Pulseless electrical activity, or PEA, is a cardiac arrest rhythm in which the heart’s electrical system still generates organized signals, but the heart muscle does not contract strongly enough to produce a detectable pulse or meaningful blood flow. It is one of the four recognized rhythms that can cause sudden cardiac arrest, alongside ventricular fibrillation, pulseless ventricular tachycardia, and asystole. The electrical activity looks organized on a monitor, yet no blood is circulating to the brain or vital organs. Without immediate CPR and treatment, PEA is fatal.
What Is A Pulseless Electrical Activity?
PEA is defined by a specific mismatch. The heart’s electrical conduction system continues to fire in an organized pattern, but the mechanical pumping action fails. On a cardiac monitor, the rhythm can look almost normal — regular QRS complexes at a reasonable rate. But when a clinician checks for a pulse, there is none.
This is different from asystole, where there is no electrical activity at all. In PEA, electricity is present. The problem is that the electrical signal is not producing effective muscle contraction.
The term “pulseless electrical activity” replaced an older name, “electromechanical dissociation,” because it is more precise. Electrical activity and mechanical activity are dissociated — one is happening without the other.
PEA is not a disease. It is a final common pathway that many different catastrophic events can produce. That is why identifying the underlying cause is the central challenge in treating it.
What Causes Pulseless Electrical Activity?
PEA has many possible causes, and they fall into two broad categories: cardiac and non-cardiac. The cardiac causes directly impair the heart’s ability to pump. The non-cardiac causes interfere with the heart indirectly — by reducing blood return to the heart, by starving it of oxygen, or by creating mechanical obstruction.
In emergency medicine, clinicians use the mnemonic “Hs and Ts” to remember the reversible causes. These are the conditions that, if identified and corrected quickly, offer the best chance of restoring circulation.
The Hs
- Hypovolemia — severe blood or fluid loss reduces the volume returning to the heart, so there is nothing to pump
- Hypoxia — lack of oxygen to the heart muscle
- Hydrogen ion (acidosis) — severe acid buildup in the blood
- Hypokalemia or hyperkalemia — dangerously low or high potassium levels, which disrupt cardiac muscle function
- Hypothermia — severely low body temperature
- Hypoglycemia — very low blood sugar
The Ts
- Tension pneumothorax — air trapped in the chest cavity compresses the heart and great vessels
- Tamponade — fluid around the heart prevents it from filling properly
- Toxins — drug overdose or poisoning
- Thrombosis (coronary or pulmonary) — a blood clot blocking a coronary artery or the pulmonary arteries
- Trauma — severe injury causing blood loss or direct cardiac damage
In hospitalized patients, PEA is often the terminal rhythm seen after prolonged shock, respiratory failure, or metabolic collapse. In out-of-hospital cardiac arrest, causes like hypoxia from respiratory arrest, pulmonary embolism, and severe bleeding are common.
The distribution of causes matters because treatment is cause-directed. CPR alone rarely restores a pulse in PEA. The rhythm converts only when the underlying problem is reversed.
How Is PEA Different From Other Cardiac Arrest Rhythms?
The four cardiac arrest rhythms differ in what the monitor shows and in how they respond to treatment.
Ventricular fibrillation shows chaotic, disorganized electrical activity. The heart muscle quivers rather than pumps. It responds to defibrillation.
Pulseless ventricular tachycardia shows a fast, organized electrical pattern from the ventricles. It also responds to defibrillation.
Asystole shows a flat line or nearly flat line. There is no electrical activity to shock.
PEA shows organized electrical activity — but no pulse. Like asystole, it is not a shockable rhythm. Defibrillation does not help because the electrical system is already organized. The problem is mechanical, not electrical.
This distinction is critical. A monitor can display a rhythm that looks reassuringly normal. But if the patient has no pulse, the rhythm is PEA, and the patient is in cardiac arrest. Treating the monitor instead of the patient is a recognized and dangerous error.
What Does PEA Look Like on a Monitor?
On a cardiac monitor, PEA can appear as a narrow-complex rhythm with a normal rate, a wide-complex rhythm, or a slow, irregular pattern. The rate may be fast or slow. The QRS complexes may be narrow or wide.
What all PEA rhythms share is that they produce no palpable pulse and no effective blood pressure.
