Lessons Learned from Death and Near Death Experiences 2

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Published on The Doomstead Diner on June 12, 2017

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LESSONS LEARNED FROM DEATH AND NEAR DEATH EXPERIENCES

Part 2: Complete Heart Block and Ventricular Asystole, true and false “brown pants cases”

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

Cardiac arrest refers to the sudden cessation of effective pumping action of the heart due to either an extremely rapid heart rate or, less commonly, due to complete ventricular standstill.

Malignant, extremely rapid ventricular arrhythmias, most commonly VF, are the main cause of sudden cardiac death. Rarely, supraventricular arrhythmias can mimic ventricular arrhythmias and cause sudden death (eg atrial flutter or atrial fibrillation conducting rapidly down an accessory pathway resulting in a ventricular rate of 300/min or more. The ECG of this particular supraventricular arrhythmia resembles a ventricular arrhythmia because of “aberrant conduction”).

At the opposite end of the spectrum, primary ventricular asystole or ventricular standstill is another cause of sudden cardiac death, although rather uncommon. The electrical, and hence mechanical, activities of the ventricles, the main pumping chambers, literally just stop. The patient flatlines. Contrary to Hollywood dramas, ventricular asystole does NOT respond to DC shock, you cannot “jump start” a heart in asystole. We sometimes try DCC anyway if we suspect the patient is in “fine VF” – when the amplitude of the VF is so small it might mimic a flat line. But true asystole does not respond to DCC.

Cardiac arrest in the context of a myocardial infarction is usually due to VF. Flatlining is only seen at the very end of a failed resuscitation when the heart muscle has experienced prolonged starvation of oxygen and energy, and is essentially dead. This is secondary ventricular asystole, secondary to the heart muscle being dead.

Patients who develop complete heart block or CHB (when electrical impulses between atria and ventricles are blocked) have slow heart rates, perhaps between 25 to 40 beats per minute depending on the level of the new intrinsic pacing focus, the “escape” focus, which has taken over from the normal intrinsic pacing focus, the sinus node. CHB may first be discovered by the doctor when it is already chronic (ie persistent and well established). The patient may present with fatigue and breathlessness with a very slow heart rate and those symptoms are fully reversed after they have pacemaker implantation.

Before CHB becomes chronic however, it tends to be intermittent. If the heart rate abruptly drops from a normal rate of, say 100/min during activity, to just 30/min, the patient may feel very dizzy or even blackout. Often there is a pause, there is ventricular standstill, in the transition between the normal rate and new slow rate, before the new escape pacing focus kicks in. This pause is primary ventricular asystole. If the pause is brief eg 4 or 5 seconds duration, the patient may just feel dizzy, but if it is about 7 seconds or longer the patient will lose consciousness. If upright, they will have a sudden “drop” attack.

Patients with untreated CHB have high rates of sudden death. This high mortality rate can be completely reversed by permanent pacemaker implantation. The mechanism of sudden death in untreated CHB is probably primary ventricular asystole, but that is difficult to prove because their deaths tend to be unmonitored deaths occurring in the community. Nowadays whenever we see any hint of CHB picked up by ECG monitoring and there is no reversible underlying cause (eg medications, hypothyroidism, acute phase of inferior MI), the patient very quickly gets a PPM before they come to any harm. A simple and low risk procedure which is incredibly cost effective, hence worth doing even for a 90+ year old patient.

All the background information above is necessary to understand my attitudes and approach towards certain tricky cardiac situations. It is always stressful if a patient has a cardiac arrest in front of you. Hopefully when that happens, you switch to cold, clinical, analytical mode and act according to the dictates of your emergency algorithms. After the event, even if the outcome has been 100% successful, exhaustion kicks in and you feel drained, a lot has been taken out of you, you need to sit down and take a few deep breaths.

I have a term for such cases. I call them “brown pants cases”. That does not refer to the patients themselves but more to an imagined consequence of their potential effect on me. Whereas I tended to designate most “brown pants cases” in retrospect, because their malignant arrhythmia or ventricular standstill occurred unexpectedly out of the blue, some potential BPCs may be anticipated in advance.

In my third year as an advanced cardiology trainee, my bosses made me responsible, as sole operator, for the permanent pacemaker implantation list. Implantation of a brand new pacemaker system involved transvenous placement of the the atrial and ventricular electrodes in the right side of the heart, which after testing for correct positioning, were then connected to the implantable pulse generator (the IPG contains the battery and microprocessor) which itself was placed in a subcutaneous pocket under the clavicle (usually left clavicle, for right handed patients). It was a routine procedure which I did not find stressful. Paradoxically, the much simpler and faster procedure of IPG replacement only (where the original pacing electrodes are retained) was potentially much more stressful for me.

