The ventilatory response to carbon dioxide and sustained hypoxia is enhanced after episodic hypoxia in OSA patients

2006 ◽  
Vol 150 (2-3) ◽  
pp. 122-134 ◽  
Author(s):  
Bradley Khodadadeh ◽  
M. Safwan Badr ◽  
Jason H. Mateika
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Response ◽  
Episodic Hypoxia ◽  
Sustained Hypoxia

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.

Ventilatory sensitivity to carbon dioxide before and after episodic hypoxia in women treated with testosterone

2007 ◽  
Vol 102 (5) ◽  
pp. 1832-1838 ◽  
Author(s):  
Deepti Ahuja ◽  
Jason H. Mateika ◽  
Michael P. Diamond ◽  
M. Safwan Badr
Keyword(s):  
Carbon Dioxide ◽  
Ventilatory Threshold ◽  
Minute Ventilation ◽  
Premenopausal Women ◽  
Oxygen Levels ◽  
Carbon Dioxide Rebreathing ◽  
Episodic Hypoxia ◽  
Before And After ◽  
Testosterone Administration ◽  
Sustained Hypoxia

We hypothesized that the ventilatory threshold and sensitivity to carbon dioxide in the presence of hypoxia and hyperoxia during wakefulness would be increased following testosterone administration in premenopausal women. Additionally, we hypothesized that the sensitivity to carbon dioxide increases following episodic hypoxia and that this increase is enhanced after testosterone administration. Eleven women completed four modified carbon dioxide rebreathing trials before and after episodic hypoxia. Two rebreathing trials before and after episodic hypoxia were completed with oxygen levels sustained at 150 Torr, the remaining trials were repeated while oxygen was maintained at 50 Torr. The protocol was completed following 8–10 days of treatment with testosterone or placebo skin patches. Resting minute ventilation was greater following treatment with testosterone compared with placebo (testosterone 11.38 ± 0.43 vs. placebo 10.07 ± 0.36 l/min; P < 0.01). This increase was accompanied by an increase in the ventilatory sensitivity to carbon dioxide in the presence of sustained hyperoxia (VSco2hyperoxia) compared with placebo (3.6 ± 0.5 vs. 2.9 ± 0.3; P < 0.03). No change in the ventilatory sensitivity to carbon dioxide in the presence of sustained hypoxia (VSco2 hypoxia) following treatment with testosterone was observed. However, the VSco2 hypoxia was increased after episodic hypoxia. This increase was similar following treatment with placebo or testosterone patches. We conclude that treatment with testosterone leads to increases in the VSco2hyperoxia, indicative of increased central chemoreflex responsiveness. We also conclude that exposure to episodic hypoxia enhances the VSco2 hypoxia, but that this enhancement is unaffected by treatment with testosterone.

Carbon dioxide effects on the ventilatory response to sustained hypoxia

1988 ◽  
Vol 64 (4) ◽  
pp. 1451-1456 ◽  
Author(s):  
P. A. Easton ◽  
N. R. Anthonisen
Keyword(s):  
Carbon Dioxide ◽  
Young Adults ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Initial Response ◽  
Initial Increase ◽  
Additional Increase ◽  
End Tidal ◽  
End Tidal Co2 ◽  
Sustained Hypoxia

We examined the interrelation between CO2 and the ventilatory response to moderate (80% arterial saturation) sustained hypoxia in normal young adults. On a background of continuous CO2-stimulated hyperventilation, hypoxia was introduced and sustained for 25 min. Initially, with the introduction of hypoxia onto hypercapnia, there was a brisk additional increase in inspiratory minute ventilation (VI) to 284% of resting VI, but the response was not sustained and hypoxic VI declined by 36% to a level intermediate between the initial increase and the preexisting hypercapnic hyperventilation. Through the continuous hypercapnia, the changes in hypoxic ventilation resulted from significant alterations in tidal volume (VT) and mean inspiratory flow (VT/TI) without changes in respiratory timing. In another experiment, sustained hypoxia was introduced on the usual background of room air, either with isocapnia or without maintenance of end-tidal CO2 (ETCO2) (poikilocapnic hypoxia). Regardless of the degree of maintenance of ETCO2, during 25 min of sustained hypoxia, VI showed an initial brisk increase and then declined by 35-40% of resting VI to a level intermediate between the initial response and resting room air VI. For both isocapnia and poikilocapnic conditions, the attenuation of VI was an expression of a diminished VT. Thus the decline in ventilation with sustained hypoxia occurred regardless of the background ETCO2, suggesting that the mechanism underlying the hypoxic decline is independent of CO2.

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

Effects of dopamine and domperidone on ventilatory sensitivity to hypoxia after 8 h of isocapnic hypoxia

1999 ◽  
Vol 86 (1) ◽  
pp. 222-229 ◽  
Author(s):  
Michala E. F. Pedersen ◽  
Keith L. Dorrington ◽  
Peter A. Robbins
Keyword(s):  
Confidence Interval ◽  
Lower Limit ◽  
Analysis Of Variance ◽  
Significant Interaction ◽  
Low Dose ◽  
Ventilatory Response ◽  
Hypoxic Ventilatory Response ◽  
Dopaminergic Activity ◽  
Sustained Hypoxia

Acclimatization to altitude involves an increase in the acute hypoxic ventilatory response (AHVR). Because low-dose dopamine decreases AHVR and domperidone increases AHVR, the increase in AHVR at altitude may be generated by a decrease in peripheral dopaminergic activity. The AHVR of nine subjects was determined with and without a prior period of 8 h of isocapnic hypoxia under each of three pharmacological conditions: 1) control, with no drug administered; 2) dopamine (3 μg ⋅ min−1 ⋅ kg−1); and 3) domperidone (Motilin, 40 mg). AHVR increased after hypoxia ( P ≤ 0.001). Dopamine decreased ( P ≤ 0.01), and domperidone increased ( P ≤ 0.005) AHVR. The effect of both drugs on AHVR appeared larger after hypoxia, an observation supported by a significant interaction between prior hypoxia and drug in the analysis of variance ( P ≤ 0.05). Although the increased effect of domperidone after hypoxia of 0.40 l ⋅ min−1 ⋅ %saturation−1[95% confidence interval (CI) −0.11 to 0.92 l ⋅ min−1 ⋅ %−1] did not reach significance, the lower limit for this confidence interval suggests that little of the increase in AHVR after sustained hypoxia was brought about by a decrease in peripheral dopaminergic inhibition.

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