# Pulseless Electrical Activity

Manage pulseless electrical activity as a nonshockable arrest: deliver uninterrupted high-quality CPR, give early epinephrine, verify true pulselessness, and simultaneously identify a reversible mechanical, metabolic, toxic, thrombotic, or hypoxic cause.

**Clinical question:** How should clinicians resuscitate PEA while rapidly identifying and treating its reversible cause?

Updated: 2026-09-15T22:55:21.085327+00:00

## What matters in practice
- PEA is a nonshockable cardiac-arrest rhythm: do not defibrillate unless the rhythm converts to ventricular fibrillation or pulseless ventricular tachycardia. [12][15]
- Prioritize high-quality CPR, early IV/IO epinephrine, and parallel cause-directed treatment; PEA and asystole share this initial management framework. [15][22]
- Use the arrest context, QRS width, waveform capnography, and focused ultrasound during planned pulse checks to prioritize mechanical versus metabolic causes without prolonging interruptions in compressions. [4][14][19]
- Do not give calcium, sodium bicarbonate, or magnesium routinely in PEA; reserve calcium for suspected hyperkalemia, hypermagnesemia, or calcium-channel-blocker overdose. [14][22]
- After ROSC, obtain a 12-lead ECG, treat seizures if present, consider EEG for patients not following commands, and perform emergent coronary angiography when ST-segment elevation indicates suspected coronary occlusion. [13][22]

## What to do immediately in PEA

Treat electrical activity without a definite pulse as cardiac arrest while checking for rapidly correctable mimics and causes.

Confirm unresponsiveness, absent normal breathing, and no definite central pulse, then activate the resuscitation response and begin high-quality CPR. PEA is nonshockable; continue CPR rather than delivering a shock. Reassess rhythm and pulse at scheduled pauses, and switch to the shockable-arrest pathway only if ventricular fibrillation or pulseless ventricular tachycardia appears. [12][15]

Obtain IV or IO access and administer epinephrine as early as possible in the nonshockable-arrest pathway. Epinephrine is recommended for cardiac arrest; high-dose epinephrine is not recommended routinely. Continue to search for and treat the precipitant during CPR rather than waiting for repeated rhythm checks. [15][22]

Assign one clinician to a focused reversible-cause screen each cycle: prearrest trajectory, witnessed collapse versus respiratory deterioration, trauma or procedure, dialysis or renal failure, toxin exposure, anticoagulation, chest pain, known venous thromboembolism, severe asthma or obstructive lung disease, and hypothermic exposure. The Hs and Ts remain the core differential: hypovolemia, hypoxia, acidosis, potassium disorder, hypothermia, tension pneumothorax, tamponade, toxins, pulmonary or coronary thrombosis. [13][14]
- Use continuous waveform capnography when an advanced airway is placed; low or falling ETCO2 should trigger reassessment of compression quality and ventilation, while an abrupt rise can support ROSC recognition. [4][14][23]
- Avoid routine calcium, sodium bicarbonate, and magnesium during undifferentiated cardiac arrest. [22]

*Immediate PEA priorities and actions. [12][14][15][22]*

| Finding or task | Immediate action | Decision consequence |
| --- | --- | --- |
| Organized rhythm with no definite pulse | Treat as nonshockable arrest; begin/continue CPR and do not defibrillate. [12][15] | Defibrillation is reserved for conversion to VF/pulseless VT. [12] |
| IV/IO access established | Give epinephrine early. [15][22] | Continue cause-directed interventions in parallel with CPR. [15] |
| Low or decreasing waveform ETCO2 | Reassess compression quality, ventilation, and airway position. [4][14][23] | Do not interpret ETCO2 without accounting for ventilation and compression variation. [4] |
| Suspected hyperkalemia, hypermagnesemia, or calcium-channel-blocker overdose | Give IV/IO calcium as an adjunct: calcium chloride 10% 5-10 mL or calcium gluconate 10% 15-30 mL. [14] | Calcium is indication-specific, not routine PEA treatment. [14][22] |

## Use the rhythm pattern and arrest context to focus the differential

A narrow- versus wide-complex PEA pattern can prioritize the first cause-directed intervention, but does not replace the Hs-and-Ts screen.

