Pulseless Electrical Activity

Description

Pulseless electrical activity (PEA), previously known as electromechanical dissociation (EMD), is defined as electrical depolarization of the heart in the absence of synchronous cardiac myocyte shortening. New evidence suggests that it is a heterogenous clinical condition with varying levels of BP and cardiac activity:
- Pseudo PEA: Severe hypotension, no clinically detectable pulses, residual cardiac activity.
- True PEA: BP and cardiac wall motion are completely absent.
Treatment requires initiation of advanced cardiac life support (ACLS) with concurrent diagnosis and treatment of the underlying cause; this approach has not evolved in decades. Recent increases in the incidence of PEA have aroused interest and the development of animal models to better understand the pathogenesis in order to improve therapies and survival.
Anaesthetists must be aware of potential, common perioperative events that could incite PEA such as hypoxia, hypovolemia, potassium abnormalities, hypothermia, acidosis, and concomitant beta-blocker and calcium-channel blocker use; as well as pulmonary embolism, hypoglycemia, cardiac tamponade, tension pneumothorax, and coronary artery thrombosis.

Epidemiology

Incidence

Comprises ~35–40% of all in-hospital cardiac arrests
Comprises ~22–30% of all out-of-hospital cardiac arrests
Pseudo-PEA data not available

Morbidity/Mortality

In-hospital PEA cardiac arrests: 11% survival, of which 62% had good neurologic outcomes.
Out-of-hospital arrests: 2.5% survival to discharge.
Outcomes following PEA were slightly better than those following asystole.

Etiology/Risk Factors

PEA and other forms of cardiac arrest are often caused by a set of reversible conditions conveniently referred to as the "H’s" and "T’s." These factors should be considered and corrected as quickly as possible while life-saving efforts are being performed.

Hypoxia (common perioperative cause)
Hyperkalemia or hypokalemia
H⁺ ions (acidemia)
Hypovolemia (common perioperative cause)
Hypothermia
Hyperglycemia
Tamponade
Tension pneumothorax
Thrombosis, coronary
Thrombosis, pulmonary
Toxins (poisoning)
Trauma

Physiology/Pathophysiology

Electrical depolarization is typically followed by mechanical contraction and blood ejection from the ventricles. This sequence is fast and elegant; however, there are several clinical conditions that can impede it.
The H's and T's involve cardiac, respiratory, and metabolic disturbances with a common end-point: Electrical activity without a meaningful pulse. The exact pathogenesis remains unclear; however, evidence suggests that myocardial ischemia is the common pathophysiologic insult, either by decreased preload or cardiac contractility.
- Decreased preload may result from hypovolemia, tension pneumothorax, tamponade, or pulmonary thrombosis.
- Decreased cardiac contractility may result from hypoxia, hypothermia, potassium abnormalities, acidosis, or coronary thrombosis.
Global myocardial ischemia can consequently result in hypoxia, acidosis, and increased vagal tone. These disturbances are believed to cause depolarization and the uncoupling of excitation and contraction with resultant PEA.
- Hypoxia results in anaerobic metabolism and lactic acidosis, with resultant hyperkalemia. It has negative inotropic effects.
- Intracellular acidosis from hypoxia and the build-up of metabolic by-products may be responsible for impairing calcium affinity to troponin C. It has negative inotropic effects.
- Increased vagal tone can reduce heart rate and BP.
Animal studies have suggested that calcium uptake following reperfusion may be involved in, or is the result of, PEA. A significant uptake of calcium into myocardial cells is followed by swelling, damage to mitochondria and myofibrils, and deposits of intramitochondrial calcium phosphate. The increased calcium uptake has been postulated to impair voltage-gated calcium ion channels, calcium stores in the sarcoplasmic reticulum, and affinity of calcium to troponin C (1).
Beta-blocker and calcium-channel blocker use has been associated with an increased incidence of PEA and a concomitant decrease in ventricular fibrillation. The etiology has been attributed to their negative inotropic effects (2).

