Shown below is an example of an ECG showing tall T waves in V1 seen in Left bundle branch block and left ventricular hypertrophy. Shown below is an EKG demonstrating typical negative T waves post anterior myocardial infarction.
This patient also shows QTc prolongation. Whether this has an effect on prognosis is debated. Copyleft images obtained - courtesy of ECGpedia, [3]. Template:WikiDoc Sources. The American Journal of Emergency Medicine.
PMID Retrieved Japanese Circulation Journal. Pathologic evidence of myocardial damage following acute brain injuries. Heart-Brain Interactions. Critical Care Medicine. Stroke; a Journal of Cerebral Circulation. Vnitr Lek in Czech. Heart Rhythm.
Cookies help us deliver our services. By using our services, you agree to our use of cookies. Namespaces Home Page Discussion. Views Read View source View history Help. T waves can appear tall in the setting of an otherwise normal ECG. This typically occurs in young patients and athletes and manifests as a tall T wave in the anterior precordial leads V2-V4 with an asymmetric base consisting of a gradual upslope and abrupt downslope. Tall T waves in the setting of left ventricular hypertrophy as well as associated conditions giving rise to LVH such as hypertrophic cardiomyopathy and aortic stenosis can have similar morphology with the tall, upright T waves present in leads with dominant negative voltage.
Myocardial ischemia is a common cause of inverted T waves. Inverted T waves are less specific than ST segment depression for ischemia, and do not in and of themselves convey a poor prognosis as compared to patients with an acute coronary syndrome and ST segment depression.
Despite this fact, inverted T waves in the setting of an appropriate clinical history are very suggestive of ischemia. Ischemia can be due to an acute coronary syndrome caused by rupture of an atherosclerotic plaque or due to factors increasing oxygen demand or decreasing oxygen supply such as severe anemia or sepsis.
The acute coronary syndromes associated with inverted T waves include unstable angina and non-ST elevation myocardial infarction, the prime distinction between the two syndromes being the absence or presence of serum biomarkers of myocyte necrosis such as troponin, CK and CK-MB. One particularly important ischemic syndrome associated with inverted T waves is Wellens Syndrome. 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. This occurs because the last cells to depolarize are located in the subepicardial region of the ventricles and these cells have shorter action potentials than found in the subendocardial regions of the ventricular wall. So, although the depolarization of the subepicardial cells occurs after the subendocardial cells, the subepicardial cells undergo phase 3 repolarization before the subendocardial cells.
Therefore, repolarization waves generally are oriented opposite of depolarization waves green versus red arrows in figure , and repolarization waves moving away from a postive recording electrode produce a positive voltage. The T wave is longer in duration than the QRS complex that represents depolarization.
The longer duration occurs because conduction of the repolarization wave is slower than the wave of depolarization.
The reason for this is that the repolarization wave does not utilize the high-velocity bundle branch and purkinje system, and therefore primarily relies on cell-to-cell conduction. Sometimes a small positive U wave may be seen following the T wave not shown in figure at top of page. This wave represents the last remnants of ventricular repolarization. Inverted T waves or prominent U waves indicates underlying pathology or conditions affecting repolarization.
The QT interval represents the time for both ventricular depolarization and repolarization to occur, and therefore roughly estimates the duration of an average ventricular action potential. This interval can range from 0. At high heart rates, ventricular action potentials shorten in duration, which decreases the QT interval. Because prolonged QT intervals can be diagnostic for susceptibility to certain types of tachyarrhythmias, it is important to determine if a given QT interval is excessively long.
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