Sudden cardiac death (SCD) is an abrupt loss of heart function in a person who may or may not have diagnosed heart disease. The event stems from an electrical disturbance within the heart that disrupts its pumping action, stopping blood flow to the brain and other organs. This is different from a heart attack, which is a circulatory or “plumbing” problem caused by a blockage. SCD, in contrast, is an “electrical” problem, though a heart attack can damage the heart muscle and subsequently trigger a lethal electrical malfunction.
Underlying Causes
The direct cause of sudden cardiac death is an abnormal heart rhythm, or arrhythmia. The most common life-threatening arrhythmia is ventricular fibrillation (VF), where the heart’s lower chambers quiver chaotically instead of pumping blood. This disorganized electrical activity stops blood delivery to the body, and death occurs within minutes without intervention. Ventricular fibrillation is triggered by pre-existing heart conditions that create an unstable electrical environment.
The leading underlying cause is coronary artery disease (CAD), responsible for about 80% of SCD cases. In CAD, arteries that supply blood to the heart are narrowed or blocked, which can lead to a heart attack. A heart attack can damage the heart muscle, creating scar tissue that disrupts the normal flow of electrical impulses and makes dangerous arrhythmias more likely. The risk of SCD is higher during the first six months following a heart attack.
Structural heart problems are another contributor. Cardiomyopathies, diseases of the heart muscle, can make the heart prone to electrical instability. For example, hypertrophic cardiomyopathy (HCM) is a genetic condition causing the heart muscle to become abnormally thick, which can interfere with its electrical system. This condition is a leading cause of SCD in young athletes, and other issues like congenital heart defects can also set the stage for fatal arrhythmias.
A smaller percentage of SCD cases arise from primary electrical disorders in a structurally normal heart. These conditions, known as channelopathies, are inherited genetic defects affecting the function of ion channels—the microscopic pores in heart cells that control electrical signals. Conditions like Long QT syndrome and Brugada syndrome fall into this category, causing disturbances that can lead to ventricular fibrillation.
Identifying At-Risk Individuals
The most significant risk factor is a previous heart attack, as about 75% of SCD cases are linked to one. The presence of coronary artery disease, even without a full-blown heart attack, is also a major predictor.
A clinical indicator of risk is the heart’s ejection fraction (EF), which measures the percentage of blood pumped out of the main chamber with each beat. A low ejection fraction, 35% or less, signals a weakened heart muscle that is more susceptible to life-threatening rhythms. People with heart failure, a condition characterized by low EF, are six to nine times more likely to experience ventricular arrhythmias that can lead to SCD.
Family history is an important risk factor. A history of sudden cardiac death in a close relative, like a parent or sibling, can indicate an inherited predisposition from conditions like hypertrophic cardiomyopathy or Long QT syndrome. Unexplained fainting spells (syncope) can also be a warning sign of an undiagnosed heart rhythm disorder.
Lifestyle and external factors also elevate risk. Substance abuse, particularly with stimulants like cocaine or methamphetamines, can provoke dangerous arrhythmias. Severe electrolyte imbalances, such as low potassium or magnesium in the blood, can disrupt the heart’s electrical stability and trigger an event. Traditional cardiovascular risk factors like smoking, high blood pressure, and diabetes also contribute by promoting the development of coronary artery disease.
Screening and Proactive Management
The initial step in screening involves non-invasive tests to evaluate the heart’s structure and electrical function. An electrocardiogram (ECG or EKG) records the heart’s electrical activity and can detect abnormal rhythms or clues to underlying conditions like hypertrophic cardiomyopathy or Long QT syndrome.
An echocardiogram, which uses ultrasound waves to create images of the heart, provides a more detailed view. This test can assess the heart muscle’s thickness, the size of its chambers, and its pumping function, including the ejection fraction. If an arrhythmia is suspected but not captured on a standard ECG, a Holter monitor—a portable device worn for 24 hours or more—can continuously record the heart’s rhythm during daily activities. A stress test may also be recommended to assess how the heart responds to physical exertion.
The most effective intervention for high-risk individuals is the implantable cardioverter-defibrillator (ICD). An ICD is a small device surgically placed under the skin with wires connected to the heart. It continuously monitors the heart’s rhythm and delivers an electrical shock to restore a normal heartbeat if it detects a dangerous arrhythmia like ventricular fibrillation.
Medications like beta-blockers and other antiarrhythmic drugs can help control heart rate and reduce the likelihood of dangerous rhythms. For some patients, catheter ablation is an option. In this procedure, a catheter is threaded to the heart to locate the tissue causing abnormal electrical signals, which is then scarred using heat or cold energy to block the faulty pathway.
Immediate Intervention During an Event
Should an SCD event occur, a bystander’s actions in the first few minutes can be the difference between life and death. The signs are sudden and clear: the individual will collapse, become unresponsive, and will not be breathing normally, or may only be gasping for air. There will be no pulse, which indicates the heart has stopped circulating blood effectively.
The first step is to call emergency services immediately, as survival rates decrease by 7% to 10% for every minute without treatment. If another person is present, one should call while the other begins cardiopulmonary resuscitation (CPR). By performing chest compressions at a rate of 100 to 120 per minute, a bystander can manually pump blood to the brain and other organs. This keeps them oxygenated until more advanced help arrives.
As soon as an Automated External Defibrillator (AED) is available, it should be used. AEDs are portable devices designed for public use and are often found in places like schools and airports, providing clear voice prompts. The user attaches two adhesive pads to the person’s bare chest as shown in the diagrams on the pads. The AED then analyzes the heart’s rhythm to determine if a shock is needed.
If a shock is advised, the AED will instruct the user to ensure no one is touching the person and to press the button to deliver it. This shock is intended to stop the chaotic electrical activity, giving the heart a chance to reset its natural rhythm. After the shock, or if none is advised, the bystander should resume CPR until emergency medical personnel take over.