ST depression, a finding on an electrocardiogram (EKG), refers to a downward shift of the tracing segment connecting the heart ventricles’ electrical contraction to their recovery phase. This deviation is common, but its meaning is highly variable. While it can signal a serious cardiac event, ST depression can also occur in healthy individuals. Determining if the finding is “normal” requires careful evaluation of the patient’s symptoms, medical history, and the EKG tracing characteristics.
Understanding ST Segment Deviation
The ST segment represents the period on the EKG between the completion of ventricular depolarization (contraction) and the start of ventricular repolarization (electrical recovery). Normally, this segment should be isoelectric, resting on the baseline of the EKG tracing. The point where the QRS complex ends and the ST segment begins is called the J-point.
ST depression is measured as the vertical distance of the J-point below the established baseline, often the PR or TP segment. A depression of \(0.5\) millimeters or more below the baseline in at least two adjacent leads is considered a significant finding. The specific shape, or morphology, of the depressed segment is a crucial factor in determining its clinical importance.
The morphology of the ST depression is classified into three types: upsloping, horizontal, or downsloping. An upsloping segment dips down but quickly rises back toward the baseline before the T-wave begins. A horizontal depression maintains a level path below the baseline, while a downsloping depression continues to angle downward. Horizontal or downsloping patterns are much more commonly linked to serious conditions than upsloping ones.
Pathological Causes Linked to Heart Disease
The most serious consideration when ST depression is present is myocardial ischemia, a mismatch between the heart muscle’s oxygen supply and demand, often due to coronary artery disease. This finding is especially concerning when the depression is horizontal or downsloping, correlating strongly with insufficient blood flow to the inner heart wall (subendocardial ischemia). A depression of \(0.5\) millimeters or more in two or more contiguous leads is a widely accepted threshold for indicating myocardial ischemia.
Horizontal or downsloping ST depression is a primary indicator for diagnosing Non-ST-Elevation Myocardial Infarction (NSTEMI) or unstable angina, both forms of acute coronary syndrome. When accompanied by symptoms like chest pain, shortness of breath, or fainting, this EKG finding suggests a high probability of an ongoing heart attack. ST depression can also appear as a reciprocal change in leads opposite to the location of a significant ST elevation myocardial infarction (STEMI).
ST depression can also be a secondary finding in other serious cardiac conditions caused by structural issues. Severe left ventricular hypertrophy, where the main pumping chamber is thickened, can cause secondary ST depression and T-wave changes. Very fast heart rhythms (tachycardias) can also cause transient ST depression due to increased oxygen demand.
Functional and Non-Cardiac Factors
ST depression is frequently observed in healthy individuals, particularly during periods of increased heart rate, making the distinction from disease challenging. The most common “normal” cause is physical exercise or a high heart rate (tachycardia). During a stress test, a benign upsloping ST depression is often seen. This depression is typically less than \(1\) millimeter and rapidly resolves within the first few minutes after exercise stops.
This exercise-induced upsloping depression is often called J-junctional depression because it is confined to the J-point. It is not considered a positive sign for ischemia unless the depression is slow-rising, significant, or persists into the recovery phase. Hyperventilation, often occurring during panic or anxiety, can also produce a similar benign EKG pattern.
Non-cardiac conditions and medications can also cause ST depression unrelated to coronary artery blockages. An imbalance of electrolytes, particularly low potassium (hypokalemia), can alter the heart’s electrical recovery. Additionally, the heart medication digitalis, used for heart failure and rhythm problems, characteristically causes a scooped or concave-shaped ST depression, known as the “digitalis effect.”
Interpreting Results and Next Steps
The clinical interpretation of ST depression requires a thorough correlation with the patient’s overall clinical picture, including symptoms and medical history. The presence of symptoms such as active chest pain, profuse sweating, or significant shortness of breath alongside ST depression warrants an immediate medical evaluation to rule out acute ischemia. If symptoms are absent, a physician will investigate potential non-ischemic causes, such as medication use or electrolyte abnormalities.
A standard next step for unexplained ST depression is often a cardiac stress test, using exercise or pharmacological agents to increase the heart’s workload. This test determines if the ST depression is load-dependent, suggesting underlying coronary artery disease, or if it is a benign, functional response to a high heart rate. If the EKG changes resolve quickly after the heart rate normalizes, or if the depression is mildly upsloping, it is less likely to indicate significant heart disease.
If the ST depression is a secondary effect of an underlying condition, such as ventricular hypertrophy or a medication, the focus shifts to managing the primary cause. For example, correcting hypokalemia may resolve the EKG abnormality. Patients without symptoms who have mild, isolated ST depression should follow up with their primary care provider for ongoing monitoring.