Pulseless electrical activity

Pulseless electrical activity
Other names: Electromechanical dissociation (EMD)
A drawing of what a rhythm strip of PEA could look like
Specialty	Emergency medicine, cardiology
Symptoms	Loss of consciousness, no pulse
Complications	Brain injury, rib fractures, limb ischemia
Types	True, pseudo
Causes	Hs and Ts: hypoxia (50%), hypovolemia, hydrogen ions, hyperthyroidism, hypothermia, tension pneumothorax, trauma, tamponade, toxins, pulmonary thrombosis, cardiac thrombosis
Diagnostic method	ECG monitor, pulse check
Differential diagnosis	Severe peripheral vascular disease, obesity
Treatment	Cardiopulmonary resuscitation
Medication	Epinephrine
Prognosis	Poor
Frequency	25% of cardiac arrests

Pulseless electrical activity (PEA) is when there is no pulse despite a rhythm strip showing organized beats. Those affected are in cardiac arrest and are generally not responsive. Complications may include brain injury, rib fractures, and limb ischemia. Outcomes are often poor, including among those who survive.

The underlying causes which are occasionally reversible include the Hs and Ts: hypoxia (50%), hypovolemia, hydrogen ions, hyperthyroidism, hypothermia, tension pneumothorax, trauma, tamponade, toxins, pulmonary thrombosis, and cardiac thrombosis. Other causes include intracranial bleeding. The underlying mechanism involves insufficient contraction of the heart despite electrical activity. Diagnosis is by ECG monitor and pulse check. It is divided into two types: "true" in which there is no heart movement and "pseudo" in which some movement is present.

Cardiopulmonary resuscitation (CPR) is the initial treatment, while potential causes are looked for and treated. The medication epinephrine is typically given every 3 to 5 minutes. Specific treatments may include needle decompression for a pneumothorax and pericardiocentesis for tamponade. Survival is about 6% at one month; though, may be 20% at discharge if the event occurs in hospital. About half of those who initially survive have a poor outcome at one year. Pulseless electrical activity is found initially in about 20% of out-of-hospital and 33% of in-hospital cardiac arrests.

Signs and symptoms

Pulseless electrical activity leads to a loss of cardiac output, and blood supply to the brain. As a result a person loses consciousness and stops breathing. This is confirmed by examining the airway for obstruction, observing the chest for respiratory movement, and feeling the pulse (usually at the carotid artery) for a period of 10 seconds.

Causes

These possible causes are remembered as the Hs and Ts.

• Hypovolemia
• Hypoxia
• Hydrogen ions (acidosis)
• Hyperkalemia or Hypokalemia
• Hypoglycemia
• Hypothermia
• Tablets or Toxins
• Cardiac Tamponade
• Tension pneumothorax
• Thrombosis (e.g., myocardial infarction, pulmonary embolism)
• Tachycardia
• Trauma (e.g., hypovolemia from blood loss)

The possible mechanisms by which the above conditions can cause pulseless in PEA are the same as those recognized as producing circulatory shock states. These are (1) impairment of cardiac filling, (2) impaired pumping effectiveness of the heart, (3) circulatory obstruction and (4) pathological vasodilation causing loss of vascular resistance and excess capacitance. More than one mechanism may be involved in any given case.

Diagnosis

Pulseless electrical activity, it is possible to observe by invasive blood pressure (red) the transition from a normal mechanical activity of the heart, which progressively changes in rhythm and contractile quality to asystole, even in the presence of normal electrical activity (green), also confirmed by the pulse oximeter detection even if with artifacts (blue)

The absence of a pulse generally confirms a diagnosis of cardiac arrest, with PEA distinguished from other types of arrest by a electrocardiography (ECG). In PEA, there is organised or semi-organised electrical activity as opposed to asystole (flatline) or to the disorganised electrical activity of either ventricular fibrillation or ventricular tachycardia.

A narrow QRS duration <0.12 may point towards tamponade, tension pneumothorax, hypovolemia, or pulmonary embolism. While a wide QRS duration > 0.12 may point towards hyperkalemia or hypocalcemia.

Treatment

Cardiopulmonary resuscitation (CPR) should be initiated promptly to maintain cardiac output until the PEA can be corrected. The approach to treatment is directed at the underlying cause, if known (e.g. relieving a tension pneumothorax). Where an underlying cause cannot be determined and reversed, the treatment is similar to that for asystole. There is no evidence that external cardiac compression increases cardiac output in situations such as bleeding, in which poor cardiac filling is the underlying mechanism.

Part of resuscitation is placement of an intravenous or intraosseous line for epinephrine (adrenaline) 1 mg every 3–5 minutes. Although previously the use of atropine was recommended for PEA/asystole, this recommendation was withdrawn in 2010 by the American Heart Association due to lack of evidence of benefit. Epinephrine too has a limited evidence base, and it is recommended on the basis of its mechanism of action.

Sodium bicarbonate 1 mEq per kilogram may be considered in this rhythm as well, although there is little evidence to support this practice. Its routine use is not recommended in this context, except in special situations (e.g. preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdose). Defibrillators is not effective, as the problem lies in the response of the myocardial tissue to electrical impulses.

External links

Classification	ICD-10: I46.9 ICD-9-CM: 427.9 DiseasesDB: 4166
External resources	eMedicine: med/2963