Why the Hypoxic Drive Theory Sucks Wind……..
As an RT student I never could quite
resolve my understanding of the CO2 retainer/hypoxic drive theory. The more I tried, the less sense it seemed
to make. Finally the theory's armor
started chipping away, eventually collapsing into a sea of absurdity. One day I looked at this whole issue and
could say to myself that this is one emperor who is indeed butt naked. This is
an issue I feel strongly about and would therefore like to make a post
regarding this issue--- to see where others stand and ask where we should go
from here.
It is my experienced opinion that one
of the causes of an overabundance of both clinical silliness and suffering is
the persistence of the CO2 Retainer/Hypoxic Drive theory. This is the theory maintaining that any patient with a compensated chronic
respiratory acidosis must rely on the hypoxic drive for a stimulus to
ventilate----that somehow the CO2 sensors have become blunted or useless. The theory further maintains that if you
give one of these patients "too much oxygen" they will "stop
breathing".
I feel this theory is essentially
garbage. There may be patients who do
have a defunct hypercarbic drive. Some
of them may even be CO2 retainers. The
regulation of ventilation is certainly complicated and vies with that of blood
pressure in complexity. Indeed now I am
fantasizing two physiologists at a divided chalkboard, each with chalk in
hand. Each physiologist takes a
progressively revved up turn diagramming either blood pressure or ventilation
as dueling banjoes plays in the background (from the movie
"Deliverance").
If this CO2 Retainer/hypoxic drive
theory had any real merit, then where are the legions of patients arriving in
ERs whom have turned up their home O2?
Where are the episodes on "Murder She Wrote", as then home
oxygen would be the perfect murder weapon (the evidence would disappear after
the heinous crime) for any greedy relatives of a CO2 retainer? Has any malpractice suit ever been won on
the grounds of giving a CO2 retainer too much oxygen? If so then that case should now be reviewed/reversed in light of
recent studies and a newer approach which actually makes some sense.
I would refer anyone interested in
this subject to the following articles…..
"_Debunking
myths of chronic obstructive lung disease [editorial; comment]_ AUTHOR: Hoyt JW SOURCE: Crit Care Med 1997
Sep;25(9):1450-1 NLM CIT. ID: 97441579
_O2-induced change in ventilation and ventilatory drive in COPD._
AUTHOR: Dick CR; Liu Z; Sassoon CS;
Berry RB; Mahutte CK AUTHOR AFFILIATION: Department of Medicine, University of
California, Irvine, USA. SOURCE: Am J Respir Crit Care Med 1997
Feb;155(2):609-14 NLM CIT. ID: 97184400
_Influence of inspired oxygen concentration on deadspace,
respiratory drive, and PaCO2 in intubated patients with chronic obstructive
pulmonary disease [see comments]_ AUTHOR: Crossley DJ; McGuire GP; Barrow PM; Houston PL AUTHOR
AFFILIATION: Department of Anaesthesia, Toronto Hospital, ON, Canada. SOURCE:
Crit Care Med 1997 Sep;25(9):1522-6 NLM CIT. ID: 97441594
And there is the
Critical Care Medicine article,1996 Vol. 24, No1 by Hanson, Marshall, Frasch,
Marshall, entitled, "Causes of hypercarbia with oxygen therapy in patients
with chronic obstructive pulmonary disease". To quote the ending paragraph, "The development of Haldane
deadspace and loss of the mitigating effects of hypoxic pulmonary
vasoconstriction are sufficient to account predominately for the changes in
PaCO2 seen in patients with severe COPD when treated with oxygen.".
And for more discussion of this issue,
look at pages 838-9 in Martin Tobin's
book, "Principles and Practice of Mechanical Ventilation". The chapter is by Robert Lodato.
As the article and chapter may be
confusing to some, I would like to try my hand in explaining the mechanisms
here.....
.
V/Q MISTMATCH--. Picture the alveolar air equation as a form
of a battle plan whereby an army of O2 soldiers know they will take certain
losses on their way to link up with the Hgb.
