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Topics for study:

1. General Introduction to ST-T and U Wave Abnormalities
2. ST Segment Elevation
3. ST Segment Depression

1. General Introduction to ST, T, and U wave abnormalities

 Basic Concept: the specificity of ST-T and U wave abnormalities is provided more by the clinical circumstances in which the ECG changes are found than by the particular changes themselves. Thus the term, nonspecific ST-T wave abnormalities, is frequently used when the clinical data are not available to correlate with the ECG findings. This does not mean that the ECG changes are unimportant! It is the responsibility of the clinician providing care for the patient to ascertain the importance of the ECG findings.

 Factors affecting the ST-T and U wave configuration include:

 Intrinsic myocardial disease (e.g., myocarditis, ischemia, infarction, infiltrative or myopathic processes)

 Drugs (e.g., digoxin, quinidine, tricyclics, and many others)

 Electrolyte abnormalities of potassium, magnesium, calcium

 Neurogenic factors (e.g., stroke, hemorrhage, trauma, tumor, etc.)

 Metabolic factors (e.g., hypoglycemia, hyperventilation)

 Atrial repolarization (e.g., at fast heart rates the atrial T wave may pull down the beginning of the ST segment)

 Ventricular conduction abnormalities and rhythms originating in the ventricles



 "Secondary" ST-T Wave changes (these are normal ST-T wave changes solely due to alterations in the sequence of ventricular activation)

 ST-T changes seen in bundle branch blocks (generally the ST-T polarity is opposite to the major or terminal deflection of the QRS)

 ST-T changes seen in fascicular block

 ST-T changes seen in nonspecific IVCD

 ST-T changes seen in WPW preexcitation

 ST-T changes in PVCs, ventricular arrhythmias, and ventricular paced beats



 "Primary" ST-T Wave Abnormalities (ST-T wave changes that are independent of changes in ventricular activation and that may be the result of global or segmental pathologic processes that affect ventricular repolarization)

 Drug effects (e.g., digoxin, quinidine, etc)

 Electrolyte abnormalities (e.g., hypokalemia)

 Ischemia, infarction, inflammation, etc

 Neurogenic effects (e.g., subarrachnoid hemorrhage causing long QT)

2. Differential Diagnosis of ST Segment Elevation

 Normal Variant "Early Repolarization" (usually concave upwards, ending with symmetrical, large, upright T waves)

 Example #1: "Early Repolarization": note high take off of the ST segment in leads V4-6; the ST elevation in V2-3 is generally seen in most normal ECG's; the ST elevation in V2-6 is concave upwards, another characteristic of this normal variant.

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 Ischemic Heart Disease (usually convex upwards, or straightened)

 Acute transmural injury - as in this acute anterior MI

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 Persistent ST elevation after acute MI suggests ventricular aneurysm

 ST elevation may also be seen as a manifestation of Prinzmetal's (variant) angina (coronary artery spasm)

 ST elevation during exercise testing suggests extremely tight coronary artery stenosis or spasm (transmural ischemia)



 Acute Pericarditis

 Concave upwards ST elevation in most leads except aVR

 No reciprocal ST segment depression (except in aVR)

 Unlike "early repolarization", T waves are usually low amplitude, and heart rate is usually increased.

 May see PR segment depression, a manifestation of atrial injury



 Other Causes:

 Left ventricular hypertrophy (in right precordial leads with large S-waves)

 Left bundle branch block (in right precordial leads with large S-waves)

 Advanced hyperkalemia

 Hypothermia (prominent J-waves or Osborne waves)

3. Differential Diagnosis of ST Segment Depression

 Normal variants or artifacts:

 Pseudo-ST-depression (wandering baseline due to poor skin-electrode contact)

 Physiologic J-junctional depression with sinus tachycardia (most likely due to atrial repolarization)

 Hyperventilation-induced ST segment depression



 Ischemic heart disease

 Subendocardial ischemia (exercise induced or during angina attack - as illustrated below)

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Note: "horizontal" ST depression in lead V6

 ST segment depression is often characterized as "horizontal", "upsloping", or "downsloping"

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Note: "Upsloping" ST depression is not an ischemic abnormality

 Non Q-wave MI

 Reciprocal changes in acute Q-wave MI (e.g., ST depression in leads I & aVL with acute inferior MI)



 Nonischemic causes of ST depression

 RVH (right precordial leads) or LVH (left precordial leads, I, aVL)

 Digoxin effect on ECG

 Hypokalemia

 Mitral valve prolapse (some cases)

 CNS disease

 Secondary ST segment changes with IV conduction abnormalities (e.g., RBBB, LBBB, WPW, etc)