The Ventilatory Response to CO2 of Patients with Diffuse Pulmonary Infiltrations or Fibrosis

1972 ◽  
Vol 43 (1) ◽  
pp. 55-69 ◽  
Author(s):  
J. M. S. Patton ◽  
S. Freedman
Keyword(s):  
Ventilatory Response ◽  
Normal Subjects ◽  
Work Rate ◽  
Mechanical Work ◽  
Respiratory Response ◽  
Co2 Sensitivity ◽  
Venous Pco2 ◽  
Pulmonary Infiltration ◽  
Rebreathing Method ◽  
Ventilatory Response To Co2

1. We have used the rebreathing method to examine the respiratory response to CO2 in five normal subjects and twelve patients with diffuse pulmonary infiltration or fibrosis. The response to CO2 was measured in terms of both ventilation and mechanical work rate. 2. The response to CO2 was, on average, reduced in the patients compared with the normals but the patients had to perform more mechanical work to achieve a given level of ventilation. 3. Six patients had an abnormally low resting mixed venous Pco2 and four of these also had an abnormally low response to CO2. 4. The pattern of breathing was identical in patients and normals. 5. The results indicate that the reduced ventilatory response represents a true loss of CO2 sensitivity and is not simply due to mechanical limitation; but the paradox in some patients of resting hyperventilation and a low level of CO2 responsiveness is unexplained.

Ventilatory Response to Exercise and to Co2 Rebreathing in Normal Subjects

1972 ◽  
Vol 43 (6) ◽  
pp. 861-867 ◽  
Author(s):  
A. S. Rebuck ◽  
N. L. Jones ◽  
E. J. M. Campbell
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
O2 Uptake ◽  
Co2 Output ◽  
Exercise Ventilation ◽  
Progressive Exercise ◽  
Response To Exercise ◽  
Rebreathing Method ◽  
Ventilatory Response To Co2

1. Changes in ventilation during progressive exercise were measured in eleven normal subjects. Ventilatory response to carbon dioxide at rest was measured in the same subjects using a rebreathing method. 2. The range of ventilatory response to exercise was 16·6–32·0 litres min−1 (litres CO2 min−1)−1 (mean 22·7; SD 5·35); response to O2 uptake was 17·0–43·9 litres min−1 (litres O2 min−1)−1 (mean 29·02; SD 9·07). Ventilatory response to CO2 (Sco2) ranged from 0·81 to 3·22 litre min−1 mmHg−1 (mean 1·87; SD 0·62). 3. There was a highly significant (P < 0·001) correlation between the changes in response to increasing CO2 output or O2 uptake, and Sco2. 4. The results are compatible with the suggestion that ventilation during exercise in normal subjects is directly related to their chemosensitivity to CO2, those having the highest sensitivity showing the greatest exercise ventilation.

The effect of Airway Anaesthesia on the Control of Breathing and the Sensation of Breathlessness in Man

1985 ◽  
Vol 68 (2) ◽  
pp. 215-225 ◽  
Author(s):  
A. J. Winning ◽  
R. D. Hamilton ◽  
S. A. Shea ◽  
C. Knott ◽  
A. Guz
Keyword(s):  
Tidal Volume ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Cough Reflex ◽  
Before And After ◽  
Median Diameter ◽  
Receptor Block ◽  
Normal Man ◽  
End Tidal ◽  
Ventilatory Response To Co2

1. The effect on ventilation of airway anaesthesia, produced by the inhalation of a 5% bupivacaine aerosol (aerodynamic mass median diameter = 4.77 μm), was studied in 12 normal subjects. 2. The dose and distribution of the aerosol were determined from lung scans after the addition to bupivacaine of 99mTc. Bupivacaine labelled in this way was deposited primarily in the central airways. The effectiveness and duration of airway anaesthesia were assessed by the absence of the cough reflex to the inhalation of three breaths of a 5% citric acid aerosol. Airway anaesthesia always lasted more than 20 min. 3. Resting ventilation was measured, by respiratory inductance plethysmography, before and after inhalation of saline and bupivacaine aerosols. The ventilatory response to maximal incremental exercise and, separately, to CO2 inhalation was studied after the inhalation of saline and bupivacaine aerosols. Breathlessness was quantified by using a visual analogue scale (VAS) during a study and by questioning on its completion. 4. At rest, airway anaesthesia had no effect on mean tidal volume (VT), inspiratory time (Ti), expiratory time (Te) or end-tidal Pco2, although the variability of tidal volume was increased. On exercise, slower deeper breathing was produced and breathlessness was reduced. The ventilatory response to CO2 was increased. 5. The results suggest that stretch receptors in the airways modulate the pattern of breathing in normal man when ventilation is stimulated by exercise; their activation may also be involved in the genesis of the associated breathlessness. 6. A hypothesis in terms of a differential airway/alveolar receptor block, is proposed to explain the exaggerated ventilatory response to CO2.

