I wasn't always like this.
Ask co-interns and they will tell you I was the most notorious minutiae-obsessed physiology manipulator west of the Mississippi.
What changed? Well, I
grew up and realized that micromanaging physiology is most often a fool's
errand. Evolution was indeed a brilliant
chemist (Max Perutz), and I recognize my impotence in one-upping him. I can order zero ABGs or a dozen ABGs in a
week and little changes but the volume of blood that is flushed down the
drain.
So, using an example from earlier in the day, I'll lead you
through a stream of consciousness explanation of why I can most often do
without an ABG.
A man in his 30s is admitted for alcohol withdrawal (WD) for
the sixth time in 12 months. About half
of these times, his WD has been severe and he has required ICU admission. Overnight, during the administration of
benzodiazepines for his WD symptoms, he has become progressively tachycardic
and tachypneic and his oxygen needs have been steadily increasing. His saturation on the monitor displays a good
tracing at 95%. BIPAP is applied. I
can hear his respiratory rate at about 25, and based on the flow I hear from
the BIPAP machine, I can guess that his minute ventilation is about 15 liters
per minute (these guesses could be confirmed with RT).
Knowing nothing else about his case, I am asked if an ABG should be
ordered to assess his respiratory status.
Should it?
Well, I think it should only if the results are likely to
influence my decision making. Simply
"to see where he's at" is not sufficient reason for me. I would rather think through where I think
he's at based on what I already know, and if it all adds up and nothing is
unusual, I don't need an ABG. When I see
someone running and breathing heavy, I don't wonder what the ABG would
show. I understand the physiology of
running and there is no need for further investigation in any particular case
unless something unusual is happening.
Like the runner collapses.
The next part of the explanation can serve as an introduction
of Bayesian Decision Making applied to clinical decisions. I need to know nothing more than the
information above to make some very good inferences about what's going on with
this man's clinical status. I need only
think about what is common, and in particular what is common in this particular
scenario. What is this man predisposed
to that will affect his lungs?
[An aside here - I used to implore medical students on their
second year H&P rotation to think of a patient as a person who is exposed
to various things in his or her environment.
In fact, the whole past medical, surgical, social, family, OBGyn,
medication, occupational, travel and vaccination history is simply an exercise
in revealing what exposures a patient has had that increase or decrease the
prior probability of various disease states.
This is a very useful exercise and makes the importance of a past
medical history paramount. Another
clinical saw that derives from Bayes' Theorem:
The most likely diagnosis is one that is common, or that is related to
something we already know the patient has.]
Well, I expect one of two things (or both) to happen to a
young man with WD who gets progressively hypoxemic overnight during the first 8
hours of admission, based on what I know about the natural history of this
disease process. (For a case synopsis of
ETOH WD, see this recent Case Records of the Massachusetts General Hospital.) One, I expect that he may
develop atelectasis as he is given benzos for his WD. Two, also related to the benzos, I expect
that he may develop micro- or macro-aspiration, or that any pre-existing
aspiration may blossom into lung injury and full-blown pneumonia as he receives
fluids for resuscitation. Quite simply,
I look at his exposures both prior to and during the hospitalization and
determine what he's most likely to get.
But what if I'm wrong?
I know that I could be, and in the
back of my head, I'm thinking of other possibilities, ready to revise my
initial suspicions as soon as there is something out of place or I "smell
a rat" or new information becomes available. One of my favorite adages for clinical
decision making is that the most common reason for missing a diagnosis is
failure to consider it. This is
self-evident, so much so that the message fails to be internalized. This is no place to enumerate and elaborate
all kinds of decision making biases, but it is important to point out that the
list of possibilities should remain
broad, but the list of probabilities
should be ordered and succinct.
This guy could have Langerhan's Cell Granulomatosis or
sarcoidosis after all is said and done, but this is no time to be ordering CTs,
biopsies, ACE levels and ANAs. But what
other possibilities warrant consideration as probabilities at this
juncture? Well, what other things is an
alcoholic exposed to? Things that
crossed my mind are community acquired pneumonia such as S. pneumo and Klebsiella
and it's influenza season - he could surely have that. He could have an alcoholic cardiomyopathy
with congestive heart failure and cardiogenic pulmonary edema. He could have asthma. He could have a bronchial foreign body. All of these are possible, some maybe even
probable in the right scenario, but none fits with his deterioration after admission as well as progressive
atelectasis and/or aspiration does. (And
yes, anybody can have PE, but I'm not going there because of what I reveal
below. PE need rarely be investigated in
patients without a swollen leg and who have parenchymal opacities on CXR that sufficiently
explain the gas exchange abnormalities, and the last thing I want to do is give
this alcoholic guy an anticoagulant anyway.
All these are reasons to dismiss this -at least for now.)
