Lessons Learned from Death & Near Death Experiences 4

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Published on The Doomstead Diner on June 29, 2017

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Part 4: PEA or EMD and a tale with a twist

By Geoffrey Chia, MBBS, MRCP, FRACP, July 2017

Sudden death may be due to causes other than malignant arrhythmias or ventricular asystole. Catastrophic events may lead to a clinical state known as “pulseless electrical activity” a term which replaced the old but entirely adequate term “electromechanical dissociation”. Simply put, PEA or EMD is a state where there seems to be adequate electrical activity of the heart (eg sinus or junctional rhythm at, say, 50 beats per minute) as displayed on the ECG monitor, but there is little or no mechanical output of blood from the heart. There is no pulse (or a barely palpable pulse, prior to complete loss of the pulse). Obviously the patient will be unconscious at the time and if the situation cannot be redeemed within a few minutes, the patient will die.

If a patient presents out of the blue with PEA and we know nothing of preceding events, we teach medical students to always think first of three classical diagnoses, another unholy trinity of scary conditions: cardiac tamponade, tension pneumothorax and massive pulmonary embolism.

(Fig 1: Circulation)

Cardiac tamponade is a situation where there is massive accumulation of fluid in the pericardial sac surrounding the heart. This sac cannot expand rapidly outwards like a balloon and thus the fluid compresses and collapses the (thin walled, low pressure) right ventricle, thus preventing blood from entering the right ventricle. (see diagram in Part 3) Hence there is no output from the RV, no flow into the pulmonary vessels, no input into the LV, no output from the LV and no pulse. If the tamponade occurs relatively gradually as in the case of “malignant effusion” due to underlying cancer, the patient will present with progressive breathlessness and there is usually sufficient time to make a diagnosis with an echocardiogram and time to drain the fluid and hence provide acute relief. In some situations however, fluid enters the pericardial sac extremely rapidly, specifically in the case of a pericardial bleed, causing sudden collapse. This may occur in a type A aortic dissection (discussed in part 3) or a ventricular rupture (a rare catastrophe in the context of a “full thickness” myocardial infarct), in which case the patient can present ab initio with PEA. Pericardial haemorrhage from either cause is almost always fatal

Tension pneumothorax is a situation where a “ball valve” mechanism forces air, with every breath the patient takes, into the pleural cavity (the space surrounding a lung). This can occur if there has been a penetrating chest wound, in which case the diagnosis is obvious (Fig 2: Open Pneumothorax). However it can also occur in the absence of an open chest wound (Fig 3: Closed Pneumothorax). In tension pneumothorax, high air pressure builds up in one pleural cavity, collapsing the lung on that side and pushing the heart and lungs toward the other side. The squashing of the pulmonary vessels obstructs output o f blood from the right ventricle. Furthermore, external pressure on the right ventricle impairs its filling as well. Both lead to reduction of cardiac output. Diagnosis is usually not a problem here: there may be a history of trauma, the patient presents with sudden severe breathlessness, on auscultation there is no air entry on one side of the chest and immediate relief is conferred by inserting a chest tube on the side of the pneumothorax.

Pulmonary embolism is a condition where a clot detaches, usually from a deep vein in a leg, and passes through the right side of the heart and gets lodged in a pulmonary artery. If the embolus is small and lodges in a peripheral pulmonary arterial branch, it can cause an infarct (circumscribed cell death) of that particular lung segment. That damaged, inflamed peripheral segment can irritate the external lining of the lung or pleura, causing “pleuritic” chest pain. Rupture of the blood vessels in that damaged segment can cause bleeding into a bronchial tube and the patient may cough up some blood (Fig 4: DVT and PE). At the other extreme of PE, if a massive clot detaches from a leg and suddenly blocks the main pulmonary artery or lodges at the branching of main pulmonary artery to RPA/LPA, a so-called “saddle embolus”, output of blood from the right ventricle will be obstructed and the patient may collapse, present with PEA and die suddenly (Fig 5: Saddle Embolus). Sometimes the chest compression of CPR may fragment the clot, allowing successful resuscitation. We have all heard horror stories where a person after a long distance flight, perhaps a young female on the pill (who may also have an undiagnosed “thick blood” disorder), got off the plane, walked a few steps then dropped dead. Such cases have been confirmed by post mortem to be due to massive PE. Thankfully they are exceedingly rare but are highly memorable because they are so unexpected and tragic.