Narrow-complex PEA more often indicates a mechanical obstruction to forward flow, particularly tamponade, tension pneumothorax, mechanical hyperinflation, or pulmonary embolism. In a patient with abrupt collapse, distended neck veins, chest trauma, invasive thoracic procedure, obstructive lung disease, or severe dyspnea before arrest, prioritize a mechanical cause while maintaining CPR. [19]

Wide-complex PEA more often suggests a metabolic cause, particularly potassium derangement, severe acidosis, or sodium-channel-toxic exposure. Obtain targeted history from staff, family, medication records, dialysis records, and the prearrest ECG; use an immediately available blood gas and electrolyte measurement to direct correction when feasible without delaying resuscitation. [19]

Do not let QRS morphology exclude other diagnoses. Pulmonary or coronary thrombosis, profound hypoxia, hemorrhagic hypovolemia, hypothermia, and toxicologic causes may present with variable electrical patterns, so the working diagnosis must be revised with each new bedside finding. [13][14][19]

*Etiology-directed PEA branching framework. [13][14][19]*

| Priority branch | Clues during arrest | Focused test or maneuver | Cause-directed next action |
| --- | --- | --- | --- |
| Mechanical obstruction | Narrow-complex PEA; abrupt collapse; trauma, thoracic procedure, obstructive lung disease, or suspected venous thromboembolism. [19] | Focused bedside ultrasound during a planned pulse check; chest examination and ventilation assessment. [14][19] | Treat suspected tamponade, tension pneumothorax, mechanical hyperinflation, or pulmonary embolism immediately while CPR continues. [14][19] |
| Metabolic or toxic cause | Wide-complex PEA; renal failure or dialysis history; medication or overdose history; preceding metabolic deterioration. [19] | Point-of-care blood gas and electrolytes when immediately available; review prearrest ECG and exposure history. [13][19] | Correct potassium, acidosis, or toxin-specific physiology; use calcium only when hyperkalemia, hypermagnesemia, or calcium-channel-blocker toxicity is suspected. [14] |
| Hypovolemia or hypoxia | Hemorrhage, fluid loss, respiratory failure, submersion, or prolonged hypoxemia before arrest. [13][14] | Assess oxygen delivery, ventilation, airway placement, chest movement, and bleeding source. [13][14] | Restore oxygenation and address volume loss or hemorrhage during ongoing CPR. [13][14] |
| Coronary thrombosis | Chest discomfort, acute heart failure, ischemic ECG changes before arrest, or ROSC with ST-segment elevation. [13][22] | Obtain 12-lead ECG after ROSC. [13][22] | Perform emergent coronary angiography when post-ROSC ECG shows ST-segment elevation and coronary occlusion is suspected. [22] |

## Use POCUS and ETCO2 without extending CPR pauses

Monitoring should improve CPR quality or reveal a treatable cause; it must not become a reason for prolonged hands-off time.

Integrate focused cardiac and thoracic POCUS only during an already planned rhythm or pulse check. In PEA, ultrasound can identify findings that support tamponade, massive pulmonary embolism, or hypovolemia and can help distinguish pseudo-PEA from true absence of cardiac mechanical activity. [6][14][19]

Treat POCUS as a decision aid, not an isolated prognosis test. In nonshockable arrest, focused ultrasound may provide etiologic and prognostic information, but rapid recognition and treatment of reversible causes remain the purpose of imaging during resuscitation. [7][14]

Interpret ETCO2 trends in their physiologic context. Ventilation rate, compression depth, airway type, and sex affect absolute values; in one out-of-hospital manual-CPR cohort, standardized ETCO2 was higher with ROSC than without ROSC, and ETCO2 trajectory differed before ROSC versus non-ROSC. A low or downward trend should first prompt correction of CPR and ventilation delivery rather than termination based on a single measurement. [4]
- If ultrasound image acquisition repeatedly delays chest compressions, stop intra-arrest imaging and return to the standard nonshockable algorithm. [14][15]
- Use waveform capnography to confirm and monitor advanced-airway placement and to reassess CPR quality when PETCO2 is low or falling. [23]

*Interpretation of intra-arrest monitoring in PEA. [4][14][19][23]*

| Tool | Useful finding | What it changes | Pitfall |
| --- | --- | --- | --- |
| Focused POCUS | Pericardial fluid, cardiac activity, or findings consistent with hypovolemia, pulmonary embolism, or thoracic pathology. [14][19] | Prioritizes an immediate mechanical-cause intervention or recognition of pseudo-PEA. [6][14] | Image acquisition must be limited to planned pauses and should not interrupt CPR. [14] |
| Waveform capnography | Low or decreasing PETCO2 during CPR. [4][23] | Reassess compression quality, ventilation rate, and advanced-airway position. [4][23] | Absolute ETCO2 values vary with ventilation and compression characteristics. [4] |
| Waveform capnography | Abrupt ETCO2 rise. [24] | Assess promptly for ROSC at the next appropriate rhythm/pulse check. [24] | An ETCO2 value alone should not be used as the sole determinant of prognosis. [4][21] |

## Which medications to use and avoid in PEA

Medication selection should follow the arrest algorithm and a specific reversible-cause hypothesis.

