What Are the Common Underlying Causes of PEA Arrest?

Pulseless electrical activity, or PEA, is a form of cardiac arrest in which the heart’s electrical system continues firing in an organized pattern, but the muscle itself fails to pump blood effectively enough to produce a detectable pulse.¹ The underlying causes are classically organized into two groups known as the “Hs and Ts,” a mnemonic that covers everything from massive blood loss to blood clots in the lungs. But PEA is not a single disease. It is the final common pathway of many different emergencies, and figuring out which one is responsible during active CPR is one of the hardest problems in emergency medicine.

Why Finding the Cause Is the Entire Game

In a cardiac arrest caused by ventricular fibrillation, the treatment is relatively straightforward: deliver a shock. PEA, by contrast, is not a shockable rhythm. The electrical tracing on the monitor can look deceptively normal, sometimes even resembling a healthy heartbeat, yet no blood is moving. Standard CPR buys time, but the only real path to survival is identifying and correcting the specific problem that made the heart stop pumping. Without that, the drugs and chest compressions are treating a symptom rather than the disease.

This is why clinicians train to run through the Hs and Ts mentally during resuscitation. The mnemonic is not just academic. Each letter points to a distinct, potentially fixable catastrophe. PEA that goes unexplained almost never responds to resuscitation alone. It is the arrests where someone correctly diagnoses a tension pneumothorax or a massive pulmonary embolism in real time that end with the patient walking out of the hospital.

The “H” Causes

The “H” side of the mnemonic captures conditions that disrupt the heart’s internal environment, whether by starving it of volume, oxygen, or the right chemical balance. Six causes traditionally make the list.

Hypovolemia: Severe blood loss is one of the most common triggers. Trauma patients who lose enough circulating volume can slip into PEA because the heart simply has nothing left to pump. Massive internal bleeding from a ruptured abdominal aortic aneurysm, for instance, can present as sudden PEA arrest with no obvious external hemorrhage.² Non-hemorrhagic causes such as severe dehydration or septic shock can also deplete circulating volume to the point of arrest.
Hypoxia: When oxygen delivery to the heart muscle drops below a critical threshold, the heart can no longer contract effectively even though its electrical system remains intact. Drowning, airway obstruction, and severe asthma attacks are classic scenarios. In mechanically ventilated patients, a particular problem called dynamic hyperinflation can trap air in the lungs, compress blood vessels, and cut off blood return to the heart, sometimes triggering PEA arrest.³ Briefly disconnecting the ventilator to let trapped air escape has been described as a potential intervention in these cases.⁴
Hydrogen ion excess (acidosis): Severe metabolic acidosis, from conditions like diabetic ketoacidosis or kidney failure, can depress heart function enough to cause PEA. The heart cells become progressively less able to contract as the blood’s pH drops.
Hyperkalemia: Dangerously high potassium levels interfere with the heart’s electrical conduction system and can produce PEA arrest. One clue on the monitor is a widened QRS complex. In a study of cardiac arrest patients, those presenting with wide QRS PEA had significantly higher potassium levels than those with narrow QRS PEA, and roughly half of the wide QRS group had frank hyperkalemia compared to about a quarter in the narrow QRS group.⁵ Kidney failure, crush injuries, and certain medications are typical culprits.
Hypothermia: As the body’s core temperature drops, cardiac electrical conduction slows and becomes increasingly unstable. A systematic review of experimental and clinical data found that progressive cooling prolongs certain intervals on the heart tracing and that severe hypothermia is commonly associated with dangerous rhythm disturbances or cardiac arrest.⁶ Drowning victims, outdoor exposure patients, and those undergoing prolonged surgery can all present this way.
Hypoglycemia: Critically low blood sugar, while more commonly associated with seizures or loss of consciousness, can occasionally precipitate cardiac arrest. It is probably the least common of the Hs, but it is the easiest to check and fix, which is why it stays on the list.

The “T” Causes

The “T” side of the mnemonic generally involves mechanical obstructions or toxic insults. These tend to be more dramatic and, in some cases, more immediately treatable.

