Sudden cardiac death (SCD) is an unexpected death caused by a loss of heart function. It is different from a heart attack, which is caused by a blockage in the heart’s blood vessels. SCD is an electrical problem where the heart’s signaling system malfunctions, causing it to beat erratically and then stop. The primary tool used to assess the heart’s electrical system is the electrocardiogram (ECG), a non-invasive test that provides a snapshot of the electrical impulses coordinating each heartbeat.
Underlying Causes of Sudden Cardiac Death
The causes of sudden cardiac death fall into two main categories: structural abnormalities and primary electrical disorders. Structural problems alter the heart’s physical form, which can disrupt the flow of electrical signals. Conditions like hypertrophic cardiomyopathy (a thickening of the heart muscle) and arrhythmogenic cardiomyopathy (where muscle is replaced by scar tissue) create an unstable electrical environment that can lead to dangerous rhythms.
Primary electrical disorders, or channelopathies, are different because the heart’s structure may appear normal. The problem lies within the microscopic channels that control the flow of ions in and out of heart cells. When the genes for these channels have mutations, it can lead to conditions like Long QT syndrome or Brugada syndrome, which affect the heart’s ability to reset between beats.
Regardless of the cause, the final pathway for most SCD cases is a life-threatening arrhythmia called ventricular fibrillation. During this event, the heart’s lower chambers (the ventricles) quiver chaotically instead of pumping blood. This disorganized activity means no blood is sent to the brain or other organs, and without immediate intervention, death occurs within minutes.
How an ECG Detects Risk Factors
An electrocardiogram detects the heart’s collective electrical activity through electrodes placed on the skin. Each heartbeat is triggered by an electrical impulse that travels through the heart in a coordinated sequence. This progression of electrical waves is captured by the ECG and translated into a waveform.
The different parts of the ECG trace correspond to specific electrical events. For instance, the P wave represents the electrical activation of the atria, the QRS complex shows the activation of the ventricles, and the T wave marks the recovery phase of the ventricles. The timing and shape of these components are consistent in a healthy heart.
Structural heart diseases and electrical disorders create identifiable deviations in this normal pattern. A scarred area might conduct electricity more slowly, while malfunctioning ion channels can delay the heart’s recovery phase. These changes alter the shape and duration of the ECG trace, indicating a vulnerability to life-threatening arrhythmias.
Specific ECG Patterns Indicating High Risk
Several specific ECG patterns indicate a high risk for SCD:
- Brugada Syndrome: This genetic disorder is identified by an abnormality in the right precordial leads (V1-V3). The “Type 1” pattern shows a “coved” shape where the ST segment is elevated and slopes downward. This pattern is caused by a faulty sodium channel and indicates a risk for ventricular fibrillation, especially during sleep or fever.
- Long QT Syndrome (LQTS): The hallmark is a prolonged QTc interval, which measures the time for the ventricles to contract and recharge. In this genetic condition, the recharging period is abnormally long, leaving the heart vulnerable to a dangerous rhythm. A QTc interval over 460 milliseconds in females and 440 in males is a warning sign.
- Wolff-Parkinson-White (WPW) Syndrome: This is identified by a short PR interval and a “delta wave.” An extra electrical pathway between the atria and ventricles causes the signal to arrive too early (short PR interval). The delta wave is a slurring at the beginning of the QRS complex from this premature activation, which can create a short circuit leading to rapid heart rates.
- Hypertrophic Cardiomyopathy (HCM): While an echocardiogram is needed for diagnosis, the ECG often provides the first clue. Signs include high QRS voltage, reflecting the thickened heart muscle, combined with “strain” patterns like ST-segment depression and T-wave inversions. These findings suggest the heart muscle is overworked, increasing arrhythmia risk.
Screening and Follow-Up Procedures
ECG screening for SCD risk is performed in specific populations, including competitive athletes, individuals with a family history of unexplained sudden death, or people with symptoms like fainting or palpitations. The goal of screening is not to provide a final diagnosis but to identify individuals who warrant further investigation.
An abnormal ECG finding is a risk marker that prompts a more detailed evaluation. A pattern like a long QTc interval does not mean a person will experience SCD, but it signifies their risk is higher than the general population. The result must be interpreted in the context of the individual’s personal and family medical history.
Following an abnormal screening ECG, the next step is a referral to a cardiologist or an electrophysiologist, a specialist in heart rhythms. They will recommend further testing to confirm a diagnosis and assess risk. An echocardiogram is commonly used to visualize the heart’s structure and function, looking for issues like hypertrophic cardiomyopathy.
Other follow-up tests may include a stress test, where the ECG is monitored during exercise, or ambulatory ECG monitoring (like a Holter monitor) that records the heart’s rhythm over 24-48 hours. If an inherited channelopathy is suspected, genetic testing can identify mutations for conditions like Long QT or Brugada syndrome. This evaluation guides treatment, which may include lifestyle changes, medications, or implantable devices.