scholarly journals Ventilatory response to CO2 rebreathing at rest in the ama.

1981 ◽  
Vol 31 (3) ◽  
pp. 423-426 ◽  
Author(s):  
Miharu MIYAMURA ◽  
Taizo TSUNODA ◽  
Noriaki FUJITSUKA ◽  
Yoshiyuki HONDA
1993 ◽  
Vol 74 (3) ◽  
pp. 1419-1424 ◽  
Author(s):  
M. J. Mador

Partial vagal blockade produced by inhalation of a local anesthetic aerosol has enhanced CO2 responsiveness in some studies but not in others. The effect of inhaled local anesthetic may depend on the amount of drug depositing in the central airways, i.e., the degree of airway anesthesia. We examined the ventilatory response to CO2 rebreathing in 11 healthy subjects before and after inhalation of 4% lidocaine and a normal saline control solution. Lidocaine and control solutions were aerosolized via two different nebulizers: one produced particles with a mass median aerodynamic diameter of 5.28 microns, and the other produced particles with a mass median aerodynamic diameter of 1.76 microns. The ventilatory response to CO2 was not affected by the control solution. In contrast, the ventilatory response to CO2 was significantly increased after aerosolized lidocaine when administered via the moderate-particle-size nebulizer (2.13 +/- 0.66 vs. 1.83 +/- 0.54 l.min-1.Torr-1 during control, P = 0.01) but not via the small-particle-size nebulizer (1.96 +/- 0.82 vs. 1.94 +/- 0.84 l.min-1.Torr-1 during control, P = NS). The increase in ventilation was achieved predominantly by an increase in frequency (P = 0.01) while tidal volume was unchanged. In conclusion, airway receptors accessible to inhaled local anesthetic play a role in the control of breathing during CO2 rebreathing. Previous negative studies may be due to differences in nebulizer technique, affecting the amount of drug depositing within the central airways.


1986 ◽  
Vol 6 (1) ◽  
pp. 188
Author(s):  
T. Labaille ◽  
F. Clergue ◽  
K. Samii ◽  
C. Ecoffey ◽  
A. Berdaux

PEDIATRICS ◽  
1986 ◽  
Vol 77 (3) ◽  
pp. 390-395
Author(s):  
Ch. Maayan ◽  
C. Springer ◽  
Y. Armon ◽  
E. Bar-Yishay ◽  
V. Shapira ◽  
...  

Two siblings, a 14.5-year-old boy and his 11.5-year-old sister, with congenital nemaline myopathy presented with severe respiratory failure and, in the case of the older patient, with cor pulmonale and systemic hypertension. The children were treated initially by continuous mechanical ventilation, but after a few weeks they only required ventilation at night. At the start of treatment, both were found to have a decreased ventilatory response to CO2 which apparently improved during 4 to 5 years of follow-up treatment. It has not been possible to wean them from nocturnal mechanical ventilation, but during the daytime they attend school and function almost normally. It is postulated that respiratory failure in nemaline myopathy may not be related to the severity of the muscle weakness but may result from a disturbance of the feedback required for normal control of breathing.


1991 ◽  
Vol 39 (1) ◽  
pp. 13-19 ◽  
Author(s):  
Jan Zandbergen ◽  
Henk Pols ◽  
Cathrien de Loof ◽  
Eric J.L. Griez

1990 ◽  
Vol 70 (Supplement) ◽  
pp. S383 ◽  
Author(s):  
R. J. Sperry ◽  
P. L. Bailey ◽  
N. L. Pace ◽  
S. Eldredge ◽  
K. Johnson ◽  
...  

1985 ◽  
Vol 68 (2) ◽  
pp. 215-225 ◽  
Author(s):  
A. J. Winning ◽  
R. D. Hamilton ◽  
S. A. Shea ◽  
C. Knott ◽  
A. Guz

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.


1983 ◽  
Vol 55 (4) ◽  
pp. 1064-1071 ◽  
Author(s):  
H. Gautier ◽  
M. Bonora

Adult intact conscious or anesthetized cats have been exposed to either hypoxia or low concentrations of CO in air. In addition, the ventilatory response to CO2 was studied in air, hypoxic hypoxia, and CO hypoxia. The results show that 1) in conscious cats, low concentrations of CO (0.15%) induce a slight decrease in ventilation and higher concentrations of CO (0.20%) induce first a small decrease in ventilation and then a characteristic tachypnea similar to the hypoxic tachypnea described in carotid-denervated cats; 2) in anesthetized cats, CO hypoxia induces only mild changes in ventilation; and 3) the ventilatory response to CO2 is increased in CO hypoxia in both conscious and anesthetized animals but differs from the increase observed during hypoxia. It is concluded that the initial decrease in ventilation may be caused by some brain stem depression of the respiratory centers with CO hypoxia, whereas the tachypnea originates probably at some suprapontine level. Conversely, the possible central acidosis may account for the potentiation of the ventilatory response to CO2 observed in either conscious or anesthetized animals.


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