Pulseless electrical activity
| Pulseless electrical activity | |
| ICD-10 | I46.9 |
|---|---|
| DiseasesDB | 4166 |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Synonyms and keywords: PEA; electromechanical dissociation; EMD; non-perfusing rhythm
Overview
Pulseless electrical activity is defined as the absence of a pulse or cardiac contractility despite the presence of electrocardiographic activity. The most common causes are respiratory failure and hypovolemia.
Classification
True PEA
There are no cardiac contractions despite electrical activity.
Pseudo PEA
There are very weak cardiac contractions present that fail to generate a blood pressure compatible with systemic perfusion and life despite electrical activity.
Post Defibrillation PEA
Following defibrillation, there can be a period of electromechanical dissociation where electrocardiographic complexes do not generate a pulse. As a result of post defibrillation PEA, it is often useful to continue CPR for up to one minute following restoration of a perfusing rhythm.
Pathophysiology
There is often a downward spiral in the pathophysiology of PEA. A severe initial insult often reduces cardiac output which may in turn cause myocardial ischemia, left ventricular failure, hypoxia and metabolic acidosis. These pathophysiologic disturbances further reduce cardiac output further exacerbating the downward spiral. With loss of cardiac output; hypotension, loss of consciousness and apnea rapidly ensue.
Reduced Preload and Inadequate Filling of the Left Ventricle or
PEA may be due to inadequate filling of the left ventricle with blood to stretch the cardiac sarcomeres adequately to result in a cardiac contraction (i.e. there is inadequate preload). Examples include rapid fluid or blood loss as occurs in major trauma. Cardiac tamponade, pneumothorax, and pulmonary embolism are other examples.
Elevated Afterload
Elevated afterload is rarely a cause of PEA.
Electromechanical Dissociation
In some cases, PEA may be caused by electromechanical dissociation. The normal condition when electrical activation of muscle cells precedes mechanical contraction is known as electromechanical coupling. This coupling is lost in some forms of PEA, and this is known as electromechanical dissociation.
Reduced Contractility
Contraction of the myocardium depends upon the integrity of the troponin subunits.
Reduced Calcium Influx
Calcium binding to troponin is required for contractility. This binding can be reduced in calcium channel blocker overdoses.
Reduced Affinity of Troponin for Calcium
In the setting of hypoxia, calcium binds less avidly to troponin.
Causes
Common causes of PEA include preceding respiratory failure in 40% to 50% of cases, and hypovolemia.
The goal of treatment of PEA is to treat the underlying cause. These possible causes are remembered as the Hs and Ts.[1][2][3]
- Hypovolemia
- Hypoxia
- Hydrogen ions (Acidosis)
- Hypothermia
- Hyperkalemia or Hypokalemia
- Hypoglycemia
- Tablets or Toxins (Drug overdose) such as beta blockers, tricyclic antidepressants, or calcium channel blockers
- Cardiac Tamponade
- Tension pneumothorax
- Thrombosis (Myocardial infarction)
- Thrombosis (Pulmonary embolism)
- Trauma (Hypovolemia from blood loss)
As noted by repeated balloon inflations in the cardiac catheterization laboratory, transient occlusion of the coronary artery does not cause PEA.
Risk Factors
The administration of beta blockers and calcium channel blockers is associated with an increased risk of PEA. This may be due to their effect on Ca / troponin interactions, and their inhibition of myocardial contractility.
Differentiating PEA From Other Disorders Causing Cardiac Arrest
- Asystole: In asystole, there is cessation of any cardiac activity and lack of cardiac output on this basis. In PEA, electrical activity is present.
- Ventricular fibrillation: There is no organized electrical activity present. There are only fine fibrillatory waves present in ventricular fibrillation. In PEA, there is organized electrical activity.
- Peripheral arterial disease: The inability to feel a peripheral pulse may be due to severe peripheral arterial disease.
