EtCO2 Monitoring and Capnography Waveforms
End-tidal CO2 (etCO2) monitoring or capnography has been a valuable tool in a clinical setting for many decades (see medical reviews: Bhende MS, LaCovey, 2001; Cambra & Pons, 2003; Zwerneman, 2006). It has been also applied for breathing retraining. It provides additional information about the progress of a person in their breathing normalization. Sometimes, however, etCO2 monitoring is used as a feedback or biofeedback mechanism. Can capnometers improve the effectiveness of breathing exercises or could it worsen the outcomes? What is the scope of correct application of capnometers and capnography in breathing retraining? First, let us consider expected etCO2 values in people with chronic diseases.
Minute ventilation rates (chronic diseases)
| All references or
click below for abstracts
|Normal breathing||6 L/min||-||Medical textbooks|
|Healthy Subjects||6-7 L/min||>400||Results of 14 studies|
|Heart disease||15 (~+mn~4) L/min||22||Dimopoulou et al, 2001|
|Heart disease||16 (~+mn~2) L/min||11||Johnson et al, 2000|
|Heart disease||12 (~+mn~3) L/min||132||Fanfulla et al, 1998|
|Heart disease||15 (~+mn~4) L/min||55||Clark et al, 1997|
|Heart disease||13 (~+mn~4) L/min||15||Banning et al, 1995|
|Heart disease||15 (~+mn~4) L/min||88||Clark et al, 1995|
|Heart disease||14 (~+mn~2) L/min||30||Buller et al, 1990|
|Heart disease||16 (~+mn~6) L/min||20||Elborn et al, 1990|
|Pulm hypertension||12 (~+mn~2) L/min||11||D'Alonzo et al, 1987|
|Cancer||12 (~+mn~2) L/min||40||Travers et al, 2008|
|Diabetes||12-17 L/min||26||Bottini et al, 2003|
|Diabetes||15 (~+mn~2) L/min||45||Tantucci et al, 2001|
|Diabetes||12 (~+mn~2) L/min||8||Mancini et al, 1999|
|Diabetes||10-20 L/min||28||Tantucci et al, 1997|
|Diabetes||13 (~+mn~2) L/min||20||Tantucci et al, 1996|
|Asthma||13 (~+mn~2) L/min||16||Chalupa et al, 2004|
|Asthma||15 L/min||8||Johnson et al, 1995|
|Asthma||14 (~+mn~6) L/min||39||Bowler et al, 1998|
|Asthma||13 (~+mn~4) L/min||17||Kassabian et al, 1982|
|Asthma||12 L/min||101||McFadden, Lyons, 1968|
|COPD||14 (~+mn~2) L/min||12||Palange et al, 2001|
|COPD||12 (~+mn~2) L/min||10||Sinderby et al, 2001|
|COPD||14 L/min||3||Stulbarg et al, 2001|
|Sleep apnea||15 (~+mn~3) L/min||20||Radwan et al, 2001|
|Liver cirrhosis||11-18 L/min||24||Epstein et al, 1998|
|Hyperthyroidism||15 (~+mn~1) L/min||42||Kahaly, 1998|
|Cystic fibrosis||15 L/min||15||Fauroux et al, 2006|
|Cystic fibrosis||10 L/min||11||Browning et al, 1990|
|Cystic fibrosis*||10 L/min||10||Ward et al, 1999|
|CF and diabetes*||10 L/min||7||Ward et al, 1999|
|Cystic fibrosis||16 L/min||7||Dodd et al, 2006|
|Cystic fibrosis||18 L/min||9||McKone et al, 2005|
|Cystic fibrosis*||13 (~+mn~2) L/min||10||Bell et al, 1996|
|Cystic fibrosis||11-14 L/min||6||Tepper et al, 1983|
|Epilepsy||13 L/min||12||Esquivel et al, 1991|
|CHV||13 (~+mn~2) L/min||134||Han et al, 1997|
|Panic disorder||12 (~+mn~5) L/min||12||Pain et al, 1991|
|Bipolar disorder||11 (~+mn~2) L/min||16||MacKinnon et al, 2007|
|Dystrophia myotonica||16 (~+mn~4) L/min||12||Clague et al, 1994|
Note that advanced stages of asthma can lead to lung destruction, ventilation-perfusion mismatch,
and arterial hypercapnia causing further reduction in body oxygen levels.
It is obvious that, since nearly 100% of people with chronic diseases suffer from chronic hyperventilation, they should have reduced etCO2 levels and the purpose of breathing retraining is to normalize end-tidal and alveolar CO2 levels so as to improve oxygen transport.
Capnography waveforms and etCO2 and breathing patterns
Capnography measures etCO2 and this end-tidal CO2, in conditions of normal breathing (6 L/min, 12 breaths/min, 500 ml for tidal volume) is very close to alveolar CO2. Since problems with lungs are not common and gas exchange between alveoli and the blood is very fast and effective, alveolar CO2 reflects arterial CO2. Hence, capnography can define CO2 level in the arterial blood. However, since modern people do not have normal diaphragmatic breathing at rest, etCO2 can be misleading due to various factors.
The first problem with etCO2 monitoring relates to chest breathing. During normal diaphragmatic breathing (shown by the capnography waveforms graph), we get a nice alveolar plateau. As a result, it is easy to find the alveolar CO2 pressure that corresponds to the top of this plateau. (In this case, the alveolar CO2 is about 5% or 38 mm Hg, which is common for some modern normals.)
