltage, nonspecific ST-T abnormalities
Negative T waves in precordial leads in an anterior subepicardial ischemic pattern is the most frequent ECG abnormality of massive PE.
While pulmonary embolism frequently may not generate electrocardiographic changes or only subtle nonspecific abnormalities, there are characteristic findings that may indicate right ventricular pressure overload. These electrocardiographic findings may include T wave inversion in V1–V3 or a characteristic S1Q3T3 with an S wave in lead I and new Q waves and T-wave inversions in lead III. Sinus tachycardia is frequently seen, and atrial fibrillation may also be observed (Figure 102-10).
This 47-year-old gentleman presented with dyspnea and had multiple filling defects on contrast-enhanced computed tomography of the chest, consistent with pulmonary emboli. T-wave inversions in the anterior precordial leads are suggestive of right-sided dysfunction, as was confirmed echocardiographically.