760 torr minus the water vapor = 713.
Times .21 = 150. Then minus 1.2
times the PaCO2. Well if the PaCO2 is
40, then that's 150 minus 48 = 102. Now
imagine one real poorly ventilated alveoli where the PaCO2 has built up to 120
torr in that unit. Now,with an RE of .8
that O2 army is fighting an effective back pressure of 144 torr so the PAO2 is
only 6 in that alveoli. Well when the
pulmonary circulation gets exposed to that low of an oxygen level (below 60
torr) in it's venous circulation it constricts. Blood is then sent to better ventilated(and thereby oxygenated
also) lung units.
But if the patient is on 100% O2 then
the PAO2 would be 569. The pulmonary
circulation wouldn't constrict (unless the CO2 climbed to about 6-700), and the
resultant CO2 would backwash into the systemic circulation. This phenomenom can
also affect the V/Q matching of asthmatics whom are placed on a NRB mask, or on
100% O2 as initial ventilator settings.
HADANE EFFECT--. The Haldane effect is
where increasing oxygen levels drive CO2 off the RBC—increasing O2 levels
decrease the affinity of Hgb for CO2.
This is so O2 from the alveoli will drive CO2 off the RBCs and it will
be then ventilated. The opposite is the
Bohr effect at the tissue level where increasing CO2 levels drive O2 off the
RBC (or more correctly put—decrease the affinity of Hgb for O2). .
Remember that stereotypical "blue bloater" with a
chronic PaO2 of 50, SpO2 of 85%, and a compensated PaCO2 of say 70. Usually those patients had a fairly high
Hct, let's say 50%. What is attached to the Hgb more now with a lower
PaO2? It's CO2. Their blood carries a chronic CO2
reservoir .And the patient has more
blood to boot also. So if that patient
has their FIO2 increased then that CO2 will be driven off the blood and into
the circulation. Your or I would just
breathe a little deeper and faster, no big deal. But the compromised COPDpatient's ventilatory ability can't
handle it, especially now when they've arrived in the ER with an increased temp
and a rapid RR.
. When hypercarbia associated with
hyperoxemia is seen, it's not so much that you've knocked out the patient's
hypoxic drive. Rather you've driven in
a hypercarbic potential.
Some may say, "what does it
matter the mechanism if the result is still increased respiratory acidosis with
O2 administration?". To the extent
that V/Q mismatch is the culprit, now we can be safe with a SpO2 of 97 as
opposed to trying to hover in the high 80's to very low 90's. To the extent that the Haldane effect is the
culprit....well if the patient comes in with a PaO2 of 32 on RA with a PaCO2 of
80 with a pH of 7.34 and a RR of 48, just get that ET tube or Bipap ready. For every SpO2 increase with O2 therapy you
will be driving moreCO2 out and challenging further a ventilatory system
already on the verge of collapse. But
if that same patient is at home and resting while watching the ball game on TV
as their O2 accidentally gets turned up by 1 l/m---- well they won't stop
breathing and that's why I've never met an ambulance with such a patient on
board. .
And some people say,
"but I've seen it happen....No you didn't really see all that theory
happen. You witnessed a series of
clinical events interspersed with some lab data and then chose to invoke a certain theory to tie it
all together. For eons people have
believed that they've seen various unscientific superstitions come true and
"happen" as lightning, thunder,and earthquakes have wreaked havoc
with our psyche and compelled people to come up with some explanation for what
they witnessed.
Where is the RT report room
where stories don't echo off the walls--- telling the tale of the "stupid
nurse who almost killed the COPD patient by turning up his oxygen"(notice
that the patient is always "almost" killed). Or one of my favorites, "I couldn't
wake him up after his O2 was turned up".
Why did you need to wake him up?
Perhaps his hypoxemia was finally relieved so the patient could get a
good rest? Was it time for a sleeping
pill?
