I am a trained anesthesiologist who has become a fan of CO2 in the recent years. I have read most of Ray Peat's works and I truly believe that CO2 is key to life.
There is only one point I was struggling with: When boosting metabolism and increasing body temperature, CO2 rises. That sounds good. But unfortunately it seems like the ventilatory drive is also increasing. I have experienced this from myself as well as with some patients. Now I have had a look at the literature and found this 2000 study:
I just wanted to let you know of this study as I was reading this forum and came across this question at some point.
On my own clinical experiences:
I have closely observed patients with chronic hyperventilations syndrome during general anesthesia. Unless I block their respiration with muscle relaxants or high doses of opioids, they just KEEP their (low) CO2 setpoint. When I increase their temperature with a heating device (e.g. from 36°C to 37,5°C during a long surgery), their minute ventilations just RISES until I limit that with muscle relaxants or an opioid. Even after days on the intensive care unit with an opioid depressed ventilation, most of these patients return after the extubation just to their 'normal' hyperventilating breathing patterns.
Unfortunately, I am still looking the the 'magic bullet' to improve CO2 tolerance. Volatile anesthetics, high dose benzodiazepines and high dose opioid do work, but this is certainly not for everyday use. Alternatives like Tianeptin seem to have a neglect-able effect with its normal dose (like reducing mean breathing frequency from 18.3 to 18.1). If you do have any experience with a drug that increases CO2 tolerance, please share this with me.
I have equipped some patients with a Spire device which tracks the breathing frequency and alarms patients when their breathing becomes 'tense'. This sometimes helps patients to perform Buteyko-like exercises at the right moment. Some of these patients report of far less Asthma symptoms. I an can also confirm that Buteyko was right on the breathing frequency correlating with the CO2. At least the etCO2 in my patients who reported a reduced breathing frequency on their Spire device also had more normal (higher) etCO2 levels when I checked.
There is only one point I was struggling with: When boosting metabolism and increasing body temperature, CO2 rises. That sounds good. But unfortunately it seems like the ventilatory drive is also increasing. I have experienced this from myself as well as with some patients. Now I have had a look at the literature and found this 2000 study:
Boden AG, Harris MC, Parkes MJ: A respiratory drive in addition to the increase in CO(2) production at raised body temperature in rats. - PubMed - NCBI
Mammals that use the ventilatory system as the principal means of increasing heat loss, i.e. that pant, show two fundamental changes in the control of breathing at raised temperatures. First, alveolar ventilation increases by more than, rather than in proportion to, the increase in CO2 production. Second, hypocapnia no longer causes apnoea. Rats do not use the ventilatory system as the principal means of increasing heat loss, so we have investigated whether rats also show these two changes at raised temperatures. Breathing was detected from diaphragmatic electromyogram (EMG) activity. Anaesthesia and hyperoxia were used to minimise behavioural and hypoxic drives to ventilation and arterial PCO2 (Pa,CO2) was controlled using mechanical ventilation. At 36.6 +/- 0.1 >C, breathing was absent as long as Pa,CO2 was held below a threshold level of 32.9 +/- 0.7 mm Hg (n = 14) under steady-state conditions. When body temperature in rats was raised above 37 >C, both fundamental changes in the control of breathing became apparent. First, at 39 >C the mean Pa,CO2 level during spontaneous breathing (39.6 +/- 5.4 mm Hg, n = 4) fell by 3.9 +/- 1.4 mm Hg (P < 0.05, Student's paired t test). Second, at 39.9 +/- 0.1 >C breathing was present when mean Pa,CO2 levels were only 18.2 +/- 1.5 mm Hg (n = 14), the lowest mean Pa,CO2 level we could achieve with mechanical ventilation. We calculate, however, that at 39.9 >C, the drive to breathe from the increased CO2 production alone would not sustain breathing below a Pa,CO2 level of 27.8 +/- 1.4 mm Hg (n = 13). In rats at raised body temperatures therefore a respiratory drive exists that is in addition to that related to the increase in CO2 production.
Mammals that use the ventilatory system as the principal means of increasing heat loss, i.e. that pant, show two fundamental changes in the control of breathing at raised temperatures. First, alveolar ventilation increases by more than, rather than in proportion to, the increase in CO2 production. Second, hypocapnia no longer causes apnoea. Rats do not use the ventilatory system as the principal means of increasing heat loss, so we have investigated whether rats also show these two changes at raised temperatures. Breathing was detected from diaphragmatic electromyogram (EMG) activity. Anaesthesia and hyperoxia were used to minimise behavioural and hypoxic drives to ventilation and arterial PCO2 (Pa,CO2) was controlled using mechanical ventilation. At 36.6 +/- 0.1 >C, breathing was absent as long as Pa,CO2 was held below a threshold level of 32.9 +/- 0.7 mm Hg (n = 14) under steady-state conditions. When body temperature in rats was raised above 37 >C, both fundamental changes in the control of breathing became apparent. First, at 39 >C the mean Pa,CO2 level during spontaneous breathing (39.6 +/- 5.4 mm Hg, n = 4) fell by 3.9 +/- 1.4 mm Hg (P < 0.05, Student's paired t test). Second, at 39.9 +/- 0.1 >C breathing was present when mean Pa,CO2 levels were only 18.2 +/- 1.5 mm Hg (n = 14), the lowest mean Pa,CO2 level we could achieve with mechanical ventilation. We calculate, however, that at 39.9 >C, the drive to breathe from the increased CO2 production alone would not sustain breathing below a Pa,CO2 level of 27.8 +/- 1.4 mm Hg (n = 13). In rats at raised body temperatures therefore a respiratory drive exists that is in addition to that related to the increase in CO2 production.
I just wanted to let you know of this study as I was reading this forum and came across this question at some point.
On my own clinical experiences:
I have closely observed patients with chronic hyperventilations syndrome during general anesthesia. Unless I block their respiration with muscle relaxants or high doses of opioids, they just KEEP their (low) CO2 setpoint. When I increase their temperature with a heating device (e.g. from 36°C to 37,5°C during a long surgery), their minute ventilations just RISES until I limit that with muscle relaxants or an opioid. Even after days on the intensive care unit with an opioid depressed ventilation, most of these patients return after the extubation just to their 'normal' hyperventilating breathing patterns.
Unfortunately, I am still looking the the 'magic bullet' to improve CO2 tolerance. Volatile anesthetics, high dose benzodiazepines and high dose opioid do work, but this is certainly not for everyday use. Alternatives like Tianeptin seem to have a neglect-able effect with its normal dose (like reducing mean breathing frequency from 18.3 to 18.1). If you do have any experience with a drug that increases CO2 tolerance, please share this with me.
I have equipped some patients with a Spire device which tracks the breathing frequency and alarms patients when their breathing becomes 'tense'. This sometimes helps patients to perform Buteyko-like exercises at the right moment. Some of these patients report of far less Asthma symptoms. I an can also confirm that Buteyko was right on the breathing frequency correlating with the CO2. At least the etCO2 in my patients who reported a reduced breathing frequency on their Spire device also had more normal (higher) etCO2 levels when I checked.
) every day.
