Carbon Dioxide Myth

[BLADEMDA]

So, are we hyperventilating our patients during surgery and causing harm? Dr. Lewis Coleman seems to think so.

50 Years Lost in Medical Advance: The Discovery of Hans Selye’s Stress Mechanism Kindle Edition​

by Lewis coleman

Many of his ideas are unconventional but seem convincing and certainly worth examining in more detail.

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[BLADEMDA]

Standards and guidelines for CO2 management during anesthesia
are urgently needed.2 The harmful habit
of hyperventilation depletes CO2 tissue reserves and disrupts oxygen transport
and delivery.3 It is inherently
harmful and confers no benefits,4 but it has been
“gospel” in anesthesia practice ever since the founder of the profession, Dr.
Ralph Waters, characterized CO2 as “toxic waste, like urine” that must be “rid
from the body.” His underlying motive was political, not medical.5,6

The anesthesiology profession is poised to realize priceless public prestige by performing long term outcome studies that test and confirm the validity of stress theory and reforming itself.


1 Coleman, L. S. 50 Years Lost in Medical Advance: The Discovery of Hans Selye’s Stress Mechanism. (The American Institute of Stress Press, 2021).
2 Coleman, L. S. A call for standards on perioperative CO(2) regulation. Can J Anaesth (2011). https://doi.org/10.1007/s12630-011-9469-7
3 Coleman, L. S. Oxygen Transport and Delivery. (2022). <>.
4 Coleman, L. S. Intraoperative Hyperventilation May Contribute to Postop Opioid Hypersensitivity. apsf Newsletter Winter 2009-2020 (2010). <Intraoperative Hyperventilation May Contribute to Postop Opioid Hypersensitivity>.
5 Coleman, L. S. Four Forgotten Giants of Anesthesia History. Journal of Anesthesia and Surgery 3, 1-17 (2015). <Four Forgotten Giants of Anesthesia History>.
6 Coleman, L. S. The Great Medical Hoax of the 20th Century. (2022). <Amazon product>.

 

[MirrorTodd]

Hyperventilation has gone away according to my relatively recent training. I was taught to keep the patient somewhere in their normal range for PaCO2 (estimating from their ETCO2 (assuming normal V/Q matching)).

 

[BLADEMDA]

Hyperventilation has gone away according to my relatively recent training. I was taught to keep the patient somewhere in their normal range for PaCO2 (estimating from their ETCO2 (assuming normal V/Q matching)).

Should be we permitting some mild hypercarbia like a CO2 of 45-50 in order to augment the offloading of oxygen? Many times I see providers keeping the Co2 around 30-32. Does this have implications for renal blood flow? The author seems to think it does.

 

[BLADEMDA]

Intraoperative Hyperventilation May Contribute to Postop Opioid Hypersensitivity

To the Editor I read Dr. Stoelting’s recent editorial entitled “Dangers of Postoperative Opioids—Is There A Cure?” I believe that iatrogenic

www.apsf.org

Critical Care specialists have already embraced permissive hypercarbia. Anesthesiologists could profit from their example. The simple remedy of replacing hyperventilation with permissive hypercarbia that enhances respiratory drive can improve safety and outcome by preventing unexpected respiratory depression, rendering opioids more predictable, and facilitating greater opioid dosage to control stress.

Lewis S. Coleman, MD
Bakersfield, CA

 

[BLADEMDA]

Four Forgotten Giants of Anesthesia History​

Lewis Coleman

Abstract​

The anesthesiology profession may one day serve as a cautionary tale of how power, politics and privilege can perturb science and progress. Previous anesthesia practitioners possessed a superior understanding of physiology and pharmacology, but overenthusiastic CO2 supplementation with inadequate monitors and machines caused asphyxiation disasters that were improperly attributed to CO2 toxicity. Dr. Ralph Waters founded the anesthesiology profession on the basis of a practical new anesthetic technique that introduced elective intubation and hyperventilation to eliminate CO2 toxicity, but mechanical hyperventilation dangerously depletes CO2 tissue reserves and exaggerates morbidity and mortality. The benefits of CO2 supplementations were forgotten, and consequent CO2 confusion has derailed research, discouraged opioid treatment, damaged patient safety, and disrupted professional progress. Anesthesiologists can no longer claim to provide superior service, and hospital administrators are replacing them with nurses. Professional membership is in decline, and professional survival is in question. Modern machines have eliminated asphyxiation, and modern monitoring enables safe and beneficial hypercarbia that complements opioid treatment and minimizes surgical morbidity and mortality. CO2 reform promises revolutionary advance but faces formidable opposition.