Augmentation of ventilatory response to asphyxia by prochlorperazine in humans

1982 ◽  
Vol 53 (3) ◽  
pp. 637-643 ◽  
Author(s):  
L. G. Olson ◽  
M. J. Hensley ◽  
N. A. Saunders
Keyword(s):  
Ventilatory Response ◽  
Blocking Agent ◽  
Control Value ◽  
Before And After ◽  
Venous Pco2 ◽  
Hypercapnic Hypoxia ◽  
Dopamine Hydrochloride ◽  
Response Line ◽  
Arterial O2 Saturation ◽  
Ventilatory Response To Co2

The effect of the dopamine-receptor blocking agent prochlorperazine on the ventilatory response to hypercapnic hypoxia was studied in six healthy adults. Repeated episodes of transient hypoxia were induced at the mixed venous PCO2 level by a nonrebreathing technique in five males and one female before and after an intravenous bolus injection of prochlorperazine mesylate (12.5 mg = 10 mg base). The ventilatory response to CO2 was also studied before and after drug administration. Prochlorperazine produced a modest (15%) increase in resting ventilation (P less than 0.05) but a marked increase in the ventilatory response to asphyxia such that the group mean response was double the control value [2.0 +/- 0.7 vs. 4.2 +/- 1.5 l . min-1 . % arterial O2 saturation (%SaO2); P less than 0.001]. Two-thirds of this change in ventilatory response was due to an increase in frequency response to hypoxia (0.34 +/- 0.20 vs. 0.81 +/- 0.52 breaths . min-1 . %SaO2; P less than 0.001). The position of the ventilatory response line, as judged by the computed ventilation at 95% SaO2, was increased by prochlorperazine (22.2 +/- 9.6 vs. 35.9 +/- 10.9 l . min-1; P less than 0.01) due to an increase in both tidal volume (P less than 0.05) and frequency of breathing (P less than 0.0125). The ventilatory response to CO2 was unchanged by drug injection. In separate experiments prochlorperazine was shown to 1) increase the ventilatory response to steady-state eucapnic hypoxia (P less than 0.01) demonstrating that the drug effect was not dependent on either the presence of hypercapnia or rapidly changing states of arterial oxygenation; and 2) reverse the depressant effect of intravenously infused dopamine hydrochloride (5 micrograms . kg-1 . min-1) on the ventilatory response to transient asphyxia (P less than 0.01). We conclude that prochlorperazine augments hypoxic responsiveness in humans. The mechanism may be blockade of dopaminergic receptors that modulate carotid body discharge.

Luft's syndrome: O2 cost of exercise and chemical control of breathing

1975 ◽  
Vol 39 (5) ◽  
pp. 857-859 ◽  
Author(s):  
N. H. Edelman ◽  
T. V. Santiago ◽  
H. L. Conn
Keyword(s):  
Chemical Control ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Control Of Breathing ◽  
O2 Consumption ◽  
Arterial Blood ◽  
Skeletal Muscle Mitochondria ◽  
Ventilatory Response To Co2

The oxygen cost of exercise and chemical control of breathing were studied in a subject with Luft's syndrome, a disorder in which skeletal muscle mitochondria have a high “resting” O2 consumption which is imcreased only slightly by stimulation with excess phosphate acceptor, but a normal P/O ratio. The O2 consumption was more than three times normal (1.05 1/min) at rest but could be doubled when stimulated by maximal exercise. The O2 cost of exercise was similar to that of normal subjects. At rest, arterial blood PCO2 and ventilatory response to CO2 were normal, while ventilatory response to hypoxia was four times the predicted value. The data 1) confirm, in vivo, the normal respiratory efficiency of skeletal muscles in this disorder; 2) suggest that in vitro estimates of the extent to which mitochondrial respiration can be stimulated may not correlate with in vivo determinations; and 3) suggests that hypermetabolism per se can cause the ventilatory adjustments which are associated with exercise in normal subjects.