Epinephrine is the routine vasoactive medication in PEA cardiac arrest; administer it early after IV/IO access is obtained. Vasopressin alone or combined with methylprednisolone may be considered in combination with epinephrine, but it is not a substitute for epinephrine. [22]

Do not reflexively administer calcium, sodium bicarbonate, or magnesium in undifferentiated PEA. Calcium is appropriate as an adjunct when the presentation suggests hyperkalemia, hypermagnesemia, or calcium-channel-blocker overdose; listed IV/IO doses are calcium chloride 10% 5-10 mL or calcium gluconate 10% 15-30 mL. [14][22]

Consider extracorporeal CPR for refractory arrest only in systems with appropriate equipment and trained staff. ECPR is a systems-dependent escalation, not a substitute for prompt conventional ACLS and immediate treatment of reversible causes. [22]
- Amiodarone and lidocaine are options for defibrillation-refractory VF/pulseless VT, not for persistent PEA. [22]
- If the rhythm changes to VF/pulseless VT, transition immediately to the shockable-arrest pathway. [12][15]

*Medication and escalation decisions in PEA. [14][22]*

| Intervention | Use in PEA | Restriction or trigger |
| --- | --- | --- |
| Epinephrine | Administer early in cardiac arrest after IV/IO access. [22] | High-dose epinephrine is not recommended routinely. [22] |
| Calcium chloride or calcium gluconate | Use as an adjunct for suspected hyperkalemia, hypermagnesemia, or calcium-channel-blocker overdose. [14] | Do not use calcium routinely in undifferentiated PEA. [14][22] |
| Sodium bicarbonate or magnesium | Do not administer routinely. [22] | Use only if a specific cause-directed indication is established. [22] |
| ECPR | Reasonable for refractory cardiac arrest where trained staff and equipment are available. [22] | Requires institutional capability and should run in parallel with standard ACLS. [22] |

## Post-ROSC priorities after PEA

ROSC changes the task from intra-arrest diagnosis to stabilization, cause confirmation, and prevention of recurrent arrest.

Obtain a 12-lead ECG promptly after ROSC to guide coronary evaluation. Perform emergent coronary angiography for patients with suspected coronary cause and ST-segment elevation; angiography is also reasonable without ST elevation when the likelihood of significant coronary artery disease and potential benefit from revascularization are high. [13][22]

Normalize oxygenation, ventilation, and glucose control after ROSC, and provide lung-protective ventilation. Continue the etiologic workup initiated during arrest, including targeted assessment for pulmonary embolism, tamponade, tension pneumothorax, toxic exposure, electrolyte abnormality, hemorrhage, or hypoxic respiratory failure. [13]

Treat clinically evident seizures after ROSC. For patients who do not follow commands, EEG may be used to detect seizures; routine seizure prophylaxis is not recommended. In patients with spontaneous hypothermia who remain unresponsive to verbal commands, do not routinely rewarm faster than 0.5°C per hour. [22]
- Reassess for recurrent arrest and for the original reversible cause until it has been definitively corrected. [12][13]
- Document the initial rhythm, suspected etiology, rhythm transitions, interventions, ETCO2 trajectory, and ROSC timing to support post-arrest decision-making and quality review. [4][20]

*Post-ROSC actions relevant to PEA survivors. [13][22]*

| Post-ROSC finding or status | Action | Purpose |
| --- | --- | --- |
| ST-segment elevation with suspected coronary cause | Perform emergent coronary angiography. [22] | Identify and revascularize an acute coronary culprit when present. [22] |
| No ST-segment elevation but high likelihood of significant coronary disease | Consider coronary angiography. [22] | Evaluate a potentially reversible coronary cause. [22] |
| Not following commands | Consider EEG; treat detected or clinical seizures. [22] | Detect and manage post-arrest seizures; do not use routine prophylaxis. [22] |
| Spontaneous hypothermia and unresponsive to verbal commands | Avoid routine rewarming faster than 0.5°C per hour. [22] | Avoid overly rapid rewarming. [22] |

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## Editorial note

Prepared from cited clinical literature using Astra's research workflow. Verify recommendations against current guidance and patient-specific factors.