 

[BLADEMDA]

Respiratory acidosis
  Hypoventilation accumulates CO2 in blood and tissues, causing “respiratory acidosis” that is benign and beneficial in the absence of hypoxia. CO2 enhances the release of oxygen into tissues via the Bohr effect, stimulates respiratory chemoreceptors, reduces blood viscosity, improves cardiac efficiency, and reversibly interacts with water in blood to form harmless carbonic acid that reduces blood pH and stimulates the respiratory drive of consciousness via pH receptors in brain ventricles. Harmless hypoventilation occurs during both normal sleep and anesthesia when respiratory drive becomes dependent on respiratory chemoreceptors, causing mild respiratory acidosis that enhances tissue perfusion, tissue oxygenation, and organ function.



Yandell Henderson, PhD (1873-1944) was the director of the Yale laboratory of applied physiology and the most prominent gas physiologist in his era. Like Crile, he was an idealist who believed that science should serve the public interest[62]. He opposed American involvement in WWIT. He testified before congress about the dangers of automobile exhaust pollution, though his views were not accepted until long after his death[63].

In 1911 Henderson famously led a team of international experts that studied respiratory physiology at the top of Pike’s Peak[64]. His research demonstrated that spontaneous hyperventilation during anesthesia (due to inadequately controlled surgical stimulation) can cause cardiopulmonary collapse or unexpected postoperative respiratory arrest. He showed how CO2 supplementation stabilizes hemodynamic function, stimulates respiratory drive, enhances cardiac efficiency, improves tissue oxygenation, and prevents postoperative atelectasis, pneumonia, nausea, vomiting, and unexpected respiratory arrest[30,65,66]. Henderson also demonstrated that CO2 supplementation effectively treats myocardial infarction, angina, strokes, pneumonia, asthma, influenza, breathing problems in newborn babies, carbon monoxide poisoning, drowning, and smoke inhalation[30,67,68]. His work inspired the installation of CarbogenU, which was a mixture of oxygen and carbon dioxide, on fire trucks in New York City, Chicago, and other major cities. Carbogen was widely embraced by physicians as an effective treatment, and it was credited with saving many lives, but unfounded fears of CO2 toxicity caused it to disappear from use.

In 1912 Dr. Henderson chaired a five-member Committee on Anesthesia that reported to the American Medical Association’s House of Delegates. It forcefully stated :“Anesthesia should cease to be regarded as merely an adjunct of surgery. It should be in charge of those whose principal aim is, not to see as much of the operation as possible, but to administer anesthesia in such a manner as to bring the patient through with the least possible loss of vitality.” Coming just two years after the Flexner Report, this recommendation had little effect on anesthesia practice, but it did put the AMA on record as supporting improvement in anesthesia practiceV.

Lewis Coleman, MD

 

[periopdoc]

I usually run my patients at a PaCO2 between 45 and 50, unless I'm dealing with a tight brain

 

[BLADEMDA]

I think that getting all providers to understand this CO2 paradigm is like the time when we went to "low flow" anesthesia. My hunch is that most of you are still keeping the CO2 in the 30-35 range as are most CRNAs. This has been the practice for the past 70 years and I am guilty of it myself. That said, there should be a limit on how high we allow the CO2 to go up during a case. Is that 50 or 55? I still feel quite uncomfortable with a CO2 above 50 even if Dr. Lewis Coleman thinks that is not only acceptable but recommended.

