CO2 Levels in the Lungs and in the Blood

This section is not essential reading in order to master Buteyko Exercises. It is included mainly for the benefit of the more technically minded and for Buteyko practitioners who are often puzzled by an apparent contradiction concerning the method. The aim of the method is to decrease lung ventilation in order to increase alveolar CO2. However, many asthmatics have high blood CO2. This leads doctors to recommend the opposite – increased lung ventilation – in order to reduce blood CO2, because the high CO2 is due to insufficient ventilation. However, increased breathing will reduce alveolar CO2 and usually provokes bronchospasm. This presents a dilemma for doctors.

In 1962 Dr. Buteyko, for the first time, resolved this paradox. He explained that the difference between blood CO2 and lung CO2 that exists in some asthmatics is caused by damage to lung tissue resulting in a deterioration of the gas exchange process in the lung. In this case the increased ventilation causes a deficiency only in lung CO2 resulting in hypertonicity of the smooth muscle in the walls of the bronchi, provoking bronchospasm.

The diagram below approximately represents the gas exchange in the lungs with normal indices of CO2 and O2 in alveolar air and blood.

But in asthma these indices are not normal. Usually asthmatics have consistently very low levels of CO2 in alveolar air while the CO2 in the blood can be low, normal or high depending on the severity of asthma. The consistently low level of alveolar CO2 is a result of chronic alveolar hyperventilation. The high level of CO2 in the blood is a result of destroyed or damaged lung tissue resulting in a deterioration of the gas exchange process in the lung. The following illustrates how alveolar and blood CO2 can vary in asthmatics.

Normal CO2

In healthy individuals or in individuals with early stage asthma, alveolar and blood CO2 are the same. This assumes that the lung tissues are normal and that normal gaseous exchange takes place through the alveolar membranes.

Low CO2

Alveolar membranes are normal, while both alveolar and blood CO2 are low. In healthy individuals the alveolar CO2 level is around 40mm Hg. It is never this high in asthmatics. The reason for the low level of CO2 found in the lungs is chronic hyperventilation.

High CO2

In severe asthma alveolar CO2 is always very low. CO2 in the blood is high in severe asthma and occasionally in mild -to-moderate asthma. This results from destroyed tissue in the lungs and a deterioration of gas exchange in the lung. Pulmonary emphysema and pneumosclerosis can often cause arteriovenous shunting in the lung. With this condition the destruction of the lung tissue in some areas prevents normal gas exchange, resulting in the venous blood from these areas, with its high CO2 and low O2 content, effectively being shunted back into the arteries.

Alveolar CO2 should be measured at the end of a normal exhalation. It often happens that end tidal CO2 measurements appear to show higher than usual CO2 levels in alveolar air. This happens when there is an unnaturally long exhalation. In this event the air closest to the blood which is richer in CO2 enters the gas analyzer, which will show a higher percentage of CO2 in the alveoli than the average value. For this reason it is important to measure CO2 correctly after a normal exhalation, especially if there is normal gas exchange in the lungs.

	Back to: The Book Index Table of Contents Excerpt: Buteyko-Land Excerpt: How to measure the Control Pause correctly		CO2 Levels in the Lungs and in the Blood This section is not essential reading in order to master Buteyko Exercises. It is included mainly for the benefit of the more technically minded and for Buteyko practitioners who are often puzzled by an apparent contradiction concerning the method. The aim of the method is to decrease lung ventilation in order to increase alveolar CO2. However, many asthmatics have high blood CO2. This leads doctors to recommend the opposite – increased lung ventilation – in order to reduce blood CO2, because the high CO2 is due to insufficient ventilation. However, increased breathing will reduce alveolar CO2 and usually provokes bronchospasm. This presents a dilemma for doctors. In 1962 Dr. Buteyko, for the first time, resolved this paradox. He explained that the difference between blood CO2 and lung CO2 that exists in some asthmatics is caused by damage to lung tissue resulting in a deterioration of the gas exchange process in the lung. In this case the increased ventilation causes a deficiency only in lung CO2 resulting in hypertonicity of the smooth muscle in the walls of the bronchi, provoking bronchospasm. The diagram below approximately represents the gas exchange in the lungs with normal indices of CO2 and O2 in alveolar air and blood. But in asthma these indices are not normal. Usually asthmatics have consistently very low levels of CO2 in alveolar air while the CO2 in the blood can be low, normal or high depending on the severity of asthma. The consistently low level of alveolar CO2 is a result of chronic alveolar hyperventilation. The high level of CO2 in the blood is a result of destroyed or damaged lung tissue resulting in a deterioration of the gas exchange process in the lung. The following illustrates how alveolar and blood CO2 can vary in asthmatics. Normal CO2 In healthy individuals or in individuals with early stage asthma, alveolar and blood CO2 are the same. This assumes that the lung tissues are normal and that normal gaseous exchange takes place through the alveolar membranes. Low CO2 Alveolar membranes are normal, while both alveolar and blood CO2 are low. In healthy individuals the alveolar CO2 level is around 40mm Hg. It is never this high in asthmatics. The reason for the low level of CO2 found in the lungs is chronic hyperventilation. High CO2 In severe asthma alveolar CO2 is always very low. CO2 in the blood is high in severe asthma and occasionally in mild -to-moderate asthma. This results from destroyed tissue in the lungs and a deterioration of gas exchange in the lung. Pulmonary emphysema and pneumosclerosis can often cause arteriovenous shunting in the lung. With this condition the destruction of the lung tissue in some areas prevents normal gas exchange, resulting in the venous blood from these areas, with its high CO2 and low O2 content, effectively being shunted back into the arteries. Alveolar CO2 should be measured at the end of a normal exhalation. It often happens that end tidal CO2 measurements appear to show higher than usual CO2 levels in alveolar air. This happens when there is an unnaturally long exhalation. In this event the air closest to the blood which is richer in CO2 enters the gas analyzer, which will show a higher percentage of CO2 in the alveoli than the average value. For this reason it is important to measure CO2 correctly after a normal exhalation, especially if there is normal gas exchange in the lungs.


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