Certainly the unholy trinity above must be considered when confronted with undiagnosed PEA. However the commonest situation in which we encounter PEA is one where the diagnosis is known and we are familiar with the preceding events, specifically in the context of failed cardiac resuscitation following myocardial infarction. The usual scenario is one where the patient was admitted for an MI and while in hospital goes into VF unremittingly. The patient is repeatedly electrically defibrillated back to normal rhythm in between chest compressions but VF keeps recurring. The resuscitation attempt is prolonged and the patient eventually appears to re-establish an adequate heart rate and rhythm on ECG monitor, but the heart is not actually contracting mechanically. The patient remains pulseless and unconscious. The patient may make gasping movements, so-called “agonal” respiration, however there is no actual air entry into the lungs. This is a pre-terminal dying reflex. What has happened is that during the prolonged resuscitation attempt, there has been inadequate supply of oxygen to the heart muscle (and brain) which is now irreversibly damaged. Hence even though electrical activity of the heart may appear to have recovered, mechanical activity has not and there is PEA. What follows after that is a flat line, ventricular asystole. The “agonal” respiration ceases and time of death is called.

The medical information above is a necessary prelude to describing my most memorable early experience of resuscitating a patient. This was back in the dark ages when I was a wet-behind-the-ears young medical graduate. I had completed one year as a hospital intern (AKA general dogsbody and menial donkey worker) and another year as an army medical officer, which mainly involved deskwork at army HQ medical services. Fortunately, for my upcoming final year as an army MO, I was to be posted to a rural army base in a third world country where, apart from my official army MO duties, I would have the opportunity to provide a basic clinic service to the local villagers. In preparation for that solo stint in the wilderness, the army released me back for intensive hospital training for a few months, rapidly rotating me through several disciplines, in an attempt to pick up basic speciality skills, not only in general surgery and general medicine but also in sub-disciplines such as ophthalmology and ENT (ear, nose and throat) basic procedures. I had just completed my ENT stint and was now on my final one month rotation in general medicine before being deployed overseas. I was attending a tutorial in a hospital ward (TPH) with some of my contemporaries who were also relatively new medical graduates. We were being taught by a medical registrar. I myself aspired to become a registrar in internal medicine, which required a great deal more study and experience on my part and was keen to absorb whatever wisdom I could from this senior colleague. Becoming a medical registrar was an essential step on the path to specialisation. We were interrupted in the middle of our tutorial (held in an annex to the ward), by a nurse who called an emergency because a patient in the ward had suddenly collapsed. This was a general medical ward, consisting mostly of non-cardiac patients with a few convalescing cardiac patients, none of whom were on heart monitors. We all rushed to the bedside and saw a gasping semi conscious elderly lady who was blue around the lips. The registrar called for a defibrillator to be brought to the bedside, which would double as an ECG monitor and determine if she was in a malignant arrhythmia which may require cardioversion. Her pulse was weak, so, as she lapsed into unconsciousness, the registrar commenced CPR and directed others to “bag and mask” the patient with oxygen. When the defibrillator arrived, we placed the electrodes on her and found she was in a normal heart rhythm, not VT or VF, hence shocking her heart was inappropriate. CPR did not improve her situation and she remained unconscious. After what seemed an interminable time, ongoing efforts seemed hopeless. She continued to have apparently satisfactory ECG complexes on the monitor, however her heart rate was now very slow, which is a common pre-terminal event. She exhibited gasping chest movements with no audible air entry to the lungs, which the registrar felt was agonal breathing. We had no idea what caused the collapse. Did she have sudden cardiac tamponade? Did she have massive pulmonary embolism? The registrar decided to cease CPR and call it. While we were moving away from the bedside, one of my contemporaries (another junior doctor), Dr KML, noticed an apple core on the patient's bedside table. She wondered aloud to everybody if that had anything to do with the patient's collapse. Even without performing the Heimlich manoeuvre, also known as "abdominal thrusts" (not recommended by the Australian Resuscitation Council these days*), a solid food bolus lodged in the larynx should in theory have been expelled by the chest compressions of CPR anyway, hence the registrar felt the apple core was not particularly relevant. Being the smart arse that I was however, and having just completed an ENT stint, I asked permission to try something. There was nothing to lose anyway, so the registrar had no objection. I grabbed a direct laryngoscope and a pair of right angled forceps from the resuscitation trolley. Using the direct laryngoscope I was able to visualise the patient's larynx and sure enough there was a piece of apple lodged on it, which I was able to extract using the right angled forceps. The patient immediately restarted normal breathing, followed shortly by return of normal colour to her lips and full consciousness. She recovered fully.