 

[BLADEMDA]

The Shortcomings of Pulse Oximetry​

Few nurses, doctors, and even anesthesiologists appreciate the complicated characteristics and deceptive shortcomings of pulse oximetry, which is the most common means to monitor oxygen in hospitals and clinics. It does not measure the partial pressure of oxygen in tissues, which is the critical measure of cellular oxygenation. Instead, it determines blood oxygen saturation using an algorithm that assesses light frequencies reflected from oxygen in blood. Unfortunately, it cannot distinguish between oxygen bound to hemoglobin and oxygen saturated in plasma, and it can be “fooled” by numerous circumstances. For example, it cannot detect hypoventilation when patients are breathing 100% oxygen, and it cannot detect cellular oxygen starvation caused by mechanical hyperventilation that depletes carbon dioxide and disrupts the release of oxygen from hemoglobin into tissues. This happens routinely when patients are hyperventilated during surgery, based on the false belief that carbon dioxide is a “waste gas” that must be removed from the body.

Lewis Coleman, MD

 

[GravelRider]

I’ve been doing permissive hypercarbia since residency (~10 years). The hyperventilation never really made sense to me. My guess is that hyperventilation came about as a margin of safety against a patient making respiratory efforts that might bother a surgeon. With sugammadex now, most people feel more comfortable keeping the patient more deeply paralyzed and thus the need to hyperventilate might go away. Although, like many things in anesthesia, old habits die hard. I tend to keep my ETCO2 in the upper 40s to low 50s. If someone gives me a break or takes over for me, they first thing they usually do is “fix” my ventilation for me.

 

[pgg]

Seems like much ado about nothing.

Nobody's really pushing for hyperventilation even in cranis any more, unless it's brief and a specific action for a brain that is noted to be tight right then.

Permissive hypercapnia has been regarded as safe and OK since I was an intern 20 years ago.

There's usually a gradient of at least ~5 or so between ETCO2 and PACO2 so I don't think it's cause for concern if someone runs their ETCO2 in the 30s.


For some reason our ventilators are all preset with a RR of 16 and TV of 425. Occasionally I'll see an ETCO2 in the 20s because someone forgot to adjust it in a 45 kg old person, but I don't often see inappropriate deliberate hyperventilation.


They're going to have to produce some extraordinary data to convince me that a CO2 of 35 is harmful in any way.

 

[Beeftenderloin]

No offense, but I think you’re showing your age here Blade. Unless they have a tight brain or a sick RV, nobody ever stressed hyperventilation as a baseline modus operandi in the OR when I trained. And even with those disease states, the goal is normocapnea, not hypocapnea.

And to actually counter your argument: since I trained in the post ARDSNET era of lung protective ventilation and robotic surgery, the concept of permissive HYPERcapnea was far more commonly discussed and employed.

 

[BLADEMDA]

No offense, but I think you’re showing your age here Blade. Unless they have a tight brain or a sick RV, nobody ever stressed hyperventilation as a baseline modus operandi in the OR when I trained. And even with those disease states, the goal is normocapnea, not hypocapnea.

And to actually counter your argument: since I trained in the post ARDSNET era of lung protective ventilation and robotic surgery, the concept of permissive HYPERcapnea was far more commonly discussed and employed.

Sure, it's easy to say I am old and out of touch but the purpose of my posting this thread was to point out that maybe a CO2 of 50, with an average AA gradient of 5, so a real arterial CO2 of 55, would be beneficial in most situations. I doubt most providers are actually setting their vents for a Co2 of 50.

As for me, I readily admit I use a CO2 of 35-40 for the vast majority of my cases. It's what I have been doing for decades. I don't "hyperventilate" but rather seek a normal, physiologic CO2. With an A-A gradient of 5 that means set the ventilator to obtain a CO2 in 35-40 range. This thread is about whether we should be setting it to get a 50 CO2 on ET readings. Again, I doubt that 90% of you are doing that at this time. Perhaps, 45 on the EtCo2 reading will become my new norm for my cases.

I'm fully aware of the literature of permissive hypercapnia in Critical Care. We use it all the time with our LMA cases (whether we believe in it or not). The question still remains should we set the EtCo2 to 50 for our routine cases especially our ASA 3 and 4 cases.

