Lessons Learned From Death & Near Death Experiences

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Published on The Doomstead Diner on June 6, 2017

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Part 1: Malignant Ventricular Arrhythmias

by Geoffrey Chia, MBBS, MRCP, FRACP, June 2017

Advances in Cardiology over the past several decades have been nothing short of astonishing. The first major advance arose from the realisation that most deaths in the acute phase of myocardial infarction or MI (heart attack) were due to ventricular fibrillation or VF (a lethal cardiac rhythm) which could be reverted with prompt DC Cardioversion (electrical defibrillation). DCC applied within seconds of onset of VF is virtually always successful, leaving no detriment to the brain or other vital organs. With each minute of delay however, the likelihood that DCC will fail and hence the patient will die increases exponentially. Even if belated DCC is successful, with each minute of delay the likelihood of subsequent brain damage due to oxygen deprivation increases exponentially. 1

 

The risk of VF declines markedly after the first 48 hours following an MI, as the electrical instability of the heart muscle settles. The understanding of this particular mechanism of cardiac death led to the creation of coronary care units or CCUs in the 1970s, staffed by specially trained cardiac nurses who continuously monitor the cardiac rhythms of "early MI" patients and administer immediate DCC if a patient goes into VF. This was the first major mortality advance for in-hospital cardiac care.

Resources are finite and it is highly inappropriate to utilise CCU beds for patients with non-cardiac chest pain, which could deprive genuine cardiac patients of life saving monitoring. Appropriate patient selection requires high diagnostic accuracy which still remains an art more than a science. "Unstable" or "crescendo" angina, which can precede myocardial infarction, may not manifest any blood or ECG abnormalities when the patient initially turns up at the emergency department. Back in the Dark Ages when I was a cardiology trainee, I remember receiving a phone call from the A&E registrar about a middle aged man who presented with fluctuating indigestion type pain and the ECG done when he happened to be free of pain was normal. The entire story however did not sit comfortably with me and instead of agreeing to send him home, I told them to admit him to a CCU bed. Later that night, I received a phone call from a CCU nurse telling me she had just shocked the patient out of a VF arrest, thus saving his life. We then set into motion full fledged MI therapy for him, rather than the basic medication and monitoring originally initiated. I shuddered to think what would have happened had I allowed the patient to go home. He would certainly have died.2

The ONLY treatment for VF is DCC, electrical defibrillation. True VF NEVER spontaneously reverts back to normal rhythm, it is always relentless and unremitting and the ONLY action which can revert it back to normal is DCC. CPR is only a bridge to keeping the patient (barely) alive till they can be shocked. If DCC can be applied within seconds of onset of VF, CPR should be avoided.

Some patients have such severe MIs that their heart muscle becomes so electrically unstable that the situation is irredeemable. They exhibit multiple recurrent bursts of VF, each requiring DCC and in between shocks we try to stabilise them with medications such as amiodarone. Only once did I go through the entire gamut of drastic drugs, eventually reaching to the agent of last resort, bretylium, which also failed to stabilise the patient, who went into refractory VF which did not respond to further DC shocks, ending up with a flat line. Thankfully in this day and age, advances in preventive cardiology have rendered such scenarios very uncommon.3

Ventricular tachycardia or VT is a beast somewhat different from VF, yet it can also be quite similar. VT can lead to VF. VT can be categorised into monomorphic and polymorphic VT, which in turn have their own subcategories. If the onset of rapid VT is witnessed on the heart monitor and if the patient is still conscious, then urgently telling the patient to cough forcefully may revert the VT back to normal rhythm. If not, and the patient lapses into unconsciousness, then a precordial thump (slamming your fist onto the patient's sternum), can sometimes revert it. If that does not work, the patient must have immediate DCC.

In the bad old days when we used ionic contrast media for coronary angiography, it was not uncommon to provoke a burst of VT especially when injecting the right coronary artery. The staff would then shout in unison at the patient to "COUGH". The cardiologist might even poise their gloved fist over the patient's chest, ready to thump it if coughing did not work, an appalling image. Thankfully such bursts of VT during angiography were usually self limiting and very brief. On rare occasions when the VT deteriorated to VF, DCC would be promptly applied, leaving no bad sequelae for the patient (a defibrillator is always charged up and ready to go in every cardiac catheterisation lab).