Picture that COPDer whom arrives in
the ER SOB with a RR 45 and initial PaO2 44, PaCO2 66, pH 7.35 on RA. So someone places them on a 8 l/m simple
mask and draws another ABG---now they are PaO2 110 PaCO2 80, pH 7.25 The patient's RR is now 26 and the patient's
respiratory effort is much less labored.
Did we really knock out that patient's drive to breathe? Or did we relieve the patient's hypoxemia
sufficient that the patient could practice their own form of permissive
hypercapnea? If we intubated that
patient and considered his auto-peep we may be happy with the latter ABGs also. Why should the patient suck anymore than we
now blow?
When I bring up my arguments against
the hypoxic drive,often I feel as if I am arguing religion and not
science. To walk into a report room of
old-timer RTs and challenge this theory is akin to walking into a group of
holy-rollers on good Friday and announcing that Easter has been cancelled as
they've found the body. Sadly enough, for too many, this hypoxic drive theory
represents the high water mark of their theoretical RT development.
It may be hard for some to let go of
this theory. After all, some of us have
been berating others for years. It made
us the keepers of the O2 Black Art, especially when oxygen was a lucrative
ancillary service. The essence of
groupthink.
I may offend some by opening up
against this outdated theory with both barrels. But I feel this assault is exactly what is needed in order to
flush this issue out of the obscure corners where it is presently being
debated. The damage is happening daily everywhere.
I have asked local RT instructors
their opinion. One said, "I don't
believe in it (CO2 retainer/hypoxic drive theory), but I've got to teach
it".
This theory causes clinical silliness
as we try with oximetry to maintain CO2 retainers in some magic SpO2 range of
88-90%.
This theory causes clinical suffering
as hypoxemic patients are often denied the very oxygen which would relieve
their dyspnea.
The hypoxic drive theory is already
dead. It's ghost still lives on in
clinical practice. But the body is beginning to smell. Our profession was instrumental in bringing
this theory to life. It is now our
responsibility to drive the nails in the coffin, say a few words, and bury it.
------------------------------
It seems everyone has about 1 or 2
clinical stories where the hypoxic drive theory has happened. I have my own, but the patient was not a
COPDer.
Let’s consider the typical patient
whom is alleged to have had their hypoxic drive suppressed.
She was in borderline respiratory
failure, fatigued, then when the NRB 100% was put on her, her hypoxemia was
relieved(especially if her SpO2 on NRB mask was still only 92%). Perhaps she rested her muscles. Perhaps she
was practicing Patient Permissive Hypercapnea? If she were then intubated and mechanically ventilated, given
her emphyzematic obstructive lung mechanics and auto-peep potential, would we
settle for a PaCO2 around 90 and the resultant pH?
Was she policythemic? If so then the O2 drove off that CO2
reservoir normally carried on her arterial and venous Hgb. Her CO2 load was then increased, perhaps at
the very time she was having trouble handling her normal load (and was her temp
increased already also? had she had a
big bowl of pasta before admission?)
Was there a significant component of
increased airway resistance/bronchospasm to her pre-NRB clinical
presentation? If so then the NRB O2 may
have released hypoxic pulmonary vasoconstriction in the most poorly ventilated
lung units. That's another problem of the
CO2 Retainer/Hypoxic drive theory---it tends to blind us to the real danger of
giving severe asthmatics 100% O2 needlessly.
As a counterpoint though, in that asthmatic setting, perhaps the extra
O2 prevents a kind of reverse absorption atelectasis and resultant mucous
plugging which must occur in the face of widespread pulmonary vasoconstriction
----decreased perfusion, decreased ventilation, decreased alveolar gas of any
kind from either the atmosphere or the circulation. Just a thought.
Perhaps this patient actually had a
compromised hypercapneic drive? If so,
was it related to her chronic PaCO2 level in the 50s? Patients with lung disease have various degrees of blunted drives
and responses of dyspnea. This all gets
complicated real fast. I just think we
need to replace a new, better theory for an older outdated one which causes so
much harm and needless work.
For my story,....
Years ago in one of the worst
hospitals and RT Depts...
This patient had abdominal surgery,
was extubated and re-intubated several times.