Epidemiology and Demographics
PEA accounts for approximately 20% of out of hospital cardiac arrests, and accounts for about a third of inhospital cardiac arrests. [4] PEA is responsible for 10% of in-hospital deaths.[5]
Gender
There is a slight female preponderance of PEA. It is unclear if this is mediated by a direct influence of gender on the pathophysiology, or if female gender is a confounder.
Age
Patients with PEA tend to be older.
Natural History, Complications, Prognosis
PEA is associated with a poor prognosis, particularly if the underlying cause is not readily identifiable and treated. The presence of a QRS interval > 0.20 seconds is associated with a poorer prognosis. The survival of in hospital PEA is only 11.2%.[4] The survival for out of hospital occurrence of PEA is higher (19.5%) than for in hospital PEA, likely due to the higher incidence of reversible causes among patients with out of hospital arrest. The survival of PEA as a presenting rhythm is poorer than ventricular tacycardia or ventricular fibrillation.[6]
Diagnosis
Symptoms
Physical Examination
A rapid physical examination should be performed to identify rapidly reversible causes of PEA:
Neck
- Distended neck veins suggests cardiac tamponade
- Tracheal deviation suggests tension pneumothorax
Lungs
- Unilateral absence of breath sounds suggests tension pneumothorax
Electrocardiogram
The appearance of the electrocardiogram in the setting of PEA varies, but several common patterns exist. There may be a normal sinus rhythm or sinus tachycardia, with discernible P waves and QRS complexes. Sometimes there is a bradycardia, with or without P waves, and often there is a wide QRS complex.[7] The presence of a QRS interval > 0.20 seconds is associated with a poorer prognosis. The EKG should be carefully evaluated for signs of:
- Hyperkalemia (peaked T waves, complete heart block, a ventricular escape rhythm)
- ST segment elevation MI should be ruled out
- Osborne waves suggest hypothermia
- QRS interval prolongation suggests tricyclic antidepressant overdose
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.
Laboratory Studies
- Hyperkalemia should be ruled out
- A stat arterial blood gas will provide information regarding the presence of hypoxia and acidosis
- A stat hematocrit can also be checked on the arterial blood gas to evaluate the patient for exsanguination
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.[8]
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.[9] [10]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.[8]
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).[8]
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.
References
- ↑ ACLS: Principles and Practice. p. 71-87. Dallas: American Heart Association, 2003. ISBN 0-87493-341-2.
- ↑ ACLS for Experienced Providers. p. 3-5. Dallas: American Heart Association, 2003. ISBN 0-87493-424-9.
- ↑ "2005 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care - Part 7.2: Management of Cardiac Arrest." Circulation 2005; 112: IV-58 - IV-66.
- ↑ 4.0 4.1 Nadkarni VM, Larkin GL, Peberdy MA, Carey SM, Kaye W, Mancini ME, Nichol G, Lane-Truitt T, Potts J, Ornato JP, Berg RA (2006). "First documented rhythm and clinical outcome from in-hospital cardiac arrest among children and adults". JAMA : the Journal of the American Medical Association. 295 (1): 50–7. doi:10.1001/jama.295.1.50. PMID 16391216. Retrieved 2012-09-16. Unknown parameter
|month=ignored (help) - ↑ Raizes G, Wagner GS, Hackel DB (1977). "Instantaneous nonarrhythmic cardiac death in acute myocardial infarction". The American Journal of Cardiology. 39 (1): 1–6. PMID 831417. Retrieved 2012-09-16. Unknown parameter
|month=ignored (help) - ↑ Meaney PA, Nadkarni VM, Kern KB, Indik JH, Halperin HR, Berg RA (2010). "Rhythms and outcomes of adult in-hospital cardiac arrest". Critical Care Medicine. 38 (1): 101–8. doi:10.1097/CCM.0b013e3181b43282. PMID 19770741. Retrieved 2012-09-16. Unknown parameter
|month=ignored (help) - ↑ Foster B, Twelve Lead Electrocardiography, 2nd edition, 2007
- ↑ 8.0 8.1 8.2 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
|month=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)