Patients with chest pain, dyspnea or other symptoms consistent with an acute coronary syndrome (ACS) often do not have an obvious STEMI on their presenting ECG. Sometimes, the initial ECG only shows “nonspecific ST-depressions” or “T-wave abnormalities.”
The differential diagnosis of ST-segment depressions includes acute coronary syndrome (non-STEMI or unstable angina), ST-segment depressions that are reciprocal to a less-obvious STEMI, pulmonary embolism, left ventricular hypertrophy with repolarization abnormalities (strain pattern), digitalis effect, various cardiomyopathies, electrolyte disturbances and other miscellaneous conditions.
ST-segment depressions that are horizontal or downsloping and ST-depressions that are ≥ 0.5 mm in V2–V3 or ≥ 1.0 mm in other leads are most likely due to ischemia. ST-depressions are especially diagnostic of acute ischemia (or non-STEMI) if they are present in two or more contiguous leads or are found in multiple ECG leads or if they are dynamic (appearing or increasing during episodes of chest pain and disappearing during asymptomatic periods). In ischemia, the T-waves may or may not be inverted.
The “digitalis effect” includes a sagging ST-segment depression, said to resemble “Salvador Dalí’s mustache” or the cables of a suspension bridge. Other ECG manifestations of digitalis effect include bradycardia or PR-segment lengthening, reduced-amplitude or even inverted T-waves, QT-interval shortening and the appearance of U-waves.
ST-segment depressions and T-wave inversions are also common in patients with left ventricular hypertrophy (LVH). LVH is recognized by a combination of criteria, including increased QRS amplitude in left-facing limb and precordial leads, left axis deviation, poor R-wave progression, left atrial enlargement and widening of the QRS complex. The “strain pattern” is characterized by ST-segment depressions and T-wave inversions in these high-voltage, left-facing leads. Characteristically in patients with LVH, the ST-segments descend gradually into an inverted T-wave. The inverted T-wave usually has asymmetric limbs with a much sharper terminal upstroke. The ST-segments are frequently elevated in the right precordial leads (V1–V3), leading to overdiagnosis of acute anterior wall STEMI.
The differential diagnosis of T-wave inversions includes: pulmonary embolism; intracranial hemorrhage; myocardial ischemia (coronary T-waves, or Wellens’ syndrome); cardiomyopathies or myocarditis; electrolyte abnormalities, especially hypokalemia; and normal variants.
Ischemic T-wave inversions are classically symmetric. Often, they appear in an anatomic (regional) pattern. Even minor T-wave inversions may be significant if they are disproportionate to the voltage of the QRS complex.
T-wave inversions may signify acute intra-cerebral hemorrhage. Often, the inverted T-waves are wide and bizarre with asymmetric and widely splayed limbs (“grotesque T-wave inversions”). QT prolongation, U-waves and bradycardia are often present.
After sinus tachycardia, T-wave inversions in the right precordial leads (V1, V2 and V3) are the most common ECG abnormality in patients with pulmonary embolism. They correlate with more extensive pulmonary vascular clot burden and acute right ventricular dysfunction. T-wave inversions that appear simultaneously in the anterior and inferior leads are a strong clue to acute pulmonary embolism.
In earlier chapters of this atlas, we covered several important electrocardiographic emergencies, including inferior, anterior and posterior wall ST-elevation myocardial infarctions (STEMIs) and various causes of shortness of breath – in particular, pulmonary embolism, myocarditis and pericardial effusion. In most cases of STEMI, the diagnosis comes quickly: ST-segment elevations are present on the initial ECG; there is a regional (that is, anatomic or coronary vascular) distribution; and usually, the ST-elevations are accompanied by reciprocal ST-segment depressions in the opposite-facing leads.
But these are the easy cases. Frequently, our patients present with chest pain or dyspnea, and the ECG demonstrates only ST-segment depressions or T-wave inversions. How should we respond? Are these ST-segment depressions important? Or are they simply “nonspecific ST-T-wave changes,” signifying nothing? How do we know if there is acute disease?
Emergency and critical care clinicians must have an organized approach to patients who have chest pain, dyspnea or similar symptoms, where the electrocardiogram demonstrates ST-segment depressions or T-wave inversions without clear evidence of a STEMI.