In a patient with an old pacemaker system, the battery will need replacement after, say, 8 years (sooner if the IPG paces constantly, but later if the IPG only paces intermittently). Some patients are mostly in their own normal intrinsic rate and rhythm and only exhibit CHB intermittently, at which time the PPM senses the slow rate and paces the heart at a “demand” pacing rate, which may be set to perhaps 50/min. In other patients however, the PPM paces the heart 100% of the time. When you test the PPM with a programming device and reduce the “demand” pacing rate to 30/min, if the PPM still continues to pace with no evidence of the patient's own intrinsic rhythm kicking in, we designate such patients as “pacemaker dependent”. Why is this important? Because if you disconnect the old IPG (with the depleting battery) from the electrodes in a non pacemaker dependent patient, their intrinsic heart rate and rhythm will take over and all will remain stable while you take your time to connect the brand new IPG to the electrodes. In a pacemaker dependent patient however, when you disconnect the old IPG, the patient is likely to flatline. You therefore only have a few seconds to connect the new IPG to the old electrodes and restart the pacing, or TS will HTF. I used to have nightmares about fumbling around, dropping both old and new IPGs on the floor and the patient flatlining all that time, with chaos reigning supreme. It never happened of course, and I never took me more than 2 or 3 seconds to disconnect the old IPG and connect the new IPG to the electrodes, but I had nightmares about it. It is best to avoid trouble by anticipating problems in advance. Hence before performing routine IPG replacements, I used to go through the printout of the patient's last PPM check to see if that patient was pacemaker dependent. If they were, I would write on the top right hand corner of the front page of the patient's notes: BPC. That was a reminder to me when I next saw their notes again in OT just before the procedure, to be extra careful and extra quick.

LESSON LEARNED: It is best to anticipate problems in advance in order to prevent them from occurring, or to be prepared to act quickly and effectively if the anticipated problem does, in fact, occur. To be forewarned is to be forearmed.

 

I would now like to describe one memorable false alarm, a false BPC if you will. As it was not a true emergency it was not a stressful event, merely an interesting learning experience. This was an example of fake ventricular asystole a long time ago in a patient in whom I had just implanted a permanent pacemaker at the Royal Brisbane Hospital*. It is normal practice after PPM implantation for the patient to be monitored overnight in CCU just in case early lead displacement inadvertently occurs. Shortly after implanting the PPM in that patient I was doing an evening round in CCU and the nurse in charge calmly mentioned to me that the patient's bedside monitor was persistently sounding the alarm of ventricular asystole and the ECG tracing on the monitor was a flatline. The commonest cause of flatlining is inadvertent detachment of one or more skin electrodes, perhaps when the patient turns over in bed, however this is easily detected as such by the machine and is displayed as "leads off" on the monitor. In this patient, all electrode wires were securely attached. The patient himself was however fully conscious, felt perfectly fine and his pulse and BP were perfectly normal. What was going on? Before answering the question, some background information is necessary.

If you are not a health worker, you may wish to skip the following explanation in green, because it is rather technical. The surface electrocardiogram or ECG is a record of electrical activity of the heart, sampled via "sticky dot" electrodes placed on the skin of the limbs and trunk. Each spike of electrical activity (either a "depolarisation" or "repolarisation") is a vector having magnitude, measured in millivolts, and direction (by convention described only in two planes, the coronal and transverse planes). The direction of the main vector, the QRS complex, which represents summary depolarisation of both ventricles, is termed the "cardiac axis". Various "leads" or "channels" look at cardiac electrical discharges from different directions, for example in the standard twelve lead ECG, leads II, II and aVF look at the heart from below, the so-called inferior leads. The "V" chest leads look at the heart from the front and left side, the so-called anterolateral precordial leads.

Old fashioned "dumb" ECG machines merely capture the basic magnitude and direction of each electrical vector, which is displayed on paper or on a monitor. There is no processing of the raw vectors. "Smart" ECG monitors with microprocessors, particularly the newer CCU monitors which were proliferating at that time, not only captured the basic data but also performed software modification before displaying the ECG.

Electrical activity of the pacemaker also has magnitude and direction, but pacemaker "spikes" tend to be much smaller than electrical discharges from the heart muscle. The pacemaker spikes may be too small to be detected by a "dumb" ECG machine. This cannot be resolved by simply increasing the sensitivity of the ECG machine because that could result in indiscriminately amplifying all sorts of electrical "noise" from skeletal muscle activity, making the ECG impossible to read. The way around that is to "tell" the smart ECG monitor that the patient has a pacemaker. The machine then looks, with extremely high sensitivity, at the time window just before each QRS complex and is thus able to detect the pacemaker spike, which by software processing it then magnifies for display. This selective magnification of a tiny electrical spike during an extremely short time window avoids the indiscriminate magnification of other tiny electrical impulses during the rest of the cardiac cycle. In that particular older "smart" monitor, I suspect the detection of the augmented pacemaker spike, being a post data acquisition event, may have been inadvertently inserted on the ECG tracing late and coincided with the cardiac QRS depolarisation (rather than being just before it).

