An electrocardiogram (ECG or EKG) is a non-invasive test that records the heart’s electrical activity using electrodes placed on the skin. The machine translates the electrical impulses that trigger each heartbeat into a series of waves and spikes on a graph, providing a visual representation of the heart’s rhythm and function. Analyzing this tracing helps healthcare providers determine if the heart’s electrical system is working correctly. An “abnormal” ECG shows a variation from the standard pattern, indicating an electrical issue, a structural change, or an influence from outside the heart. This result requires further investigation, but it is not a final diagnosis of a specific disease.
Problems with Heart Rhythm and Rate
One of the most frequent reasons for an abnormal ECG involves issues with the heart’s rhythm (arrhythmia) or its speed. The heart’s electrical cycle is initiated by the sinus node, the natural pacemaker, and follows a precise pathway through the heart chambers. Disruptions to this conduction system lead to irregularities in the timing and appearance of the recorded electrical waves.
A heart rate that is too fast, known as tachycardia, generally exceeds 100 beats per minute in adults at rest. This can manifest as ventricular tachycardia, a serious condition where rapid electrical impulses originate in the lower chambers. Conversely, bradycardia occurs when the heart rate is too slow, typically under 60 beats per minute.
Irregular rhythms, where the timing between heartbeats is inconsistent, also produce distinct patterns. Atrial fibrillation (AFib), a common arrhythmia, is characterized by the absence of clear P waves, which represent atrial contraction. The ECG shows an irregularly irregular pattern of QRS complexes, reflecting a breakdown in the organized transmission of electrical signals.
Muscle Damage and Blood Flow Issues
Insufficient blood flow (ischemia) or actual muscle death (myocardial infarction or heart attack) significantly alters the heart’s electrical properties. Damaged heart muscle cannot conduct electricity normally. These changes are often focused on the ST segment and the T wave, which represent the repolarization, or electrical resetting, of the ventricles.
Acute, severe ischemia affecting the full thickness of the heart wall often causes ST segment elevation, indicating an ongoing injury. Less severe ischemia may present as ST segment depression or T-wave inversion, where the T wave points downward. These deviations occur because the affected tissue repolarizes at a different rate than the healthy muscle.
A past heart attack leaves a permanent electrical scar detected as a pathological Q wave. While a normal Q wave is a small, downward deflection, a pathological Q wave is wider and deeper. This represents an electrically silent area of dead tissue that no longer contributes to the recorded electrical activity, helping providers determine a heart attack occurred previously.
Changes in Heart Structure
Chronic physical changes to the heart muscle, particularly the thickening of the walls, can alter the path and magnitude of the electrical signal. The most common example is ventricular hypertrophy, often resulting from long-standing conditions like high blood pressure or valve disease. This increased workload causes the muscle cells to grow larger, increasing the overall mass of the chamber wall.
When the ventricular walls thicken, the larger muscle mass requires a stronger electrical impulse for depolarization. This translates into an increased amplitude, or height, of the QRS complex on the ECG. For instance, left ventricular hypertrophy typically causes taller R waves and deeper S waves, and the electrical axis of the heart may shift.
The thickened muscle can also take longer to depolarize and repolarize, sometimes causing a slight prolongation of the QRS complex duration. The immense strain on the muscle can lead to a secondary “strain pattern,” characterized by ST segment depression and T-wave inversion in the affected area.
Non-Cardiac Causes and External Factors
Not all abnormal ECG results originate from a primary heart problem; various factors outside the heart can significantly disrupt its electrical function. Electrolyte imbalances, particularly involving potassium and calcium, are common external causes. These charged minerals are fundamental to the heart muscle cell’s depolarization and repolarization phases.
For example, high potassium levels (hyperkalemia) cause the T wave to appear tall and peaked, and rising levels progressively widen the QRS complex. Low potassium (hypokalemia) can flatten the T wave and cause a prominent U wave. Imbalances in calcium can affect the QT interval, the time required for the ventricles to fully repolarize.
Certain medications, even non-cardiac drugs, can alter the ECG, most notably by prolonging the QT interval. This prolongation increases the risk of a dangerous arrhythmia called Torsades de Pointes. Systemic diseases also influence electrical activity; severe thyroid disease, for instance, can cause either a fast rate (hyperthyroidism) or a slow rate (hypothyroidism). An acute problem like a large pulmonary embolism can cause a pattern of right heart strain due to the sudden increase in pumping pressure.