ST depression refers to a finding on an electrocardiogram.[1][2]
Measurement[edit]
ST segment depression may be determined by measuring the vertical distance between the patient's trace and the isoelectric line at a location 2[3]-3 millimeters from the QRS complex.
It is significant if it is more than 1 mm in V5-V6, or 1.5 mm in AVF or III.
In a cardiac stress test, an ST depression of at least 1 mm after adenosine administration indicates a reversible ischaemia, while an exercise stress test requires an ST depression of at least 2 mm to significantly indicate reversible ischaemia.[4]
Physiology[edit]
For non-transmural ischemia, the pathophysiological cause of ST depression is a slightly elevated resting potential in myocardial cells, but with the ST segment less affected, as it represents a depolarized state. Still, the resting potential is the reference line in ECG, making it display an apparent ST depression rather than an elevation of the other segments.
Causes[edit]
It is often a sign of myocardial ischemia, of which coronary insufficiency is a major cause. Other ischemic heart diseases causing ST depression include:
- Subendocardial ischemia[5] or even infarction.[3] Subendocardial means non full thickness ischemia. In contrast, ST elevation is transmural (or full thickness) ischemia
- Non Q-wave myocardial infarction[5]
- Reciprocal changes in acute Q-wave myocardial infarction (e.g., ST depression in leads I & aVL with acute inferior myocardial infarction)[5]
Depressed but upsloping ST segment generally rules out ischemia as a cause.
Also, it can be a normal variant or artifacts, such as:
- Pseudo-ST-depression, which is a wandering baseline due to poor skin contact of the electrode[5]
- Physiologic J-junctional depression with sinus tachycardia[5]
- Hyperventilation[5]
Other, non-ischemic, causes include:
- Side effect of digoxin[3][5]
- Hypokalemia[3][5]
- Right or left ventricular hypertrophy[5]
- Intraventricular conduction abnormalities (e.g., right or left bundle branch block, WPW, etc.)[5]
- Hypothermia[3]
- Tachycardia[3]
- Reciprocal ST elevation[3]
- Mitral valve prolapse[5]
- CNS disease[5]
Mnemonic[edit]
DEPRESSED ST ---> D - Drooping valve (MV Prolapse) E - Enlargement of the left ventricle P - Potassium loss R - Reciprocal ST Depression (e.g. Inferior MI) E - Encephalon Hemorrhage S - Subendocardial Infarct S - Subendocardial Ischemia E - Embolism (Pulmonary) D - Dilated Cardiomyopathy S - Shock T - Toxicity (Digitalis/Quinidine)
See also[edit]
ST depression be can caused by stroke (especially subarachnoid haemorrhage) (http://www.gpnotebook.co.uk/simplepage.cfm?ID=597295149)
References[edit]
- ^ Okin PM, Devereux RB, Kors JA, et al. (April 2001). "Computerized ST depression analysis improves prediction of all-cause and cardiovascular mortality: the strong heart study". Ann Noninvasive Electrocardiol 6 (2): 107–16. doi:10.1111/j.1542-474X.2001.tb00094.x. PMID 11333167.
- ^ Okin PM, Roman MJ, Lee ET, Galloway JM, Howard BV, Devereux RB (April 2004). "Combined echocardiographic left ventricular hypertrophy and electrocardiographic ST depression improve prediction of mortality in American Indians: the Strong Heart Study". Hypertension 43 (4): 769–74. doi:10.1161/01.HYP.0000118585.73688.c6. PMID 14769809.
- ^ a b c d e f g madscientist software > MicroEKG Manual Retrieved September 2010
- ^ Yap, L. B.; Arshad, W.; Jain, A.; Kurbaan, A. S.; Garvie, N. W. (2005). "Significance of ST depression during exercise treadmill stress and adenosine infusion myocardial perfusion imaging". The International Journal of Cardiovascular Imaging 21 (2–3): 253–258; discussion 258–60. doi:10.1007/s10554-004-2458-y. PMID 16015437.
- ^ a b c d e f g h i j k l X. ST Segment Abnormalities Frank G. Yanowitz, MD. University of Utah School of Medicine
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