Ventricular tachycardia occurring in the early, irritable phase of an MI may manifest as multiple, brief, self limiting bursts which may be suppressed by medications such as lignocaine or amiodarone. It is also essential to correct electrolyte disturbances. If VT deteriorates into VF then the only treatment is DCC. Specific arrhythmias require specific treatment.4 This is why all CCU staff need to know how to read ECGs.

There is one particular type of monomorphic VT, due to a re-entrant pathway (electrical short circuit) in an otherwise normal heart, which is benign in the sense it may be relatively slow, say 160/min, is well tolerated, does not deteriorate into VF and usually responds well to oral medication. It can also be completely cured by an ablation procedure. On the other hand, very rapid, sustained monomorphic VT, especially in the context of an acute MI, can cause collapse and should be treated with immediate DCC, just like VF. However VT caused by drug toxicity such as flecainide or digoxin overdose can be notoriously unresponsive to DCC – which might even precipitate fatal, refractory cardiac arrest. Identifying the underlying cause of the monomorphic VT is of vital importance in managing the patient.5

Polymorphic VTs are of various types as well. Polymorphic VT may appear so chaotic on ECG that it may be confused with VF, however like monomorphic VT, polymorphic VT may occur in self limiting bursts and may respond to a vigorous cough or a precordial thump. If a prolonged run of polymorphic VT causes collapse, it should be treated with DCC anyway.6

There is a specific type of polymorphic VT called "torsade de pointes" VT, which also has subcategories. The French name means "twisting about the points" and I personally liken the summary ECG appearance to a "double sine wave" pattern. The commonest type of TDP is "acquired" in the sense that it tends to manifest in middle age or later, usually in females and is related to having a background slow heart rate. Various "QT prolonging" medications (and there are many of them) can predispose patients to this arrhythmia.

TDP had previously been described as "self limiting VF" by some early investigators because short bursts could appear similar to VF, but that was a misnomer. TDP can present as self limiting bursts of abnormal rhythm causing dizzy spells or even blackouts, but there is a substantial risk that any one single burst can become continuous, leading to cardiac arrest and death. In that situation, the TDP requires prompt DCC. VF on the other hand is never self limiting. Once VF occurs, it always persists and it never self reverts. The only treatment for VF is DCC.

All this information may be confusing to a lay person. However such background knowledge is essential in order to understand why and how certain experiences have profoundly influenced my thinking, my beliefs and my actions. Cardiology is not a dry esoteric academic field. It deals with life and death situations. But it does require specific knowledge, applied with common sense.

One of my most memorable patients was a lady in her 60s I encountered long ago when I was a cardiology trainee. She presented with dizzy spells and her ECG monitor in hospital showed bursts of TDP. Her background ECG when in sinus (normal) rhythm showed a slow rate around 40+/min with a "prolonged QTc", the latter being a classical marker for the predisposition to TDP. Immediate treatment was intravenous magnesium, then a search for and elimination of any background medications which could prolong her QTc, the commonest being sotalol. Despite that, she continued to exhibit bursts of TDP, hence I placed a temporary pacing wire in her heart and set the demand pacing rate at 70/min. This completely suppressed further TDP. It was now obvious that the only way to protect her in the long term was with a permanent pacemaker (this was in the days before implantable defibrillators became routine). PPM implantation was one of my routine responsibilities as a cardiology registrar so I scheduled her on the list. Our protocol required intravenous antibiotics immediately before the operation, usually a broad spectrum cephalosporin (which is related to penicillin). She however gave a history of a previous severe allergy to penicillin, hence I established her on an alternative agent in our protocol, intravenous erythromycin. Within minutes of starting that drip however, just as we were about to wheel her from the prep room into the OT, her previously rock solid stable paced rhythm at 70/min became unstable, with bursts of TDP yet again. I was completely taken aback by this, not really knowing what was going on, but decided to cease the erythromycin, then increased the pacing rate of her temporary pacemaker to 100/min and gave her another shot of i/v magnesium. This stabilised things. I swapped the erythromycin for another antibiotic, implanted her PPM, removed her temporary wire and sent her back to CCU. When I later explored the literature about TDP, I found, in the fine print, among the long list of medications which could potentially predispose a patient to TDP, erythromycin. The intravenous erythromycin had, in mere minutes, further prolonged her QT interval, thus raising her heart rate threshold for the development of TDP, such that even being paced at 70/min did not sufficiently protect her. This event more than any other highlighted to me how even small details buried deep within a mountain of other medical information can make the difference between life and death.7

Medical information derived from peer reviewed scientific research which has been reproducibly validated and summarised in textbooks, informs us about objective reality. We ignore, dismiss or remain ignorant of such scientific knowledge at our peril. It is impossible for any one single person to know everything, which is why specialisation is necessary. But hyper specialisation can result in tunnel vision, which is why specialists must talk with each other and why "specialist generalists" (specialists in general internal medicine) are also needed to help join the dots and offer us a big picture. Not only that, doctors must talk with scientists and policy makers must be informed by scientists to make rational, enlightened policy decisions.

