Pulseless Electrical Activity

OVERVIEW

Pulseless electrical activity (PEA) occurs when organised or semi-organised electrical activity of the heart persists but the product of systemic vascular resistance and the increase in systemic arterial flow generated by the ejection of the left ventricular stroke volume is not sufficient to produce a clinically detectable pulse

  • In the ALS algorithm, PEA was formerly known as EMD (electromechanical dissociation)
  • In reality, pulseless electrical activity encompasses a very heterogeneous variety of severe circulatory shock states ranging in severity from pseudo-cardiac arrest to true electro-mechanical dissociation with cardiac standstill
  • The ‘one size fits all’ approach of current ALS algorithms may be inappropriate given the heterogeneity of PEA states
  • Overall, prognosis of PEA far less favourable than VF/VT, prognosis for out-of-hospital cardiac arrests (OOHCA) with initial asystole or pulseless electrical activity is <3% survival… though excpetions may include PEA with heart rate >60/min and ‘pseudo-PEA’
  • Need to seek and treat the underlying cause
  • In Victoria, Australia, ~12% of OOHCA with a non-shockable rhythm is PEA (the majority are asystole)

CAUSES OF PEA

The causes of PEA are widely thought of as the 4Hs and 4Ts

  • Hypovolaemia
  • Hypoxia
  • Hyper/hypokalaemia and metabolic disorders
  • Hyper/hypothermia
  • Toxicity
  • Tension pneumothorax
  • Tamponade (cardiac)
  • Thromboembolism – MI or PE

However, this list is incomplete – for instance, non-ischemic cardiac disorders and intracranial haemorrhage occurred in 8.3% and 6.9% of PEA cases (Beun et al, 2015)

The Littman algorithm use ECG waveform and echo findings to help stratify likely causes (Littman et al, 2014):

  • Step 1: Determine if the PEA is narrow (QRS duration <0.12) or wide (QRS duration ≥0.12) on ECG monitor
  • Step 2: Narrow-complex PEA is generally due to mechanical problems caused by right ventricular inflow or outflow obstruction
  • Step 3: Wide-complex PEA is typically due to metabolic problems, or ischemia and left ventricular failure (or the above causes with co-existent conduction abnormality)

MANAGEMENT OF PEA

ACLS protocol

  • ABCDE approach
  • continuous CPR (100 compressions/min, 10 breaths/min, 30:2 ratio if unintubated)
  • intubation + ventilation, IV access
  • adrenaline 1mg IV immediately upon recognition of PEA then every 2nd cycle (q4min)
  • address 4Hs and 4Ts

Specific therapy to treat cause:

  • Hypovolaemia – fluid, blood products, stop bleeding, clamp vessels
  • Hypoxia – intubation and ventilation (FiO2 1.0)
  • Hypokalaemia – K+ replacement
  • Hyperkalaemia – treat cause, Ca2+ gluconate 10mL 10%, insulin-dextrose, salbutamol, NaHCO3
  • Metabolic disorders – Mg2+ if low, Ca2+ if low, consider bicarbonate for acidaemia (e.g. with normal anion gap)
  • Hyperthermia – cool, dantrolene for malignant hyperthermia
  • Hypothermia– warm
  • Toxicity – stop absorption, increase elimination, antidote to specific drug
  • Tension pneumothorax – decompress (needle or finger thoracostomy prior to intercostal catheter)
  • Tamponade – pericardiocentesis, open chest
  • Thromboembolism – thrombolysis (proven or suspected pulmonary embolus) +/- surgical embolectomy

PROGNOSIS OF PEA

Overall, OOHCA patients with PEA have poor outcomes (Andrew et al, 2014)

  • survival to hospital discharge was 5.9% for PEA (compared with 1.1% for asystole)
  • in survivors with 12-month follow-up data, the combined rate of death, vegetative state or lower severe disability was 44.7% (95% CI 30.2-59.9%) (compared with 67% for asystole)

OOHCA patients with PEA and heart rate >60/min may have better outcomes, comparable to OOHCA patients with shockable rhythms

  • Weiser et al (2018) found that the >60/min group showed a 30-days-survival rate of 22% and a good neurological outcome in 15% of all patients in Vienna, Austria

PSEUDO-PEA

Pseudo-PEA is essentially a severe shock state and is distinct from true electro-mechanical dissociation

  • Pseudo-PEA can be detected in the absence of a palpable pulse by:
    • arterial line placement during cardiac arrest (identified by the presence of a blood pressure)
    • high ETCO2 readings in intubated patients
    • echocardiography or Doppler ultrasound demonstrating cardiac pulsatility
  • In animal models asynchronous CPR during pseudo-PEA is harmful
    • raised mean intrathoracic pressure due to chest compression can be expected to reduce rather than to increase cardiac filling

