![]() ![]() Additionally, pulseless electrical activity (PEA) can cease and become asystole. Asystole typically occurs as a deterioration of the initial non-perfusing ventricular rhythms: ventricular fibrillation (V-fib) or pulseless ventricular tachycardia (V-tach). 2008 36:391–396.Asystole, colloquially referred to as flatline, represents the cessation of electrical and mechanical activity of the heart. Simplifying the diagnosis and management of pulseless electrical activity in adults: a qualitative review. A Simplified and Structured Teaching Tool for the Evaluation and Management of Pulseless Electrical Activity. Survey of junior hospital doctors’ attitudes to cardiopulmonary resuscitation. First documented rhythm and clinical outcome from in-hospital cardiac arrest among children and adults. Nadkarni VM, Larkin GL, Peberdy MA, et al.I like the approach because it makes me think differently and takes into account the very thing we are looking at throughout this whole scenario…the ECG trace. Please remember that this system is an academic proposal and as the author himself writes, there are some limitations, especially with patients with a pre-existing left bundle branch block or a massive PE, where the complexes may appear wide. If Na channel blockade is suspected, give NaHCO3. ![]() If Hyperkalaemia is suspected give NaHCO3 and Calcium.If a Tension pneumothorax then decompress.If there is over ventilation, disconnect.The echocardiogram can give the rest of the solution Start Fluid- Normal Saline and be aggressive as these causes may respond to fluid.How To Use This Approach In A Narrow QRS Complex PEA The proposed approach doesn’t specifically use hypothermia or toxins but assumes that given the history of presentation, that these causes will be picked up. This approach doesn’t take into account hyperaemia, hypokalaemia, or hypoglycaemia, however the frequency of progression to PEA of these patients is very rare(4). This is usually due to a metabolic problem or ischaemia and heart failure. In a 2014 paper, Littmann et al(3) proposed a new tool that simplified the approach to PEA by simply looking at the width of the QRS complex and dividing the causes based on QRS width. We now use echocardiography and certainly our appreciation of electrocardiographic tracings has much improved, yet neither ECG tracings nor echocardiography appear anywhere in these protocols. Things have changed since these guidelines were produced. That’s been my approach since I can remember. ….Then I’ve got to think of the others…….Could they be having a PE or MI or is there a cardiac tamponade?.I personally have an approach that is as follows: In fact the literature shows that it is difficult during an arrest to remember them all(2), so you and I are not alone. ![]() I don’t know about you but I see people trying to think of them during an arrest and having trouble. When confronted by the PEA patient, ACLS guidelines require us to quickly evaluate the potential cause by citing the H’s and T’s. ![]() More on this will follow in the next few blogs. More recently, the term pseudo-PEA, is used for those patients where we can’t find an output by feeling for a pulse, but there may in fact be one, when we view the heart by echocardiography. Given that it’s not a shockable rhythm, it has a very poor prognosis, especially when associated with acute myocardial Infarction(MI)(1). Pulseless Electrical Activity(PEA) occurs in about 30% of cardiac arrest cases. ![]()
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