Effect of 30% Oxygen on Local Matching of Perfusion and Ventilation in Chronic Airways Obstruction

1977 ◽  
Vol 53 (4) ◽  
pp. 387-395 ◽  
Author(s):  
Noemi M. Eiser ◽  
Hazel A. Jones ◽  
J. M. B. Hughes
Keyword(s):  
Chronic Bronchitis ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Systematic Change ◽  
Lung Field ◽  
Arterial Pco2 ◽  
Oxygen Breathing ◽  
Airways Obstruction ◽  
Hypoxic Vasoconstriction ◽  
Change In The Mean

1. Sixteen patients with chronic bronchitis and airways obstruction were given radioactive nitrogen (13N) by intravenous injection and by inhalation, while breathing air and after 10–20 min breathing 30% oxygen. The clearance of 13N from four zones of each patient's whole lung field was monitored. 2. The 13N clearance of each region in these patients with chronic bronchitis was much slower than in normal subjects. Oxygen breathing produced a significant delay in the clearance of intravenously administered 13N in 23 zones in 10 patients but no systematic change in clearance after inhaled 13N. 3. With inhalation of 30% oxygen there was no significant change in the mean minute ventilation, tidal volume or arterial Pco2. 4. The results suggest that local hypoxic vasoconstriction is present in some patients on breathing air and that this is relieved by 30% oxygen, resulting in a diversion of local blood flow from well-ventilated to more poorly ventilated areas. The fall in V̇A/Q̇ on 30% oxygen is insufficient to increase arterial Pco2.

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.

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.

Semistarvation and exercise

1986 ◽  
Vol 60 (6) ◽  
pp. 2035-2039 ◽  
Author(s):  
C. Weissman ◽  
S. Goldstein ◽  
J. Askanazi ◽  
S. H. Rosenbaum ◽  
J. Milic-Emili ◽  
...  
Keyword(s):  
Amino Acids ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Response Characteristic ◽  
Mechanical Efficiency ◽  
Co2 Production ◽  
Arterial Pco2 ◽  
Amino Acid Infusion ◽  
Response To Exercise ◽  
Dextrose Infusion

Nutritional intake plays an important role in determining metabolic and respiratory demands during both rest and exercise. This study examines the effects in normal subjects of 4 days of semistarvation with 440 kcal/day of intravenously infused dextrose followed by the infusion of 480 kcal/day of amino acids for 48 h on the metabolic and ventilatory response to exercise (1.25, 2.50, and 5.0 kg . m/s.). After 4 days of the dextrose infusion, arterial PCO2 (P less than 0.05), and the ventilatory equivalent for CO2 (VE/VCO2, P less than 0.05) were decreased at rest compared with control measurements made prior to the dextrose infusion. During all three levels of steady-state exercise, arterial PCO2 was significantly lower (P less than 0.05) than observed before the start of the dextrose infusion. The subsequent infusion of amino acids resulted in increases in O2 consumption (V02; P less than 0.05) and minute ventilation (VE; P less than 0.05), a decrease in arterial PCO2 (P less than 0.05), and little change in CO2 production (VCO2) at rest. During low levels of exercise, compared with the values obtained following the 4 days of dextrose infusion, there were larger increases in VE and VO2, whereas VCO2 changed little. Mechanical efficiency (kcal work/kcal energy utilized) during exercise increased after 4 days of dextrose and returned to near control levels with the amino acid infusion. The adaptive response characteristic of semistarvation with dextrose appears to be altered when isocaloric amounts of amino acids are subsequently administered for short periods.

Effect of posture on the ventilatory response to CO2

1982 ◽  
Vol 53 (3) ◽  
pp. 761-765 ◽  
Author(s):  
C. Weissman ◽  
B. Abraham ◽  
J. Askanazi ◽  
J. Milic-Emili ◽  
A. I. Hyman ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Sitting Position ◽  
Breathing Patterns ◽  
Arterial Pco2 ◽  
Air Breathing ◽  
Supine Posture ◽  
The Relationship ◽  
Ventilatory Response To Co2

The effect of sitting and supine posture on breathing patterns and gas exchange during room air breathing and administration of 2 and 4% CO2 was studied in nine normal subjects using a noninvasive canopy system. During air breathing minute ventilation (VE) was 21% (P less than 0.005) higher in the sitting position. Tidal volume (VT) and mean inspiratory flow (VT/TI) were also greater in the sitting position. With the administration of 4% CO2, VE was 13.9 and 20.0 1/min in the supine and seated position, respectively. The relationship between VE and VT was the same in both cases. For any given level of VE, VT/TI was higher in the seated position. No difference in response to CO2 as measured by delta VE/delta PaCO2 and (delta VT/TI)/delta PaCO2 was observed. However, arterial PCO2 was lower both in the resting and stimulated states when sitting.