Some PEA rhythms are described as “pseudo-PEA.” In pseudo-PEA, the heart is actually generating a small amount of mechanical contraction — enough to produce a weak blood pressure that may be detectable with an arterial line or ultrasound, but not enough to produce a palpable pulse. Some research suggests pseudo-PEA may have a somewhat better prognosis than true PEA, though distinguishing the two in real time can be difficult and the evidence on outcomes is not definitive.
Point-of-care ultrasound is increasingly used during cardiac arrest to assess whether the heart is contracting at all. This can help distinguish true PEA from pseudo-PEA and can sometimes identify a specific cause, such as cardiac tamponade or a massively dilated right ventricle suggesting pulmonary embolism. However, ultrasound must not delay CPR or other interventions.
How Is PEA Treated?
Treatment follows established cardiac arrest protocols. The priorities are high-quality CPR, rapid identification of reversible causes, and epinephrine administration.
High-quality chest compressions maintain some blood flow to the brain and heart while the team works to find and fix the underlying problem. Compressions should be started immediately and continued with minimal interruption.
Epinephrine is given as soon as possible in PEA and asystole. The standard cardiac arrest dose is 1 mg of epinephrine (0.1 mg/mL concentration) administered intravenously or intraosseously every 3 to 5 minutes. This is the established dose in current resuscitation guidelines.
PEA is not shockable. Defibrillation is not indicated and may worsen the situation by interrupting compressions.
The most important intervention is finding and reversing the cause. If the cause is tension pneumothorax, needle decompression is needed. If it is tamponade, pericardiocentesis may be required. If it is hypovolemia, rapid volume replacement is needed. If it is opioid overdose, naloxone may reverse the respiratory depression driving the arrest. If it is hyperkalemia, calcium and other agents may be given.
Without correcting the underlying cause, PEA rarely converts to a perfusing rhythm. This is the central fact that separates PEA from shockable rhythms.
What Is the Survival Rate for PEA?
Survival from PEA is generally lower than survival from shockable rhythms like ventricular fibrillation. This is because PEA often reflects a severe underlying condition — massive blood loss, pulmonary embolism, or prolonged hypoxia — that is harder to reverse than an isolated electrical problem.
Survival also depends heavily on where the arrest occurs. In-hospital arrests tend to have better outcomes than out-of-hospital arrests, partly because trained staff and equipment are immediately available. Witnessed arrests with immediate bystander CPR have better outcomes than unwitnessed arrests.
Specific survival percentages vary widely across studies and depend on the population, the cause, and the speed of intervention. No single number applies to all cases. What is consistent across the evidence is that early, high-quality CPR and rapid correction of reversible causes give the best chance of survival.
What Should You Do If You Witness a Cardiac Arrest?
Call 911 immediately. Start chest compressions if you are trained or willing. Push hard and fast in the center of the chest. Do not stop until emergency responders arrive or until the person shows clear signs of life.
If an automated external defibrillator (AED) is available, use it. The AED will analyze the rhythm and advise whether a shock is needed. If the rhythm is PEA, the AED will not advise a shock — but it will still guide you to continue CPR.
You cannot diagnose PEA without a monitor and a pulse check. What you can do is recognize that someone who is unresponsive, not breathing normally, and has no pulse is in cardiac arrest, regardless of the underlying rhythm. Bystander CPR doubles or triples survival from out-of-hospital cardiac arrest compared with no CPR, according to the American Heart Association.
The distinction between PEA and other rhythms matters to clinicians choosing treatments. For bystanders, the action is the same: call for help, start compressions, and use an AED if one is available.
Frequently Asked Questions
Is PEA a shockable rhythm?
No. PEA is not shockable because the electrical system is already organized. Defibrillation is used for ventricular fibrillation and pulseless ventricular tachycardia, not for PEA or asystole.
What is the difference between PEA and asystole?
PEA has organized electrical activity on the monitor but no pulse, while asystole has no electrical activity at all. Both are non-shockable cardiac arrest rhythms.
Can someone survive pulseless electrical activity?
Survival is possible but generally lower than for shockable rhythms, and it depends on how quickly CPR starts and whether the underlying cause can be reversed. Early bystander CPR and rapid treatment of reversible causes give the best chance.
What is the first drug given for PEA?
Epinephrine is given as soon as possible, at a dose of 1 mg intravenously or intraosseously every 3 to 5 minutes. The most important intervention, however, is identifying and correcting the underlying cause.