I came on the night shift after she had been re-tubed her second
time. I looked at her pre-admission
ABG. It was something like pH
7.38/PaCO2 54/PaO2 58. She had no lung
disease. She was rather obese, and had
a lot of upper airway tissue. She
probably had sleep apnea contributing to her ABG portfolio and respiratory
drive. As I worked the night shift
others told me that when they turned down her SIMV rate she just "wouldn't
breathe".
So that night I got the only oximeter
we had(which, at that time everyone was afraid to use so it was kept in a
closet). As I slowly turned down her
FIO2 until her SpO2 reached 89% I watched her then start to spontaneously
ventilate. Her post
extubation/pre-reintubation ABGs all showed PaO2s into the 100s with a
respiratory acidosis. I returned her to
her previous FIO2 and mentioned all this to the young intern on duty that
night. He asked, "What's an
oximeter".
Later the next day I heard they put
her on CPAP on the same FIO2 after someone had accidentally turned off her
Cardiac Monitor alarms. She arrested
in the ICU with an unknown down time. I
heard there was a lawsuit going on...Dah...
Ironic and sad. The only known time where perhaps the
suppression of the hypoxic drive resulted in a fatal outcome and the patient
was ....
on a ventilator
not a COPDer.
How can we bridge the gap
between complicated studies appearing in Critical Care involving computerized
models of compartmental systems and the present wholesale clinical belief
structure?
My objective in posting my opinion is
to call for an overhaul of the present pervasive belief in the hypoxic drive as
the cause of the hypercapnea which may be associated with oxygen therapy.
The hypoxic drive is still on the
exams and believed as gospel by many RTs and treated as an occult phenomenom by
many RNs.
I am not suggesting that we just give
O2 with wanton disregard, rather that we make some effort to eradicate the
pervasive belief that any hypoxic drive suppression is the culprit.
I mentioned a SpO2 of 97 as, all
things(pH,temp,etc) being equal, a SpO2
of 97 is usually about a PaO2 of 97. So
if for every 10 torr rise in PaO2 a PaCO2 will rise 1-5 torr, then a rise of
PaO2 60 to 97(let's round off to 100) will cause the PaCO2 to climb 4-20 torr.
So if the patient looks worse with a PaCO2 of 97, back off to 94%. But do they need to be 88%? I just think that in most cases we can have
our cake and eat it too (relieve hypoxemia and not raise PaCO2 through
worsening V/Q mismatch and/or Haldane effect).
It's when the patient is on really high FIO2 with a SpO2 99-100 (and in
crisis) that I would get worried. And
again, let's worry a little about that asthmatic also. (Does high FIO2s for
asthmatics, especially children, contribute to the RML atelectasis syndrome
through absorption atelectasis combined with decreased collateral ventilation?)
For a patient to have a chronic
compensated PaCO2 level shouldn't be a sentence for hypoxemia. And let's face it, if we settle for a PaO2
of 60 then they're gonna be far lower a lot of the time. When you consider all the variables in low
flow O2 (and how many patients at home or in the hospital will really
chronically wear a Venti-mask), the changes in patient position and activity
levels, plus the time for ventilation and perfusion to equilibrate in response
to any change in FIO2 (even IF the patient is stable during that time frame),
then it really becomes an impossible task to keep a patients PaO2 just above
the hypoxemic boundary. To even try is silly. We have to chose---over a little
or under alot.
I don't think just putting a NRB mask
flush on a COPD patient in crisis is a benign thing to do. But I also don't think they need to cruise
the hypoxic boundary to maintain a drive to breathe.
The question is.......what can we do
about the current theory being so pervasive, so wrong, and so harmful?
Is our profession mature enough to
make a widespread change in such an entrenched belief structure? Is there a good enough educational
background among the vast numbers of RTs in this country to understand how V/Q mismatch
and the Haldane effect could be causing this phenomenon when it does
occur? Can we pull the tablecloth off
without breaking too many dishes?
