Link To YouTube Video From PulmCrit-“10 minute talk on hypoxemia physiology”

Posted on October 16, 2021 by Tom Wade MD

In this post, I link to and embed Dr. Josh Farkas‘ PulmCrit YouTube video, 10 minute talk on hypoxemia physiology, Sept. 8, 2021, from

I recommend that you watch Dr. Farkas lecture on YouTube [link is to the YouTube video] because, on the YouTube video, you can follow along with the excellent autogenerated transcript.

All that follows is from the above resource.

Here is a 10-minute video I [Dr. Josh Farkas] made for the Cooper Critical Care Conference.  It explores some basic & useful concepts about hypoxemia physiology, including how to apply this at the bedside.  The algorithms in the video aren’t intended to be strictly followed, but rather merely as general conceptual schemas.

related

  • For more information about the disutility of ABGs in evaluating the cause of respiratory failure, see this prior blog.
  • A more detailed discussion about hypoxemia physiology in the context of shunting may be found here.

What follows are some screenshots from Dr. Farkas’ YouTube video with accompanying text from the autogenerated YouTube transcript. I do this just because it helps me remember the material. Readers of this blog should go to the YouTube video and watch it and follow along with the autogenerated text on the YouTube site.

00:22-00:28
There are only really three mechanisms
of hypoxemia that you need to worry
about: hypoventilation, vq mismatch, and
shunting.
00:28-02:38
Shunting in hypoventilation the alveoli
and the bronchi are working perfectly
and the problem is simply there’s not
enough ventilation getting to the lung
so the alveoli are burning through
oxygen faster than they’re getting
oxygen probably the most commonly
encountered cause of hypoventilation is
a central brain drive problem where the
brain is simply not stimulating the body
00:48
to breathe and we’re most familiar with
00:50
this probably in the context of opioid
00:52
intoxication so folks come in their
00:53
respiratory rate is low they’re
00:55
substantially altered they’re not
00:56
breathing this is relatively easy to
00:58
diagnose other causes of central
01:00
hypoventilation are folks with brain
01:02
stem strokes or substantial brain
01:04
pathology and once again relatively
01:05
straightforward to diagnose on the basis
01:07
of substantially altered mental status
01:09
so the second type of hypoventilation is
01:11
a respiratory mechanical problem where
01:13
the brain is stimulating the body to
01:15
breathe but the body is unable to
01:16
breathe either due to a tracheal
01:18
obstruction or upper airway obstruction
01:20
or neuromuscular problem involving the
01:22
diaphragm in the chest ball for patients
01:24
with acute respiratory mechanical
01:25
problem they will compensate for this
01:27
with tachypnea and they will only
01:29
develop hypercapnia and hypoxemia when
01:32
they’re really on the brink of death so
01:34
most of these patients will present with
01:35
tachypnea and they’ll be struggling to
01:37
breathe but they won’t necessarily be
01:39
substantially hypercapnic nor hypoxemic
01:41
and things of this nature would include
01:42
epiglottitis acute transverse myelitis
01:45
gumbray syndrome neuromuscular problems
01:47
things like periodic hypokalemic
01:49
paralysis so some sort of acute
01:50
neuromuscular or airway catastrophe and
01:53
once again these patients are not really
01:55
going to present with hypoxemia usually
01:57
they will present with almost like an
01:59
exfixial problem so the last cause of
01:59
exfixial problem so the last cause of
02:01
hypoventilation is a chronic respiratory
02:03
mechanical problem and this can be very
02:04
difficult to diagnose so these are folks
02:06
with for example chronic muscular
02:08
dystrophy or chronic obesity
02:10
hypoventilation syndrome and what
02:11
happens here is that the brain adapts to
02:14
a higher level of paco2 so the brain is
02:16
kind of okay with this and it doesn’t
02:18
really stimulate the patient to drive
02:20
their respiratory rate too too high so
02:22
patients may show up on a couple liters
02:24
of oxygen and they’re not an extremist
02:26
they don’t look too bad most of these
02:27
patients can be diagnosed because they
