Patients with Wellens syndrome manifest deep, symmetrically inverted T waves in the anterior precordial leads. These T waves are suggestive of a severe stenosis of the proximal left anterior descending coronary artery and, left untreated, can progress to a large anterior ST elevation infarction. Thus, recognition of this syndrome on the ECG is critically important. Severe insult to the central nervous system can cause deep, symmetric T wave inversions on the ECG, usually diffuse rather than limited to one ECG territory.
Prolongation of the QT interval is also seen. These abnormalities are thought to be due to sympathetic discharge from the central nervous system. Specific disease entities associated with cerebral T waves include subarachnoid hemorrhage, massive ischemic stroke, subdural hematoma, and traumatic brain injury.
Medications such as digoxin, class I, and class III anti-arrhythmics, and psychoactive medications can cause T wave inversion as can severe hypokalemia, hypomagnesemia, and hypocalemia. The abnormalities are diffuse rather than localized to a coronary territory. As noted above in the section on tall T waves, left or right ventricular hypertrophy can cause abnormalities of the T wave. Leads that evince t wave inversion are typically the leads with large positive voltage, and the T wave will deflect opposite that of the QRS complex.
Left or right bundle branch block results in abnormal repolarization of the myocardium and can be associated with T wave inversion.
In the setting of right bundle branch block, T wave inversions are expected in leads V1-V3. In the setting of left bundle branch block, the T waves should deflect opposite the major deflection of the QRS for example, one expects T waves to be inverted in leads V6 and 1 if left bundle branch block is present. Later stages of pericarditis can manfest with diffuse T wave inversions on the 12 lead ECG.
The sequence of ECG changes in acute pericarditis evolves over weeks. The initial changes include ST segment elevation that is concave upwards. Subsequently, T wave become inverted.
The ST segment next returns to baseline, leaving diffuse T wave inversions as the isolated abnormality which normalize thereafter. Acute pulmonary embolism large enough to cause right ventricular pressure overload can cause multiple abnormalities on the 12 lead ECG.
This pattern is seen in a minority of pulmonary embolism cases. Septal and anterior T wave inversions can also be associated with large pulmonary embolism and represent an acute right ventricular strain pattern, sometimes with associated right bundle branch block. The most common ECG abnormality seen in pulmonary embolism, however, is simply sinus tachycardia. Finally, hyperventilation can cause deep, reversible ST segment abnormalities.
The diagnostic approach to T wave abnormalities identified on the 12 lead ECG includes first considering the indication for performing the ECG in the first place.
Was the tracing performed to assist in diagnosis of a chest pain syndrome? In response to electrolyte abnormalities noted on the chemistry panel? As a routine screening tracing prior to initiation of a new medication? Each of these indications influences the pre-test probability of the diseases listed above in the differential diagnosis and will affect interpretation accordingly. Second, comparison of the tracing to a prior tracing will provide valuable information as to the chronicity of the abnormalities.
If tall T waves are identified, the presence or absence of chest pain, dyspnea, nausea, diaphoresis, or other symptoms suggestive of an acute myocardial infarction can suggest hyperacute T waves associated with myocardial infarction. The presence of known or suspected renal failure, dialysis dependence, and review of the medication list can service as important clues to the diagnosis of hyperkalemia.
Similarly, if T wave inversions are identified, symptoms of cardiac ischemia should be actively delineated if present. Characteristic history of pleuritic chest pain, or dyspnea, cough, and hemoptysis could suggest pericarditis or pulmonary embolism respectively. Headache or report of new neurologic deficit would implicate cerebral T waves as the cause of the T wave inversions. A review of the medication list and prior serum chemistries, if available, is a valuable diagnostic aid.
The physical examination may be unrevealing or may provide additional clues to the diagnosis. Persistent ST-segment elevation suggests aneurysm formation. Early in the course of AMI, biochemical markers may not be elevated, although this may be changing in the era of highly sensitive troponin assays.
In the early stages of MI, prior to the development of necrosis, the myocardium is suffering from ischemia. Timely revascularization may actually prevent complete infarction and death of the affected portion of the myocardium. Therefore, recognizing ACS early is beneficial because patients have improved outcome the timelier revascularization occurs [3], and delay to reperfusion causes larger infarction size and worse functional outcomes [4]. It is well known that new ST-segment elevation represents complete vessel occlusion and transmural infarct.
However, the STEMI criteria have limited sensitivity in diagnosing coronary artery occlusion [5, 6, 7]. Of course, it is important to recognize an obvious STEMI, but patients may present initially with only subtle ECG changes and minimal ST-segment elevation they may not meet the official criteria. It is true that more ST elevation indicates a larger area of infarcted myocardium, however patients with subtle ST elevation MI experience similar functional outcomes and mortality rates as those with obvious STEMI [10].
Some experts would argue that patients with subtle findings of coronary vessel occlusion should be treated as expeditiously as patients with obvious STEMI [10]. The T-wave is often the first deflection on the ECG to change in acute vessel occlusion. Initial changes to the T-wave are straightening of the ST-segment and enlargement of the T-wave height and width. The T-wave becomes disproportionately large when compared to the QRS. The prominent T-waves seen early in coronary vessel occlusion are called hyperacute T-waves.
