Reciprocal ST elevation
Bundle Branch Block
The shape of the ST segment & whether the abnormality is localized to leads looking at one area of the heart, often allows the cause of ST depression to be diagnosed.|
Also be a reciprocal ST elevation showing an inverted view of what's happening @ another place in the heart.
ST segment depression is considered significant if the segment is @ least one box below baseline, as measured 2 boxes after the end of the QRS.
As with infarction, the location of the ischemia is reflected in the leads in which the ST depression occurs.
When ST segment depression is transient, it's almost always due to acute myocardial ishemia. Signs of EKG ischemia may come & go fairly quickly like possibly minutes.|
ST segment depression is most specific for ischemia if the segment slopes down from the "J point".
Horizontal or flat STs are also quite suspicious for ischemia. Upsloping ST depression is only about 60% accurate for diagnosing ischemia.
"J point" depression @ the beginning of the QRS complex is not significant if the location of measurement (2 boxes past the QRS) finds the ST segment has risen back to 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 thru the ventricular wall (non-transmural). Subendo infarctions involve small areas of injured tissues, with larger areas of overlying ischemia. These infarctions my show ST depression (rather than elevation) because of the larger areas of ischemia.|
ST depression can also be seen as a "mirror" of what's happening on the other side of the heart. EXample: the inferior leads may show ST depression as a reflection of what's 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 & T-wave abnormalities are commonly seen in leads I,L, & V4-V6.
Right ventricular hypertrophy or acute ventricular strain can produce changes in the right precordial leads, V1-V2.
Left bundle branch block (LBBB)produces ST depression & inverted T-waves in leads I,L,&V5-V6.|
The ST will slope away from the direction of the QRS: a large wide R-wave will have down-sloping ST ending in an inverted T, whicle a deep wide S-wave will have a up-sloping ST ending in an upright T-wave.
OF ST ABNORMALITY:
Patients on digitalis often show mild ST depression....usually <1mm, & produces a scooped appearance. These ST adnormalities are seen in multiple leads.|
Hypothermia & severe hypokalemia (low potassium) routinely cause ST depression in multiple leads. Hypothermia will tend to lenghten all EKG intervals, including PR & QT.
Hypokalemia will often lengthen the PR while shortening the ST segment slightly.
ST depression is called "nonspecific ST abnormality" rather than "ST depression" if the ST are less than 1mm depressed & are accompanied by a normal T-wave.
ST elevation is usually attributed to impending infarction, but can also be due to pericarditis or varient angina.In some healthy young adults, a form of ST elevation can be normal.|
Height of the ST segment is measured @ a point 2 boxes after the end of the QRS complex. St elevation is significate if it exceeds imm in a limb lead or 2mm in a precordial lead.
In transmural infarction, ST elevation will be among the first manifestations.|
ST segment elevation will be seen in those leads involved in impending infarction.
ST elevation decreases as T-wave inversion begins.
ST may remain elevated when ventricular aneurysm develops. ST segment elevation that persists beyond 3 months following MI suggests ventricular aneurysm. ST elevation will be present in about 1/3 of ventricular aneuryms.
Missed diagnoses of impending MI vs aneurysm with acute chest pain is to get a baseline EKG (& use of non-needed thrombolytic drugs).
||ST elevation can be seen in a severe type of ischemia called vasospastic or Prinzmetal's angina. While exercise angina involves the subendocardium, vasospasticangina causes severe transmural loss of blood flow. ST elevation simply indicates injury, whether due to coronary thrombosis with impending infarction, or coronary spasm (Prinzmetal's angina). At this point, the injury is reversible.|
Pericarditis is the inflammation of the space between the pericardial sack & outer surface of the heart which causes widespread ST segment elevation.|
Damage & irritation of the heart's surface produces a "current of injury" in all EKG leads.
Generalized ST elevation, unrelated to the distribution of any coronary artery, implies pericarditis. Must be careful in diagnosing pericarditis from the EKG.
For example, an inferolateral transmural infarction with pre-existing junctional ST elevation in the anterior leads, could produce widespread ST elevation that could be confused with pericarditis.
Later in the course of pericarditis, ST 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.|
T-wave begins early adding elevation to the ST segment.
Usually early repolarization shouws elevation of the J point (junction between the end of the QRS & ST segment) & 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 EKG, but can be seen in limb leads to a lesser degree.
Early repolarization cannot always be differentiated from MI. In the chest pain patient, it's safest to assume ST elevation to be infarction until proven otherwise by reviewing a previous EKG or by obtaining serial EKGs.
T-wave abnormalities can provide added evidence. The T-wave must be considered along with QRS & ST segnment abnormalities.|
Except for hyperkalemia, T-wave abnormality alone is not diagnostic of any particular condition.
T-waves will usually be abnormal in ventricular hypertrophy, LBBB, chronic pericarditis, & in electrolyte abnormality.
Tall, peaked T-waves occur due to hyperkalemia. If the tall T-waves are seen throughout the EKG, 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 MI. The tall T's are due to potassiium leak thru damaged membranes in the area of the infarction.
Infarction if localized.
Acute cerebral disease.
Other cardiac disease.
Flattened & non-specific.
In chronic pericarditis, T-waves show wide-spread inversion, not corresponding to any coronary artery distribution. General inversion of T-waves can be due to an evolving global subendocardial infarct.|
Inverted T-waves are seen during the evolution of MI. 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 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 & V2. The T-wave will be inverted over right heart leads showing evidence of hypertrophy & strain.
LBBB can cause ST depression & inverted T-waves in leads I, L & V5-V6. the T-wave tends to be oriented opposite QRS in LBBB.
Flat T-waves can be seen in many conditions, including ischemia, cardiac scar, evolving infarction, & electrolyte abnormality.
In acute cerebral disease, such as intracranial hemorrhage, elongated or bizzare T-waves may be seen. These Ts are often biphasic or deeply & sharply inverted. The QT interval is often dramatically lengthed (0.5-0.7 seconds).