Human respiratory control at high ambient pressures and inspired gas densities

1980 ◽  
Vol 48 (3) ◽  
pp. 528-539 ◽  
Author(s):  
R. Gelfand ◽  
C. J. Lambertsen ◽  
R. E. Peterson
Keyword(s):  
Pressure Range ◽  
Ventilatory Response ◽  
Respiratory Control ◽  
Co2 Concentration ◽  
Density Range ◽  
Respiratory Response ◽  
Gas Density ◽  
Ventilatory Responses ◽  
Nitrogen Narcosis ◽  
Ventilatory Response To Co2

Four men, exposed to the pressure equivalent of 1,200 ft of seawater (37 ATA) for 6 days in a CO2-free, normoxic helium-oxygen environment (Predictive Studies III-1971, Aviation Space Environ. Med. 4: 843-855, 1977), had no evident respiratory distress at work, at rest, or asleep. Ventilatory responses of two men to CO2 were measured in 20-min acute exposures to mixtures of oxygen (173 Torr) with nitrogen, crude neon, and helium over a gas density range of 0.4-22 g/l and a pressure range of 1-37 ATA during stepwise compression of 37 ATA. Analysis of delta V/delta PACO2 as functions of pressure, of density, and of density-to-viscosity ratios shows that increased gas density, but not nitrogen narcosis, is associated with gross diminution of the ventilatory response to CO2. A small ventilatory response to CO2 is predicted for liquid breathing when viscosity is included as a parameter in the analysis. Other findings associated with increased gas densities and progressive elevation of inspired CO2 concentration are disruption of the normal patterns of tidal volume and frequency of breathing and reduction in the range of linear respiratory response to CO2.

The Ventilatory Response to CO2 after Administration of Frusemide in Normal Man

1972 ◽  
Vol 43 (1) ◽  
pp. 47-54 ◽  
Author(s):  
H. W. Iff ◽  
D. C. Flenley
Keyword(s):  
Ventilatory Response ◽  
Normal Subjects ◽  
Oxygen Balance ◽  
Co2 Response ◽  
Small Shift ◽  
Normal Man ◽  
Slight Rise ◽  
End Tidal ◽  
The Right ◽  
Ventilatory Response To Co2

1. We have determined the ventilatory response to CO2 inhaled in 30% oxygen (balance nitrogen) in eight normal subjects (1) before and during 4 days of 80 mg of oral frusemide daily and (2) within 55–75 min of 80 mg of frusemide orally. 2. Over 4 days the drug decreased serum potassium concentrations, but increased end tidal (and arterial) Pco2 and serum bicarbonate, thus inducing a mild metabolic alkalosis with an appropriate but small shift in CO2 response to the right without a significant change in the slope of the response. The CO2 response was unaltered by oral frusemide 55–75 min earlier. 3. This slight rise in Pco2 during 4 days of frusemide therapy contrasts with the absence of rise in Pco2 after treatment with thiazide diuretics, as reported by others. 4. We discuss possible implications of these results for the selection of an appropriate diuretic in patients with CO2 retention at various phases of their illness.

Ventilatory response of the sleeping newborn to CO2 during normoxic rebreathing

1991 ◽  
Vol 71 (1) ◽  
pp. 168-174 ◽  
Author(s):  
G. Cohen ◽  
C. Xu ◽  
D. Henderson-Smart
Keyword(s):  
Rem Sleep ◽  
Ventilatory Response ◽  
Relative Magnitude ◽  
Quiet Sleep ◽  
Volume Response ◽  
The Mean ◽  
Arterial O2 Saturation ◽  
Arterial Po2 ◽  
Rebreathing Method ◽  
Ventilatory Response To Co2

