scholarly journals VENTILATORY RESPONSE TO CARBON DIOXIDE DURING EXTRADURAL ANAESTHESIA WITH LIGNOCAINE AND FENTANYL

1989 ◽  
Vol 63 (1) ◽  
pp. 97-102 ◽  
Author(s):  
P. MORISOT ◽  
J.F. DESSANGES ◽  
J. REGNARD ◽  
A. LOCKHART
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response

Ventilatory responses to carbon dioxide at low and high levels of oxygen are elevated after episodic hypoxia in men compared with women

2004 ◽  
Vol 97 (5) ◽  
pp. 1673-1680 ◽  
Author(s):  
Chris Morelli ◽  
M. Safwan Badr ◽  
Jason H. Mateika
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
High Oxygen ◽  
Set Point ◽  
Ventilatory Responses ◽  
Episodic Hypoxia ◽  
Before And After ◽  
Oxygen Gas ◽  
End Tidal

We hypothesized that the acute ventilatory response to carbon dioxide in the presence of low and high levels of oxygen would increase to a greater extent in men compared with women after exposure to episodic hypoxia. Eleven healthy men and women of similar race, age, and body mass index completed a series of rebreathing trials before and after exposure to eight 4-min episodes of hypoxia. During the rebreathing trials, subjects initially hyperventilated to reduce the end-tidal partial pressure of carbon dioxide (PetCO2) below 25 Torr. Subjects then rebreathed from a bag containing a normocapnic (42 Torr), low (50 Torr), or high oxygen gas mixture (150 Torr). During the trials, PetCO2 increased while the selected level of oxygen was maintained. The point at which minute ventilation began to rise in a linear fashion as PetCO2 increased was considered to be the carbon dioxide set point. The ventilatory response below and above this point was determined. The results showed that the ventilatory response to carbon dioxide above the set point was increased in men compared with women before exposure to episodic hypoxia, independent of the oxygen level that was maintained during the rebreathing trials (50 Torr: men, 5.19 ± 0.82 vs. women, 4.70 ± 0.77 l·min−1·Torr−1; 150 Torr: men, 4.33 ± 1.15 vs. women, 3.21 ± 0.58 l·min−1·Torr−1). Moreover, relative to baseline measures, the ventilatory response to carbon dioxide in the presence of low and high oxygen levels increased to a greater extent in men compared with women after exposure to episodic hypoxia (50 Torr: men, 9.52 ± 1.40 vs. women, 5.97 ± 0.71 l·min−1·Torr−1; 150 Torr: men, 5.73 ± 0.81 vs. women, 3.83 ± 0.56 l·min−1·Torr−1). Thus we conclude that enhancement of the acute ventilatory response to carbon dioxide after episodic hypoxia is sex dependent.

Peripheral chemoreflex responsiveness is increased at elevated levels of carbon dioxide after episodic hypoxia in awake humans

2004 ◽  
Vol 96 (3) ◽  
pp. 1197-1205 ◽  
Author(s):  
Jason H. Mateika ◽  
Chris Mendello ◽  
Dany Obeid ◽  
M. Safwan Badr
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
High Oxygen ◽  
Recruitment Threshold ◽  
Episodic Hypoxia ◽  
Before And After ◽  
Carbon Dioxide Levels ◽  
Peripheral Chemoreflex ◽  
Long Term Facilitation ◽  
Ventilatory Response To Hypoxia

We hypothesized that the acute ventilatory response to hypoxia is enhanced after exposure to episodic hypoxia in awake humans. Eleven subjects completed a series of rebreathing trials before and after exposure to eight 4-min episodes of hypoxia. During the rebreathing trials, subjects initially hyperventilated to reduce the partial pressure of carbon dioxide (PetCO2) below 25 Torr. Subjects then breathed from a bag containing normocapnic (42 Torr), low (50 Torr), or high oxygen (140 Torr) gas mixtures. During the trials, PetCO2 increased while a constant oxygen level was maintained. The point at which ventilation began to rise in a linear fashion as PetCO2 increased was considered to be the ventilatory recruitment threshold. The ventilatory response below and above the recruitment threshold was determined. Ventilation did not persist above baseline values immediately after exposure to episodic hypoxia; however, PetCO2 levels were reduced compared with baseline. In contrast, compared with baseline, the ventilatory response to progressive increases in carbon dioxide during rebreathing trials in the presence of low but not high oxygen levels was increased after exposure to episodic hypoxia. This increase occurred when carbon dioxide levels were above but not below the ventilatory recruitment threshold. We conclude that long-term facilitation of ventilation (i.e., increases in ventilation that persist when normoxia is restored after episodic hypoxia) is not expressed in awake humans in the presence of hypocapnia. Nevertheless, despite this lack of expression, the acute ventilatory response to hypoxia in the presence of hypercapnia is increased after exposure to episodic hypoxia.

