A Simplified and Structured Teaching Tool for the Evaluation and Management of Pulseless Electrical Activity

Abstract

Cardiac arrest victims who present with pulseless electrical activity (PEA) usually have a grave prognosis. Several conditions, however, have cause-specific treatments which, if applied immediately, can lead to quick and sustained recovery. Current teaching focuses on recollection of numerous conditions that start with the letters H or T as potential causes of PEA. This teaching method is too complex, difficult to recall during resuscitation, and does not provide guidance to the most effective initial interventions. This review proposes a structured algorithm that is based on the differentiation of the PEA rhythm into narrow- or wide-complex subcategories, which simplifies the working differential and initial treatment approach. This, in conjunction with bedside ultrasound, can quickly point towards the most likely cause of PEA and thus guide resuscitation.

The 10 Commandments of Resuscitation

“…There is increasingly more certainty regarding the fact that wide and slow complexes are of coronary aetiology, secondary to severe hyperkalemia or severe sodium channel blocker toxicity (these are agonal rhythms or that require urgent coronary intervention), unlike narrow fast rhythms, which are due to mechanical causes (cardiac tamponade, tension pneumothorax, pulmonary embolism) or hypovolemia [16]. The current use of point of care ultrasound (POCUS) has an excellent indication in the case of rhythm change with a pulse in order to rule out mechanical causes or hypovolemia as the factors leading to cardiac arrest [17].…”

Improving Survival From Cardiac Arrest: A Review of Contemporary Practice and Challenges

“…35,36,62,64 The causes of pulseless electrical activity have been classically listed as the H's and T's (Table 3), but some authors have developed simpler approaches to its diagnosis. 62,[65][66][67] Pulseless electrical activity can be broadly divided into reversible states in which the arterial pressure generated by cardiac contraction is inadequate to produce a palpable pulse (termed "pseudo-pulseless electrical activity") and irreversible states of electromechanical dissociation when the electrical activation of the heart fails to produce a mechanical contraction. 62,65-67 Pseudo-pulseless electrical activity is the end stage of any form of profound shock.…”

“…Hypoxemia and acidosis typically contribute to persistent or recurrent pulseless electrical activity during prolonged cardiac arrest, although hypoxemia may cause almost 25% of arrests attributed to pulseless electrical activity. 65,66,68,69 The pulse rate and QRS width on ECG can provide useful clues in regard to the cause of nontraumatic pulseless electrical activity (Figure 1). 62 Reversible causes (pseudopulseless electrical activity from profound shock) often produce tachycardia with visible P waves and a narrow QRS complex (tachycardic pulseless electrical activity with a supraventricular rhythm).…”

“…62 Reversible causes (pseudopulseless electrical activity from profound shock) often produce tachycardia with visible P waves and a narrow QRS complex (tachycardic pulseless electrical activity with a supraventricular rhythm). [65][66][67] Electromechanical dissociation and irreversible causes of pulseless electrical activity typically manifest bradycardia without visible P waves and a wide QRS complex (bradycardic pulseless electrical activity with a ventricular escape rhythm). 65,67 Causes of wide or slow bradycardic pulseless electrical 62 Littmann et al, 65 Desbiens, 66 and Mehta and Brady.…”

“…[65][66][67] Electromechanical dissociation and irreversible causes of pulseless electrical activity typically manifest bradycardia without visible P waves and a wide QRS complex (bradycardic pulseless electrical activity with a ventricular escape rhythm). 65,67 Causes of wide or slow bradycardic pulseless electrical 62 Littmann et al, 65 Desbiens, 66 and Mehta and Brady. 67 activity include hyperkalemia (expect characteristic ECG changes), sodium channel blocker toxicity (suggested by the clinical scenario), postshock pulseless electrical activity, massive myocardial infarction, hypoxemia, and metabolic causes, such as acidosis, hypothermia, prolonged arrest, and multiorgan failure.…”