Cardiac arrest happens when the heart’s electrical system malfunctions, causing it to stop pumping blood. Unlike a heart attack, which is a blockage in blood flow to the heart, cardiac arrest is an electrical failure that shuts down the heartbeat entirely. Within seconds, blood stops reaching the brain, lungs, and other organs. Without immediate CPR, it is fatal.
The Electrical Malfunction Behind Cardiac Arrest
Your heart beats because of a coordinated wave of electrical signals that tells each section of muscle when to contract. Cardiac arrest occurs when that coordination breaks down. The most common electrical disturbance is ventricular fibrillation, where the lower chambers of the heart receive rapid, chaotic electrical impulses instead of steady ones. Rather than contracting in rhythm, the heart quivers uselessly and can’t push blood forward.
A related problem is ventricular tachycardia, where the lower chambers beat dangerously fast. If it isn’t corrected quickly, ventricular tachycardia often deteriorates into fibrillation. In either case, the result is the same: the heart stops functioning as a pump, and organs begin losing their blood supply.
Coronary Artery Disease Is the Leading Cause
Coronary artery disease accounts for more than 75% of sudden cardiac death cases in the developed world. Over time, fatty deposits narrow the arteries that feed the heart muscle. When blood flow drops low enough, sections of heart tissue are damaged or die. That damaged tissue disrupts the heart’s electrical pathways, creating the conditions for a fatal rhythm disturbance.
Autopsy studies find that up to 64% of people who die from sudden cardiac arrest have a blood clot blocking a coronary artery. In other words, a heart attack can trigger cardiac arrest. The blocked artery starves heart tissue of oxygen, and the injured tissue fires off erratic electrical signals that throw the whole heart out of rhythm. This is why the two events are so closely linked, even though they’re fundamentally different problems.
Cardiomyopathy and Structural Heart Disease
Diseases that change the shape or thickness of the heart muscle also raise the risk of cardiac arrest, even without blocked arteries.
In hypertrophic cardiomyopathy, the heart muscle grows abnormally thick. The most common cause of death in these patients is ventricular fibrillation. Scarring within the thickened muscle creates zones where electrical signals loop back on themselves instead of traveling in a straight line, generating dangerous rhythms. Research using cardiac MRI has shown that when scar tissue makes up 15% or more of the heart’s muscle mass, the risk of sudden cardiac death roughly doubles, even in patients otherwise considered lower risk.
Dilated cardiomyopathy, where the heart stretches and weakens, carries a similar threat. About 30% of these patients have bands of scar tissue running through the wall of the heart, typically in the septum (the divider between the left and right sides). These scar bands act as a substrate for the same kind of looping electrical circuits that trigger fatal arrhythmias. Certain genetic mutations, particularly in a protein called lamin, make dilated cardiomyopathy especially dangerous by combining a high risk of rhythm problems with progressive heart failure.
Inherited Electrical Disorders
Some people have structurally normal hearts that still carry a hidden risk. Inherited conditions called channelopathies affect the tiny gates (ion channels) on heart cells that control the flow of sodium, potassium, and calcium. When these channels don’t open or close properly, the electrical cycle of each heartbeat is subtly altered, making the heart vulnerable to fibrillation.
The most well-known of these conditions are long QT syndrome and Brugada syndrome. Long QT syndrome delays the electrical reset between heartbeats, and Brugada syndrome creates abnormal signaling patterns in the heart’s right ventricle. Both can cause sudden cardiac arrest in adolescents and young adults who appear otherwise healthy. Other inherited conditions in this family include catecholaminergic polymorphic ventricular tachycardia, where intense exercise or strong emotions trigger dangerous rhythms, and short QT syndrome, which speeds up the heart’s electrical reset to an unstable degree.
Electrolyte Imbalances
Your heart’s electrical system depends on precise levels of minerals in the blood, especially potassium and magnesium. When those levels swing too high or too low, the heart’s rhythm can become unstable enough to cause arrest.
- Potassium too high (above 6 to 7 mEq/L): Progressively slows and distorts the heart’s electrical signals. If untreated, the heartbeat degrades into ineffective rhythms and eventually stops altogether.
- Potassium too low (below 2.5 mEq/L): Can trigger a state where the heart’s electrical activity continues but fails to produce an actual heartbeat, or the heart simply flatlines.
- Magnesium too high: Slows the heart rate and can suppress the electrical signals enough to cause full cardiorespiratory arrest.
- Magnesium too low: Triggers a specific type of chaotic rhythm called torsades de pointes, where the heart twists through rapidly shifting electrical patterns that prevent effective pumping.
These imbalances often develop in people with kidney disease, severe dehydration, eating disorders, or as a side effect of certain medications. They’re a correctable cause of cardiac arrest when caught in time.
Chest Impact: Commotio Cordis
A blow to the chest at exactly the wrong moment can cause cardiac arrest in a person with a completely normal heart. This is called commotio cordis. The impact, estimated at about 50 joules of energy (easily delivered by a thrown baseball), physically distorts the heart muscle and forces open ion channels that should be closed. If this happens during a specific sliver of the heartbeat’s electrical cycle, roughly 1% of the total cycle, it triggers ventricular fibrillation.
The risk peaks when the object is traveling around 40 miles per hour. Faster impacts tend to cause structural damage to the chest wall or heart itself rather than isolated electrical disruption. Smaller projectiles concentrate force on a smaller area, increasing the likelihood of commotio cordis. This is why it’s most often seen in youth sports, where participants have thinner chest walls and are hit by baseballs, hockey pucks, or lacrosse balls. The proportion of the cardiac cycle vulnerable to this effect increases with higher heart rates, making it more likely during physical exertion.
Cardiac Arrest in Children
Cardiac arrest looks fundamentally different in children than in adults. In adults, the heart’s own disease is almost always the starting point. In children, the cause is usually something happening outside the heart that eventually overwhelms it. Respiratory failure is the dominant trigger, accounting for about 76% of pediatric cardiac arrests. Conditions like airway obstruction, severe asthma, pneumonia, drowning, and suffocation starve the body of oxygen until the heart can no longer maintain its rhythm.
When a child does collapse suddenly without any preceding breathing difficulty, cardiac causes deserve immediate consideration. Undiagnosed structural heart defects, coronary artery abnormalities, and inherited channelopathies are the usual suspects. Some of these defects, like certain malformations of the heart’s chambers or major blood vessels, can go undetected through infancy and childhood until they cause a crisis.
What Happens in the Minutes After Arrest
Once the heart stops pumping, the clock starts. Bystander-witnessed cardiac arrests where CPR is started immediately have a 13% survival rate to hospital discharge. When the arrest is unwitnessed, that drops to 7.6%. Despite the stakes, only about 42% of people who collapse from cardiac arrest outside a hospital receive bystander CPR.
The brain is the organ most sensitive to lost blood flow. Earlier estimates suggested brain cells die within 5 to 10 minutes of cardiac arrest, but more recent evidence from NYU Langone Health’s research suggests that brain cells actually die slowly, over hours to days, if left without intervention. This finding has shifted how researchers think about the window for meaningful resuscitation, but it doesn’t change the urgency: every minute without CPR or defibrillation reduces the chance of a good outcome. CPR keeps some blood moving to the brain, and a defibrillator delivers a shock that can reset the heart’s chaotic electrical activity back to a normal rhythm.