02:29
may be carrying some sort of chronic or
02:31
obvious diagnosis of a neuromuscular
02:34
problem but occasionally very rarely you
02:36
might encounter this for the first time
02:39
it can be a little tricky to find this.
The following picture sums up the above part of the transcript.
The next section of the transcript discusses V/Q mismatch.
02:40 – 03:32
02:40
so getting back to the mainstream here
02:41
vq mismatch this basically involves a
02:44
partial obstruction of flow or partial
02:47
dysfunction of some alveoli so some
02:49
alveoli are hogging all of the
02:51
ventilation and other alveoli or getting
02:53
inadequately ventilated now the problem
02:55
is that the ventilation hogs here are
02:57
wasting this ventilation they don’t need
02:58
that ventilation they are saturating 100
03:01
before getting the extra ventilation the
03:02
extra ventilation does nothing for them
03:04
meanwhile the other alveoli are starved
03:06
for ventilation they become hypoxemic
03:08
and the net effect is that overall blood
03:10
becomes hypoxemic so vq mismatch is the
03:12
answer to everything in pulmonary
03:14
medicine if you’re ever asked for a
03:15
question on you know the boards or
03:18
rounding and you know why is this
03:19
patient hypoxemic you can always guess
03:21
vq mismatch and you’re generally going
03:23
to be right so this includes patients
03:24
with asthma copd pulmonary embolism most
03:26
patients with bronchodomonia where they
03:28
have kind of like some obstruction of
03:29
the bronchi but the lung is basically
03:31
functioning most of your heart failure
03:32
patients most of your interstitial lung
Next comes shunt
03:34 – 04:02
03:34
disease patients so our final cause of
03:36
hypoxemia shunting this involves some
03:38
situation where the blood does not come
03:40
in contact with oxygen and there is no
03:43
way for the blood to ever come in
03:45
contact with oxygen the most common way
03:46
that this occurs is an alveolar filling
03:49
process for example some alveoli are
03:51
filled completely with plus in the case
03:53
of pneumonia and no matter how much
03:56
oxygen you give this patient no matter
03:57
how much that patient breathes there is
03:59
not going to get any oxygen to the
04:00
alveolus and all the blood going to that
04:02
alveolus is going to be deoxygenated.
Vascular Shunting
04:04 – 04:56
04:04
another cause of shunting is a vascular
04:07
or intracardiac shunt and what’s going
04:09
on here is deoxygenated blue blood from
04:12
the right side of the heart is pouring
04:13
directly into the left side of the heart
04:15
without ever coming in contact with the
04:17
alveoli so even if the alveoli may be
04:20
functioning perfectly this patient will
04:22
still desaturate so shunts may be caused
04:24
by alveolar filling processes most
04:26
commonly things like socketing pneumonia
04:28
severe adolexis with total on collapse
04:30
ards sometimes you can see folks with
04:33
kind of a diffuse infiltrate on their
04:34
chest x-ray but what they have are kind
04:36
of just patchy areas where the alveoli
04:38
are totally dysfunctional in args and
04:40
that can cause a shunts you can have
04:42
folks with bronchial obstruction of a
04:43
large process and that’s probably what’s
04:45
going on in the icu when you have an
04:47
intubated patient who suddenly
04:48
desaturates and they get suctions and
04:50
then their saturation pops right up
04:52
those are intermittent kind of bronchial
04:53
obstruction due to mucus plugging and of
04:55
course vascular shunting like
04:56
intracardiac shots in pulmonary avms
How To Use This Information Clinically
04:58 – 06:06
04:58
we talked about hypoventilation vq
05:00
mismatch and shunting so how can we
05:02
actually use this information clinically
05:03
so let’s think about what will happen if
05:05
we expose patients with hypoventilation
05:08
vq mismatch or shunting to a hundred
05:10
percent oxygen or a very high inhaled
05:12
amount of oxygen in hypoventilation and
05:14
vq mismatch if we’re flooding these
05:16
patients with oxygen there’s so much
05:18
oxygen in their trachea that even if
05:19
there’s not like a huge bulk flow going
05:21
to these alveoli in hypoventilation or
05:24
even if there’s like an obstruction here
05:25
