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Scientific Research
Clinical Trials Report or Abstract

Clinical Trials and Research undertaken into the Buteyko Method and related issues.

Ventilation Test In Patients With Bronchial Asthma
Source: Buteiko KP, Odintsova MP, Nasonkina NS. Vrach Delo. 1968 Apr; 4:33-6. PMID: 5664602 [PubMed - indexed for MEDLINE]

* Translated by: Tamer Y. EL MAYS, MD. Cardiovascular/Respiratory Sciences, Faculty of Medicine, University of Calgary. 3330 Hospital Drive NW, Calgary, Alberta, Canada T2N 4N1
Tel:(403)220-3044, Fax:(403)270-8928, E-mail: mtyel@ucalgary.ca


Experiments on animals showed the influence of carbonic acid (gas) in inhaled air on bronchial tone (Broun, 1885; Lor, 1924; Tienze, 1929; Peter, 1955 and others). Lloyd (1963) established in healthy individuals a negative dependence between the degree of bronchial constriction and the level of CO2 in alveoli.

According to the data of several investigators on patients with bronchial asthma in periods of exacerbation of the disease, an increase in pulmonary ventilation was observed (A. I. Dziuba, 1963; P. K. Bulatov, 1964 and others). Increased pulmonary ventilation without changes in the main exchange should result in decreased pCO2 in alveoli. That is why an interest arises in studying in patients with bronchial asthma, the dependence of bronchial tone on the pulmonary ventilation and partial pressure of carbonic acid (gas) in alveoli (pCO2A).

Investigating 44 patients with bronchial asthma during exacerbation and without exacerbation, age from 10 to 70 year, 15 men, 29 women, duration of the disease from 3 to 20 years.

Patients underwent tests in which they voluntarily increased pulmonary ventilation during 1 to 3 minutes until the appearance of negative symptoms. Then they decreased depth and frequency of their breathing until disappearance of the negative symptoms that resulted from hyperventilation. During the test, 22 patients had a non-stop recording of carbopneumograms (partial pressure of carbonic acid (gas) in alveoli pCO2A) on a “capnograph” from “Godart” company, and pneumotachograms. pCO2A was determined every 10 seconds, as well as the gain of pCO2A along the alveolar plateau of the carbopneumogram per 1 sec. (ΔpCO2A mmHg/sec., which can characterize irregularity of alveolar ventilation, depending on narrowing of bronchial opening in several parts), respiratory frequency, tidal volume, minute ventilation. In all patients, subjective symptoms and the time of their onset were taken into consideration. The dynamics of indicators of external breathing and pCO2A are reflected in table 1.

Table 1:
Measurement indicators Unit of measurement Initial values Test with hyperventilation Test with decreased ventilation
Respiratory frequency Per 1min 16 22 13.5
Tidal volume L 0.523 0.764 0.430
Minute ventilation L/min 8.324 23.220 5.620
pCO2A mmHg 36.3 26 29
ΔpCO2A mmHg/sec 5.9 6.4 4.84


Initial values: pCO2A = 36.3 mmHg, respiratory frequency = 16/min, tidal volume = 0.523L, minute ventilation = 8.324 L/min, Δ pCO2A = 5.9 mmHg/sec.

As a result of hyperventilation (mean duration of the tests : 1min.45sec) pCO2A dropped to 26 mmHg, respiratory frequency increased to 22/min, tidal volume to 0.764 L, minute ventilation to 23.22L/min, Δ pCO2A to 6.4 mmHg/sec. In 32 of 44 persons in an average of 105 seconds after the beginning of hyperventilation, several signs of bronchospasm appeared (dyspnoea, wheezes, breathlessness, and cough). Besides bronchospasm symptoms 11people had headache, ten had dizziness, five had pain in the heart region, two had palpitation, one had weakness, and one had numbness of fingers.

As a result of reduced pulmonary ventilation pCO2A increased to 29 mmHg, respiratory frequency decreased to 13.5/min, tidal volume to 0.430 L, minute ventilation to 5.620 L/min, Δ pCO2A to 4.84 mmHg/sec. symptoms of bronchospasm disappeared in all patients within an average duration of 105 seconds.

Besides the above-mentioned indicators, in 18 patients, using the pneumotachograph, and by means of overlapping air stream at the pitch of inspiration and expiration bronchial resistance was defined. The resistance of bronchial tree (R) was determined by the formula P/V, where P is the pressure in the bronchi at the overlapping moment, V is the velocity of air movement at the moment of overlapping.

Conducting cross-correlative analysis (K. P. Buteyko, D. V. Demin, 1963) interconnects pCO2A with Δ pCO2A mmHg/sec. and R on inspiration and expiration for each one investigated.

Cross-correlation between pCO2A and R on inspiration was calculated in 11 people. Positive correlation was obtained in four people. The average coefficient of correlation (r) was equal to 0.67 (from 0.32 to 0.75), the response time of bronchial resistance in response to changes in CO2 (t) was on average equal to 45sec. (from 30 to 70 sec.). Negative correlation was obtained in six people, r = -0.49 (from -0.36 to -0.80), t = 73 sec. (from 20 to 210 sec.). One patient did not show clear correlation.

Correlation between pCO2A and R on expiration was calculated in 17 people. Positive correlation was obtained in nine people: r = 0.53 (from 0.11 to 0.87); t = 57.7 sec. (from 20 to 120 sec.), negative correlation was obtained in eight people: r = -0.40 (from -0.80 to -0.89), t = 98.7 sec. (from 30 to 220 sec.).

Correlation between pCO2A and Δ pCO2A was calculated in 16 people: positive correlation was obtained in six: r = 0.50 (from 0.15 to 0.78), t = 75 sec. (from 20 to 230 sec.), negative correlation was obtained in nine: r = -0.43 (from -0.16 to -0.92), t = 44.4 sec. (from 20 to 90 sec.), clear correlation was not determined in two patients.

Thus, hyperventilation, decreasing pCO2 in alveoli, led to increased irregularities of pulmonary ventilation (Δ pCO2A) and to the appearance of some or other symptoms of bronchospasm in the majority of the patients. Decreased pulmonary ventilation resulted in decreased irregularities of alveolar ventilation (Δ pCO2A) and disappearance of symptoms of bronchospasm that appeared during hyperventilation in all patients.

In the majority of patients (in six of ten) with clear cross-correlation, negative dependence was obtained between the level of pCO2A and the resistance of bronchial tree on inspiration and between the ventilatory irregularities’ indicators (Δ pCO2A) and pCO2A (in nine of fifteen), which indicate a rise in bronchospasm in the majority of patients upon decreased pCO2A during hyperventilation.

Conclusions

1. Hyperventilation, decreasing pCO2 in alveolar air, in patients with bronchial asthma in exacerbation period, lead to increase alveolar ventilation’s irregularities and the appearance of bronchospasm symptoms in the majority of them.
2. Decreased pulmonary ventilation lead to decrease irregularities of alveolar ventilation and disappearance of bronchospasm’ symptoms that resulted from hyperventilation.
3. In the majority of patients with clear cross-correlation, negative dependence was determined between the level of partial pressure of CO2 in alveoli and the resistance of bronchial tree on inspiration; as well as between partial pressure of CO2 in alveoli and irregularity of pulmonary ventilation (Δ pCO2A).

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