Airway anesthesia effects on hypercapnic breathing pattern in humans

1983 ◽  
Vol 55 (2) ◽  
pp. 368-376 ◽  
Author(s):  
T. Y. Sullivan ◽  
P. L. Yu
Keyword(s):  
Airway Resistance ◽  
Vital Capacity ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inspiratory Time ◽  
Abrupt Increase ◽  
Thoracic Gas Volume ◽  
Before And After ◽  
Gas Volume

Minute ventilation (VE) and breathing pattern during an abrupt increase in fractional CO2 were compared in 10 normal subjects before and after airway anesthesia. Subjects breathed 7% CO2-93% O2 for 5 min before and after inhaling aerosolized lidocaine. As a result of airway anesthesia, VE and tidal volume (VT) were greater during hypercapnia, but there was no effect on inspiratory time (TI). Therefore, airway anesthesia produced an increase in mean inspiratory flow (VT/TI) during hypercapnia. The increase in VT/TI was compatible with an increase in neuromuscular output. There was no effect of airway anesthesia on the inspiratory timing ratio or the shape and position of the curve relating VT and TI. We also compared airway resistance (Raw), thoracic gas volume, forced vital capacity, forced expired volume at 1s, and maximum midexpiratory flow rate before and after airway anesthesia. A small (0.18 cmH2O X l-1 X s) decrease in Raw occurred after airway anesthesia that did not correlate with the effect of airway anesthesia on VT/TI. We conclude that airway receptors accessible to airway anesthesia play a role in hypercapnic VE.

The Pattern of Breathing in Patients with Chronic Airflow Obstruction

1979 ◽  
Vol 56 (3) ◽  
pp. 215-221 ◽  
Author(s):  
C. S. Garrard ◽  
D. J. Lane
Keyword(s):  
Tidal Volume ◽  
Vital Capacity ◽  
Breathing Pattern ◽  
Important Determinant ◽  
Airflow Obstruction ◽  
Inspiratory Capacity ◽  
Maximum Increase ◽  
Thoracic Gas Volume ◽  
Volume Response ◽  
Gas Volume

1. The pattern of breathing in 12 patients with severe irreversible airflow obstruction has been studied during ventilatory stimulation by rebreathing CO2. Mean maximum tidal volume response was only 1·23 ± 0·30 litres (mean ± sd); this represented 65% of mean measured vital capacity and 82% of mean measured inspiratory capacity. During the course of rebreathing mean total breath duration was reduced from 3·48 ± 0·93 to 2·44 ± 0·48 s. 2. End-expiratory thoracic gas volume (FRC) was elevated at rest in all subjects and increased significantly by a further 0·50–1·90 litres during ventilatory stimulation in 10 of the 12 subjects. The maximum increase in FRC was proportional to the degree of airflow obstruction afforded by the airways in each subject. 3. It is suggested that the increase in FRC during ventilatory stimulation is responsible for the diminished tidal volume response and is an important determinant of breathing pattern and symptomatology in patients with airflow obstruction.

Body plethysmographic measurement of thoracic gas volume without panting against a shutter

1996 ◽  
Vol 81 (2) ◽  
pp. 1007-1011 ◽  
Author(s):  
A. Agrawal ◽  
K. P. Agrawal
Keyword(s):  
Airway Resistance ◽  
Normal Subjects ◽  
Dilution Method ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Restrictive Lung Disease ◽  
Asthmatic Patients ◽  
Specific Airway Resistance ◽  
Thoracic Gas Volume ◽  
Gas Volume

When a subject breathes through a pneumotachograph in a body box, the measured value of specific airway resistance (sRaw1) is equal to the product of thoracic gas volume (TGV) and the sum of the airway resistance (Raw) and the instrument resistance (Rins). If an additional resistance (Radd) is put in the breathing path, the measured specific, airway resistance (sRaw2) exceeds sRaw1 by the product of TGV and Radd and can be used for determining TGV. With the use of a device increasing Rins by a known amount (Radd) during normal breathing, sRaw1 and sRaw2 were measured in 3 normal subjects, 16 asthmatic patients, 2 patients with chronic obstructive pulmonary disease, and 1 patient with restrictive lung disease from the slopes of the x-y plots of airflow vs. box signals obtained before and after adding Radd. TGV was calculated by dividing (sRaw2-sRaw1) bu Radd. We also determined subjects' TGV by the panting method of A. B. DuBois, S. Y. Botelho, G. N. Bedell, and J. H. Comroe, Jr. (J. Clin. Invest. 35: 322–326, 1956) and functional residual capacity by the helium-dilution method. The results of the new method were quite reproducible (coefficient of variation = 5.6) and equivalent to those obtained by the other two methods.