Prevantative Measures

Avoidance of the "H’s" and "T’s" of PEA

The history should provide information regarding possible etiologies (drug overdose, diabetes, coronary artery disease, trauma, intubation, insertion of central venous catheter, etc.)
Physical examination should include a palpation for a pulse, temperature, assessment for tracheal shifting, breath sounds, distended jugular veins.
Diagnostic procedures/Other
- Blood sugar
- Potassium level
- Arterial blood gas
- Echocardiogram to assess for cardiac tamponade, hypovolemia
- Handheld Doppler to rule out pseudo-PEA
Monitors
- Pulse oximetry, BP cuff, and arterial line indicate the lack of a pulse or mechanical contraction.
- Tachycardia and hypertension often precede onset; however, perioperatively, this lacks specificity (surgical stimulation, light anesthesia, ephedrine, etc.).
- EKG can demonstrate suggestive etiologies prior to the onset of PEA (usually applicable for intraoperative events).
  - Peaked T waves: Consider hyperkalemia
  - Inverted T waves (U waves): Consider hypokalemia
  - ST segment changes: Consider cardiac thrombosis (myocardial infarction)
  - Wide QRS: Consider myocardial injury, hyperkalemia, hypoxia
  - Wide QRS and slow: Consider drug overdose from tricyclic antidepressants, beta-blockers, calcium-channel blockers
  - Narrow QRS: Consider hypovolemia, pulmonary embolus, cardiac tamponade

Differential Diagnosis

Pseudo-PEA
Implantable pacemaker firing in asystole

ACLS for PEA.
- The goal during resuscitation is to maintain perfusion to vital organs during cardiac arrest and simultaneously diagnose and treat any underlying causes until return of spontaneous circulation (ROSC) occurs.
In the operating room, begin CPR, administer or increase oxygen delivery, attach defibrillator.
PEA is not a shockable rhythm; therefore its algorithm differs from that of ventricular fibrillation and tachycardia (3).
- Perform chest compression and ventilation for 2 minutes. The provider performing chest compressions should switch every 2 minutes.
- Administer epinephrine (1 mg IV every 3–5 minutes) or vasopressin (40 U IV) to replace the first or second dose of epinephrine.
- Note that atropine is no longer recommended for routine use in PEA/asystole.
- Check for shockable rhythm after 2 minutes.
- If shockable, follow the appropriate algorithm
- If not shockable, check for pulse. If pulse is present, begin post-resuscitation care. If absent, continue chest compressions and rhythm evaluation.
Airway management should also be addressed during the ACLS algorithm.
- In the perioperative setting, the patient's airway may already be secured; proper placement should be confirmed.
- If the patient is undergoing monitored anesthetic care (MAC), mask ventilation or intubation should be performed
- In the scenario where a supraglottic device is being utilized, consider converting to an endotracheal tube to provide positive pressure ventilation if appropriate.
- The key is to minimize interruptions in chest compressions during airway placement.
Differential diagnosis: While performing CPR, providers should review the potentially reversible "H’s" and "T’s" as possible causes and correct them when possible (4).
- Hypoxia should be treated with oxygen at a FiO₂ 100%.
- Hyperkalemia can be treated with a combination of calcium, bicarbonate, glucose, and insulin to stabilize myocardial cells and shift potassium intracellularly. Administer furosemide to enhance potassium excretion.
- Hydrogen ion excess (acidemia) may be treated with IV bicarbonate and hyperventilation.
- Hypovolemia can be corrected with IV fluid hydration or blood transfusion in cases of severe hemorrhage.
- Hypothermia can be corrected with active internal warming techniques.
- Tamponade can be treated with thoracotomy in cases of trauma or pericardiocentesis guided by echocardiography when possible.
- Tension pneumothorax should be treated with needle decompression and chest tube placement.
- Thrombosis, coronary: Thrombolytic therapy, coronary reperfusion, and emergency cardiopulmonary bypass should be considered.
- Thrombosis, pulmonary: Consider fibrinolytic therapy when pulmonary infarction is suspected or known.
- Toxins: Activated charcoal is indicated in many instances of drug overdose. Some toxins require specific correctional measures but ACLS guidelines should always be followed. Urgent toxicology consultation is recommended when ROSC occurs, if there are no other obvious causes.
- Trauma involving the head and neck requires C-spine stabilization. The jaw-thrust maneuver should be used to establish an airway.