For those 30% of patients who, with
uncontrolled O2 therapy, became unconscious and had their PaCO2 rise over 30/torr
in one hour..........weren't they in trouble already handling their CO2
load? How policythemic were they? Were their respiratory muscles already
fatigued?
Let me relate some
clinical stories about how this hypoxic drive theory is causing needless harm
to patients and silliness among clinicians....
1) Many years ago I
worked a night registry shift at a hospital across the bay. In the middle of report we were summoned
stat to a med/surg ward. By the time we
arrived the MD was in the patients room having a conversation with her. The patient was alert, appeared to have
respirations slightly labored and appeared slightly cyanotic from the
doorway. We told the charge RN to call
us back after the MD had ordered therapy. (Hey, this was in the old days,
before protocols and such). I went back
to shift report, got oriented to the hospital quickly and did my first round of
treatments.
I then stopped by the med/surg ward to
see how the patient was doing.
"She's asleep now, we did an ABG" (the regular staff RT did
the ABG).
Later on in the early AM I again
inquired as to how that patient was doing.
"Oh here's the ABG results we got back before" The patient was on 4l/m nc O2..pH 7.40/PaCO2
44/PaO2 48. "What did you
do", I asked the RN. "Oh we
found out she is a COPDer,so we turned her O2 down to 2l/m and we're doing
another ABG in the morning."
Ahhhhh..........I begged her to turn
up the O2 and let me adjust her with an oximeter. She didn't know what an oximeter was (this was awhile ago and they
were just coming out). I went to the
ICU and related the story to the staff RT who was working in the ICU with their
only oximeter.
"Don't tell them about the
oximeter, then they'll want it all the time".
Ahhhh........
Report was coming up in a half an
hour. I quickly related to the oncoming
therapist my concerns and urged her to quickly do the am ABG, etc.
The next night I returned. During my first rounds of treatments I
answered a code blue to ICU. It was
that same patient whom was now on a ventilator FIO2 .70. She didn't make it. I doubt that she had her hypoxic drive
knocked out.
2) I answer a stat call to the floor for a
patient in respiratory distress. He was
one of those patients who, by many perspectives, should have been a no-code but
wasn't. He was in distress, cyanotic,
rapid RR with audible ronchi, clearly needing NT sx to relieve his struggling
discomfort. I asked one of the RNs to
turn up the O2 from 1 l/m to 6 as I went to get the suction catheter and
lubricant.
"NO! He's a CO2 retainer and the doctor wants him only on 1 l/m"
I grabbed a bag/mask and hand
ventilated him with O2 before successfully NT sxing him.
He was a COPDer, but not even a
retainer.
I asked the RN if she planned to bag
the patient during a code with compressed air?
Later on, when it was less busy, I
came by and tried to explain the phenomenon of hyperoxic induced V/Q mismatch
and the Haldane effect. I can still
remember the paper with my bizarre scrawlings of pulmonary circulation and
little Hgbs. She got a migraine.
3) While working on a burn unit, I went to give
a HHN tx and check the O2 of a burn patient.
She was a smoker, indeed she smoked her way into the hospital in a
literal sense. In the Progress Notes it
said "probable COPD" as she had a long smoking hx. But she had had no previous hospital
admissions for lung trouble or evidence of CO2 retention per ABGs.
On 2l/m her SpO2 was 92%, but her RR
was 28 and she said she felt slightly SOB.
As often a respiratory alkalosis may raise the SpO2 via
hyperventilation, I raised her O2 from 1 l/m to 3. Her RR dropped to 18 and she no longer complained of SOB. Her SpO2 was now 96%. After the HHN tx I told the RN about how I
had raised her FIO2. The RN was
concerned as "she is a COPDer".
I find this doubly ironic given recent
discoveries of how O2 is vital to wound healing through incorporation directly
into collagen (studies by Hunt). In
this concern it's the PaO2 that's important more than the SpO2, as tissue O2
levels allow increased collagen formation and wound healing.
Maybe after checking out of the
hospital, she could then go to an oxygen bar to augment wound healing? Just leave those smokes and that Vaseline at
home!