Effect of a previous deep inspiration on airway resistance in man

1961 ◽  
Vol 16 (4) ◽  
pp. 717-719 ◽  
Author(s):  
Jay A. Nadel ◽  
Donald F. Tierney
Keyword(s):  
Airway Resistance ◽  
Healthy Adult ◽  
Transpulmonary Pressure ◽  
The Body ◽  
Deep Inspiration ◽  
Thoracic Gas Volume ◽  
Before And After ◽  
Residual Capacity ◽  
Gas Volume ◽  
Control State

We measured airway resistance and thoracic gas volume by the body plethysmograph technique, and transpulmonary pressure in seven healthy, adult subjects, before and after induction of bronchoconstriction. A deep inspiration never altered airway resistance, measured at functional residual capacity in the control state, but always reduced it for 1—2 min when bronchoconstriction was present. Discrepancies in data published on airway resistance may be due to use of methods which require a deep inspiration, or to occurrence of a spontaneous deep inspiration shortly before the test. Submitted on January 13, 1961

Breathing Pattern during and after Smoking Cigarettes

1982 ◽  
Vol 63 (5) ◽  
pp. 473-483 ◽  
Author(s):  
Martin J. Tobin ◽  
Anne W. Schneider ◽  
Marvin A. Sackner
Keyword(s):  
Breathing Pattern ◽  
Minute Ventilation ◽  
Systematic Difference ◽  
Breathing Patterns ◽  
Inspiratory Time ◽  
Stimulant Effect ◽  
Respiratory Inductive Plethysmography ◽  
Before And After ◽  
Respiratory Centre ◽  
Airway Conductance

1. The breathing patterns of ten habitual smokers were monitored in the semi-recumbent position with respiratory inductive plethysmography before and after smoking cigarettes. The subjects smoked a high-tar-content (HTC) and a low-tar-content (LTC) cigarette. The mean (±sd) values and frequency histograms of minute ventilation , tidal volume (VT), frequency (fR), inspiratory time (TI), fractional inspiratory time (TI/TTOT) and mean inspiratory flow (VT/TI) during baseline were compared with the values during and after smoking. 2. On a separate occasion, specific airway conductance (sGaw) and multiple-breath nitrogen washout were measured before and after smoking in six of the subjects. 3. One group of smokers (n = 4) had a greatly increased mean (±sd) baseline VT/TI (390 ± 39 ml/s) compared with normal non-smokers and another group (n = 6) a near normal VT/TI (246 ± 36 ml/s). The first group (‘deep inhalers’) had a significantly higher mean inhalation fraction (volume of inhaled smoke and air/vital capacity; 0·25 ± 0·05). The second group had a lower mean inhalation fraction of 0·14 ± 003 (‘moderate inhalers’). 4. VT/TI decreased to 323 ± 33 ml/s in the post-smoking period in the deep inhalers, whereas it increased to 345 ± 65 ml/s in the moderate inhalers during smoking. No systematic difference in VT/TI was noted between smoking high- and low-tar cigarettes, although the high-tar brand tended to have a greater effect on VT/TI. Deep inhalers showed a fall in VT during and after smoking. Moderate inhalers showed a decrease in TI/TTOT during and after smoking. 5. sGaw, measured in four moderate inhalers and two deep inhalers, fell in all subjects after smoking HTC (19 ± 8·7%; P < 0·01) and LTC (13·9 ± 10%) cigarettes. 6. ‘Sham’ smoking with an unlit cigarette produced no change in breathing pattern. 7. In moderate inhalers, the increase in respiratory output (as reflected by increased VT/TI) combined with a reduction in TI/TTOT appears to reflect the respiratory-centre stimulant effect of nicotine directly or indirectly through broncho-constriction. This contrasts with the reduced neural drive in deep inhalers, which may relate to some overriding satiating effect of the smoking.

Influence of prior ventilatory experience on the estimation of breathlessness during exercise

1990 ◽  
Vol 78 (2) ◽  
pp. 149-153 ◽  
Author(s):  
Rachel C. Wilson ◽  
P. W. Jones
Keyword(s):  
Exercise Test ◽  
Prior Experience ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Resistive Load ◽  
Inspiratory Time ◽  
Borg Scale ◽  
Exercise Tests ◽  
Loaded Breathing ◽  
Inspiratory Load

