Effects of CO2 breathing on ventilatory response to sustained hypoxia in normal adults

1989 ◽  
Vol 66 (3) ◽  
pp. 1071-1078 ◽  
Author(s):  
D. Georgopoulos ◽  
D. Berezanski ◽  
N. R. Anthonisen
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Inhibitory Effect ◽  
Hypoxic Exposure ◽  
Initial Increase ◽  
Co2 Levels ◽  
End Tidal ◽  
The Relationship ◽  
Sustained Hypoxia ◽  
Ventilatory Response To Co2

The relationship between CO2 and ventilatory response to sustained hypoxia was examined in nine normal young adults. At three different levels of end-tidal partial pressure of CO2 (PETCO2, approximately 35, 41.8, and 44.3 Torr), isocapnic hypoxia was induced for 25 min and after 7 min of breathing 21% O2, isocapnic hypoxia was reinduced for 5 min. Regardless of PETCO2 levels, the ventilatory response to sustained hypoxia was biphasic, characterized by an initial increase (acute hypoxic response, AHR), followed by a decline (hypoxic depression). The biphasic response pattern was due to alteration in tidal volume, which at all CO2 levels decreased significantly (P less than 0.05), without a significant change in breathing frequency. The magnitude of the hypoxic depression, independent of CO2, correlated significantly (r = 0.78, P less than 0.001) with the AHR, but not with the ventilatory response to CO2. The decline of minute ventilation was not significantly affected by PETCO2 [averaged 2.3 +/- 0.6, 3.8 +/- 1.3, and 4.5 +/- 2.2 (SE) 1/min for PETCO2 35, 41.8, and 44.3 Torr, respectively]. This decay was significant for PETCO2 35 and 41.8 Torr but not for 44.3 Torr. The second exposure to hypoxia failed to elicit the same AHR as the first exposure; at all CO2 levels the AHR was significantly greater (P less than 0.05) during the first hypoxic exposure than during the second. We conclude that hypoxia exhibits a long-lasting inhibitory effect on ventilation that is independent of CO2, at least in the range of PETCO2 studied, but is related to hypoxic ventilatory sensitivity.

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.

Transient ventilatory response to CO2 as a function of sleep state in full-term infants

1983 ◽  
Vol 54 (6) ◽  
pp. 1482-1488 ◽  
Author(s):  
J. V. Anderson ◽  
R. J. Martin ◽  
E. F. Abboud ◽  
I. Z. Dyme ◽  
E. N. Bruce
Keyword(s):  
Steady State ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Full Term ◽  
Initial Increase ◽  
Sleep State ◽  
Term Infants ◽  
Co2 Partial Pressure ◽  
End Tidal ◽  
Ventilatory Response To Co2

The influence of sleep state on the transient (i.e., initial 60 s) and steady-state ventilatory responses to 2% CO2 inhalation was studied in 19 healthy full-term infants. A nasal mask pneumotachometer was used to measure ventilation and end-tidal CO2 partial pressure (PCO2) and enabled abrupt changes in the inspired gas concentration to be made. The magnitude of the change in minute ventilation for both the transient and steady-state responses to CO2 was not statistically different between active (AS) and quiet (QS) sleep. Nonetheless the greater variability in minute ventilation during AS compared with QS continued throughout the period of CO2 inhalation and was associated with a more variable change in ventilation in the individual infants during AS. There was a greater increase in end-tidal PCO2 over the first 60 s during AS (3.3 +/- 0.3 vs. 2.6 +/- 0.2 Torr, in AS and QS, respectively, P less than 0.03). This may indicate a smaller initial increase in alveolar ventilation, relative to CO2 delivery to the lungs, in response to CO2 inhalation during AS. Asynchronous chest wall movements were more common during AS than QS (P less than 0.005) and did not change with CO2. The inconsistent transient ventilatory response to CO2 during AS compared with QS may be important in the behavior of infants to spontaneous episodes of hypercapnia occurring during AS.

