EtCO2, Capnography Waveforms, Breathing Training

EtCO2 Monitoring, Capnography Waveforms, Breathing Training

CO2 molecule 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)

Condition	Minute ventilation	Number of people	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 (±4) L/min	22	Dimopoulou et al, 2001
Heart disease	16 (±2) L/min	11	Johnson et al, 2000
Heart disease	12 (±3) L/min	132	Fanfulla et al, 1998
Heart disease	15 (±4) L/min	55	Clark et al, 1997
Heart disease	13 (±4) L/min	15	Banning et al, 1995
Heart disease	15 (±4) L/min	88	Clark et al, 1995
Heart disease	14 (±2) L/min	30	Buller et al, 1990
Heart disease	16 (±6) L/min	20	Elborn et al, 1990
Pulm hypertension	12 (±2) L/min	11	D'Alonzo et al, 1987
Cancer	12 (±2) L/min	40	Travers et al, 2008
Diabetes	12-17 L/min	26	Bottini et al, 2003
Diabetes	15 (±2) L/min	45	Tantucci et al, 2001
Diabetes	12 (±2) L/min	8	Mancini et al, 1999
Diabetes	10-20 L/min	28	Tantucci et al, 1997
Diabetes	13 (±2) L/min	20	Tantucci et al, 1996
Asthma	13 (±2) L/min	16	Chalupa et al, 2004
Asthma	15 L/min	8	Johnson et al, 1995
Asthma	14 (±6) L/min	39	Bowler et al, 1998
Asthma	13 (±4) L/min	17	Kassabian et al, 1982
Asthma	12 L/min	101	McFadden & Lyons, 1968
COPD	14 (±2) L/min	12	Palange et al, 2001
COPD	12 (±2) L/min	10	Sinderby et al, 2001
COPD	14 L/min	3	Stulbarg et al, 2001
Sleep apnea	15 (±3) L/min	20	Radwan et al, 2001
Liver cirrhosis	11-18 L/min	24	Epstein et al, 1998
Hyperthyroidism	15 (±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 (±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 (±2) L/min	134	Han et al, 1997
Panic disorder	12 (±5) L/min	12	Pain et al, 1991
Bipolar disorder	11 (±2) L/min	16	MacKinnon et al, 2007
Dystrophia myotonica	16 (±4) L/min	12	Clague et al, 1994

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 that 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.

End tidal CO2 (etCO2) capnography waveforms for diaphragmatic and chest breathing The first problem with etCO2 monitoring relates to chest breathing. During normal diaphragmatic breathing (the top 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 the 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

Young woman practicing yoga 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 (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.

Older man with artifical respiration Indeed, medical doctors also observed these dynamic effects in 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.)

Man with chest breathing 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 exactly how Dr. Buteyko viewed and described capnography monitoring in his patents and other writings.

The situation with breathing devices 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 flow 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. There are numerous restrictions and contraindications for some health problems (anxiety, diabetes, hypertension, GI problems, and so on) in relation to specific breathing exercises. In addition, pregnant women, people with organ transplants, and some other groups of people should follow special guidelines in relation to their general breathing retraining progress. Finally, there are important preliminary requirements that make breath work safe and more effective (empty stomach, good thermoregulation, and so forth). All these factors can be found in the Learning Section of this website.

Reference Web Pages: Breathing norms, Medical Graphs and Tables about Breathing Rates (Minute Ventilation) and Body Oxygen in Healthy, Normal and Sick People
Breathing norms Parameters, graph, and description of the normal breathing pattern
6 breathing myths 6 myths about breathing and body oxygenation (prevalence: over 90%)
Hyperventilation Definitions of hyperventilation: their advantages and weak points
Hyperventilation Syndrome in the Sick. Table 1. Western scientific evidence about prevalence of CHV (chronic hyperventilation) in patients with various chronic conditions (34 medical studies)
Normal Minute Ventilation in Healthy Subjects: Easy and Light Breathing (14 Studies)
Hyperventilation Prevalence Present in Over 90% of Normal People (24 medical publications)
HV and hypoxia How and why deep breathing reduces oxygenation of cells and tissues of all vital organs
Body oxygen test How to measure your own breathing and body oxygenation (a simple DIY test)
Body oxygen in healthy Table 4. CP (body oxygen level) in healthy people (27 medical studies)
Body oxygen in sick Table 5. CP (body oxygen level) in sick people (14 medical studies)
Buteyko Table of Health Zones with clinical description of most common zones
Morning HV Morning hyperventilation effect or how and why critically ill people are most likely to die during early morning hours

References: CO2 Effects Web Pages
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 tissues
Cell Oxygen Levels and oxygen transport are controlled by alveolar CO2 and breathing
Oxygen Transport depends on breathing and these two effects (Vasoconstriction-Vasodilation and the Bohr effect) are parts of two diagrams that summarize influences of hypocapnia (low CO2 content in the blood and cells) on circulation and O2 delivery
Free Radical Generation takes place due to anaerobic cell respiration caused by cell hypoxia. Hence, antioxidant defenses of the human body are also regulated by CO2 and breathing
Inflammatory Response is controlled by breathing since hypoxia leads to or intensifies chronic inflammation through over-expression of the hypoxia-inducible factor 1, while normal breathing reduces these processes
Nerve stabilization takes place due to calmative or sedative effects of carbon dioxide in neurons or nerve cells
Muscle relaxation or relaxation of muscle cells is normal at high CO2, while hypocapnia causes muscular tension, poor posture and, sometimes, aggression and violence
Brochodilation - dilation of airways (bronchi and bronchioles) by carbon dioxide, and their constriction due to hypocapnia
Blood pH regulation and regulation of other bodily fluids
CO2: Lung Damage Healer: Elevated carbon dioxide prevents injury and promotes healing of lung tissues
CO2: Skin and Tissue Healer
Synthesis of Glutamine in the Brain, CO2 fixation, and other chemical reactions
CO2 myth "CO2 is a toxic waste gas" myth
Breathing control How is our breathing regulated? Why hypocapnia makes breathing uneven and erratic

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