1. The intensity of breathlessness was measured during exercise in nine normal subjects using a modified Borg scale to examine the effect of prior experience of breathlessness on subsequent estimates of breathlessness. 2. Each subject performed four exercise tests, each of which consisted of two identical runs of workload incrementation (run 1 and run 2). An inspiratory resistive load of 3.8 cmH2O s−1 l−1 was applied during the appropriate run of the exercise test to examine the effect of (a) prior experience of ‘loaded’ breathing on breathlessness estimation during ‘unloaded’ breathing, and (b) prior experience of ‘unloaded’ breathing on breathlessness estimation during ‘loaded’ breathing. Run 1 was the conditioning run; run 2 was the run in which the effect of conditioning was measured. 3. There was a good correlation between breathlessness and minute ventilation during both unloaded’ breathing (median r = 0.93) and ‘loaded’ breathing (median r = 0.95). 4. The slope of the Borg score/minute ventilation relationship was greater during ‘loaded’ breathing than during ‘unloaded’ breathing (P < 0.01). There was no difference in mean Borg score between ‘unloaded’ and ‘loaded’ breathing. 5. After a period of ‘loaded’ breathing during run 1, estimated breathlessness was significantly reduced during ensuing ‘unloaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which ‘unloaded’ breathing was experienced throughout both run 1 and run 2. 6. After a period of ‘unloaded’ breathing in run 1, estimated breathlessness was significantly increased during ensuing ‘loaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which the inspiratory load had already been experienced in run 1. 7. Changes in the pattern of breathing (inspiratory time, expiratory time, total breath duration, inspiration time/total breath duration ratio and tidal volume) were not consistent with the changes in breathlessness. 8. We suggest that perception of breathlessness may be influenced by a subject's immediate prior experience of an altered relationship between breathlessness and ventilation.

Pulmonary response to threshold levels of sulfur dioxide (1.0 ppm) and ozone (0.3 ppm)

1985 ◽  
Vol 58 (6) ◽  
pp. 1783-1787 ◽  
Author(s):  
L. J. Folinsbee ◽  
J. F. Bedi ◽  
S. M. Horvath
Keyword(s):  
Sulfur Dioxide ◽  
Pulmonary Response ◽  
Rest Periods ◽  
Pollutant Concentrations ◽  
Thoracic Gas Volume ◽  
Exercise Ventilation ◽  
Before And After ◽  
Residual Capacity ◽  
Gas Volume ◽  
Male Subjects

We exposed 22 healthy adult nonsmoking male subjects for 2 h to filtered air, 1.0 ppm sulfur dioxide (SO2), 0.3 ppm ozone (O3), or the combination of 1.0 ppm SO2 + 0.3 ppm O3. We hypothesized that exposure to near-threshold concentrations of these pollutants would allow us to observe any interaction between the two pollutants that might have been masked by the more obvious response to the higher concentrations of O3 used in previous studies. Each subject alternated 30-min treadmill exercise with 10-min rest periods for the 2 h. The average exercise ventilation measured during the last 5 min of exercise was 38 1/min (BTPS). Forced expiratory maneuvers were performed before exposure and 5 min after each of the three exercise periods. Maximum voluntary ventilation, He dilution functional residual capacity, thoracic gas volume, and airway resistance were measured before and after the exposure. After O3 exposure alone, forced expiratory measurements (FVC, FEV1.0, and FEF25–75%) were significantly decreased. The combined exposure to SO2 + O3 produced similar but smaller decreases in these measures. There were small but significant differences between the O3 and the O3 + SO2 exposure for FVC, FEV1.0, FEV2.0, FEV3.0, and FEF25–75% at the end of the 2-h exposure. We conclude that, with these pollutant concentrations, there is no additive or synergistic effect of the two pollutants on pulmonary function.

Airway resistance measurement during any breathing pattern in man

1959 ◽  
Vol 14 (1) ◽  
pp. 89-96 ◽  
Author(s):  
R. G. Bartlett ◽  
H. F. Brubach ◽  
R. C. Trimble ◽  
H. Specht
Keyword(s):  
Body Temperature ◽  
Airway Resistance ◽  
Breathing Pattern ◽  
Continuous Measurement ◽  
Normal Subjects ◽  
Pulmonary Diseases ◽  
Alveolar Pressure ◽  
Improved Method ◽  
Compression And Expansion ◽  
Pressure Changes

A broadly applicable method for the quantitative and continuous measurement of airway resistance in man is described. It permits the simultaneous measurement of air flow (breath velocity) and alveolar pressure during any breathing pattern. Alveolar pressure is calculated from body plethysmograph pressure (plethysmogram) changes coincident with the compression and expansion of lung air during expiration and inspiration, respectively. The plethysmograph interior is maintained at body temperature and complete H2O saturation. This avoids the errors in measurement due to plethysmograph pressure changes produced by temperature and humidity changes in the inspired and expired breath and also obviates the necessity of using only a panting type breathing pattern. Data on three normal subjects at near resting and near maximum breathing efforts are presented and discussed. This improved method, permitting airway resistance measurements during any breathing pattern, should find application in diagnosis and assessment of treatment of pulmonary diseases as well as in the investigation of several basic pulmonary function problems. Submitted on June 17, 1958

Quiet-breathing vs. panting methods for determination of specific airway conductance