Living high-training low increases hypoxic ventilatory response of well-trained endurance athletes

2002 ◽  
Vol 93 (4) ◽  
pp. 1498-1505 ◽  
Author(s):  
Nathan E. Townsend ◽  
Christopher J. Gore ◽  
Allan G. Hahn ◽  
Michael J. McKenna ◽  
Robert J. Aughey ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Control ◽  
Endurance Athletes ◽  
Hypoxic Exposure ◽  
Dependent Manner ◽  
Hypoxic Ventilatory Response ◽  
Ambient Conditions ◽  
Altitude Exposure ◽  
End Tidal

This study determined whether “living high-training low” (LHTL)-simulated altitude exposure increased the hypoxic ventilatory response (HVR) in well-trained endurance athletes. Thirty-three cyclists/triathletes were divided into three groups: 20 consecutive nights of hypoxic exposure (LHTLc, n = 12), 20 nights of intermittent hypoxic exposure (four 5-night blocks of hypoxia, each interspersed with 2 nights of normoxia, LHTLi, n = 10), or control (Con, n = 11). LHTLc and LHTLi slept 8–10 h/day overnight in normobaric hypoxia (∼2,650 m); Con slept under ambient conditions (600 m). Resting, isocapnic HVR (ΔV˙e/ΔSpO2 , whereV˙e is minute ventilation and SpO2 is blood O2 saturation) was measured in normoxia before hypoxia (Pre), after 1, 3, 10, and 15 nights of exposure (N1, N3, N10, and N15, respectively), and 2 nights after the exposure night 20 (Post). Before each HVR test, end-tidal Pco 2(Pet CO2 ) and V˙e were measured during room air breathing at rest. HVR (l · min−1 · %−1) was higher ( P < 0.05) in LHTLc than in Con at N1 (0.56 ± 0.32 vs. 0.28 ± 0.16), N3 (0.69 ± 0.30 vs. 0.36 ± 0.24), N10 (0.79 ± 0.36 vs. 0.34 ± 0.14), N15 (1.00 ± 0.38 vs. 0.36 ± 0.23), and Post (0.79 ± 0.37 vs. 0.36 ± 0.26). HVR at N15 was higher ( P < 0.05) in LHTLi (0.67 ± 0.33) than in Con and in LHTLc than in LHTLi. Pet CO2 was depressed in LHTLc and LHTLi compared with Con at all points after hypoxia ( P < 0.05). No significant differences were observed for V˙e at any point. We conclude that LHTL increases HVR in endurance athletes in a time-dependent manner and decreases Pet CO2 in normoxia, without change inV˙e. Thus endurance athletes sleeping in mild hypoxia may experience changes to the respiratory control system.

Increased chemoreceptor output and ventilatory response to sustained hypoxia

1989 ◽  
Vol 67 (3) ◽  
pp. 1157-1163 ◽  
Author(s):  
D. Georgopoulos ◽  
S. Walker ◽  
N. R. Anthonisen
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Base Line ◽  
Breathing Patterns ◽  
Peripheral Chemoreceptor ◽  
Depressant Action ◽  
Before And After ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

In adult humans the ventilatory response to sustained hypoxia (VRSH) is biphasic, characterized by an initial brisk increase, due to peripheral chemoreceptor (PC) stimulation, followed by a decline attributed to central depressant action of hypoxia. To study the effects of selective stimulation of PC on the ventilatory response pattern to hypoxia, the VRSH was evaluated after pretreatment with almitrine (A), a PC stimulant. Eight subjects were pretreated with A (75 mg po) or placebo (P) on 2 days in a single-blind manner. Two hours after drug administration, they breathed, in succession, room air (10 min), O2 (5 min), room air (5 min), hypoxia [25 min, arterial O2 saturation (SaO2) = 80%], O2 (5 min), and room air (5 min). End-tidal CO2 was kept constant at the normoxic base-line values. Inspiratory minute ventilation (VI) and breathing patterns were measured over the last 2 min of each period and during minutes 3–5 of hypoxia, and nadirs in VI were assessed just before and after O2 exposure. Independent of the day, the VRSH was biphasic. With P and A pretreatment, early hypoxia increased VI 4.6 +/- 1 and 14.2 +/- 1 (SE) l/min, respectively, from values obtained during the preceding room-air period. On A day the hypoxic ventilatory decline was significantly larger than that on P day, and on both days the decline was a constant fraction of the acute hypoxic response.(ABSTRACT TRUNCATED AT 250 WORDS)

Upper airway muscle activity during sustained hypoxia in awake humans

1993 ◽  
Vol 75 (4) ◽  
pp. 1552-1558 ◽  
Author(s):  
S. Okabe ◽  
W. Hida ◽  
Y. Kikuchi ◽  
H. Kurosawa ◽  
J. Midorikawa ◽  
...  
Keyword(s):  
Muscle Activity ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Normal Subjects ◽  
Initial Increase ◽  
Fine Wire ◽  
Obstructive Sleep ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