In this chapter, we consider the following causes of ST-T changes: acute coronary syndrome (non-STEMI or unstable angina), ST-segment depressions that are reciprocal to a nonobvious STEMI, pulmonary embolism, left ventricular hypertrophy with repolarization abnormalities (“strain pattern”), digitalis effect, intracranial hemorrhage and electrolyte disturbances (Chan et al., 2005; Pollehn et al., 2001).
We do not consider the myriad case reports of ST-segment deviations and T-wave inversions purportedly caused by cholecystitis, food impaction, pancreatitis, pneumothorax and other miscellaneous conditions.
The various nonischemic causes of ST-segment elevations and prominent (upright) T-waves that masquerade as STEMIs (“coronary mimics”) are considered in Chapter 7.
ST-segment depressions may represent subendocardial ischemia in the region of the myocardium directly beneath the exploring leads. In patients with chest pain, dyspnea or similar symptoms, this is a primary consideration. At the same time, as emphasized throughout this atlas, ST-segment depressions may be reciprocal to a STEMI taking place in a myocardial zone that is anatomically and electrically opposite to the leads with the ST-depressions (Birnbaum, Wilson et al., 2014). Frequently, these ST-segment depressions are the only clue to a STEMI that is otherwise not obvious.
Apart from acute coronary syndromes (unstable angina, non-STEMI and STEMI), the differential diagnosis of ST-segment depressions also includes digitalis effect, left ventricular hypertrophy (with repolarization abnormalities, or “strain”), electrolyte abnormalities and, frequently, “nonspecific ST-segment changes.”
ST-Segment Depressions Reciprocal to an Acute ST-Elevation Myocardial Infarction
Whenever ST-segment depressions are present on the ECG, the most important first step is to verify that these ST-segment depressions are not reciprocal to an acute STEMI, even one that was not at first obvious. Don’t be fooled. As illustrated in Chapters 2, 3 and 4 and throughout this atlas:
ST-segment depressions in leads I and aVL may be early warnings of an inferior wall STEMI;
ST-segment depressions in the inferior leads may signal an early high lateral STEMI; and
ST-segment depressions in precordial leads V1–V4 (maximal in V2–V3) means that an acute posterior wall STEMI, often due to left circumflex artery occlusion, may be present, especially if the T-waves in these leads are “bolt” upright. As highlighted in Chapter 4, Posterior Wall Myocardial Infarction, this is a “STEMI equivalent” and a clear indication for “cath lab activation” (Smith et al., 2002; Pride et al., 2010; Birnbaum, 2014; Nikus et al., 2014; Ayer and Terkelsen, 2014). See Chapter 4 for clues that can help differentiate anterior wall subendocardial ischemia (unstable angina or non-STEMI) from a true posterior wall STEMI.
ST-segment depression in multiple inferior and lateral leads, when accompanied by ST-segment elevations in lead aVR, is also a “STEMI equivalent,” indicating a high likelihood of left main coronary artery obstruction, or its equivalent (Birnbaum, Nikus et al., 2014; Nikus et al., 2014; Nikus et al., 2010).
ST-Segment and T-Wave Changes Due to Ischemia or Non-STEMI
ST-segment depressions and T-wave inversions may be caused by coronary insufficiency in the absence of ST-elevation myocardial infarction. These patients are most likely to have either unstable angina or, if cardiac biomarkers are positive, a non-ST elevation MI (non-STEMI) (Amsterdam et al., 2014). In patients with acute coronary syndromes, ST-segment depressions usually represent subendocardial ischemia; as explained by Nikus, “when ischemia is confined primarily to the subendocardium, the overall ST vector typically faces the inner ventricular layer and the ventricular cavity, such that the surface ECG leads show ST-segment depressions” (Nikus et al., 2010).
Following is a brief summary of the ECG features that are most suggestive of subendocardial ischemia or a non-STEMI (Wagner and Strauss, 2014; Chan et al., 2005; Pollehn et al., 2001; Amsterdam et al., 2014; Smith et al., 2002).
ST-Segment Depressions Indicating Subendocardial Ischemia or Non-STEMI
The ST-segments are horizontal or downsloping;
The ST-segment depressions are present in two or more contiguous leads;
The ST-segment depressions are ≥ 0.5 mm in V2–V3 or ≥ 1 mm in other leads;
But lesser degrees of ST-segment depression or T-wave inversion may have diagnostic importance if they are large relative to a small-amplitude R-wave;
The T-waves may or may not be inverted.
