Pulseless Electrical Activity (PEA) is a severe medical emergency that accounts for a significant portion of cardiac arrests. It represents a profound disconnect in the heart’s function: the electrical system remains active and organized, but this activity is not followed by a mechanical pumping action sufficient to circulate blood and generate a pulse. PEA is life-threatening because the body is deprived of oxygen and blood flow, leading rapidly to cardiac death. Immediate recognition and intervention are necessary to identify and reverse the underlying cause.
Defining Pulseless Electrical Activity
Pulseless Electrical Activity is fundamentally a failure of the heart’s mechanical function, not its electrical initiation. The heart muscle receives the electrical signal, which should trigger a strong contraction to eject blood. In PEA, the electrical impulse is transmitted in an organized fashion, but the resulting muscular contraction is too weak, or entirely absent, to create enough force to push blood effectively.
This situation is sometimes referred to as electromechanical dissociation, highlighting the uncoupling of the electrical signal from the mechanical response. The heart is essentially idling, with its electrical system firing but its muscle failing to generate adequate cardiac output or a detectable pulse. Without a palpable pulse, the body’s tissues, especially the brain, quickly suffer from a lack of oxygenated blood.
PEA exists on a spectrum, ranging from “true PEA,” where there is no mechanical contraction, to “pseudo-PEA.” Pseudo-PEA involves extremely weak contractions that generate very low aortic pressure, insufficient to create a pulse that can be felt. Regardless of the specific contraction strength, the patient is in cardiac arrest, requiring immediate intervention.
Identifying PEA on a Cardiac Monitor
The diagnosis of Pulseless Electrical Activity relies on combining two distinct observations: the appearance of the heart rhythm on a monitor and the absence of a detectable pulse. Unlike ventricular fibrillation (VF) or asystole, the electrocardiogram (ECG) displays an organized or semi-organized electrical pattern. This rhythm can resemble a normal heart rate, a fast rate (tachycardia), or a slow rate (bradycardia).
The rhythm may look like a sinus rhythm, atrial fibrillation, or an idioventricular rhythm—patterns where a pulse would typically be expected. The defining characteristic is that the rhythm is organized and is not one of the “shockable” rhythms like VF or pulseless ventricular tachycardia (pVT). If the monitor shows organized electrical activity, the next step is to check for a pulse.
The clinical diagnosis of PEA is confirmed only when the patient is unresponsive and no pulse can be felt, despite the organized electrical activity on the monitor. Providers must always treat the patient, not just the monitor, as a seemingly “normal” rhythm can be misleading.
Underlying Causes (The H’s and T’s)
Identifying the cause of PEA is paramount, as survival depends almost entirely on reversing the underlying problem. The common causes are grouped into a mnemonic known as the “H’s and T’s,” which represents the most frequent and reversible etiologies.
The H’s (Physiologic/Metabolic)
The H’s primarily represent physiologic or metabolic issues:
- Hypovolemia: Severe blood or fluid loss, leading to insufficient blood volume to fill the heart chambers. Without adequate volume, the heart cannot pump enough blood to generate a pulse.
- Hypoxia: A lack of oxygen in the body, which is a major contributor often resulting from respiratory failure.
- Hydrogen ion excess (Acidosis): Impairs the heart muscle’s ability to contract effectively, reducing its mechanical strength.
- Hypo- or hyperkalemia: Imbalances of potassium that destabilize the electrical gradient necessary for strong muscle contraction, often presenting with changes on the ECG.
- Hypothermia: A dangerously low body temperature that slows all metabolic processes, including the heart’s ability to contract forcefully.
The T’s (Mechanical/Toxic)
The T’s generally represent mechanical or toxic causes:
- Tension pneumothorax: Air pressure builds up in the chest, compressing the great vessels and heart, preventing blood return and filling.
- Cardiac tamponade: Fluid accumulation in the sac around the heart squeezes it and prevents it from expanding and filling with blood.
- Thrombosis: Includes massive pulmonary embolism (a large clot in the lungs) or coronary thrombosis (a heart attack). These cause PEA by blocking blood flow or causing severe muscle damage.
- Toxins: Drug overdose or poisoning that can directly suppress the heart muscle’s contractility or interfere with electrical pathways.
Emergency Response and Survival Rates
The immediate response to PEA follows the Advanced Cardiac Life Support (ACLS) protocols, which prioritize high-quality Cardiopulmonary Resuscitation (CPR). CPR is started immediately to manually circulate oxygenated blood to the brain and heart while the cause is being sought. Unlike ventricular fibrillation, PEA is a non-shockable rhythm, meaning a defibrillator will not correct the underlying problem.
A vasopressor medication, typically epinephrine (adrenaline), is administered every three to five minutes to induce vasoconstriction, which helps increase blood flow to the vital organs during CPR. The most crucial aspect of the emergency response is the rapid identification and treatment of the specific cause from the H’s and T’s list. For instance, a tension pneumothorax requires needle decompression, while severe hypovolemia requires rapid fluid or blood administration.
The prognosis for PEA is significantly less favorable than for shockable rhythms. Survival rates to hospital discharge for out-of-hospital cardiac arrests presenting with PEA are generally low, often falling between 2% and 5%. This low survival rate reflects the fact that PEA is often the result of a profound physiological collapse that is difficult to reverse. Favorable outcomes are typically seen only when the underlying cause is identified and corrected quickly.