This good outcome was due to the coincidental convergence of various factors. The registrar followed normal, standard resuscitation procedures which any competent doctor would have done. Only one person in our group, Dr KML, had the acute observational skill to point out the apple core at the bedside. More importantly, she refused to accept the situation as hopeless. As for the rest of us, to paraphrase Dr A Conan Doyle, “we saw but we did not observe”. I was lucky I had recently picked up certain relevant ENT skills before joining this medical rotation, skills which I otherwise would not have had, were it not for dumb luck.

One big question arises from this story. What if such an event occurred outside hospital, say in a restaurant (with no laryngoscope or right angled forceps available) and if CPR/chest thrusts failed to dislodge the food bolus, as happened in this case? Could the patient still be saved from choking to death? The answer is yes, the patient's life could easily be saved by a simple but somewhat barbaric procedure called a cricothyrotomy, which is easily accomplished with a sharp steak knife (or pen knife) and an empty pen casing** (which is used as a breathing tube). It can be done by a layperson without medical training. Step by step instructions regarding this procedure can be found from reputable medical sites on the internet, however it should not be attempted without making a correct diagnosis first. It should not be performed on a person who has merely fainted or has had a seizure, or indeed on anyone who has collapsed from any cause other than laryngeal obstruction. It could do them serious damage. Knowledge and situational awareness are key and presumably the reader will have achieved some measure of these after repeated reading of this series of articles. Fig 6: Palpation of cricothyroid membrane

Even within the hospital context, if the cause of the laryngeal obstruction is not a lodged food bolus but is due to laryngeal fracture or laryngeal swelling or spasm (as in a severe allergic reaction), availability of a laryngoscope or a right angled forceps will not help and endotracheal intubation may be impossible. This type of laryngeal obstruction, if severe, can only be alleviated by a cricothyrotomy (or emergency tracheostomy, if the equipment and expertise are available). The diagnosis of laryngeal oedema caused by an allergy is usually obvious because the patient will often have puffy eyelids and itchy hives on their skin. In the case of allergy, adrenaline, antihistamines and steroids should also be administered ASAP.



  1. What appears to be PEA may not always be PEA.

  2. I cannot emphasize enough that making the correct diagnosis is crucial to taking correct and effective action and is crucial to whether a patient lives or dies.

  3. The so-called "leaders" of our societies are spouting flawed diagnoses based on fake news as to what truly ails humanity (or simply paying lip service to the problems while effectively ignoring them) and this monstrous ignorance, stupidity and negligence will vastly exacerbate the looming great die-off.

G. Chia, July 2017


* https://resus.org.au/faq/choking/ "The ARC does not recommend the use of abdominal thrusts as there is considerable evidence of harm caused by this procedure."

see also: https://www.accreditedfirstaid.com.au/2014/08/22/the-heimlich-manouevre-why-dont-we-use-it/

** an empty pen casing, kept in a first aid kit, can also be used as a chest tube for a patient with tension pneumothorax. No underwater seal is needed, just a finger stall cut from a rubber glove, which is attached with a rubber band to the end of the tube. This finger stall becomes a one way air valve. Fig 7: Treatment of Pneumothorax

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