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.

Nonrandom variability in respiratory cycle parameters of humans during stage 2 sleep

1990 ◽  
Vol 69 (2) ◽  
pp. 630-639 ◽  
Author(s):  
M. Modarreszadeh ◽  
E. N. Bruce ◽  
B. Gothe
Keyword(s):  
High Frequency ◽  
Minute Ventilation ◽  
Power Spectra ◽  
Low Frequency ◽  
Neural Mechanism ◽  
Normal Subjects ◽  
Feedback Loops ◽  
Low Frequency Oscillations ◽  
Stage 2 Sleep ◽  
Correlated Components

We analyzed breath-to-breath inspiratory time (TI), expiratory time (TE), inspiratory volume (VI), and minute ventilation (Vm) from 11 normal subjects during stage 2 sleep. The analysis consisted of 1) fitting first- and second-order autoregressive models (AR1 and AR2) and 2) obtaining the power spectra of the data by fast-Fourier transform. For the AR2 model, the only coefficients that were statistically different from zero were the average alpha 1 (a1) for TI, VI, and Vm (a1 = 0.19, 0.29, and 0.15, respectively). However, the power spectra of all parameters often exhibited peaks at low frequency (less than 0.2 cycles/breath) and/or at high frequency (greater than 0.2 cycles/breath), indicative of periodic oscillations. After accounting for the corrupting effects of added oscillations on the a1 estimates, we conclude that 1) breath-to-breath fluctuations of VI, and to a lesser extent TI and Vm, exhibit a first-order autoregressive structure such that fluctuations of each breath are positively correlated with those of immediately preceding breaths and 2) the correlated components of variability in TE are mostly due to discrete high- and/or low-frequency oscillations with no underlying autoregressive structure. We propose that the autoregressive structure of VI, TI, and Vm during spontaneous breathing in stage 2 sleep may reflect either a central neural mechanism or the effects of noise in respiratory chemical feedback loops; the presence of low-frequency oscillations, seen more often in Vm, suggests possible instability in the chemical feedback loops. Mechanisms of high-frequency periodicities, seen more often in TE, are unknown.

Pulmonary gas exchange in humans exercising at sea level and simulated altitude

1986 ◽  
Vol 61 (1) ◽  
pp. 260-270 ◽  
Author(s):  
P. D. Wagner ◽  
G. E. Gale ◽  
R. E. Moon ◽  
J. R. Torre-Bueno ◽  
B. W. Stolp ◽  
...  
Keyword(s):  
Gas Exchange ◽  
Arterial Pressure ◽  
Sea Level ◽  
Pulmonary Arterial Pressure ◽  
Minute Ventilation ◽  
Statistical Significance ◽  
Random Order ◽  
Normal Subjects ◽  
Simulated Altitude ◽  
Pulmonary Arterial

In a previous study of normal subjects exercising at sea level and simulated altitude, ventilation-perfusion (VA/Q) inequality and alveolar-end-capillary O2 diffusion limitation (DIFF) were found to increase on exercise at altitude, but at sea level the changes did not reach statistical significance. This paper reports additional measurements of VA/Q inequality and DIFF (at sea level and altitude) and also of pulmonary arterial pressure. This was to examine the hypothesis that VA/Q inequality is related to increased pulmonary arterial pressure. In a hypobaric chamber, eight normal subjects were exposed to barometric pressures of 752, 523, and 429 Torr (sea level, 10,000 ft, and 15,000 ft) in random order. At each altitude, inert and respiratory gas exchange and hemodynamic variables were studied at rest and during several levels of steady-state bicycle exercise. Multiple inert gas data from the previous and current studies were combined (after demonstrating no statistical difference between them) and showed increasing VA/Q inequality with sea level exercise (P = 0.02). Breathing 100% O2 did not reverse this increase. When O2 consumption exceeded about 2.7 1/min, evidence for DIFF at sea level was present (P = 0.01). VA/Q inequality and DIFF increased with exercise at altitude as found previously and was reversed by 100% O2 breathing. Indexes of VA/Q dispersion correlated well with mean pulmonary arterial pressure and also with minute ventilation. This study confirms the development of both VA/Q mismatch and DIFF in normal subjects during heavy exercise at sea level. However, the mechanism of increased VA/Q mismatch on exercise remains unclear due to the correlation with both ventilatory and circulatory variables and will require further study.