 

[pgg]

the purpose of my posting this thread was to point out that maybe a CO2 of 50, with an average AA gradient of 5, so a real arterial CO2 of 55, would be beneficial in most situations

Beneficial is a bold, dramatic claim.

If you said not harmful I'd casually agree but the claim that some real tangible benefit will follow from routinely running CO2s in the 50s ... care to hazard a NNT guess? What specific outcome are we improving, in theory?

 

[DesiredMemberName?]

Intentional hypercapnia vs normocapnia probably doesn’t matter much for most cases in reasonably healthy patients. I don’t know anyone who is routinely, purposefully hyperventilating patients. Is that a thing?

If the pt is so tenuous that this could have a significant beneficial effect, you should probably place an arterial line and optimize ventilation/acid-base status using gases rather than guessing the ETCO2/PACO2 gradient.

You could be running the ETCO2 at 50 for some theoretical benefit based on an a bunch of assumptions and not realize that the pH is 7.2.

 

[GassYous]

I also aim for 35-40 but with an lma I'm happy to leave them in the 50s.

 

[abolt18]

Controlled ventilation, I'm usually riding 35-40. If I'm checking blood gasses, I just titrate to normalize pH regardless of ETCO2.

If pressure support or spontaneous ventilation, I'll tolerate 60s temporarily, like if I'm just switching them to this ventilatory mode and trying to get them breathing regularly early in the case, but not close to extubation. Definitely okay with 50s.

Only time we ever hyperventilated in residency was for cranis/tumors. They did it for every single one regardless of if it was actually needed.

 

[fakin' the funk]

Sure, it's easy to say I am old and out of touch but the purpose of my posting this thread was to point out that maybe a CO2 of 50, with an average AA gradient of 5, so a real arterial CO2 of 55, would be beneficial in most situations. I doubt most providers are actually setting their vents for a Co2 of 50.

As for me, I readily admit I use a CO2 of 35-40 for the vast majority of my cases. It's what I have been doing for decades. I don't "hyperventilate" but rather seek a normal, physiologic CO2. With an A-A gradient of 5 that means set the ventilator to obtain a CO2 in 35-40 range. This thread is about whether we should be setting it to get a 50 CO2 on ET readings. Again, I doubt that 90% of you are doing that at this time. Perhaps, 45 on the EtCo2 reading will become my new norm for my cases.

I'm fully aware of the literature of permissive hypercapnia in Critical Care. We use it all the time with our LMA cases (whether we believe in it or not). The question still remains should we set the EtCo2 to 50 for our routine cases especially our ASA 3 and 4 cases.

As pgg said - a purported BENEFIT of INTENTIONAL hypercapnia is definitely different than the known REDUCTION IN HARM associated with PERMISSIVE hypercapnia in severe respiratory failure states where minimizing all forms of VILI is a good.

 

[Iso4ane]

A few thoughts, his ideas like others have mentioned are not too crazy and I'm willing to look into it further. I've read before and people smarter than me have stated that the PaCO-etCO2 gradient in most patient is at least 5mmHg and probably closer to 7mmHg, so I fully admit that I like to run them at a etCO2 targeting PaCO2 of 40 ( or with in a CO2 range that brings the pH into a more normal physiological range). I'm of the belief that pH is one of the most important factors in regulating many cellular systems, and the bicarb-carbonic acid (CO2) just happens to be the biggest buffering system in the human body, so it makes sense that CO2 can affect others systems more globally. (If you put in the pka and normal concentrations of CO2 and HCO3- in to Henderson-Hasebach you get exactly 7.4)

I do not disagree with the assertion that CO2 levels can have many effects on the body, whether that is through signalling or what not, but the idea that intentional relative hypercapnia under anesthesia is beneficial may be a step too far.

When it comes to ARDSNet, the idea of permissive hypercapnia comes more from the idea that the dangers (increased morbidity and mortality) of increased tidal volumes and hypoxemia is higher than that permissive hypercapnia, so optimize tidal volumes and oxygenation first then target CO2 levels. It's not like they want the CO2 levels that high, they had no other choice hene permissive.

So if you have no problems with tidal volumes or oxygenation, what role does hypercapnia play?