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.

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.

The Ventilatory Response to CO2 is Not Linear within The Normal Range of Alveolar PCO2

1985 ◽  
Vol 68 (s11) ◽  
pp. 36P-36P
Author(s):  
M.S. Jacoei ◽  
A.R.C. Cummin ◽  
V.I. Iyawe ◽  
C.P. Patil ◽  
K.B. Saunders
Keyword(s):  
Ventilatory Response ◽  
Normal Range ◽  
Ventilatory Response To Co2

Assessment of Responsiveness to Carbon Dioxide in Patients with Chronic Airways Obstruction by Rate of Isometric Inspiratory Pressure Development

1976 ◽  
Vol 50 (3) ◽  
pp. 199-205 ◽  
Author(s):  
A. W. Matthews ◽  
J. B. L. Howell
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Pressure Change ◽  
Significant Negative Correlation ◽  
Inspiratory Pressure ◽  
Normal Range ◽  
Ventilatory Responses ◽  
Airways Obstruction ◽  
Pressure Development ◽  
Mechanical Factors

1. Responsiveness to CO2 was measured in forty patients with chronic airways obstruction in terms of ventilation and rate of isometric inspiratory pressure change [(dP/dt)max.]. 2. The ventilatory response was below the normal range in eighteen out of twenty-two patients with normal arterial CO2 tensions and in all of eighteen patients with CO2 retention. 3. The (dP/dt)max. response was distributed throughout the normal range in all but one of the patients with normal arterial CO2 tension. In all the patients with CO2 retention the (dP/dt)max. response was either at or below the lower limit of the normal range. 4. Although the ventilatory responses correlated significantly with FEV1 there was no such correlation for the (dP/dt)max. responses. 5. The (dP/dt)max. response showed a significant negative correlation with Pa,co2. 6. It is believed that the (dP/dt)max. response to CO2 can be used to assess central CO2 responsiveness in subjects with airways obstruction independently of mechanical factors limiting their ventilation.

Ventilatory Response to Carbon Dioxide in Tetanus

1976 ◽  
Vol 50 (1) ◽  
pp. 83-86
Author(s):  
O. O. Elegbeleye ◽  
D. Femi-Pearse
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Disease State ◽  
Normal Response ◽  
Clinical Recovery

1. Ventilatory response to carbon dioxide was measured by the rebreathing technique in seven patients with mild tetanus during the disease state and after clinical recovery. 2. The ventilatory response to carbon dioxide was found to be decreased in the tetanus patients during the disease state with normal response after full clinical recovery. It is postulated that the restrictive ventilatory defect was responsible for the decreased ventilatory response to carbon dioxide.

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.

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.

Control of breathing in uremia: ventilatory response to CO2 after hemodialysis

1976 ◽  
Vol 41 (2) ◽  
pp. 216-222 ◽  
Author(s):  
R. W. Hamilton ◽  
P. E. Epstein ◽  
L. W. Henderson ◽  
N. H. Edelman ◽  
A. P. Fishman
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Respiratory Alkalosis ◽  
Similar Increase ◽  
Acid Base ◽  
Plasma Urea ◽  
Acid Base Status ◽  
Uremic Patients ◽  
Plasma Urea Concentration ◽  
Ventilatory Response To Co2

The mechanisms responsible for the transient respiratory alkalosis which follows clinical hemodialysis were evaluated by studying the ventilatory response to carbon dioxide in chronic uremic patients, and in unanesthetized normal and chronic uremic goats. A significant increase in sensitivity to CO2 was found in acidotic uremic patients immediately (within 30 min) following hemodialysis (P less than 0.01). Sensitivity to CO2 returned to the predialysis value within 24 h. Lung volume and maximal breathing capacity were unchanged. A similar increase in sensitivity to CO2 was seen in nonacidotic uremic goats following hemodialysis. In the goats, these changes in sensitivity could not be explained by changes in cerebrospinal fluid acid-base status. Adding sufficient urea to the dialysate to prevent a fall in plasma urea concentration, eliminated this increase in sensitivity to CO2 in both uremic patients and goats. These results suggests that the transient respiratory alkalosis following hemodialysis is due to an increase in the sensitivity of the ventilatory response to carbon dioxide and is a consequence of dialysis-induced osmotic disequilibrium.

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.

scholarly journals Relation Between Personality and Ventilatory Response to Carbon Dioxide in Normal Subjects: A Role in Asthma?

BMJ ◽  
1972 ◽  
Vol 1 (5802) ◽  
pp. 719-721 ◽  
Author(s):  
N. A. Saunders ◽  
S. Heilpern ◽  
A. S. Rebuck
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Normal Subjects
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