They were first described in as an early marker of coronary artery occlusion [2]. Hyperacute T-waves are often bulky, and wide at the base and are localized to an anatomic area of infarct. The widening of the T-wave may also lengthen the QT interval. It must be emphasized that hyperacute T-waves are not necessarily always tall, they may only be relatively large when compared to the R-wave. This means that even a small T-wave can still be hyperacute if paired with a low-voltage QRS.
It is important to note that there is no acceptable universal definition of hyperacute T-waves, but there can be other clues on the ECG. During the development of hyperacute T-waves, there can be associated ST-segment depression in the reciprocal leads.
Notice also the loss of R-wave height throughout the precordium and the how the T-waves are massive in comparison to the QRS complexes. Also, the Q-waves are deepening in the leads V2 and V3. Here is another example of hyperacute T-waves, this time in the inferior leads. This is the ECG of a 75 year-old woman presenting with chest pain:. Notice the large T waves in the inferior leads. The total height of the T-waves is not all that impressive, but when compared to the QRS complexes, especially in aVF, the T-wave is massive.
Her Troponin I came back slightly elevated 0. An interesting variant of hyperacute T-waves are those paired with J-point depression. This causes a T-wave takeoff point that is below the isoelectric line. It was initially postulated that these findings are not dynamic, but rather that they remain static throughout coronary vessel occlusion until the time of reperfusion [15, 16].
Regardless, these patients require immediate reperfusion. For an interesting case of the de Winter T-wave pattern occurring in a patient who initially presented with an obvious anterior STEMI, read this case on Dr.
Another interesting phenomenon of the T-waves is the pseudonormalization in AMI. This occurs when a patient with baseline T-wave inversions presents with acute coronary occlusion. Hyperacute T-waves in these patients manifest as upright T-waves, which may be confused for a normal ECG.
This finding highlights the fact that it is not solely the height, but rather the increase in positive amplitude, that signifies a hyperacute T-wave [2].
It is important to note that this pattern appears when the patient is asymptomatic because this represents a reperfusion pattern on ECG. Type A, the biphasic T-waves, are seen immediately upon reperfusion. As the artery remains open, the T-waves evolve to be more deeply inverted, a Type B pattern.
When the patient becomes symptomatic it is because the vessel re-occludes. When that happens the T-waves become upright pseudonormalization and if it remains occluded, ST-segment elevation will appear.
These lesions are unstable because the vessel can re-occlude at any time and the patient requires revascularization. Perhaps the most well known cause of prominent T-waves is the peaked T-waves seen with hyperkalemia, and they can be confused with the hyperacute T-waves of ACS. The typical progression of ECG changes in hyperkalemia is first the development of peaked T-waves, followed by decreased P-wave amplitude, widening of the QRS complex and finally development of a sine wave.
Here are the typical changes with hyperkalemia. Although the T-waves of early hyperkalemia are very tall and prominent, the key differentiator from hyperacute T-waves is the shape of the T-wave. Hyperacute T-waves are fat and wide with a more blunted peak.
Here is the ECG of a patient with a history of type I diabetes who presented with nausea and vomiting. EMS reported that the patient was in sinus tachycardia with a rate of Notice the very tall, pointy T waves, which have a narrow base and are extremely symmetric. These T-wave inversions are symmetric with varying depth. They may be gigantic 10 mm or more or less than 1 mm.
Negative U-waves my occur when post-ischemic T-wave inversions are present. T-wave inversions may actually become chronic after myocardial infarction. Normalization of T-wave inversion after myocardial infarction is a good prognostic indicator. Please refer to Figure Secondary T-wave inversions — similar to secondary ST-segment depressions — are caused by bundle branch block, pre-excitation, hypertrophy and ventricular pacemaker stimulation.
T-wave inversions that are secondary to these conditions are typically symmetric and there is simultaneous ST-segment depression. Note that the T-wave inversion may actually persist for a period after normalization of the depolarization if it occurs. This is referred to as T-wave memory or cardiac memory.
Secondary T-wave inversions are illustrated in Figure 19 as well as Figure 18 D. T-waves with very low amplitude are common in the post-ischemic period. A biphasic T-wave have a positive and a negative deflection Figure 37, panel C. Thus, a biphasic T-wave should be classified accordingly.
The T-wave vector is directed to the left, downwards and to the back in children and adolescents. This explains why these individuals display T-wave inversions in the chest leads. T-wave inversions may be present in all chest leads. However, these inversions are normalized gradually during puberty. Some individuals may display persisting T-wave inversion in V1—V4, which is called persisting juvenile T-wave pattern.
If all T-waves persist inverted into adulthood, the condition is referred to as idiopathic global T-wave inversion. T-wave progression follows the same rules as R-wave progression see earlier discussion. This article is part of the comprehensive chapter: How to read and interpret the normal ECG. No products in the cart. Sign in Sign up. Search for:. The T-wave: physiology, variants and ECG features.
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