As emphasized repeatedly, before diagnosing ischemia or non-STEMI, it is critical to verify that the ST-segment depressions are not reciprocal to a subtle posterior, inferior, lateral or other STEMI.
T-Wave Inversions Indicating Subendocardial Ischemia or Non-STEMI
When present, the T-wave inversions are symmetric;
The T-wave inversions, even if minor-appearing, are disproportionate to the low amplitude of the QRS complex; and
The T-wave inversions are especially diagnostic if LVH is not present.
T-wave inversions may also occur during the evolutionary phase of acute STEMI. As described in Chapter 3, the T-waves are often tall and upright (hyperacute) in the first minutes of a STEMI, but they typically become inverted later, frequently while the ST-segments are still elevated1 (Goldberger, 2006; Hayden et al., 2002; Goldberger, 1980).
As noted earlier, the ST-segment depressions and T-wave inversions summarized previously are especially diagnostic of an acute coronary syndrome if they are present in two or more contiguous leads. At the same time, ischemia-induced ST-segment depressions and T-wave inversion may be diffuse and not limited to a single anatomic region (Chan et al., 2005; Pollehn et al., 2001). Studies have shown that the sum of all the ST-segment depressions, across the entire ECG, is linearly related to the odds of early mortality in patients with an acute coronary syndrome (Smith et al., 2002).
These ST-T-wave changes are more likely to represent an acute coronary syndrome when they are dynamic, appearing or increasing during episodes of chest pain and abating during asymptomatic periods.
In general, acute coronary syndromes manifested only by ST-segment depressions or T-wave inversions are not an indication for routine, emergent thrombolysis. That is, unless the ST-segment depressions represent posterior wall STEMI or another “STEMI equivalent,” as summarized in Chapter 3 and later in this chapter.
Risk stratification of patients with possible acute coronary syndromes begins on presentation to the emergency department (or even in the prehospital setting) (Amsterdam et al., 2014). The following clinical and electrocardiographic findings are indicative of a patient at higher risk of early complications such as continuing angina, infarction, arrhythmias or death: an “unstable” or “up-tempo” pattern of chest pain (pain that is frequent, prolonged or occurring at resting or with minimal exertion); dynamic ST-T-wave changes (occurring or more pronounced with pain); ST-depressions in ≥ 3 leads; transient hypotension, ventricular ectopy, mitral insufficiency or signs of congestive heart failure; and an elevated troponin level. These unstable angina/NSTEMI patients are typically good candidates for aggressive medical therapy and, if indicated, early angiography.
ST-Segment Depressions Due to Digitalis Effect
Digitalis, at therapeutic levels, causes a unique pattern of ST-segment depression known as the “digitalis effect.” The depressed ST-segment has a sagging, upwardly concave, or scooped out, appearance that is said to resemble the cables of a suspension bridge or “Salvador Dalí’s mustache” (see Figure 6.1). The T-wave may be upright, biphasic or inverted. Even at therapeutic doses, digitalis decreases sinus node automaticity and AV nodal conduction, and it may enhance AV junctional automaticity. Prominent U-waves and prolongation of the PR-segment may appear in patients with therapeutic levels of digitalis. Shortening of the QT interval and reduction in the T-wave amplitude are also common in the presence of therapeutic digoxin levels (Chan et al., 2005; Surawicz and Knilans, 2008; Delk et al., 2007; Ma et al., 2001; Hayden et al., 2002; Pollehn et al., 2001).
Figure 6.1 Digitalis effect on the ECG.
The depressed ST-segment has a sagging, upwardly concave, or scooped out, appearance that is said to resemble the cables of a suspension bridge (or “Salvador Dalí’s mustache”). The T-wave may be upright, biphasic or inverted.
Digitalis effect may be differentiated from ischemia-induced ST-segment depressions in the following manner:
In the setting of digitalis, the ST-segments are scooped or sagging (“Salvador Dalí’s mustache” or the suspension bridge cables) with an upward concavity; the ST-depressions are most apparent in left-side leads with tall R-wave amplitude; and the QT-interval is often shortened.
The ST-segment depressions caused by ischemia are likely to be flat or downsloping, often (but not always) with symmetric T-wave inversions. Ischemic T-wave inversions are usually found in a regional (anatomic) pattern; often, in ischemia, there is QT-segment prolongation (Pollehn et al., 2001).
