Friday, January 25, 2019

Limits of the Possible: Clinical Reasoning of a Harrowing Extubation

"The only way of discovering the limits of the possible is to venture a little way past them into the impossible."  -  Clark's Second Law

In prior posts here and on the Medical Evidence Blog (here, here, here, and here), I have outlined my position that the only way you can really know if a patient can breathe on their own is to let them try - a "trial of extubation".  Prediction equations get you published, but their signal to noise ratio is often poor and ignored, to patients' peril.  Indeed the reason I'm obsessed with extubation is because I think being intubated unnecessarily is one of the worst things a patient can endure, and the best thing I can do as an intensivist is identify the earliest moment when a patient can breathe on his own and extubate him.

I faced a very harrowing extubation decision recently, and I admitted to the medical students that it was the most nail-biting of my career.  But I think analyzing it, both before and after the fact can be very instructive.

A 20-something man was transferred in with asthma on the mechanical ventilator.  For the sake of brevity, assume that there is nothing special about this case other than its severity and the few nuances that I describe.  The patient had been intubated for hypercapnia, severe wheezing that began 24-48 hours prior to presentation, and, interestingly, severe hypoxemia.  He arrived from the outlying facility intubated with an 8.0 endotracheal tube, PEEP 14, FiO2 80%, Vt 380, rate set at 10, breathing at 15-30 depending upon his state of arousal, pH 7.20 PaCO2 70, SpO2 92%.  He had pan-expiratory wheezing diffusely with end inspiratory squeaks as well.  Chest X-ray showed left basilar subsegmental atelectasis.  His auto-peep was difficult to measure, but flow almost returned to baseline at end-expiration so qualitatively it was low, or at worst moderate.  The plateau pressure was likewise difficult to measure and thought to be unreliable, with peak airway pressures approximately 50 cm H2O on a peak flow of 75 liters per minute.  We administered 250mg of solumedrol per day and albuterol nebulizers 5mg every 4 hours as well as some atrovent.  The ventilator was changed to AC/VC with Vt 600 and 720 delivered (about 8 and 10 cc/kg PIBW respectively).  The measured airway pressures and qualitative autopeep did not appreciably change.  He was sedated with propofol and ketamine drips, and intermittent fentanyl boluses.

Within 24 hours, his wheezing had markedly improved, but his minute ventilation was still high at approximately 15-18 liters per minute.  He was tachycardiac at 120 beats per minute and hypertensive to systolic 155.  We decided to reduce the ketamine and replace it with intermittent ativan, start scheduled oxycodone to reduce fentanyl doses, and we changed the ventilator to pressure support 5 cm H2O and PEEP 8, with FiO2 60% at that time.  Meanwhile we had learned that there was a PFO with right to left shunt which at least partly explained his severe hypoxemia, along with the atelectasis.  While rather deeply sedated on PS 5 and PEEP 8, the Vt was 1200 cc and the respiratory rate was10-12 breaths per minute with Ve about 15 liters, and very little qualitative autopeep on the flow-time waveform.  We reasoned that he "needed some more time" for the bronchospasm to abate further and the Ve to decrease.

On hospital day #3, he had slighly less wheezing, but still had inspiratory squeaks and, off ketamine, his respiratory rate had increased to 15 with tidal volumes of 1000-1200cc.  Plateau pressures and autopeep remained difficult to measure because of patient triggering and forceful exhalation.  When we did a "sedation vacation" he awakened and followed simple commands, but with awakening, his heart rate increased from 112 to 139 beats per minute, and his respiratory rate increased to 26 -28 breaths per minute with Vt of 1000 cc and Ve 26 liters per minute!  On CPAP 5 and PEEP 8 and FiO2 60% the SpO2 was 91%.  ABG showed pH 7.43/44/60/29.  Here are the difficult questions we faced - can he be extubated, or should we continue to wait and adjust his sedation?  Why is the minute ventilation so high?  Will he "calm down" if the tube is removed?