Contrast this enlightened reality based belief and policy system with the unschooled opinions of ignorant self styled experts, principally the homoeopathic anti-vaccination delusionists who are simply malicious and despicable egotistical idiots. And yes, I include in that category Pauline Hanson, one of the most loudmouthed and stupid examples of incompetent ideological buffoonery (earlier this year she argued against the vaccination of children) and her offsiders such as the execrable and malevolent Malcolm Roberts, a monstrous denier of climate change reality. Such political opportunists are the enemies of reason, the enemies of decency and the enemies of humanity who work in the service of rightwing racist rednecks and/or the fossil fuel fraudsters and are given prominence by the prostitute mainstream media. Ditto for their American counterparts. They are a blight on humanity. They are a cancer. They are evil. I won't even talk about Mr. Orange HWAFL (which rhymes with “awful” and stands for “Hairpiece Without A Frontal Lobe”), the mere thought of whom induces projectile vomiting amongst the sapient.

CONCLUSION: LESSONS I HAVE LEARNED (numbers are referenced from above)

  1. In an emergency situation, immediate, appropriate action can make the difference between a perfect outcome and severe disability or death.

  2. The Precautionary Principle saved that man's life.

  3. Prevention is always better than cure.

  4. Making a correct diagnosis is of vital importance to enable appropriate, effective action.

  5. Identifying the underlying cause of a problem is of vital importance to enable appropriate, effective action.

  6. There are various levels of diagnosis. There is the broad diagnosis, which may be sufficient for emergency management (eg diagnosing rapid VT which requires DCC, but not necessarily identifying the subtype of VT at that time). There is the specific diagnosis, which requires identification of the underlying cause of the problem and is necessary for long term individual management (eg VT in the acute phase of an MI tends to settle after 48 hours, especially if the extent of muscle damage has been limited by PCI or thrombolysis, and does not require long term antiarrhythmic therapy. However VT unrelated to an MI and due to an unfixable abnormality eg "RV dysplasia" requires an implantable defibrillator).

  7. Science based knowledge is completely different from and is infinitely superior to other types of so-called "knowledge", such as being able to quote passages from the particular version of the Bible which suits your prejudices. Indeed the latter is not knowledge, it is anti-knowledge. It is pretentious bullshit dressed up as ancient “received wisdom”, designed to preserve the power and wealth of a patriarchal authoritarian organisation. Science based knowledge is based on objective reality, can be used for the immense benefit of ordinary people and makes the difference between life and death. Furthermore, the devil is in the detail.

Of course, the above aphorisms are already familiar to everyone, even to the extent that some may regard them as trite platitudes, "I've heard it all before, sooo booooring, let's move on". I think such sneeringly complacent people should have those aphorisms tattooed on their foreheads, laterally inverted, so they can read it every morning when they look in the mirror. Especially these days when we face existential threats to our survival which have been clearly identified by Objective Science. Especially since the source of those threats to our survival are the anti-knowledge, anti-reality fossil fuel fraudsters, armchair warmongering chickenshit politicians, mendacious economists, rapacious bankers and their media whores.

Even though I have left the days of stressful in-hospital night duty long behind me and am content to pursue non-procedural clinical work nowadays (I am not an adrenaline junkie like the emergency or ICU or surgical consultants), the hard lessons learned from my early training have been burned into my brain and continue to inform every aspect of my patient care, every single day. And they inform my wider philosophy.

One Response to Lessons Learned From Death & Near Death Experiences

  • George Robinson says:

    Hi Geoffrey,  

    I think you'd love getting to grips with My-Big-TOE by Tom Campbell.  Science is finally finding its own foundation. 

    And for a sober view of why some sapients are not altogether trusting of the international vaccination programs (because of the potential for abusive payloads they provide), William Pawelec describes here billions of bio-chips missing from a facility later bought out by Siemens:   www.youtube.com/watch?v=yytSNQ2ogD4

    We really need much more transparency in both Government and the corporate world to start trusting large scale programs again.

    Thank you for sharing your experiences in coronary medicine !  

     

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