Tension pneumothorax: When air leaks into the space around a lung and cannot escape, pressure builds up and compresses the heart and major blood vessels. The heart cannot fill, so it cannot pump. Inserting a needle or tube to release the trapped air can reverse the arrest within seconds. This cause is especially important in trauma patients and in anyone on a ventilator.
Cardiac tamponade: Fluid or blood collecting in the sac around the heart squeezes it from the outside, preventing it from filling between beats. Tamponade can result from chest trauma, cancer, infections, or, frequently, aortic dissection. In one autopsy series of patients who died suddenly from aortic dissection, the majority had blood in the pericardial sac as the final mechanism of death.⁷ Draining the fluid with a needle can restore cardiac output.
Thrombosis, pulmonary: A massive pulmonary embolism, meaning a large blood clot blocking the arteries in the lungs, is one of the most feared causes of PEA arrest. The right side of the heart suddenly cannot push blood through the lungs, so the left side has nothing to pump forward. In one series of patients with PEA arrest from confirmed massive pulmonary embolism who received clot-dissolving drugs, right heart pressures dropped substantially within 48 hours of treatment.⁸ Without aggressive treatment, survival rates for PE-related PEA are extremely low.
Thrombosis, coronary: A heart attack can cause PEA, though the mechanism varies. In animal models, acute coronary artery blockage in a heart that was already weak from prior damage produced PEA almost immediately, because the remaining muscle simply could not compensate.⁹ In patients, PEA after a heart attack has classically been blamed on rupture of the heart’s free wall, but other mechanical complications like papillary muscle rupture can also be responsible.¹⁰
Toxins: Drug overdoses and poisonings are a significant cause of PEA, especially in younger patients. Methamphetamine exposure has been reported to cause PEA arrest even in very young children.¹¹ Certain prescription medications, particularly at toxic doses, can stabilize cell membranes in a way that paralyzes the heart’s ability to contract. A case of severe venlafaxine overdose causing refractory PEA arrest was treated with intravenous lipid emulsion, a technique recommended by multiple professional societies for cardiac arrest caused by fat-soluble drug toxicity when standard treatments fail.¹² Tricyclic antidepressants, calcium channel blockers, beta blockers, and local anesthetics are among the other drugs that can cause PEA in overdose.

Why PEA Arrests Are Becoming More Common

For decades, ventricular fibrillation was the dominant arrest rhythm encountered both inside and outside the hospital. That has changed. PEA has emerged as the most common rhythm found during in-hospital cardiac arrests and is rising rapidly in out-of-hospital reports as well.¹³ The proportion of out-of-hospital cardiac arrests presenting with PEA as the initial rhythm continues to climb.¹⁴

Several factors probably explain this shift. Wider use of medications like beta blockers and implantable defibrillators has reduced the number of people who develop ventricular fibrillation as their first arrest rhythm. Meanwhile, the population is aging, and older patients with multiple chronic illnesses are more likely to arrest in PEA. Better monitoring in hospitals may also mean that fibrillation gets caught and treated before it progresses, leaving PEA as the rhythm seen by the time a full arrest is recognized. The net effect is that emergency teams are now facing PEA more often than the rhythm they were traditionally most prepared for.

True PEA Versus Pseudo-PEA

Not all PEA is the same. The traditional definition relies on a clinical finding: organized electrical activity on the monitor and no palpable pulse. But palpating a pulse during CPR is unreliable. With the spread of bedside ultrasound, clinicians have discovered that many patients diagnosed with PEA actually have some degree of cardiac wall motion visible on the screen. The heart is squeezing, just not hard enough to generate a pulse you can feel at the wrist or neck.¹⁵

This distinction matters because patients with pseudo-PEA, where the heart is weakly contracting, tend to have a better prognosis than those with true PEA, where the heart muscle is not moving at all despite electrical activity. Pseudo-PEA is more likely to be caused by something reversible like hypovolemia or tamponade, where the heart wants to pump but physically cannot because of an external constraint. True PEA, by contrast, often reflects more devastating damage such as prolonged ischemia or irreversible metabolic collapse. Recognizing which type you are dealing with can guide how aggressively to pursue specific interventions and how long to continue resuscitation.