Effect of hypothermia on ventilatory response to carbon dioxide inhalation and carbon dioxide infusion in dogs

1960 ◽  
Vol 15 (3) ◽  
pp. 397-401 ◽  
Author(s):  
John Salzano ◽  
F. G. Hall
Keyword(s):  
Carbon Dioxide ◽  
Body Temperature ◽  
Lower Order ◽  
Ventilatory Response ◽  
Water Immersion ◽  
Carbon Dioxide Tension ◽  
Order Of Magnitude ◽  
Gaseous Carbon Dioxide ◽  
Ice Water ◽  
Immersion Hypothermia

Some respiratory and circulatory responses to carbon dioxide stress during ice-water immersion hypothermia were studied in 13 dogs. Stresses were imposed by increasing the carbon dioxide tension of the inspired gas in eight animals and by intravenous infusion of gaseous carbon dioxide in five other animals. It was found that when compensation is made for the depressed ventilation exhibited at low body temperature, animals responded to the carbon dioxide stresses in essentially the same manner in the hypothermic as in the normothermia state. However, the responses are of a lower order of magnitude. Submitted on November 19, 1959

Combined ventilatory and breath-holding evaluation of sensitivity to respiratory gases

1959 ◽  
Vol 14 (3) ◽  
pp. 353-356 ◽  
Author(s):  
Robert C. Stroud
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Direct Determination ◽  
Breath Holding ◽  
Respiratory Response ◽  
Data Comparison ◽  
Direct Measurements ◽  
Respiratory Gases ◽  
Definite Role

Direct measurements of the ventilatory response to variations in CO2 tension independent of changes in O2 tension are easily obtained by breathing mixtures of carbon dioxide in 100% oxygen. Direct determination of the respiratory response to O2, however, is not possible due to alternations in CO2 tension resulting from changes in ventilation. Therefore, an attempt has been made to determine this response empirically by a combined analysis of breath-holding and ventilatory data. Comparison of experimentally determined responses to various combinations of O2 and CO2 tensions agree quite well with those predicted by this approach and indicate that oxygen plays a small but definite role in the regulation of eupnic breathing at sea level. Submitted on October 22, 1958

Effect of obesity on ventilatory adjustment to exercise

1963 ◽  
Vol 18 (1) ◽  
pp. 19-24 ◽  
Author(s):  
J. Howland Auchincloss ◽  
John Sipple ◽  
Robert Gilbert
Keyword(s):  
Carbon Dioxide ◽  
Steady State ◽  
Treadmill Exercise ◽  
Ventilatory Response ◽  
Carbon Dioxide Production ◽  
Exercise Ventilation ◽  
Expired Gas ◽  
Obese Subjects ◽  
Oxygen Tensions ◽  
Alveolar Oxygen

The ventilatory response to treadmill exercise was studied in normal and obese subjects, with an analysis of both the steady and unsteady states of exercise. Ventilation, oxygen consumption, carbon dioxide production, respiratory quotient, and alveolar and mixed expired gas concentrations were measured directly or computed. During the steady state of exercise obese subjects increased their ventilation sufficiently to maintain normal alveolar carbon dioxide tensions. During the first 2 min of exercise hypoventilation was more pronounced in obese subjects and in certain individuals resulted in mild reductions in alveolar oxygen tensions. Obese individuals exercised less efficiently than nonobese as manifested by excessive energy expenditure in relation to weight. Steady-state exercise PaCoCo2 values were higher in those subjects previously shown to be relatively insensitive to inhalation of 5% CO2 but failed to correlate with the speed of ventilatory responsiveness.

Effect of intravenous dopamine on hypercapnic ventilatory response in humans

1983 ◽  
Vol 55 (5) ◽  
pp. 1418-1425 ◽  
Author(s):  
D. S. Ward ◽  
J. W. Bellville
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Carbon Dioxide Concentration ◽  
Carbon Dioxide Tension ◽  
Model Parameters ◽  
Loop Gain ◽  
Loop Contribution ◽  
Dopamine Infusion ◽  
Hypercapnic Ventilatory Response ◽  
End Tidal

This study assessed the effect of low-dose intravenous dopamine (3 micrograms X kg-1 X min-1) on the hypercapnic ventilatory response in humans. Six normal healthy subjects were studied. By manipulating the inspired carbon dioxide concentration, the end-tidal carbon dioxide tension was raised in a stepwise fashion from 41 to 49 Torr and held at this level for 4 min. The end-tidal CO2 tension was then lowered back to 41 Torr in a stepwise fashion. The end-tidal O2 tension was held constant at 106 Torr throughout the experiment. The ventilatory response to this normoxic hypercapnic stimulus was analyzed by fitting two exponential functions, allowing the response to be separated into slow and fast chemoreflex loops. Each loop is described by a gain, time constant, and time delay. A single eupneic threshold was used for both loops. Nine control experiments and eight experiments performed during dopamine infusion were analyzed. The dopamine infusion caused the fast loop gain to be significantly (P less than 0.05) reduced from 0.64 to 0.19 l X min-1 X Torr-1, while the slow loop gain was unchanged. The fast loop contribution was reduced from 28 to 11% of the total ventilatory response. None of the other model parameters were significantly affected by the dopamine infusion. Exogenously administered dopamine substantially reduces the sensitivity of the fast chemoreflex loop to carbon dioxide.

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