A new PEA diagnostic algorithm: ECG and ultrasound

How are we supposed to remember all those pesky reversible causes of PEA arrest in the crunch of an actual arrest? Well, this article by Littman and all offers a new approach:


Farewell H & T

The traditional ALS teachings for causes of PEA arrest have been based around trying to recall a list of Hs and Ts, that, by some counts, extends to 13 by time you expand out all those acronyms. It is argued that these are not the easiest thing to remember, and include a number of conditions that are not really that likely to cause PEA arrest (especially without someone noticing it first). In addition, this does not give any guidance on how to differentiate between them based on the limited clinical information in front of you during an arrest.

3 + 3 = PEA

In 2008 Desbiens reviewed the causes of PEA arrest in the published literature, and narrowed the important causative considerations down to 3 main groups:

  1. Volume (or lack thereof)
  2. Pump failure
  3. Obstruction
    1. Tension pneumothorax
    2. Cardiac tamponade
    3. Massive PE
The 3 and 3 model [Desbiens 2008]

This is a great rationalisation of the issue, but still lacks a little clarity for newcomers (what does "pump failure" include?), and does not give an easy approach on how to differentiate between them all.

A new approach: ECG + ultrasound

Littman et al combine initial ECG morphology with clinical scenario to indicate the most likely causes, and offer further diagnostic backup using bedside ultrasound. The primary distinction is between narrow complex and wide complex PEA, with ultrasound being used to help differentiate the causes of narrow complex PEA in particular.

They offer a few simple diagrams in their article, but I thought I might try and bring it all together into a unifying algorithm:


Of the traditional Hs and Ts, they exclude trauma and other conditions that would be clinically obvious (eg hypothermia) or would likely present initially with bradycardia, hypotension or atrioventricular block prior to PEA (eg β-blockers, calcium channel blockers or digoxin). They have also excluded causes that have not been shown to actually lead to much PEA (eg hypoxia, hypokalaemia and hypoglycaemia).

I like that this is based on simple bedside information available at a PEA arrest: clinical history, ECG pattern and bedside ultrasound, and that it has prioritised the number of important causes to consider in the heat of the moment (but also provides a bit more than the Desbiens model). I think it mainly reinforces what is becoming standard practice of looking at the patient, ECG and then including a quick bedside ultrasound (such as the RUSH protocol).

This algorithm may help mainly in the narrow QRS group to help guide some decision making in where to look first with the ultrasound probe: RV collapsing, is there tamponade? If not, is there pneumothorax? RV full, are there other signs of PE or sufficient suggestion in the clinical scenario to merit empirical thrombolysis?

Choose your weapon

Which ever method takes your fancy—the 4 Hs & Ts, the 3 & 3, the ECG and ultrasound, or a combination of them all—it's worth having a framework in mind to quickly work through potential reversible causes in your arrested patient while pumping away.

So, how do you approach this in the heat of resuscitation?



Australian Resuscitation Council. Adult Cardiorespiratory Arrest Management Flowchart. 2010 [accessed August 2014]

Desbiens NA. Simplifying the diagnosis and management of pulseless electrical activity in adults: a qualitative review. Crit Care Med. 2008 Feb;36(2):391-6 

Littmann L, Bustin DJ & Haley MW. A Simplified and Structured Teaching Tool for the Evaluation and Management of Pulseless Electrical Activity. Med Princ Pract 2014;23:1–6

Seif D et al. Bedside Ultrasound in Resuscitation and the Rapid Ultrasound in Shock Protocol. Crit Care Res Pract. 2012; 2012: 503254. View the full text here


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