Can Seizures Cause Cardiac Arrest?

Seizures can cause cardiac arrest, though the pathway from one to the other is less straightforward than most people assume. People with epilepsy face roughly a threefold higher risk of sudden cardiac arrest compared to the general population, and seizure activity has been documented immediately before cardiac arrest in a substantial fraction of cases. The connection runs through several distinct mechanisms, from direct disruption of heart rhythm during a seizure to longer-term stress on the heart muscle, and even shared genetic vulnerabilities that make both the brain and heart electrically unstable.

How Seizures Disrupt the Heart

During a seizure, the brain sends a storm of electrical signals that spill beyond their intended targets. Some of those signals cascade through the autonomic nervous system, the branch of the nervous system that controls heart rate, blood pressure, and breathing without conscious effort. The result is a sudden, intense surge of adrenaline and related stress hormones. This surge can push the heart into dangerously fast rhythms, dangerously slow rhythms, or even a complete pause.

The most commonly observed cardiac change during a seizure is a spike in heart rate. A study that reviewed video-EEG recordings of seizures found a heart rate increase of at least 10 beats per minute in 73% of seizures, with the rate jump often happening right at seizure onset. ECG abnormalities showed up in about a quarter of seizures, and one patient in the study experienced a 30-second period of asystole, meaning the heart stopped beating entirely.¹

Ictal asystole, where the heart pauses during a seizure, is the most alarming direct cardiac consequence. It is rare but well-documented. The condition occurs most often in people with temporal lobe epilepsy and can cause the person to collapse from syncope on top of their seizure, leading to injuries or death if the pause is long enough.² In a study of patients with drug-resistant epilepsy who had implanted heart monitors, roughly 7% showed episodes of seizure-related slow heart rates, and three patients had cardiac pauses exceeding six seconds, long enough to require permanent pacemaker implantation.³

The Population-Level Risk

Looking beyond individual case reports, epidemiological data confirms that epilepsy itself is a risk factor for sudden cardiac arrest (SCA) in the broader population. A case-control study comparing people who experienced SCA with matched controls found that active epilepsy was associated with an almost threefold increased risk of sudden cardiac arrest. The risk appeared even higher for people under 50 and for women, though these subgroup findings were based on small numbers.⁴

A community-based study further underscored the severity of this overlap. Among people with epilepsy who experienced sudden cardiac arrest, about a third had evidence of seizure activity right before the arrest. These patients fared considerably worse than cardiac arrest patients without epilepsy: survival to hospital discharge was under 3%, compared with about 12% in the non-epilepsy group. Part of the reason was that people with epilepsy were far less likely to present with a shockable heart rhythm, the type that responds to defibrillation.⁵

Seizure-Induced Heart Muscle Damage

Beyond rhythm disturbances, seizures can directly injure heart tissue through the sheer force of the adrenaline surge. The most dramatic example is Takotsubo cardiomyopathy, sometimes called “broken heart syndrome,” where a flood of stress hormones stuns the heart muscle, causing the left ventricle to balloon out and lose pumping strength. A review of the literature identified 36 cases of seizure-triggered Takotsubo cardiomyopathy, most commonly after tonic-clonic seizures or status epilepticus. In about half of those cases, the heart dysfunction showed up immediately after the seizure, and the condition frequently presented as sudden hemodynamic collapse.⁶ The authors suggested that some unexplained deaths in epilepsy patients may actually be Takotsubo events that went unrecognized.

A more recent systematic review of Takotsubo cases in epilepsy from 2000 to 2023 confirmed that the catecholamine surge is the driving mechanism, producing a characteristic pattern of heart muscle stunning. About 39% of the patients in that review had a prior history of epilepsy, suggesting that repeated seizures over time may increase vulnerability.⁷ Takotsubo can also recur. One case report described a woman with epilepsy who developed the condition twice in 11 months, each time after a tonic-clonic seizure, with different patterns of ventricular wall involvement each time.⁸

Even when Takotsubo does not develop, seizures can leave biochemical fingerprints of cardiac stress. A study of over 700 patients admitted after epileptic seizures found that about 7% had elevated cardiac troponin, a protein released when heart muscle cells are damaged, without any other obvious cardiac explanation. Risk factors for this elevation included having vascular conditions like high blood pressure or diabetes.⁹ A separate study found that troponin elevation was more common when seizures originated in the temporal lobe and in cases of status epilepticus, though none of the patients developed symptomatic heart attacks.¹⁰

