Ecg what does t wave represent

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This relatively short duration indicates that ventricular depolarization normally occurs very rapidly. This can occur with bundle branch blocks or whenever a ventricular foci abnormal pacemaker site becomes the pacemaker driving the ventricle. Such an ectopic foci nearly always results in impulses being conducted over slower pathways within the heart, thereby increasing the time for depolarization and the duration of the QRS complex. The shape of the QRS complex in the above figure is idealized.

In fact, the shape changes depending on which recording electrodes are being used. The shape also changes when there is abnormal conduction of electrical impulses within the ventricles. The isoelectric period ST segment following the QRS and ending at the beginning of the T wave is the time at which both ventricles are completely depolarized.

This segment roughly corresponds to the plateau phase of the ventricular action potentials. The ST segment is very important in the diagnosis of ventricular ischemia or hypoxia because under those conditions, the ST segment can become either depressed or elevated. The T wave represents ventricular repolarization. Generally, the T wave exhibits a positive deflection.

The reason for this is that the last cells to depolarize in the ventricles are the first to repolarize. 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. 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. Acute ischemia may manifest with signs of heart failure such as an S3, elevated jugular venous pressure, or pulmonary rales.