Pseudo-PEA is associated with better outcomes than true EMD

  • Prosen et al, 2012
    • in a small trial, ETCO2 and echocardiography were used to confirm pseudo-PEA
    • These patients were administered vasopressin (an additional vasopressor) and had CPR ceased for 15 seconds
    • 94% of patients received ROSC and 50% had good neurological outcomes
  • Flato et al, 2015
    • rates of ROSC were 70.4% for those in pseudo-EMD, 20.0% for those in EMD, and 23.5% for those in asystole
    • Survival upon hospital discharge and after 180 days occurred only in patients in pseudo-EMD (22.2% and 14.8%, respectively)

Management of pseudo-PEA

  • Recognition of pseudo-PEA
    • early arterial line placement and ETCO2 monitoring
    • early echocardiography, provides additional information regarding intravascular volume status (ventricular volume), cardiac tamponade, mass lesions (tumour, clot), left ventricular contractility and regional wall motion
    • avoid CPR
  • narrow complex QRS
    • likely obstructive cause (e.g. tamponade, tension, dynamic hyperinflation or PE) or underfilling (e.g. hypovolaemia)
    • treat the cause of obstructive shock, administer fluids and inopressors
  • broad complex QRS
    • consider hyperkalaemia, hypocalcaemia or cardiotoxicity
    • treat hyperK with 10% calcium chloride and NaHCO3; the former will treat a low calcium and the latter will also help overcome sodium channel blockade

FAILURE OF PULSE DETECTION

  • in some patients, pulse detection may be difficult even when the patient is not in a severe shock state (e.g. morbid obesity, calcified arteries in severe peripheral vascular disease)
  • studies suggest that first responders are poor at accurately performing pulse checks during cardiac arrests

References and links

Journal articles

  • Andrew E, Nehme Z, Lijovic M, Bernard S, Smith K. Outcomes following out-of-hospital cardiac arrest with an initial cardiac rhythm of asystole or pulseless electrical activity in Victoria, Australia. Resuscitation. 2014; 85(11):1633-9. [pubmed]
  • Beun L, Yersin B, Osterwalder J, Carron PN. Pulseless electrical activity cardiac arrest: time to amend the mnemonic “4H&4T”? Swiss medical weekly. 145:w14178. 2015. [pubmed]
  • Flato UA, Paiva EF, Carballo MT, Buehler AM, Marco R, Timerman A. Echocardiography for prognostication during the resuscitation of intensive care unit patients with non-shockable rhythm cardiac arrest. Resuscitation. 92:1-6. 2015. [pubmed]
  • Hogan TS. External cardiac compression may be harmful in some scenarios of pulseless electrical activity. Medical hypotheses. 79(4):445-7. 2012. [pubmed]
  • Littmann L, Bustin DJ, Haley MW. A simplified and structured teaching tool for the evaluation and management of pulseless electrical activity. Medical principles and practice : international journal of the Kuwait University, Health Science Centre. 23(1):1-6. 2014. [pubmed] [free full text]
  • Mehta C, Brady W. Pulseless electrical activity in cardiac arrest: electrocardiographic presentations and management considerations based on the electrocardiogram. The American journal of emergency medicine. 30(1):236-9. 2012. [pubmed]
  • Myerburg RJ, Halperin H, Egan DA et al. Pulseless Electric Activity: Definition, Causes, Mechanisms, Management, and Research Priorities for the Next Decade: Report From a National Heart, Lung, and Blood Institute Workshop. Circulation. 128(23):2532-2541. 2013. [free full text]
  • Paradis NA, Martin GB, Goetting MG, Rivers EP, Feingold M, Nowak RM. Aortic pressure during human cardiac arrest. Identification of pseudo-electromechanical dissociation. Chest. 101(1):123-8. 1992. [pubmed]
  • Paradis NA, Halperin HR, Zviman M, Barash D, Quan W, Freeman G. Coronary perfusion pressure during external chest compression in pseudo-EMD, comparison of systolic versus diastolic synchronization. Resuscitation. 83(10):1287-91. 2012. [pubmed]
  • Prosen G, Križmarić M, Završnik J, Grmec S. Impact of modified treatment in echocardiographically confirmed pseudo-pulseless electrical activity in out-of-hospital cardiac arrest patients with constant end-tidal carbon dioxide pressure during compression pauses. The Journal of international medical research. 38(4):1458-67. 2010. [pubmed]
  • Weiser C, Poppe M, Sterz F, et al. Initial Electrical Frequency Predicts Survival And Neurological Outcome in Out Of Hospital Cardiac Arrest Patients with Pulseless Electrical Activity. Resuscitation. 2018; [pubmed]

FOAM and web resources


CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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