Respiratory or Cardiac? The SUDEP Debate

Sudden unexpected death in epilepsy (SUDEP) is the leading cause of death directly related to epilepsy, and for years researchers debated whether the lethal mechanism was primarily a cardiac one. The picture has shifted. Recent evidence from both animal models and clinical studies increasingly points to respiratory shutdown, not a fatal heart rhythm, as the more common final pathway. Seizures propagate through the autonomic nervous system in a way that suppresses breathing, and the resulting oxygen deprivation then leads to cardiac arrest as a secondary event.¹¹

This does not mean the heart plays no role. In some cases, post-seizure central apnea occurs at the same time as asystole, creating a combined cardiorespiratory failure. One study of epilepsy monitoring unit patients found that this simultaneous apnea-and-asystole pattern, classified as near-SUDEP, occurred at a rate of about 10 per 1,000 patient-years.¹² The current understanding is nuanced: breathing failure appears to be the more common trigger, but cardiac rhythm problems can be the primary cause in a subset of SUDEP cases, and in many cases both systems fail together.

When the Brain and Heart Share a Genetic Flaw

One of the more striking discoveries in this field is that certain gene mutations can cause both epilepsy and dangerous heart rhythms at the same time. Many of these genes encode ion channels, the tiny pores in cell membranes that control electrical signaling. Because the same types of ion channels exist in both brain and heart tissue, a single mutation can make neurons fire erratically (causing seizures) while simultaneously making heart cells prone to arrhythmias.¹³

These shared vulnerabilities involve sodium, potassium, calcium, and other channel types, as well as some non-ion-channel genes.¹⁴ The concept is sometimes called “cardiocerebral channelopathy,” and it matters practically because it means some people with epilepsy carry an inherent cardiac vulnerability that exists independently of whether they are having a seizure at any given moment. For these individuals, the risk of cardiac arrest is not purely seizure-triggered; it is built into their biology.

ECG Changes After Seizures

Even when a seizure does not cause outright cardiac arrest, it often leaves traceable changes on an electrocardiogram. A prospective study that recorded ECGs in the immediate aftermath of seizures found abnormalities in 44% of patients. About one in five had a prolonged QT interval, a finding that signals increased vulnerability to dangerous arrhythmias. A smaller but concerning number showed Brugada-type patterns, another ECG signature associated with sudden cardiac death risk.¹⁵ Arrhythmias, QT prolongation, and ST segment changes are among the most commonly reported ECG findings during or after seizures across the broader literature.¹⁶

Generalized tonic-clonic seizures, the type involving full-body stiffening and jerking, produce the most dramatic cardiac autonomic disruption. After these seizures, heart rate variability drops sharply, reflecting a tilt toward sympathetic overdrive and suppressed vagal tone. This post-seizure cardiac stress pattern is one of the most consistent risk factors identified for SUDEP.¹⁷

The Diagnostic Mix-Up That Runs Both Ways

Adding to the complexity is a practical clinical problem: seizures and cardiac events can look almost identical to an observer. A person whose heart suddenly stops or slows dramatically may collapse, lose consciousness, stiffen, and jerk, a presentation that looks exactly like a seizure. Multiple cases have been documented where patients carried an epilepsy diagnosis for years before someone captured their ECG during an episode and discovered the “seizures” were actually cardiac syncope from an arrhythmia.¹⁸

This misdiagnosis matters enormously. If the underlying problem is cardiac, anti-seizure medications will not help and may even be harmful. The reverse is also true: if a seizure triggers a cardiac pause that causes additional syncope-like symptoms, the cardiac component may go unrecognized for a long time. This is why many epilepsy specialists now advocate for cardiac monitoring alongside standard brain monitoring, especially in patients whose seizures involve loss of consciousness or unexplained falls.

Monitoring and Prevention

Implantable loop recorders, small devices placed under the skin that continuously track heart rhythm, have become an important tool for identifying dangerous seizure-heart interactions. In a landmark study, over 220,000 patient-hours were monitored across 19 patients with severe epilepsy. The recorders captured ECGs during 377 seizures. Most showed rapid heart rates, but seven patients showed episodes of dangerously slow heart rates during seizures, and four of those patients ultimately needed permanent pacemakers.¹⁹

A challenge with these monitors is that seizure-related muscle artifact can mimic dangerous rhythms on the recording, leading to a high rate of false alarms. One study found that automatic detection flagged many seizure-induced artifacts as pseudo-ventricular tachycardia or pseudo-atrial fibrillation, and that manual activation by the patient or a caregiver produced a much higher rate of true positive readings.²⁰