I want to sort out the top two probabilities and I can't
help myself. I open the CXR file and
sure enough, there are low lung volumes and discoid (plate-like)
atelectasis thereby confirming my first
suspicion. Does this rule out aspiration
and pneumonia? Surely not, and I would
opt to give him antibiotics for 3-5 days just in case, based on the threshold model of clinical decision making. (Quite simply,
the probability of harm from antibiotics for a couple of days is so low in my
model [and the consequences of untreated pneumonia so high] that the probability
of pneumonia doesn't need to be very high for me to cross the threshold and
treat. This threshold is now and usually
is a low one.)
So, back to the ABG - do I need one? Well, what information does the ABG
provide? Information about oxygen tension
in the blood (PaO2, a surrogate for what I really want to know, SpO2), the
carbon dioxide tension, and the acidity or pH.
Are any of these truly a mysterious unknown right now?
Again, what are my expectations? Firstly, I expect atelectasis, especially
that developing acutely, to cause a significant degree of hypoxemia, just like
what is happening. And I already know
it's significant because he was on high flow oxygen by mask and is now on NIPPV
with saturations below 100%, so he's either shunting or has V/Q mismatch, both
compatible with the conditions I'm considering (and indeed compatible with just
about every single disease that causes hypoxemia). I also already know that his oxygen
saturation is acceptable based on the internal algorithm of the pulse
oximeter. And I have no good reason to
trust this less than the internal algorithms of the blood gas machine which
will extrapolate from the PaO2 to derive an SaO2. So there is no need for me to gather further
information about oxygenation.
Everything I need to know is right before me already.
Secondly, I expect his pH to be somewhere near normal. He has been sedated with benzos, but they
don't depress respiration that much, and I hear a good respiratory rate and
high flows, so I think his minute ventilation is adequate to maintain normal pH
across a range of dead space and CO2 production assumptions. But I
also expect that his CO2 production is elevated during WD, and that there may
be some tendency for hyperventilation and respiratory alkalosis from agitation,
as well as a tendency for metabolic acidosis from lactate or alcoholic
ketoacidosis or saline infusion or whatever.
Bottom line is I don't believe that he's been sedated heavily enough to
have impairment of respiratory drive sufficient to cause his pH to drift that
far from normal, and the amalgam of things that are going on simultaneously and
pulling values in different directions is really beyond my ability to discern
completely with or without an ABG. The
only thing I can know with reasonable confidence is that, barring profound
respiratory depression (which I would determine from respiratory rate and
pattern), he will mostly compensate and maintain his pH close to normal.
But it doesn't matter.
Somebody else already ordered an ABG, and they bring it to me. As is my custom, I don't look at the
results. I flip it over and list my
guess of the ranges of what the values will be based on my reasoning
above. And I always guess ranges that,
if the actual values fall within them, I will not make any changes. If falling within my ranges would lead to a
change in course, my ranges are too wide. If the true values fall outside of my ranges, either I should have ordered the ABG, or my ranges are too narrow. (A discussion about the appropriate ranges of indifference could ensue, but I'll save that one for later.) Note here that this exercise affords me the
opportunity to calibrate my decision making.
It conforms to decision theory - I have domain specific knowledge, I
have had a lot of practice, and if I do this blinded and get immediate
feedback, I will be able to calibrate myself further.
Here's my guess:
7.35-7.45/28-34/60-80/18-22
Here are the results:
7.41/32/95/19; Lactate also came back 3.4, slightly elevated as suspected.
I was off quite a bit on the PaO2 (does it matter?) but the
rest of the results fall right within my comfort zone based on what I expect is
going on. And my plans don't change one
bit.
Can I always guess the results with sufficient confidence to
obviate an ABG? I don't know for sure,
but I know from years of practice that I'm pretty close and rarely
surprised. Can you achieve the same
results? Maybe, maybe not. But if you take the time and effort to think
through the problem in this fashion, you will calibrate your own medical
decision making and your guesses about the ABG results
.
When do I get an ABG?
When I can't figure out what's going on, or when things are going
against my reasonable expectations. For
me, that's the time to get more information.
Not as a knee-jerk reflex, but as an actual investigation into something
I don't understand and I need more information to try to figure it out.
Like the last post on acidosis, I'll end this one with a
little limerick:
Oh how you love to draw some blood
Send it to the lab in a hemorrhagic flood
Chase down the result
Anemia not your fault
While I just stand by, chewing my cud
Too many tests, so much confusion
Then it comes time for a bloody transfusion
Do this instead
Just use your head
Labs don't crack cases open, it's just an illusion!
This comment has been removed by a blog administrator.
ReplyDeleteOne of the best medical blogs I've ever read. You should write a book or a script for a television show.
ReplyDeleteSCott, i have been going back and reading your posts from the past. Everything you say reaffirms what I have realized througout my (ongoing) critical care fellowship, ie most stuff we do and things we test have no bearing on the patient management whatsoever... Thank you for putting it eloquently- when I have to get these concepts across to my residents, I just redirect them to your blog. Kudos..
ReplyDeleteSantosh Dhungana (PCCM fellow, University of Kentucky)