ST segment depression can be caused by ischemia, digitalis, rapid heart rate, and temperature or electrolyte abnormality. It can also be a reflected or reciprocal ST elevation (showing an inverted view of whats happening at another place in the heart). The shape of the ST segment, and whether the abnormality is localized to leads looking at one area of the heart, often allows the cause of ST depression to be diagnosed.
When ST segment depression is transient, its almost always due to acute myocardial ischemia. The ECG signs of ischemia may come and go fairly quickly over a matter of minutes.
ST segment depression is MOST specific for ischemia if the ST segment slopes down from the J point. Horizontal or flat STs are also quite suspicous for ischemia. Upsloping ST depression is only about 60% accurate for diagnosing ischemia.
J point depression at the beginning of the QRS complex is not significant if the location of measurement (two boxes past the QRS) finds the ST segment has risen back to the baseline.
ST depression can also be seen in infarction, typically in non Q-wave infarction, often called subendocardial infarction. This type of infarct does not extend through the ventricular wall (non-transmural). Subendocardial infarctions involve small areas of injured tissue, with larger areas of overlying ischemia. These infarctions may show ST segment depression (rather than elevation) because of the larger areas of ischemia.
ST depression can also be seen as a mirror of whats happening on the other side of the heart. For example, the inferior leads may show ST depression as a reflection of whats happening in the upper lateral side of the heart.
Left ventricular hypertrophy or strain commonly causes ST segment depression, often with T wave inversions. These changes are seen in the lateral leads those that record activity over the left ventricle. In LVH, ST and T wave abnormalities are commonly seen in leads I, L, and V4-V6.
Right ventricular hypertrophy or acute ventricular strain can produce changes in the right precordial leads, V1 and V2.
Left bundle branch block produces ST depression and inverted T waves in leads I, L, and V5-V6. In general, the ST will slope away from the direction of the QRS: a large wide R wave will have a down-sloping ST ending in an inverted T, while a deep wide S wave will have an upsloping ST segment ending in an upright T.
Patients on digitalis often show mild ST depression. This depression is usually less than 1 mm, and produces a scooped appearance the Salvador Dali mustache ST. These ST abnormalities are seen in multiple leads.
Hypothermia and severe hypokalemia routinely cause ST segment depression in multiple leads. Hypothermia will tend to lengthen all ECG intervals, including the PR and QT, while hypokalemia will often lengthen the PR while shortening the ST segment slightly.
ST segment elevation is usually attributed to impending infarction, but can also be due to pericarditis or vasospastic (variant) angina. In some healthy young adults, a form of ST elevation can be normal.
In transmural infarction, ST segment elevation will be among the first manifestations. The ST segment elevation will be seen in those leads involved in impending infarction.
ST segment elevation decreases as T wave inversion begins. ST segments may remain elevated when ventricular aneurysm develops.
ST segment elevation that persists beyond three months following myocardial infarction suggests ventricular aneurysm. ST elevation will be present in about 1/3 of ventricular aneurysms. When the patient with ventricular aneurism presents with acute chest pain, a baseline ECG may help avoid misdiagnosis of impending infarction (and use of non-needed thrombolytic drugs).
ST segment elevation can be seen in a severe type of ischemia called vasospastic or Prinzmetals angina. While exercise angina involves the subendocardium, vasospastic angina causes severe transmural loss of blood flow. ST elevation simply indicates injury, whether due to coronary thrombosis with impending infarction, or coronary spasm (Prinzmetals angina). At this point, the injury is reversible.
Pericarditis, an inflammation of the space between the pericardial sack and outer surface of the heart, causes widespread ST segment elevation. Physical damage and irritation of the hearts surface produces a current of injury in virtually all ECG leads.
Later in the course of pericarditis, ST segment elevation resolves, without development of Q waves. After days to months, ST elevation is replaced by widespread T wave inversions.
Early repolarization is a cause of ST elevation. This innocent condition typically occurs in young healthy males. The T wave begins early, adding elevation to the ST segment.
Usually, early repolarization shows elevation of the J point (the junction between the end of the QRS and the ST segment) and a concave upward curve towards the T wave. (Concave upward means the hollow portion of the curve is on top.)
Early repolarization is usually seen in the anterior precordial leads of the ECG, but can be seen in limb leads to a lesser degree.
T wave abnormalities can provide added evidence to support clinical diagnosis. Except for hyperkalemia, T wave abnormality alone is not diagnostic of any particular condition. The T wave must be considered along with QRS and ST segment abnormalities. T waves will usually be abnormal in ventricular hypertrophy, left bundle branch block, chronic pericarditis, and in electrolyte abnormality.
Tall, peaked T waves occur due to hyperkalemia. If the tall T waves are seen throughout the ECG, general hyperkalemia is present. P waves will be small, PR interval short.
When typical tall, peaked T waves are seen only within a specific set of cardiac leads, it suggests impending infarction. The tall Ts are due to potassium leak through damaged membranes in the area of the infarct.
In chronic pericarditis, T waves show wide-spread inversion, not corresponding to any coronary artery distribution. General inversion of T waves can also be due to an evolving global subendocardial infarct.
Inverted T waves are seen during the evolution of myocardial infarction. The T inversion appears in the leads looking at the infarcted area. Several hours after an infarct, T waves begin to invert. T wave inversion may persist for months.
Left ventricular hypertrophy or strain commonly causes T wave inversion. In strain pattern, the ST segment slopes down to an inverted T in the leads looking at the affected ventricle.
Right ventricular hypertrophy or acute ventricular strain can produce changes in the right precordial leads, V1 and V2. The T wave will be inverted over right heart leads showing evidence of hypertrophy and strain.
Left bundle branch block can cause ST depression and inverted T waves in leads I, L, and V5-V6. The ST depression is usually not great. The T wave tends to be oriented opposite the QRS in LBBB.
Flat T waves can be seen in many conditions, including ischemia, cardiac scar, evolving infarction, and electrolyte abnormality (such as hypokalemia).
In acute cerebral disease, such as intracranial hemorrhage, elongated or bizzare T waves may be seen. These Ts are often biphasic or deeply and sharply inverted. The QT interval is often dramatically lengthened (0.5 to 0.7 seconds). [Chapter Menu]
All material referenced through this menu is excerpted from copyrighted works by Bruce Argyle, MD. You are welcome to use selected portions, as long as appropriate credit is given. The credit for the text referenced through this menu is:
Copyright© Mad Scientist Software Inc. All rights reserved.