Pulseless electrical activity
Pulseless electrical activity | |
ICD-10 | I46.9 |
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DiseasesDB | 4166 |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Synonyms and keywords: PEA; electromechanical dissociation; EMD; non-perfusing rhythm
Diagnosis
Echocardiography
A rapid beside echocardiogram can identify several rapidly reversible causes of PEA such as cardiac tamponade, myocardial infarction, cardiac rupture and underfilling of the ventricle due to hypovolemia. Elevated right heart filling pressures suggest pulmonary embolism. Tension pneumothorax can also be observed on a bedside echocardiogram.
Treatment
Initial Treatment in All Patients
The current American Heart Association-Advanced Cardiac Life Support (AHA-ACLS) guidelines advise the following be undertaken in all patients:
- Start CPR immediately
- Administer 100% oxygen to reverse hypoxia
- Intubate the patient
- Establish IV access
Reverse The Underlying Cause
The mainstay of treatment is to reverse the underlying cause of PEA.
Hypovolemic Shock
The most common reversible cause is hypovolemia (i.e. hypovolemic shock) which should be treated with IV fluids or packed red blood cell transfusion.
Tension Pneumothorax
Another readily identifiable and immediately treatable causes include tension pneumothorax (not uncommon in the ICU setting). Often in the ICU, this may occur in a ventilated patient, but conscious patients may complain of the sudden onset of chest pain, there may be the sudden appearance of cyanosis, tracheal deviation, and absent breath sounds on the involved side of the chest. In patients on a ventilator, auto ̶ positive end-expiratory pressure (auto PEEP) and rupture of a bleb are more likely to occur. A thin needle can be inserted in the upper intercostal space to relieve the pressure and allow the lung to reinflate.
Cardiac Tamponade
Suspect cardiac tamponade in the patient with recent chest trauma,neoplasm, or renal failure. These patients will complain of preceding sudden onset of chest pain, palpitations, breathlessness and lightheadedness. Elevated neck veins and a quiet muffled heart are present. There may be electrical alternans of the QRS complex and other intervals on the EKG.
Cardiac Rupture
If the patient develops PEA several days after presenting with a ST elevation MI, then cardiac rupture should be considered particularly in an elderly female with hypertension.
Recurrent Myocardial Infarction
If the patient develops PEA several days after presenting with a ST elevation MI, then recurrent MI should be considered.
Hyperkalemia
Consider this in the patient with chronic renal insufficiency or in the patient on hemodialysis.
Hypothermia
"No patient is dead unless they are warm and dead." Confirm that a newly hospitalized patient is not hypothermic with a core temperature. Longer resuscitative efforts can be undertaken in the hypothermic patient.
Pulmonary Embolism
New right axis deviation on the EKG suggests PE.
Treatment in the Absence of an Identifiable Underlying Cause
If an underlying cause for PEA cannot be determined and/or reversed, the treatment of pulseless electrical activity is similar to that for asystole.[1]
Epinephrine
The mainstay of drug therapy for PEA is epinephrine 1 mg every 3–5 minutes. Higher doses of epinephrine can be administered in patients with suspected beta blocker and calcium channel blocker overdose. Otherwise high dose epinephrine has not demonstrated a benefit in survival or neurologic recovery.
Vasopressin
Vasopressin can replace epinephrine as either the first or second dose of resuscitative pharmacotherapy.[2] [3]The dose of vasopressin is 40 U IV/IO.
Atropine
Although atropine was previously recommended in the treatment of PEA/asystole, this recommendation was withdrawn in 2010 by the American Heart Association due to lack of evidence for therapeutic benefit.[1] If the pulse is < 60 beats per minute, atropine can still be administered in the full vagolytic dose of 1 mg IV q3-5min, up to 3 doses. After atropine administration, it can become difficult to assess neurologic recovery.
Na Bicorbonate
Sodium bicarbonate at a dose of 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 for patients in this context, except in special situations (e.g. preexisting metabolic acidosis, hyperkalemia, tricyclic antidepressant overdose).[1]
CPR
All of these drugs should be administered along with appropriate CPR techniques.
Defibrillation
Defibrillation is not used to treat this rhythm, as the problem lies in the response of the myocardial tissue to electrical impulses.
Pacemaker Insertion
External and internal pacing have not been shown to improve outcome and are not recommended. There may be capture of the signals, but there is no improvement in contractility.
References
- ↑ 1.0 1.1 1.2 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (2010). "Part 8: Adult Advanced Cardiovascular Life Support". Circulation. 122 (18 Suppl): S729–S767. doi:10.1161/CIRCULATIONAHA.110.970988. PMID 20956224. Unknown parameter
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ignored (help) - ↑ Grmec S, Strnad M, Cander D, Mally S (2008). "A treatment protocol including vasopressin and hydroxyethyl starch solution is associated with increased rate of return of spontaneous circulation in blunt trauma patients with pulseless electrical activity". International Journal of Emergency Medicine. 1 (4): 311–6. doi:10.1007/s12245-008-0073-8. PMC 2657262. PMID 19384647. Retrieved 2012-09-16. Unknown parameter
|month=
ignored (help) - ↑ Kotak D (2009). "Comment on Grmec et al.: a treatment protocol including vasopressin and hydroxyethyl starch solution is associated with increased rate of return of spontaneous circulation in blunt trauma patients with pulseless electrical activity". International Journal of Emergency Medicine. 2 (1): 57–8. doi:10.1007/s12245-008-0079-2. PMC 2672974. PMID 19390921. Retrieved 2012-09-16. Unknown parameter
|month=
ignored (help)