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.
ecg_12lead004z.gif
click here to view
Ischemic Heart Disease (usually convex upwards, or straightened)
Acute transmural injury - as in this acute anterior MI
ecg_12lead027z.gif
click here to view
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)
ecg_12lead006z.gif
click here to view
Note: "horizontal" ST depression in lead V6
ST segment depression is often characterized as "horizontal", "upsloping", or "downsloping"
ecg_st.gif
click here to view
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)
2007-02-11 17:14:35
·
answer #3
·
answered by Dr.Qutub 7
·
0⤊
0⤋