Calculation of the VD/VT ratio by the helium washout technique

1986 ◽  
Vol 70 (6) ◽  
pp. 565-569 ◽  
Author(s):  
J. Jordanoglou ◽  
G. Tatsis ◽  
Z. Bissiouli
Keyword(s):  
Pulmonary Fibrosis ◽  
Chronic Bronchitis ◽  
Bronchial Asthma ◽  
Conventional Method ◽  
Normal Subjects

1. In four normal subjects and 51 patients with chronic bronchitis-emphysema, bronchial asthma and pulmonary fibrosis, the VD/VT ratio was measured by a helium washout technique (w VD/VT) and by the conventional Bohr's method using the arterial CO2 tension (VD/VT). 2. In 16 patients the w VD/VT ratio was compared with that calculated from Bohr's equation with the alveolar CO2 tension measured by the rebreathing technique (A VD/VT). 3. It was found that the values for the VD/VT ratio obtained by the helium washout technique were very close to those obtained by the conventional method using the Paco2 or P¯Aco2 values.

Site of airway obstruction in pulmonary disease: direct measurement of intrabronchial pressure

1992 ◽  
Vol 72 (3) ◽  
pp. 1016-1023 ◽  
Author(s):  
M. Yanai ◽  
K. Sekizawa ◽  
T. Ohrui ◽  
H. Sasaki ◽  
T. Takishima
Keyword(s):  
Chronic Bronchitis ◽  
Bronchial Asthma ◽  
Airway Resistance ◽  
Lateral Pressure ◽  
Airflow Obstruction ◽  
Lower Lobe ◽  
Transpulmonary Pressure ◽  
Normal Subjects ◽  
Peripheral Airway ◽  
The Right

To partition the central and peripheral airway resistance in awake humans, a catheter-tipped micromanometer sensing lateral pressure of the airway was wedged into the right lower lobe of a 3-mm-ID bronchus in 5 normal subjects, 7 patients with chronic bronchitis, 8 patients with emphysema, and 20 patients with bronchial asthma. We simultaneously measured mouth flow, transpulmonary pressure, and intra-airway lateral pressure during quiet tidal breathing. Total pulmonary resistance (RL) was calculated from transpulmonary pressure and mouth flow and central airway resistance (Rc) from intra-airway lateral pressure and mouth flow. Peripheral airway resistance (Rp) was obtained by the subtraction of Rc from RL. The technique permitted identification of the site of airway resistance changes. In normal subjects, RL was 3.2 +/- 0.2 (SE) cmH2O.l-1.s and the ratio of Rp to RL was 0.24 during inspiration. Patients with bronchial asthma without airflow obstruction showed values of Rc and Rp similar to those of normal subjects. Although Rc showed a tendency to increase, only Rp significantly increased in those patients with bronchial asthma with airflow obstruction and patients with chronic bronchitis and emphysema. The ratio of Rp to RL significantly increased in three groups of patients with airflow obstruction (P less than 0.01). These observations suggest that peripheral airways are the predominant site of airflow obstruction, irrespective of the different pathogenesis of chronic airflow obstruction.

Reversibility of Airways Obstruction in Chronic Bronchitis

1972 ◽  
Vol 42 (6) ◽  
pp. 725-733 ◽  
Author(s):  
T. W. Astin
Keyword(s):  
Muscle Contraction ◽  
Chronic Bronchitis ◽  
Lung Volume ◽  
Normal Subjects ◽  
Atropine Sulphate ◽  
Airways Obstruction ◽  
Chest Disease ◽  
Before And After ◽  
Airways Resistance ◽  
Intravenous Atropine

1. Airways resistance and lung volume were measured in twenty-five patients with chronic bronchitis and fifteen patients without chest disease before and after the inhalation of isoprenaline. Similar measurements were made on fourteen of these patients with chronic bronchitis and twelve other patients without chest disease before and after the intravenous injection of atropine sulphate. 2. There were significant decreases in airways resistance after isoprenaline inhalation and intravenous atropine both in patients with bronchitis and normal subjects but the decreases were greater in the patients with chronic bronchitis. 3. The decrease in resistance was proportional to the degree of initial airways resistance. 4. The results are considered to indicate that bronchial muscle contraction increases the airways resistance of patients with chronic bronchitis and contributes to the airways obstruction; its contribution increases with increasing severity of the condition. A significant part of the increased airways resistance in these patients is potentially reversible and nervously mediated.

Byssinosis: Differential Diagnosis from Bronchial Asthma and Chronic Bronchitis

2009 ◽  
Vol 173 (6) ◽  
pp. 761-768 ◽  
Author(s):  
H. Arnoldsson ◽  
A. Bouhuys ◽  
S.-E. Lindell
Keyword(s):  
Differential Diagnosis ◽  
Chronic Bronchitis ◽  
Bronchial Asthma

scholarly journals Effect of inhaled procaterol on cough receptor sensitivity to capsaicin in patients with asthma or chronic bronchitis and in normal subjects.

Thorax ◽  
1993 ◽  
Vol 48 (6) ◽  
pp. 615-618 ◽  
Author(s):  
M Fujimura ◽  
S Sakamoto ◽  
Y Kamio ◽  
T Bando ◽  
K Kurashima ◽  
...  
Keyword(s):  
Chronic Bronchitis ◽  
Normal Subjects ◽  
Receptor Sensitivity ◽  
Cough Receptor

Mechanism of transient nocturnal hypoxemia in hypoxic chronic bronchitis and emphysema

1985 ◽  
Vol 59 (6) ◽  
pp. 1698-1703 ◽  
Author(s):  
J. R. Catterall ◽  
P. M. Calverley ◽  
W. MacNee ◽  
P. M. Warren ◽  
C. M. Shapiro ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Chronic Bronchitis ◽  
Rem Sleep ◽  
Normal Subjects ◽  
Arterial Pco2 ◽  
Content Difference ◽  
Nocturnal Hypoxemia ◽  
Voluntary Hypoventilation ◽  
Arterial Po2 ◽  
Mixed Venous

In five patients with hypoxic chronic bronchitis and emphysema we measured ear O2 saturation (SaO2), chest movement, oronasal airflow, arterial and mixed venous gas tensions, and cardiac output during nine hypoxemic episodes (HE; SaO2 falls greater than 10%) in rapid-eye-movement (REM) sleep and during preceding periods of stable oxygenation in non-REM sleep. All nine HE occurred with recurrent short episodes of reduced chest movement, none with sleep apnea. The arterial PO2 (PaO2) fell by 6.0 +/- 1.9 (SD) Torr during the HE (P less than 0.01), but mean arterial PCO2 (PaCO2) rose by only 1.4 +/- 2.4 Torr (P greater than 0.4). The arteriovenous O2 content difference fell by 0.64 +/- 0.43 ml/100 ml of blood during the HE (P less than 0.05), but there was no significant change in cardiac output. Changes observed in PaO2 and PaCO2 during HE were similar to those in four normal subjects during 90 s of voluntary hypoventilation, when PaO2 fell by 12.3 +/- 5.6 Torr (P less than 0.05), but mean PaCO2 rose by only 2.8 +/- 2.1 Torr (P greater than 0.4). We suggest that the transient hypoxemia which occurs during REM sleep in patients with chronic bronchitis and emphysema could be explained by hypoventilation during REM sleep but that the importance of changes in distribution of ventilation-perfusion ratios cannot be assessed by presently available techniques.

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