How Bedside Ultrasound Has Changed the Equation

The classic approach to PEA arrest involves mentally running through the Hs and Ts while performing CPR, looking for clinical clues, and making an educated guess about the cause. That approach misses a lot. Point-of-care ultrasound has emerged as a tool that can detect reversible causes in real time, including tamponade, pulmonary embolism, tension pneumothorax, and hypovolemia.¹⁶

In one comparative study, ultrasound identified reversible causes of arrest in about 73% of cases, compared to roughly 43% using standard assessment alone, an absolute improvement of 30 percentage points.¹⁷ Tamponade and pulmonary embolism were detected substantially more often with ultrasound, which makes sense: these are conditions where the diagnosis can be nearly invisible to physical exam alone but obvious on a quick ultrasound view of the heart. The technology also distinguishes between true PEA and pseudo-PEA, as described above, which can change the entire management strategy.

The challenge is integrating ultrasound into CPR without interrupting chest compressions for too long. Most protocols now recommend brief imaging windows during the pulse-check pauses that are already built into the resuscitation cycle. Even a few seconds of ultrasound during those pauses can reveal a collapsing right ventricle, suggesting massive PE, or fluid around the heart, pointing to tamponade.

Survival Trends

PEA arrest has historically carried a grim prognosis, better than asystole but far worse than ventricular fibrillation. That gap has been narrowing. A 16-year study in a large U.S. community tracked survival across different arrest rhythms over four time periods and found that PEA survival increased from about 6% in the earliest period to roughly 14% in the most recent, a meaningful upward trend.¹⁸ Ventricular fibrillation survival also improved over the same period, from about 28% to 37%, while asystole survival remained essentially flat.

The study attributed the improvement in PEA outcomes to enhancements in the emergency medical services system’s management of PEA arrests specifically. That likely reflects better recognition of reversible causes, faster targeted treatments, and possibly wider ultrasound adoption. The survival numbers remain sobering. Even at 14%, most PEA arrests are still fatal. But the trajectory suggests that the cause-focused approach to PEA is working and that further gains are possible as diagnostic tools improve.

When Pre-Existing Heart Disease Sets the Stage

One underappreciated factor in PEA arrest is the state of the heart before the acute event. A heart that is already weakened by prior damage is far more vulnerable to PEA than a healthy one. In an animal model, acute coronary artery blockage in hearts with normal function led to ventricular fibrillation in most cases. But when the same blockage was induced in hearts with severe pre-existing dysfunction, every single animal developed PEA instead, and it happened almost immediately, within about two minutes of the blockage.⁹

The implication is that PEA in the setting of a heart attack may be a marker of how much reserve the heart had going in. A patient with advanced heart failure who suffers even a modest new coronary event may go directly into PEA because the remaining muscle cannot compensate at all. This also helps explain the epidemiological shift toward more PEA: as the population ages and more people survive initial heart attacks only to live with reduced heart function, the substrate for PEA arrest becomes more common. It’s a paradox of success in cardiology. Better treatment of acute events creates a population more susceptible to a different, harder-to-treat form of arrest down the line.

Vascular Catastrophes That Mimic Other Causes

Two major vascular emergencies deserve specific mention because they can masquerade as other PEA causes and because they require surgical rather than medical treatment. Aortic dissection, where the inner wall of the aorta tears and blood tracks along the vessel, can kill by producing tamponade when blood leaks backward into the pericardial sac. In one autopsy series of patients who died suddenly from aortic problems, eight of twelve dissection cases had blood in the pericardium.⁷ The remaining cases had bleeding into the chest or mediastinum. A clinician draining pericardial fluid in a PEA arrest might temporarily restore a pulse only to find that the sac refills almost immediately because the dissection is still actively bleeding.

Ruptured abdominal aortic aneurysm presents a different diagnostic trap. The bleeding is in the abdomen, not the chest, and the patient often arrives in profound shock before suddenly losing a pulse. In one reported case, a patient found unresponsive in his car went into PEA arrest in the emergency department, and bedside ultrasound revealed a large abdominal mass consistent with an aneurysm.¹⁹ Without imaging, the cause might never have been identified during resuscitation. Both of these emergencies require surgery, not just medications, which makes rapid diagnosis critical and highlights another reason ultrasound has become so valuable during PEA arrests.

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