Chest breathing leads to abnormally high etCO2 readings due to inhomogeneous (or uneven) lung ventilation. As the lower capnography waveforms show, there is no plateau since the last part of the exhalation has the gas coming from the CO2-rich bottom of the lungs, and it is hard to tell what is the real alveolar CO2. (As you can see on the graph, the etCO2 is the same or about 5% or 38 mm Hg, but respiratory frequency is higher: about 15 breaths/min instead of 12.)
From a physiological viewpoint, if we compare these 2 breathing patterns, the normal breathing pattern (the top capnography waveforms graph) and chest breathing with hyperventilation (the lower capnography waveforms graph), chest breathing may have both reduced arterial CO2 and reduced arterial O2 tensions due to hyperventilation with ventilation/perfusion mismatch. (Heavy breathing still removes too much CO2, but uneven gas exchange compromises blood oxygenation.)
Capnography waveforms and end tidal CO2
biofeedback monitoring during breathing exercises
If a person breath holds, his etCO2 reading is going to show zero (no CO2 exhaled). Obviously, his alveolar and arterial CO2 values increase during breath holding. If the person has a very shallow breathing pattern (with the tidal volume as his dead space or about 200-250 ml), there would be almost no gas exchange (very limited gas exchange will take place due to diffusion). Hence, his capnography end-tidal CO2 pressure will be small, but the alveolar and arterial CO2 pressures will be much greater and increasing in time. Hence, any changes in breathing patterns, as during breathing exercises and any other dynamic situations, should be analyzed with caution.
This effect could be also understood from the viewpoint of CO2 accumulation. If a person holds his breath, his body accumulates CO2 and etCO2 is going to be zero. If a person performs a Buteyko reduced breathing exercise (breathing about 15-20 % less air with reduced minute ventilation), it will take several minutes before stable CO2 values will be shown by the capnometer since large amounts of CO2 can be dissolved in the blood, and intra- and extra-cellular fluids. Hence, it will take several minutes (up to 5-7 min) for the stable waveforms to appear. Would etCO2 represent arterial CO2?
Let us look in more detail. If the person practices Buteyko reduced breathing exercise with strong air hunger (both minute ventilation and tidal volume are reduced about 2 times), end tidal CO2 monitoring is not going to reflect the alveolar CO2 concentration. Physiological studies have also found that people with larger tidal volume and reduced respiratory frequency have abnormally high etCO2 values. Since reduced breathing in the sick (those with less than 20 s for the body oxygen test or more than 12 L/min for minute ventilation at rest) is done with increased respiratory frequency and reduced tidal volume, they can get low etCO2 numbers, while in reality their alveolar and arterial CO2 will be increasing during the whole session (e.g., 10-15 minutes).
Vice versa, if a person starts a deep breathing exercise with increased minute ventilation with deliberate extended exhalations (to push all high-CO2 air out from the lungs), their etCO2 capnography monitoring will show increased etCO2 levels, while alveolar and arterial CO2 concentrations will be less and less.
Indeed, medical doctors also observed these dynamic effects during anesthesia. A large review of medical literature resulted in an article "Misleading end-tidal CO2 tensions" (Wahba & Tessler, 1996). The authors wrote, "End-tidal PCO2 is often not indicative of PaCO2. Also, changes in PETCO2 do not always accurately indicate the direction and extent of the change in PaCO2." They explained that "... hemodynamic instability have an increased Pa-PETCO2 gradient".
Finally, there are purely psychological factors that can seriously distort etCO2 capnography results. When someone holds a capnometer under your nose, it is difficult to maintain the automatic breathing pattern. Our breathing parameters undergo large changes as soon as we pay attention to our breath.
For example, most Buteyko breathing students, since they know that hyperventilation is not good and they practiced the reduced breathing hundreds of times in the past, may start reducing breathing as soon as there is something under their nose. (Many Buteyko teachers even say to their students, "Japanese samurai had a feather under their nose for 1 hour every day to train their breath. The goal was to have this feather motionless." Hence, the capnometer could immediately trigger this image.)
Other people may have a fantasy about the importance of deep breathing and they may start practicing deep breathing as soon as someone holds a device under their nose.
The effects will be opposite: the Buteyko student will get abnormally low etCO2 (and higher arterial CO2), while a "deep breather" will get abnormally high etCO2 with reduced arterial CO2 concentrations.
Hence, etCO2 monitoring and capnography are not useful as biofeedback, but can be used in the long run (e.g., once per day or once per week), as an additional tool for breathing retraining control. This is how Dr. Buteyko viewed and described capnography.
The situation with the application of breathing devices (such as the Frolov breathing or the DIY breathing device) is different since the practicing person has to have large diaphragmatic inhalations and exhalations, while the capnometer can be used to measure CO2 inside the breathing device or near the place where air leaves the device. In this application (e.g., for the Frolov breathing device therapy), the results will show real CO2 values in the container at the end of exhalations and etCO2 monitoring and capnography waveforms can be used as biofeedback.
Warning. Breathing exercises can cause powerful cleansing reactions and can be dangerous for pregnant women, people with organ transplants, GI problems, and panic attacks, as well as those who take medication for diabetes, hypertension, hypothyroidism, and other conditions. Consult your health care provider and follow special guidelines, which can be found in the Module Restrictions, limits, and temporary contraindications.
Reference pages: Breathing norms and the DIY body oxygen test:
- Breathing norms: Parameters, graph, and description of the normal breathing pattern
- Body-oxygen test (CP test) : How to measure your own breathing and body oxygenation (two in one) using a simple DIY test
References: pages about CO2 effect:
- Vasodilation: CO2 expands arteries and arterioles facilitating perfusion (or blood supply) to all vital organs
- The Bohr effect: How and why oxygen is released by red blood cells in body tissues
- Nerve stabilization: Carbon dioxide has powerful calmative and sedative effects on brain neurons and nerve cells
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