The ventilatory response of the newborn to CO2 was studied using a rebreathing method that minimized changes in arterial PO2 during the test. The aim was to study the variability of the ventilatory response to CO2 and take this into account to assess the relative magnitude of the response to CO2 during rapid-eye-movement (REM) sleep and quiet sleep (QS). Five full-term babies aged 4–6 days were given 5% CO2 in air to rebreathe for 1.5–3 min. O2 was added to the rebreathing circuit to maintain arterial O2 saturation and transcutaneous PO2 (Ptco2) at prerebreathing levels. Tests were repeated four to five times in REM sleep and QS. Mean Ptco2 levels varied between individuals but were similar during REM sleep and QS tests for each subject. The mean coefficient of variability of the ventilatory response was 35% (range 15–77%) during QS and 120% (range 32–220%) during REM sleep. PtcO2 fluctuations during tests [6.0 +/- 3.0 (SD) Torr, range 1–13 Torr] were not correlated with ventilatory response. Overall the ventilatory response was significantly lower in REM sleep than in QS (12.2 +/- 3.0 vs. 38.7 +/- 3.0 ml.min-1.Torr-1.kg-1, P less than 0.001; 2-way analysis of variance) due to a small (nonsignificant) fall in the tidal volume response and a significant fall in breathing rate. In 12 REM sleep tests there was no significant ventilatory response; mean inspiratory flow increased significantly during 8 of these 12 tests. We conclude that there is a significant decrease in the ventilatory response of the newborn to CO2 rebreathing during REM sleep compared with QS.

scholarly journals Ventilatory response to CO2 with Read's rebreathing method in normal infants

2020 ◽  
Author(s):  
Yosuke Yamada ◽  
Henmi Nobuhide ◽  
Hisaya Hasegawa ◽  
Shio Tsuruta ◽  
Yusuke Suganami ◽  
...  
Keyword(s):  
Body Weight ◽  
Steady State ◽  
Ventilatory Response ◽  
Minute Volume ◽  
Respiratory Center ◽  
Steady State Method ◽  
Examination Time ◽  
Rebreathing Method ◽  
Ventilatory Response To Co2 ◽  
Birth Body Weight

Background Methods of evaluating the ventilatory response to CO2 (VRCO2) of the respiratory center include the steady-state and the rebreathing method. Although the rebreathing method can evaluate the respiratory center more in detail, the steady-state method has been mainly performed in infants. The aim of this study was to investigate whether we could perform the VRCO2 with the rebreathing method in normal infants. Methods The subjects were 80 normal infants. The gestational age was 39.9（39.3-40.3）weeks, and the birth body weight was 3,142 (2,851-3,451) grams. We performed the VRCO2 with Read’s rebreathing method, measuring the increase in minute volume (MV) in response to the increase in EtCO2 by rebreathing a closed circuit. The value of VRCO2 was calculated as follow: VRCO2 (mL/min/mmHg/kg) = ΔMV / ΔEtCO2 / Body weight. Results We performed the examination without adverse events. The age in days at examination was 3 (2-4), and the examination time was 150±38 seconds. The maximum EtCO2 was 51.1 (50.5-51.9) mmHg. The value of VRCO2 was 34.6 (29.3-42.8). Tidal volume had a greater effect on the increase in MV than respiratory rate (5.4 to 14.3 mL/kg, 44.1 to 55.9 /min, respectively). Conclusion This study suggests that the rebreathing method can evaluate the ventilatory response to high blood CO2 in a short examination time. We conclude that the rebreathing method is useful even in infants. In the future, we plan to measure the VRCO2 of preterm infants, and evaluate the respiratory center of infants in more detail.

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.

Patterns of Ventilatory Response to Carbon Dioxide during Recovery from Severe Asthma

1971 ◽  
Vol 41 (1) ◽  
pp. 13-21 ◽  
Author(s):  
A. S. Rebuck ◽  
John Read
Keyword(s):  
Carbon Dioxide ◽  
Lower Limit ◽  
Severe Asthma ◽  
Ventilatory Response ◽  
Normal Subjects ◽  
Normal Range ◽  
Clinical Recovery ◽  
Time Of Presentation ◽  
Ventilatory Response To Co2

1. Ventilatory response to CO2 was measured regularly by a rebreathing technique in nineteen patients with severe asthma from the day of presentation to the time of clinical recovery. 2. Ventilatory response to CO2 increased during recovery in sixteen patients and the increased ventilatory response correlated well with increase of FEV1. Among these sixteen patients only one showed elevation of arterial CO2 tension at the time of presentation. 3. Ventilatory response to CO2 failed to increase during recovery in three patients despite increases in FEV1. All three patients showed elevation of arterial CO2 tension at the time of presentation. 4. In five patients (including three of the four with initial hypercapnia) ventilatory response to CO2 after recovery remained below the previously reported lower limit for normal subjects. The limits of normality were explored by examining ventilatory response to CO2 in seventeen outstanding athletic performers. Values for ventilatory response to CO2 both above and below the previously defined ‘normal range’ were found. The normal ventilatory response to CO2 covers a 14-fold range from 0.57 to 8.17 1 min−1 mmHg−1Pco2.

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