Ventilatory and occlusion pressure responses to helium breathing

1983 ◽  
Vol 54 (6) ◽  
pp. 1525-1531 ◽  
Author(s):  
E. L. DeWeese ◽  
T. Y. Sullivan ◽  
P. L. Yu
Keyword(s):  
Breathing Circuit ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Mouth Pressure ◽  
Partial Pressure Of Co2 ◽  
Lung Resistance ◽  
Balloon Technique ◽  
Resistive Loads ◽  
End Tidal ◽  
Airway Tone

To characterize the ventilatory response to resistive unloading, we studied the effect of breathing 79.1% helium-20.9% oxygen (He-O2) on ventilation and on mouth pressure measured during the first 100 ms of an occluded inspiration (P100) in normal subjects at rest. The breathing circuit was designed so that external resistive loads during both He-O2 and air breathing were similar. Lung resistance, measured in three subjects with an esophageal balloon technique, was reduced by 23 +/- 8% when breathing He-O2. Minute ventilation, tidal volume, respiratory frequency, end-tidal partial pressure of CO2, inspiratory and expiratory durations, and mean inspiratory flow were not significantly different when air was replaced by He-O2. P100, however, was significantly less during He-O2 breathing. We conclude that internal resistive unloading by He-O2 breathing reduces the neuromuscular output required to maintain constant ventilation. Unlike studies involving inhaled bronchodilators, this technique affords a method by which unloading can be examined independent of changes in airway tone.

Pulmonary gas exchange in humans during exercise at sea level

1986 ◽  
Vol 60 (5) ◽  
pp. 1590-1598 ◽  
Author(s):  
M. D. Hammond ◽  
G. E. Gale ◽  
K. S. Kapitan ◽  
A. Ries ◽  
P. D. Wagner
Keyword(s):  
Gas Exchange ◽  
Sea Level ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Inert Gas ◽  
Diffusion Limitation ◽  
O2 Uptake ◽  
Heavy Exercise ◽  
Blood Temperature ◽  
O2 Diffusion

Previous studies have shown both worsening ventilation-perfusion (VA/Q) relationships and the development of diffusion limitation during exercise at simulated altitude and suggested that similar changes could occur even at sea level. We used the multiple-inert gas-elimination technique to further study gas exchange during exercise in healthy subjects at sea level. Mixed expired and arterial respiratory and inert gas tensions, cardiac output, heart rate, minute ventilation, respiratory rate, and blood temperature were recorded at rest and during steady-state exercise in the following order: rest, minimal exercise (75 W), heavy exercise (300 W), heavy exercise breathing 100% O2, repeat rest, moderate exercise (225 W), and light exercise (150 W). Alveolar-to-arterial O2 tension difference increased linearly with O2 uptake (VO2) (6.1 Torr X min-1 X 1(-1) VO2). This could be fully explained by measured VA/Q inequality at mean VO2 less than 2.5 l X min-1. At higher VO2, the increase in alveolar-to-arterial O2 tension difference could not be explained by VA/Q inequality alone, suggesting the development of diffusion limitation. VA/Q inequality increased significantly during exercise (mean log SD of perfusion increased from 0.28 +/- 0.13 at rest to 0.58 +/- 0.30 at VO2 = 4.0 l X min-1, P less than 0.01). This increase was not reversed by 100% O2 breathing and appeared to persist at least transiently following exercise. These results confirm and extend the earlier suggestions (8, 21) of increasing VA/Q inequality and O2 diffusion limitation during heavy exercise at sea level in normal subjects and demonstrate that these changes are independent of the order of performance of exercise.

Ventilatory response to medroxyprogesterone acetate in normal subjects: time course and mechanism

1978 ◽  
Vol 44 (6) ◽  
pp. 939-944 ◽  
Author(s):  
J. B. Skatrud ◽  
J. A. Dempsey ◽  
D. G. Kaiser
Keyword(s):  
Medroxyprogesterone Acetate ◽  
Time Course ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Maximum Effect ◽  
Adult Males ◽  
Stimulant Effect ◽  
Unbound Fraction ◽  
Arterial Pco2 ◽  
Lumbar Cerebrospinal Fluid

The time course of ventilatory adaptation to medroxyprogesterone acetate (MPA) and potential mediators of this response in plasma and lumbar CSF were determined in five healthy adult males. A significant decrease in arterial PCO2 (PACO2) at rest and exercise was noted within 48 h of drug administration with the maximum effect reached within 7 days and amounting to a 5-Torr decrement in PACO2. Blood and lumbar cerebrospinal fluid pH because significantly alkaline to control as soon as the ventilatory resporse was noted and remained alkaline during the treatment period. The ventilatory and dP/dt max response to exogenous CO2 was unchanged but their response to moderate exercise was increased after MPA. MPA-rlated materials were detected in both the plasma and CSF as soon as the ventilatory response was noted. The increase in CSF MPA-related materials approximated the unbound fraction determined in plasma. We conclude that [H+] in plasma and CSF is a function rather than a cause of ventilator acclimatization to MPA. MPA-related materials are capable of crossing the blood-brain barrier and could potentially exert their ventilatory stimulant effect by some central mechanism.

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