Ventilatory Response to Carbon Dioxide in Tetanus

1976 ◽  
Vol 50 (1) ◽  
pp. 83-86
Author(s):  
O. O. Elegbeleye ◽  
D. Femi-Pearse

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.

1971 ◽  
Vol 41 (1) ◽  
pp. 13-21 ◽  
Author(s):  
A. S. Rebuck ◽  
John Read

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.


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

2004 ◽  
Vol 97 (5) ◽  
pp. 1673-1680 ◽  
Author(s):  
Chris Morelli ◽  
M. Safwan Badr ◽  
Jason H. Mateika

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.


2004 ◽  
Vol 96 (3) ◽  
pp. 1197-1205 ◽  
Author(s):  
Jason H. Mateika ◽  
Chris Mendello ◽  
Dany Obeid ◽  
M. Safwan Badr

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.


1960 ◽  
Vol 15 (3) ◽  
pp. 397-401 ◽  
Author(s):  
John Salzano ◽  
F. G. Hall

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


1959 ◽  
Vol 14 (3) ◽  
pp. 353-356 ◽  
Author(s):  
Robert C. Stroud

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


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