Intraoperative arrests with ROSC: The decision to proceed with the surgery depends on whether the initiating event has been resolved (or will recur) and the level of urgency/emergency of the procedure. Postoperatively, patients should be admitted to an intensive care unit for surveillance and ongoing therapy as indicated.
Out of OR arrests with ROSC: Patients should be transferred to an intensive care unit for further stabilization and ongoing treatment, as indicated. Unresponsive patients should be considered for transfer to a facility that can provide a comprehensive care plan that includes rigorous cardiac, neurologic, and metabolic monitoring (5).
Avoid hyperventilation. Hyperventilation also increases intrathoracic pressure and inversely lowers cardiac output (5).
Induced hypothermia may be considered for neural and visceral protection
Coronary angiography and PCI are indicated when necessary and may be helpful even in comatose patients who do not show signs of ST segment elevation on ECG (5).

Larabee TM , Paradis NA , Bartsch J , et al. A swine model of pseudo-pulseless electrical activity induced by partial asphyxiation. Resuscitation. 2008;78(20):196–199.
Youngquist ST , Kaji AH , Niemann JT. Beta-blocker use and the changing epidemiology of out-of-hospital cardiac arrest rhythms. Resuscitation. 2008;288:3308–3013.
Neumar RW , Otto CW , Link MS , et al. Part 8: Adult advanced cardiovascular life support: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122(18 suppl 3):S729–S767.
Paradis NA , Halperin HR , Kem K. Cardiac arrest: The science and practice of resuscitation medicine. Cambridge University Press.
Peberdy MA , Callaway CW , Neumar RW , et al. Part 9: Post-cardiac arrest care: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122(18 suppl 3):S768–S786.

ACLS algorithm
Desbiens NA : Simplifying the diagnosis and management of pulseless electrical activity in adults: A qualitative review. Crit Care Med. 2008;36(2):391–396
Vanden Hoek TL , Morrison LJ , Shuster M , et al. Part 12: Cardiac arrest in special situations: 2010 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2010;122(18 suppl 3):S829–S861.

See Also (Topic, Algorithm, Electronic Media Element)

Hyperkalemia
Cardiac Tamponade
Pneumothorax
Pulmonary Embolism
Hypothermia
ACLS Anesthesia Management

ICD9

427.5 Cardiac arrest

ICD10

I46.9 Cardiac arrest, cause unspecified
I46.8 Cardiac arrest due to other underlying condition

PEA refers to a heterogenous group of cardiac rhythm disorders; all characterized by pulselessness in the presence of some types of electrical activity other than VT or VF.
Treatment involves institution of the ACLS algorithm with concurrent diagnosis and treatment of the inciting cause.
Although the causes vary greatly, there appears to be a shared pathophysiologic cascade. Following an initial global myocardial ischemic event, hypoxia, acidosis, and increased vagal tone ensue. The pathogenesis is not completely understood at this time; however, there appears to be a renewed interest, given the increased incidence of PEA in cardiac arrests. A greater understanding may improve therapy and prognosis.

J. Scott Bluth , DS

Nina Singh-Radcliff , MD

section name header

Basics ⬇

Incidence

Morbidity/Mortality

Diagnosis ⬆ ⬇

Treatment ⬆ ⬇

Follow-Up ⬆ ⬇

References ⬆ ⬇

Additional Reading ⬆ ⬇

Codes ⬆ ⬇

Clinical Pearls ⬆ ⬇

Author(s) ⬆