The ECG manifestations of digitalis toxicity are quite different and may include both excitatory as well as inhibitory findings. The excitatory effects include accelerated junctional rhythms, atrial tachycardia with block, ventricular ectopy, ventricular tachycardia and bidirectional ventricular tachycardia (Yang et al., 2012; Surawicz and Knilans, 2008; Chan et al., 2005; Delk et al., 2007; Ma et al., 2001). Inhibitory effects include sinus bradycardia, AV nodal block and slowing and regularization of the ventricular response in atrial fibrillation.
Examine ECG 6.1 for an example of the “digitalis effect.”
ECG 6.1 A 65-year-old female presented to the emergency department after a mechanical fall.
The sagging, scooped and upwardly concave ST-segments (best seen in lead II and precordial leads V4–V6) are classic findings of digitalis effect. They resemble “Salvador Dalí’s mustache.”
There is no AV nodal block, ventricular ectopy, bradycardia, junctional rhythms or other ECG indication of a supra-therapeutic level of digitalis.
Her serum digoxin level was 1.3. There was no evidence of an acute coronary syndrome or other acute medical emergency.
ST-Segment Depressions Accompanying Left Ventricular Hypertrophy
Left ventricular hypertrophy (LVH) appears commonly on routine electrocardiograms and in patients presenting with chest pain, dyspnea and other cardiovascular complaints. LVH usually represents chronic volume or pressure overload, caused by systemic hypertension, heart failure or valvular heart disease. Frequently, left ventricular hypertrophy is accompanied by ST-segment depressions and T-wave inversions. The combination is referred to as “LVH with repolarization abnormalities” or, formerly, “LVH with strain.”
The “LVH with strain” pattern is a major reason for confusion and misdiagnosis. LVH is a common cause of over-diagnosis of STEMI and false-positive “cath lab activation” in patients with chest pain (Chan et al., 2005; Ayer and Terkelsen, 2014). In some studies, 30 percent of patients presenting to emergency departments with chest pain have LVH on their presenting ECGs (Chan et al., 2005). And, of course, electrocardiographic evidence of LVH is a risk factor for symptomatic coronary artery disease, development of congestive heart failure and premature death.
The problem for emergency and critical care clinicians is that the ECG pattern of “LVH with repolarization abnormalities” can masquerade as acute ischemia, anteroseptal STEMI, Wellens’ warning and other acute coronary syndromes. And ECGs that demonstrate LVH, if not interpreted carefully, can just as easily hide an acute STEMI.
There are numerous published criteria and scoring systems for making the electrocardiographic diagnosis of left ventricular hypertrophy (Hancock et al., 2009; Surawicz and Knilans, 2008; Goldberger, 2006; Wagner and Strauss, 2014). Table 6.1 lists some of the commonly accepted QRS voltage criteria for LVH in the left column and other signs (repolarization abnormalities, left axis deviation, left atrial enlargement and others) in the right column.
The published diagnostic criteria for LVH have variable sensitivity and specificity for detecting LVH (compared with the gold standard of echocardiography or magnetic resonance imaging), and they also have varying ability to predict later cardiovascular complications (Hancock et al., 2009). For example, the precordial lead voltage criteria are much less specific for LVH in patients less than 35 years of age. Gender, race, body habitus, and, of course, lead placement also affect QRS amplitudes measured on the routine ECG (Wagner and Strauss, 2014; Goldberger, 2006).
However, the accuracy of the LVH scoring criteria is not our concern in emergency and critical care settings. Detecting LVH with optimal sensitivity and specificity is not the critical issue. Rather, what is important is that the ECG findings of “LVH with repolarization abnormalities” have to be differentiated from acute coronary syndromes and other cardiorespiratory emergencies. In addition, LVH and the “strain pattern” can hide acute STEMIs and other emergencies. For these reasons, treating physicians must be adept at determining whether “LVH with repolarization abnormalities” is the only abnormality – no matter what the ECG computer algorithm says.
For the most part, these ECG manifestations of LVH are easily explained. When left ventricular hypertrophy develops, the increased mass of the left ventricle rotates in a more leftward and posterior direction. Thus, (a) the QRS voltage is increased in the leftward-facing leads (I, aVL and V5–V6); (b) there is often poor R-wave progression; (c) the QRS voltage in lead V6 may be taller than the voltage in V5 (This abnormal finding is similar to the bedside observation that the point of maximal impulse [PMI] is shifted leftward and posteriorly); (d) the QRS duration is slightly widened, reflecting slower conduction through the thicker left ventricle; and (e) left atrial enlargement and left axis deviation are often present.