My first thought was, the underlying disease has abated a good deal based on his wheezing on exam.  And the fact that his asthma came on quickly gave me a reason to believe that it should abate quickly as well.  The fact that he can move so much air (Ve 26 lpm) suggests that the obstruction must not be that severe.  Nonetheless, this is a lot of air to move through constricted airways, and if high minute ventilation persisted after extubation it was going to make us all worry that it could not be sustained and he would probably be reintubated for "work of breathing" if not by our team then by nigh coverage.

So, why the very high minute ventilation?  This was a major concern.  With a pH of 7.43, there are only three explanations:  high Vd/Vt or high CO2 production, or both.  Even when he was sedated his lowest Ve was about 12 liters per minute.  But it more than doubled to 26 lpm during our "sedation vacation".  Is that all increased CO2 production from arousal?  Or is Vd/Vt also very high?  The former seemed more likely, since Vd/Vt should not increase with agitation.  My favorite example of this is that of Luke Aikins skydiving from 25,000 feet without a parachute and landing in a net (a first in human history).  In this video, his heart rate during free fall is 148 (at about 40 seconds into the video), due to sheer terror alone.  If you have not previously seen this video, I recommend you watch it.

If you use the general guide that an increase in heart rate of 10 beats per minute represents approximately a 10% increase in metabolic rate, it can be inferred that Luke's metabolic rate and hence his CO2 production has increased by about 100% from baseline due to sheer terror alone.

Thus it is possible that my patient's Ve has increased from 12-15 lpm while sedated to 26 lpm from increased CO2 production during arousal and with agitation and fighting against restraints.  But, how much is driven by arousal alone and how much is driven by the presence of the ETT and the inability to speak, and the frustration and anger that all this causes?  That is, if these changes in Ve are all driven by CO2 production, how much will they change if the ETT is removed?  Like Luke, my patient's heart rate was in the 140s, but it had rarely been below 100, and he's receiving albuterol which may be driving it, and he's probably not a trained athlete like Luke so it probably doesn't represent a 100% increase from baseline CO2 production - or does it?  How much of any increased CO2 production is due to respiratory distress and metabolic activity of a diaphragm under heavy loads?  Finally, I will add this:  he looked pretty terrible as far as extubation candidacy goes - pan-tachy, freaking out quite a bit.

Then there's the hypoxemia.  It can be attributed to shunt from atelectasis and PFO, but what if much of it is V/Q mismatch from severe asthma?  And how much of it is from high oxygen consumption in the periphery of a patient resisting restraints which is worsening venous admixture for a given level of Qs/Qt (shunt fraction)?  

How can we know any of these things?  We can't.  The traditional approach would be to re-sedate the patient because he failed almost all indices of weaning:  very high minute ventilation, tachycardia, tachypnea, ongoing wheezing, hypertension, FiO2 60% on PEEP 8.  Interestingly, the f//Vt is only about 20, and the FVC criterion of ~1000 cc is met with the tidal volumes alone.

The next thing we considered was what would be the consequences of extubating if he failed and needed reintubated?  He had an OGT which was to suction evacuating the stomach.  Unfortunately we did not have the intubation records from the outside hospital, but his significant other said that the physicians there did not report difficulty with intubation.  (This is, I think, one of the most important and most frequently neglected considerations of an extubation - how difficult was the intubation?)  He had a good thyromental and thyromandibular distances, normal mouth opening and normal neck mobility.  So, we ought to be able to reintubate him.  I reinforced to the trainees that in a case like this, if we extubate and he does not markedly improve afterwards, our test has failed.  The hypothesis is:  he is breathing at Ve 26 liters because of high CO2 production from agitation which is due to the endotracheal tube.  If Ve doesn't decrease after extubation, this hypothesis is rejected and he should be expeditiously reintubated without equivocation and especially without denial.

So we decided to extubate the patient.  Then we got the intubation equipment arranged, VL in the room, ketamine and propofol drawn up......and we extubated him.

Previously I have reported on both successful and failed "extreme extubations".  Would you like to venture a guess which category this case falls into?  I will entertain comments below and on twitter before I follow-up on the results of this case.  Please let me know what you would have done!

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