But we don't want to knock out that
hypoxic drive!
4) We had a real live CO2 retainer come in for
a lung resection. His chronic
compensated PaCO2 was in the high 70s.
The previous RT had adjusted his O2 to 2/m via oxymizer for a SpO2 of 89%
while he was on his left side. He had
left lower lobe atelectasis. He was on
a continuous oximeter. In the middle of
the night I looked in on him. He was
now laying on his right side (bad lung up now), still on the 2l/m O2, RR 20,
with a SpO2 of 98%. I changed nothing.
I didn't try to wake him up. In
the morning I stopped by and the patient told me that he had gotten a good
night's sleep.
So in this situation, if the hypoxic
drive theory was real, I guess we'd have to servo the O2 flowmeter to the
oximeter to compensate for his body position changes as well as changes in his
ventilation and perfusion? Otherwise he'd stop breathing.
And in closing-----when hypercapnea
occurs with oxygen therapy---it's not because you've knocked out their hypoxic
drive. You've driven in a hypercarbic
potential.
It's
an important distinction.
Jeff
Whitnack RRT/RPFT
whitnack@pacbell.net
Post
script……………
As obstuction worsens, the lungs are
filled with areas of both increased deadspace and increased compensatory
hyper-ventilation. The result is always
that a higher mixed venous PvCO2 then becomes a lower mixed arterial PaCO2
after traversing the pulmonary circulation.
But in between, the vascular bed that this CO2 load must traverse will
constrict if subjected to a PaO2 of less than 60 torr. So, depending on both the level of the FIO2
and the various differences in deadspace and hyperventilatory compensation
going on, at a certain level of PvCO2/FIO2 a crossover point will be reached
whereby certain lung units, those with the most deadspace and resultant high
PACO2 plus a lower PAO2 dropping below 60, will be subjected to pulmonary
vasoconstriction. And meanwhile, those
lung units with less deadspace will have a higher than 60 PAO2 and remain
unconstricted. This will help to
facilitate better ventilation/perfusion matching. The pulmonary circulation will be sent to those areas with both
the best oxygenation and ventilation.
Unless uncontrolled hyperoxia completely overides this compensatory
mechanism.
At room air, the adjusted RE PACO2 at
which this starts to occur is 90 torr (150-90 =60) or a PvCO2 of 72. Thus, for
every bit of extra oxygen we provide to an obstructed patient in severe
distress whose CO2 load is climbing over 70 torr (be they an asthmatic or a
COPDer), the level of PACO2 necessary to maintain the hypoxic pulmonary vasoconstriction
in those worst ventilated lung units is also raised.
Or more to the point,....as the
combination of deadspace and CO2 load increases, the dilemna of the tradeoff between adequate oxygenation and the
effect of worsening V/Q matching secondary to the release of pulmonary hypoxic
vasoconstriction also increases. Add to
this, in patients chronically hypoxemic with elevated Hgb's, the additional
effect of a further increased CO2 load secondary to O2 administration, and the
drama continues. What's a poor
therapist to do?
In the midst of this dilemna we must
remember that hypoxia kills, hypercarbia by itself does not.
From a practical standpoint what this
means is that..
1) this issue
pertains to the patient in distress in the ER.
Not the CO2 retainer whom is home and stable while eating and watching a
ball game on TV. At all costs we must
first relieve the hypoxemia. Ideally we
will do so without increasing hypercarbia needlessly. But it is bound to happen to a degree anyway. If the level of PaCO2 becomes a clinical
problem, your local RCP should be there to assist ventilation, either in a
non-invasive fashion or with a secure airway.
2) It's not so much that our goal should be to
cruise some lower level of normal oxygenation, even in these distressed
patients. It's not so much that a PaO2
of 60 is the goal as much as it is that a PaO2 of 240 secondary to a NRB mask
will worsen V/Q matching needlessly.
3) the whole issue
isn't about the drive to breath at all!!
It is about how oxygen therapy affects the real effective CO2 load that
the patient is confronted with.
________________________