The ST-T-wave abnormalities (“strain pattern”) represent repolarization changes brought on by left ventricular pressure overload (Wagner and Strauss, 2014; Surawicz and Knilans, 2008; Hayden et al., 2002; Pollehn et al., 2001; Demangone, 2006).
A Closer Look at the “Strain Pattern”
When a patient’s ECG demonstrates voltage criteria for LVH plus ST-segment depressions and T-wave inversions, the explanation might be “LVH with repolarization abnormalities” (the “strain pattern”). Or the patient might have LVH plus an acute coronary syndrome. How do we differentiate one from the other?
To get to the right diagnosis, we first need to appreciate the classic pattern of the repolarization abnormalities associated with LVH. Examine Figure 6.2.
Figure 6.2 Differentiating LVH with repolarization abnormalities from ischemia.
In Figure 6.2, the first complex (A) demonstrates changes that are typical of myocardial ischemia (unstable angina or a non-STEMI). The ST-segment is normal in this example. However, flat or downsloping ST-segments are also commonly seen. The T-wave is symmetrically inverted. In patients with acute coronary syndromes, the ST-segment abnormalities and symmetric T-wave inversions are usually seen in a regional distribution (for example, in the anterior or inferior leads), although they may be “global,” present in multiple leads. The ST-T-wave changes are often dynamic, coming and going with changes in the patient’s chest pain or other symptoms. Patients with acute coronary syndromes may also have ST-segment depressions with upright (normal) T-waves.
Complex B depicts the strain pattern (repolarization abnormalities) due to LVH. The hallmark is the presence of inverted T-waves with asymmetric limbs (Nable and Lawner, 2015). As described by Grauer and Curry, “The typical repolarization abnormalities of strain consist of ST-segment depression with asymmetric T-wave inversions, in which the gradual descent of the sagging ST segment blends imperceptibly with the first portion of the T-wave. The final ascending portion of the T wave has a much more rapid upslope as it returns to the baseline” (Grauer and Curry, 1987). The ascent of the T-wave may even “overshoot” the baseline of the ST-segment (Chan et al., 2005).
In LVH with strain, the T-wave is always inverted in association with the descending ST-segments. The ST-segment depressions should only be seen in the same left-facing leads (I, aVL, V5 and V6) where the QRS amplitude is abnormally large (Chan et al., 2005; Demangone, 2006).
The diagnosis of “LVH with strain” is more likely if left atrial enlargement, left axis deviation, poor R-wave progression and QRS widening are present. It goes without saying that ST-segment depressions and T-wave inversions should not automatically be attributed to “LVH and repolarization abnormalities” unless the left-sided leads show increased QRS voltage consistent with LVH. Furthermore, every effort should be made to compare the presenting ECG with prior tracings; “LVH with repolarization abnormalities” is stable over time.
ECG 6.2 illustrates classic findings of “LVH with repolarization abnormalities.”
ECG 6.2 A 57-year-old female presented to the emergency department with shortness of breath.
The electrocardiogram does not explain the patient’s presenting complaint of shortness of breath. All of the changes in this ECG are consistent with “left ventricular hypertrophy with repolarization abnormalities.” For example, the left-facing limb lead voltage (leads I and aVL) is abnormally high (> 11 mm); the precordial lead voltage is also increased (for example, the sum of the S-wave voltage in lead V1 or V2 + the R-wave voltage in V5 or V6 is more than 35 mm); there is poor R-wave progression; left axis deviation is present; there is left atrial enlargement; and there is a classic strain pattern in leads I, aVL, V5 and V6 manifested by a downsloping ST-segment that blends into the inverted T-wave. As expected, the T-wave is inverted in an asymmetric fashion: the descending limb is gradual, the ascending limb is sharp, and the ascending limb even overshoots the baseline before it finally becomes electrically neutral.
Also, notice that the ST-segments are elevated in leads V2 and V3; these right precordial ST-segment elevations are probably reciprocal to the ST-segment depressions in leads V5 and V6, which, in the letting of LVH, are actually posterior, as well as lateral, leads. Not uncommonly, the ST-segments are elevated enough in leads V2 and V3 that they may suggest an acute anterior wall ST-elevation myocardial infarction.