When ictal asystole is confirmed, pacemaker implantation can be lifesaving. In one series of patients with documented ictal asystole, eight received pacemakers, and all of them remained free of seizure-related fainting during follow-up averaging six years.²¹ Current guidelines suggest considering a pacemaker when seizure-related cardiac pauses last longer than six seconds.²²

Beyond cardiac devices, seizure control itself is the most important preventive strategy. Medication nonadherence is associated with a nearly threefold increase in SUDEP risk.²³ And there is evidence that aggressive treatment with multiple anti-seizure medications may offer protection beyond simply reducing seizure frequency: a Swedish study found that taking three or more medications was associated with a roughly 70% lower SUDEP risk even after accounting for how often tonic-clonic seizures occurred.²⁴

Anti-Seizure Medications and the Heart

There is an uncomfortable irony in the seizure-cardiac arrest story: some of the medications used to prevent seizures may themselves affect the heart. Many anti-seizure drugs work by blocking sodium channels in the brain, but the same sodium channels exist in heart cells. Blocking them can slow electrical conduction through the heart, potentially leading to a widened QRS complex or prolonged QT interval on an ECG. A large Canadian study found that people with epilepsy taking sodium channel-blocking medications were roughly twice as likely to show signs of cardiac conduction delay compared to people with epilepsy on other medications. Specific drugs including carbamazepine, phenytoin, and lamotrigine all showed elevated rates.²⁵

Population data raise concern that cardiac arrhythmias and sudden cardiac death may be more common in people with epilepsy partly because of these drug effects, particularly in vulnerable populations or when sodium channel-blocking drugs are combined with other medications that affect the heart.²⁶ This does not mean these medications should be avoided. They are often the most effective options for seizure control, and uncontrolled seizures carry their own cardiac risks. But it does mean that cardiac screening, especially a baseline ECG, is worth discussing with a neurologist when starting or changing anti-seizure medications.

Wearable Devices and Early Warning

An area of active development is the use of wearable sensors to detect seizures and their cardiac consequences in real time. Beyond simply identifying that a tonic-clonic seizure has occurred, newer devices aim to track biomarkers that correlate with SUDEP risk: the duration of the tonic phase, whether the person ends up face-down, whether post-seizure immobility and slowed heart rate occur, and changes in skin conductance that reflect autonomic activation.²⁷ The hope is that if these biomarkers prove strongly predictive, they could trigger an alert to a caregiver who could intervene, for instance by repositioning the person to protect their airway or calling for emergency help during the critical minutes after a severe seizure.

How Age Changes the Cardiac Picture

The interplay between seizures and the heart looks different depending on age. Children with epilepsy appear to experience more seizure-related bradycardia and central apnea during seizures compared to adults, while adults are more prone to rapid heart rates during seizures.²⁸ After a tonic-clonic seizure, children also show greater sympathetic activation and more vagal suppression than adults, measured by skin conductance and heart rate variability.²⁹

Paradoxically, despite these more intense acute autonomic disruptions in children, SUDEP is more common in adults. One theory is that adults experience longer periods of post-seizure brain suppression, the flattening of brainwave activity that follows a severe seizure, and this prolonged suppression is what ultimately drives fatal cardiorespiratory collapse. Children’s brains may recover from this suppression more quickly, offering a window of protection even though their acute cardiac responses to seizures are more dramatic.²⁸

When Cardiac Arrest Happens During a Seizure

Emergency responders sometimes witness seizure-like activity at the moment of an out-of-hospital cardiac arrest. A Japanese study of EMS-witnessed cardiac arrests found that patients who displayed seizure-like activity at the onset of the arrest were younger on average (70 versus 79 years) and had significantly better neurological outcomes than those who did not. In that study, the seizure-like activity was itself a predictor of favorable outcomes, likely because it indicated the arrest had just occurred and the brain had not yet been without blood flow for long.³⁰

This observation carries an important caution for bystanders: convulsive movements in someone who collapses are not always a seizure. They can be the body’s response to a sudden loss of blood flow from cardiac arrest. If a person collapses, jerks briefly, and is then unresponsive and not breathing normally, calling emergency services and starting CPR may be more appropriate than waiting for what looks like a seizure to pass. The distinction between a seizure and a cardiac arrest presenting with convulsive movements can be impossible to make without medical equipment, and erring on the side of checking for a pulse and starting chest compressions when in doubt could save a life.