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One of my favorite med school professors (a surgeon and intensivist) used to say:

whenever something bad happens, we used to say "I don't know." Now we say "cy-to-kines." At least we're exercising the preservation of syllables, but the answer is really the same: we don't know.


Add to that list idiopathic (1970's) and autoimmune (1980's). Causes of many diseases in those days.

Also remember that we tend to explain according to what we can measure- before Banting and Best in the 1910's and 1920's, those who died of DKA were thought to need more sugar and often had glucose administered. Why? Because the only thing we could measure was their urine which contained copious amounts of sugar. These people must be losing sugar at a prodigious rate. Ergo, more sugar for them. Made perfect sense.


Sometimes a cigar is just a cigar...

You are too generous, my dear friend. In being so, you have conflated two very different aspects of clinical care, especially as the apply to the rapid tempo/low incidence environment of anesthesiology. I assure you (as I know you to be well aware), the hoofbeat that you hear is quite frequently the horse of inattention. Indeed, for instance, most of the arrests I know of associated with local and neuraxial anesthesia (and intercurrent IV sedation) are related to unrecognized depression of respiration. How can I say this? Because I have seen (and been a party to) such depression, which was appropriately recognized and treated, before progressing to apnea. Does this mean that ALL such catastrophic events are from inattention. Heck no. (Thanks be to the clever person who came up with the intralipid scavenging of bupivacaine...) However, whatever the mechansim of catstrophic arrest in neuraxial anesthesia, it will respond 99% of the time to a tube and a vasoconstrictor, and, if there's a non-perfusing dysrhythmia, an appropriate resuscitation featuring intralipid. The sooner it's recognized, the more likely there'll be a favorable outcome.

While we ought usually to bet on the fastest horse in a crunch, we ought not to close our minds to alternate explanations for interesting/unusual occurences. I agree that we must maintain an open mind with respect to possible mechanisms that are not heretofore recognized; my favorite is one you mentioned, optic ischemia leading to monocular blindness in long prone spinal procedures. I do lots of these, and as a consequence of the (a?) proposed mechanism; mechanical stretching of the central retinal artery, I am prone to avoid prolonged pharmacologic paralysis in those patients, in order to allow resting tone in the extraocular muscles to relieve the stretch (no, I have no evidence that this helps...) I also am very cautious about induced hypotension in this (and most) settings. Another such example is the recent proposed mechanism for massive stroke during shoulder surgery in the beach chair position with induced hypotension. One of my former partners many years ago had somebody not wake up from just such a procedure. Am I sure that this was the mechanism? No. Is it plausible? Yes.

So what?

Clinically, you and I have had colleagues who, in the heat of battle, would tarry over possible low-incidence mechanisms; intellectually fiddling while Rome burns. (I'd be glad to name names, but not here...) That some folks can't "shift gears" for M&M to a more expansive appraisal should neither surprise nor disappoint us; it is human nature. That even more people aren't comfortable that there are still things we don't know, even in the little Shire of anesthesiology, is not unexpected... You and the anesthesia intesivists, by comparison, revel in the undiscovered, living, as you do, in the dark forest of critical illness, which still teems with the lions and tigers and bears of unknown mechanisms. Being old and wooly, I have been through any number of mechanisms for sepsis and acute lung injury, and have given my share of goofy experimental poisons based on those mechanisms. It will be a happy day for the afflicted and a sad day for the seekers when it is all understood and reduced to rote...

I know that you (being a first rate intelligence) know line one of this Fitzgerald quote. But given circumstances, I like line two almost as well...


Thanks for another edifying post.

Mike O'Connor

The contrarian in me cannot be controlled.

I'm going to dis-aggregate two phenomena here:
1. cardiac arrest associated with neuraxial anesthesia and
2. respiratory arrest associated with sedation.

First, since the era of pulse oximetry began, there have been a slew of reports of cardiac arrest during neuraxial anesthesia in patient's whose pulse oximeters never indicated that they were hypoxic. Whatever this is, it is not unrecognized hypoxia and the associated bradycardic arrest. I'm not saying that unrecognized respiratory depression doesn't happen in these cases, I claim that more than a few are caused by something else.

As for the later: respiratory arrest associated with sedation. This remains a huge problem. My guess is that the frequency of the problem and its sometimes devastating consequences will increase as more and more less experienced practitioners sedate patients for procedures. Pulse oximeters are terrific tools, but monitor oxygenation, not ventilation. Hypoxia is a late sign of hypoventilation in patients being treated with supplemental oxygen. If the patient is easy to ventilate, rescue will be easy, and it is almost certain that no harm will occur. If there is any difficulty in ventilating the patient, then rescue will be a struggle, and the chances of a bad outcome increase quite substantially. Experts watch the patient and listen to the pulse ox, amateurs watch the pulse ox and listen to the radio, incompetents..... never mind....


So. I am interested in case reports associated with neuraxial anesthesia. Asystole? PEA? vtach? EHS? (exploding heart syndrome-I made that one up...)

Experts at giving aesthesia (I consider myself one, going on 60,000 hours by my reckoning) don't consciously "listen" to the pulse oximeter-they "monitor it." By which I mean, I set it to a just audible volume, and sort of consciously forget about it as I go about my tasks (line starting, charting, walking around inspecting sponges, etc); but I am hearing it; if it drops one pitch, I become aware of it. I have talked to my senior partners about this; they agree. If the room becomes noisy, I get uncomfortable almost immediately; it took me a while to figure out that I was losing the pulse ox in the room noise, although I hadn't been immediately conscious of it; now I know to just turn up the volume to compensate-anxiety alleviated. I actually use the pulse oximeter volume to modulate the room mood. If the team seems too relaxed to me, I'll turn up the volume until the whole room can hear it - it has a focusing effect. Not terribly potent; like tea rather than red bull, but it usually works, and nobody consciously notices, save the occasional really tuned-in circulator, who will look up and wink...

Along similar lines, my old tutor, Eldon Swenson, used to tell me about feeling uneasy ahead of physiologic changes in his patients; some "sixth sense." After all this time, I know what he means; sometimes, even though everything is steady, I get a funny feeling-almost always, a few minutes later something will change with the physiology; bump in BP or HR, change in rhythm, big shift in BIS. Pheromones? Since I'm by nature, a romantic, I just think it's the mystic bond.

Mike O'Connor

The comment by Chris above has niggled at me for a while.

There is in fact an 'Evil Humor of the Era'
A partial list:

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