My theory as to what caused the apparent flatline for that post PPM patient is this: In the particular directional channel we were using to monitor him at the time, it just so happened that the direction and magnitude of the (computer processed) pacemaker spike was exactly opposite and equal to that of the QRS complex, hence both cancelled each other out and the tracing in that particular channel appeared as a flatline and was interpreted as ventricular asystole by the monitor, which then triggered the alarm continuously. Hence the solution was simple, merely switch the channel of interrogation to one which looked at the heart from a different direction, in which the pacing spike and QRS vectors were not aligned. We did that with the flick of a switch and hey presto, the QRS complexes suddenly appeared, the patient was no longer in "ventricular asystole", we had resurrected him from the "dead" and the monitor no longer alarmed.

LESSON LEARNED: So-called "smart" machines can actually be incredibly dumb, can do wrong things and can make unwarranted assumptions (sort of like the predictive text on your smartphone). Irrespective of what the ECG monitor shows, always look at the patient and use your common sense before you pounce on their chest to perform CPR. You must work out problems in a logical way. Reality ALWAYS makes sense.

G. Chia June 2017

FOOTNOTE:

* This was just after I had completed my cardiology training (having previously implanted almost a hundred PPMs as sole operator) and was working as a temporary locum cardiologist in RBH, now known as RBWH. There was no full time electrophysiologist working at RBH back then, however the RBH lacked a PPM service mainly for political reasons which I will not get into here. General cardiologists with sufficient training are fully competent to implant PPMs, indeed the top pacemaker expert in Australia, Dr Harry Mond, was a general cardiologist, not an electrophysiologist. The top pacemaker expert in the world at that time, Dr Seymour Furman, was a general cardiologist, not an electrophysiologist. In the absence of an onsite PPM service, patients with heart block admitted to RBH needed to be transported onwards by ambulance, accompanied by a CCU nurse, to another hospital "just up the road" to have their PPM implantation. This would deprive the CCU team in RBH of a highly trained cardiac nurse for more than an hour. To me this was a crazy waste of resources, because we had the facilities and staff to implant PPMs in RBH. My boss at the time, Professor MF, reallocated funding to establish a pioneer PPM service in RBH and we went ahead. All proceeded well from the clinical point of view but after implanting fourteen patients with PPMs, administration got wind of our activities and I was bawled out by the medical director of RBH at the time, Dr BC, for not working according to the dictates of his administration. This was water off a duck's back to me (MF told me to ignore BC). After I left that temporary stint for a full time job in another public hospital, RBH no longer had a PPM service until they employed a full time electrophysiologist some years later.

One Response to Lessons Learned from Death and Near Death Experiences 2

  • Marty says:

    Very nice, information-filled article.

    I have often wondered about similar problems as software becomes ever more complex, from a generally Tainter-esque perspective.

    My day job is neuroimaging.  The complexity, but also helpfulness, of software has rapidly increased.  I have been responsible for some of this myself (original co-author of freesurfer).

    Because software is more and more robust and adaptable, students quickly become adept at stringing together long 'processing pipelines'.  These often involve executing the compiled result of many millions of lines of code.

    Overall, things have worked out better than I would have intuitively expected :-}

    The problems that have resulted are subtle.  They don't come from people using the software more or less as it was intended, on the problems for which it was originally designed.  Rather they come up as people find themselves in a situation where the easy gains — the 'good stuff' with large effect sizes — have been 'used up' by previous researchers.  They are driven to large increases in additional complexity of their 'pipeline' to squeeze out small additional gains, which get ever closer to the edges of statistical significance.  Or they use larger and larger sample sizes, which make it easier to find a small, but still statistically significant effect.

    The problem (mainly) isn't that scientists have suddenly become more dishonest or fad-driven or publicity-seeking.  It's simply that the 'good stuff' has mostly been used up.

    Every once in a while, a new trick is discovered that exposes some new 'good stuff' that has such a large effect size that you hardly need statistics at all.

    But a continuous supply of new 'good stuff' is not guaranteed for each new tranche of graduate students.

    Put together with the bigger picture of energy, soil, freshwater, fish, etc depletion, the prospects are somber.  Even though I have been aware of the basic energy facts for a long time (from 2002, around the second war on Iraq — also my undergraduate degree was in geology), I still sometimes get the urge to cry out to the void and send it an earnest message on all the things we found out, about where our brains came from, how we enjoy food and music, and even that we knew what would happen next.

    But like thoughts of a lost partner, the urge has no possible outlet.

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