LVH Can Resemble Anteroseptal Infarctions (and Wellens’ Syndrome)
When LVH and repolarization abnormalities are present on the ECG, it makes everything more difficult. The ST-segment depressions and T-wave inversions in the lateral precordial leads (V5 and V6) are often matched by ST-segment elevations in the right-sided precordial leads (especially V2 and V3). Often, there is poor R-wave progression or frank loss of the initial R-waves in the anteroseptal leads. The ECG may suggest acute anteroseptal STEMI, old anteroseptal infarction, Wellens’ warning or a variety of other abnormalities (Chan et al., 2005). The bottom line is that, in the presence of LVH with repolarization abnormalities, the ECG becomes much less specific. Consider the following case (ECG 6.3).
ECG 6.3 A 56-year-old female with diabetes and chronic hypertension presented with atypical chest pain.
The ECG demonstrates voltage criteria for LVH in the limb leads. (The R-wave voltage is > 11 mm in leads I and aVL.) The increased voltage in the precordial leads (the S-wave in V2 and R-wave in V5) also meets criteria for LVH. ST-segment depressions and T-wave inversions are present in the left-facing leads.
In leads I and aVL, the ST-segment depressions and T-wave inversions have the classic appearance of the strain pattern. However, the T-wave inversions in leads V5 and V6 are more symmetric, suggesting the possibility of cardiac ischemia. This is especially significant since the T-wave inversions in V4–V6 are not accompanied by any downsloping ST-segment depressions. An acute coronary syndrome is suggested.
Perhaps the most striking ECG abnormality is the presence of ST-segment elevations in leads V2 and V3, with terminal T-wave inversions, a pattern that is indistinguishable from Wellens’ warning of impending (or recently reperfused) LAD occlusion.
The entire ECG is concerning for Wellens’ warning and an early or impending STEMI, but it is also consistent with chronic, stable LVH and strain. In this case, all of the limb and precordial lead ST-T abnormalities were unchanged from prior tracings. Thus, the ECG represents a “false positive.”
How might one approach a patient with chest pain and a similar ECG? If the history is especially concerning for an acute STEMI, then consideration of emergent reperfusion therapy is appropriate. In many other cases, it may be helpful to use other diagnostic tools, including: comparison with old ECG tracings; frequent, serial ECGs and troponin levels; and an emergent echocardiogram, to rule in, or rule out, regional wall motion abnormalities (Amsterdam et al., 2014).
These are challenging cases, especially when the presenting symptoms are vague or have resolved. The best strategy may be to analyze the ECG carefully, recognize that many of the changes that normally point to a STEMI are not specific in the presence of LVH and strain, admit we don’t know for sure and consult with the interventional cardiology team.
The patient was admitted for observation. Old, baseline ECGs were obtained, which showed identical ST- and T-wave changes. There were no serum troponin elevations.
It is easy to see why “LVH with repolarization abnormalities” is such a common cause of false positive “cath lab” activations.
The T-wave is a reflection of ventricular repolarization. The differential diagnosis of T-wave inversions is broad and includes an array of cardiac and noncardiac conditions (Hayden et al., 2002; Smith et al., 2002; Goldberger, 1980).
Normal T-Wave Inversions
T-wave inversions may be normal in leads with negative QRS complexes (aVR, III, V1 and sometimes aVL) (Goldberger, 2006). Some young patients have large T-wave inversions in the right precordial leads (V1, V2 and V3). In some individuals the T-wave inversions persist into adulthood (the “persistent juvenile T-wave pattern”) (Hayden et al., 2002; Goldberger, 2006; Goldberger, 1980). In some patients, inverted or biphasic T-waves may appear in the right precordial leads, along with ST-segment elevations in a pattern that resembles Wellens’ syndrome or an acute anterior wall STEMI; this pattern is more common in athletes and young African American men, and it often disappears with exercise or other sympathetic stimulation (Hayden et al., 2002; Smith et al., 2002). T-wave inversions are also expected in patients with a right or left bundle branch block (secondary T-wave inversions), following premature ventricular contractions, in ventricular-paced rhythms, during or following tachycardias, in patients with the Wolff-Parkinson-White syndrome and in other cardiac and noncardiac conditions.
In emergency and critical care practice, it is important to consider the following conditions that may present with abnormal T-wave inversions.