1984 ◽  
Vol 57 (6) ◽  
pp. 1917-1922 ◽  
Author(s):  
W. S. Krell ◽  
K. P. Agrawal ◽  
R. E. Hyatt
Keyword(s):  
Interobserver Variability ◽  
Direct Method ◽  
Normal Subjects ◽  
Intrasubject Variability ◽  
Quiet Breathing ◽  
Thoracic Gas Volume ◽  
Coefficients Of Variation ◽  
Gas Volume ◽  
Airway Conductance

Specific airway conductance (sGaw) was measured during quiet breathing and during panting in 21 normal subjects and 10 patients with obstructive lung disease. The direct method used does not require measuring thoracic gas volume (TGV). Coefficients of variation were 5.5% for panting and 5.1% for quiet breathing. Interobserver variability was 4.7% in the quiet-breathing method and 6.3% in the panting method. The two methods gave equivalent results for sGaw. A slightly greater sGaw was found by the panting method in normal subjects with the highest sGaw values, probably due to widening of the oropharynx-glottis during panting. In six normal subjects studied for intrasubject variability over time, no significant diurnal or day-to-day variability was seen by either method. We conclude that the quiet-breathing method is a simple valid means of determining sGaw and utilizes a physiological respiratory maneuver. Obviation of the need to measure TGV is advantageous. Results are equivalent to those of the panting method and variability is similar.

Frequency dependence of plethysmographic measurement of thoracic gas volume

1984 ◽  
Vol 57 (6) ◽  
pp. 1865-1871 ◽  
Author(s):  
R. Brown ◽  
A. S. Slutsky
Keyword(s):  
Frequency Dependence ◽  
Normal Subjects ◽  
Lung Capacity ◽  
Airways Obstruction ◽  
Gas Compression ◽  
Thoracic Gas Volume ◽  
Mouth Pressure ◽  
Extrathoracic Airway ◽  
Shunt Capacitor ◽  
Gas Volume

With airways obstruction, panting frequency affects plethysmographically determined thoracic gas volume (Vtg) because the extrathoracic airway acts as a shunt capacitor. Stanescu et al. (19) suggested that in the calculation of Vtg, use of esophageal (delta Pes) rather than mouth pressure (delta Pm) swings might eliminate the problem. We measured total lung capacity (TLC) plethysmographically in 10 subjects with chronic airways obstruction (CAO) and in four normal subjects. TLC (using delta Pm) was derived from Vtg obtained from slow-(approximately 1 Hz) and fast- (approximately 4 Hz) panting frequencies. In the normal subjects and four subjects with CAO, TLC was also obtained using delta Pes. In these subjects abdominal gas compression and decompression did not contribute significantly to the frequency dependence of TLC. In CAO, TLC was frequency dependent in direct proportion to the severity of obstruction. Although the frequency dependence was greater using delta Pm to calculate Vtg, it also occurred using delta Pes. Thus it could not be explained entirely by the shunt capacitor effect of the extrathoracic airways. The residual and significant overestimations of TLC (reflected by frequency dependency of TLC derived from Vtg calculated from delta Pes) may be explained by interregional nonhomogeneities during the panting maneuver.

Role of Vagal Airway Reflexes in Control of Ventilation in Pulmonary Fibrosis

1981 ◽  
Vol 61 (6) ◽  
pp. 781-784 ◽  
Author(s):  
J. Savoy ◽  
S. Dhingra ◽  
N. R. Anthonisen
Keyword(s):  
Pulmonary Fibrosis ◽  
Breathing Pattern ◽  
Minute Ventilation ◽  
Arterial Oxygen ◽  
Control Subjects ◽  
Cough Response ◽  
Before And After ◽  
The Mean ◽  
Breath Cycle

1. in 10 patients with pulmonary fibrosis and in seven control subjects, we measured the pressure at the mouth 0.1 s after onset of an inspiration against occluded airway (P0.1), minute ventilation (VI), breathing frequency (fr), tidal volume (VT), inspiratory duration (Tl) and calculated the mean inspiratory flow (VT/Tl) and the fraction of the breath cycle devoted to inspiration (Tl/Ttot.). in the patients measurements were made at normal arterial oxygen saturations (Sao2), before and after lignocaine airway anaesthesia. 2. Efficacy of airway anaesthesia was tested by the cough response to citric acid inhalation. 3. in pulmonary fibrosis P0.1, f1 and VT/Tl were greater than in the control subjects, VT and Tl, were smaller and Tl/Ttot. and VI were not different. 4. Effective airway anaesthesia did not modify P0.1 and breathing pattern parameters observed in pulmonary fibrosis. 5. These results suggest that airway receptors do not contribute to a major extent to the control of breathing in pulmonary fibrosis.

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