in vq mismatch the oxygen concentration
05:28
is so high that enough oxygen will get
05:29
into the alveoli that the saturation
05:31
will be okay alternatively for our
05:33
patients with shunts it they don’t care
05:35
it doesn’t matter you can give these
05:37
patients 100 oxygen it’s still not going
05:39
to get to that alveolus and they will
05:40
still be hypoxemic so this is a super
05:42
important concept here hypoventilation
05:44
and vq mismatch can be fixed with oxygen
05:47
whereas supplemental oxygen will not fix
05:49
a shunt so what this means is that
05:51
refractory hypoxemia must always be due
05:54
to a shunt so when you get called that
05:55
there’s a patient who has hypoxemia
05:57
that’s not responding to oxygen you can
05:59
know over the phone right then and there
06:01
that that’s a patient with shunt
06:02
physiology even before you go down to
06:04
the emergency department to see that
06:06
patient.
06:06 – 07:04
06:06
patient so we’re going to start out with
06:08
the basic stuff we’re going to look at
06:09
their lungs with ultrasounds perhaps
06:11
we’re going to look at a chest x-ray and
06:13
most of the time we’re going to find
06:14
some sort of obvious pathology in the
06:16
lungs which will explain their hypoxemia
06:18
we can move on from there but what if
06:20
the lung ultrasound and the chest x-ray
06:22
are normal then we need to consider the
06:23
possibility of an intracardiac shunt or
06:26
vascular shots and the way that we can
06:27
evaluate those at the bedside is to
06:30
inject agitated saline while doing a
06:32
bedside pocus that’s a pretty simple
06:34
thing to do i think anyone who’s
06:36
interested in emergency medicine or
06:37
critical care should probably know how
06:38
to do that and you can identify at the
06:41
bedside patients with intracardiac
06:42
shunting or pulmonary avms you can
06:44
differentiate between those two
06:46
pathologies based on when the bubbles
06:47
show up in the left side of the heart
06:49
now what if your shunt study is negative
06:52
there are no bubbles on the left side of
06:53
the heart then you get into a weird box
06:55
here maybe this patient has a strange
06:57
bronchial obstruction perhaps they have
06:59
methemoglobinemia it’s a little outside
07:01
the scope of this talk but it’s
07:02
relatively easy to diagnose once you
07:04
think about it.
07:04 – 07:57
07:04
So let’s get back to
07:05
bread and butter here. what about our
07:07
hypoxemic patient who is responsive to
07:09
oxygen so you’re called to evaluate a
07:11
patient who is on two to four maybe five
07:13
liters of oxygen and their saturation
07:15
response to the oxygen what’s going on here
07:17
so you can know apriori that these
07:19
patients probably have either the
07:20
mismatch or hypoventilation so our
07:22
approach to a patient with hypoxemia
07:24
responsive to oxygen now first we’re
07:26
going to look at the patient if they’re
07:27
clearly not breathing maybe they’re
07:29
probably hypoventilating if they are
07:31
asphyxiating perhaps they have an upper
07:33
airway obstruction these things are
07:34
usually going to be relatively clear to
07:36
detect and honestly they’re not going to
07:38
really manifest with hypoxemia so moving
07:40
on from there most of these patients are
07:42
going to have vq mismatch so here’s
07:44
where we do our basic pulmonary workup
07:46
we listen to them we do an ultrasound so
07:48
perhaps they bronchospasm asthma copd
07:50
perhaps they have pneumonia heart
07:51
failure stuff like that this is our
07:53
bread and butter evaluation for
07:55
hypoxemia that we’re used to doing all
07:57
the time
07:57 –
07:57
if that [POCUS, CXR, and auscultation for wheezing] is negative this is
07:59
when you need to think about pulmonary
08:00
embolism so you’re going to pull out
08:01
your d-dimer your ct angio and perhaps
08:04
diagnose a pe or maybe find some sort of
08:06
subtle lung pathology that you missed
08:08
previously if that is negative then you
08:10
need to reconsider the possibility that
08:11
the patient may have hypoventilation and
08:13
check an abg to look for hypercapnia
08:16
this is a rare occurrence but
08:17
occasionally you may see this so finally

 

 

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