To examine the effects of sustained hypoxia on upper airway and chest wall muscle activity in humans, we measured genioglossus muscle (GG) activity, inspiratory intercostal muscle (IIM) activity, and ventilation during sustained hypoxia in 17 normal subjects and 17 patients with obstructive sleep apnea (OSA). The trial of sustained hypoxia was performed as follows: after an equilibration period of 3 min, isocapnic hypoxia (arterial O2 saturation = 80 +/- 2%) was maintained for 20 min. GG EMG was measured with a fine-wire electrode inserted percutaneously, and IIM EMG was measured with surface electrodes. Ventilatory response to sustained hypoxia was initially increased and subsequently decreased. Stable phasic GG activity during spontaneous tidal breathing was observed in 6 normal subjects and 10 patients with OSA. Responses of GG and IIM activities to sustained hypoxia showed a biphasic response qualitatively similar to the ventilatory response in these 16 subjects. The absolute value of the subsequent decline in GG activity was similar to that of the initial increase, whereas the subsequent decline in IIM activity was smaller than that of the initial increase. Percent GG activity was significantly lower than both percent IIM activity and percent minute ventilation during the decline and plateau phases. There were no significant differences in ventilatory and EMG responses between the normal subjects and the patients with OSA. We conclude that, during wakefulness, upper airway muscle activity declined to a greater extent than inspiratory pump muscle activity during sustained hypoxia.

Ventilatory response to sustained hypoxia in normal adults

1986 ◽  
Vol 61 (3) ◽  
pp. 906-911 ◽  
Author(s):  
P. A. Easton ◽  
L. J. Slykerman ◽  
N. R. Anthonisen
Keyword(s):  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Initial Increase ◽  
Fractional Concentration ◽  
Subsequent Decrease ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia ◽  
Normal Adults ◽  
Ventilatory Response To Hypoxia

We examined the ventilatory response to moderate (arterial O2 saturation 80%), sustained, isocapnic hypoxia in 20 young adults. During 25 min of hypoxia, inspiratory minute ventilation (VI) showed an initial brisk increase but then declined to a level intermediate between the initial increase and resting room air VI. The intermediate level of VI was a plateau that did not change significantly when hypoxia was extended up to 1 h. The relation between the amount of initial increase and subsequent decrease in ventilation during constant hypoxia was not random; the magnitude of the eventual decline correlated confidently with the degree of initial hyperventilation. Evaluation of breathing pattern revealed that during constant hypoxia there was little alteration in respiratory timing and that the changes in VI were related to significant alterations in tidal volume and mean inspiratory flow (VT/TI). None of the changes was reproduced during a sham control protocol, in which room air was substituted for the period of low fractional concentration of inspired O2. We conclude that ventilatory response to hypoxia in adults is not sustained; it exhibits some biphasic features similar to the neonatal hypoxic response.

Human ventilatory response to CO2 after 8 h of isocapnic or poikilocapnic hypoxia

1998 ◽  
Vol 85 (5) ◽  
pp. 1922-1928 ◽  
Author(s):  
Marzieh Fatemian ◽  
Peter A. Robbins
Keyword(s):  
Healthy Volunteers ◽  
Ventilatory Response ◽  
Analysis Of Covariance ◽  
Pairwise Comparisons ◽  
Air Breathing ◽  
Before And After ◽  
End Tidal ◽  
The Relationship ◽  
Ventilatory Response To Co2

During ventilatory acclimatization to hypoxia (VAH), the relationship between ventilation (V˙e) and end-tidal[Formula: see text]([Formula: see text]) changes. This study was designed to determine 1) whether these changes can be seen early in VAH and 2) if these changes are present, whether the responses differ between isocapnic and poikilocapnic exposures. Ten healthy volunteers were studied by using three 8-h exposures: 1) isocapnic hypoxia (IH), end-tidal [Formula: see text]([Formula: see text]) = 55 Torr and[Formula: see text] held at the subject’s normal prehypoxic value; 2) poikilocapnic hypoxia (PH),[Formula: see text] = 55 Torr; and 3) control (C), air breathing. TheV˙e-[Formula: see text]relationship was determined in hyperoxia ([Formula: see text] = 200 Torr) before and after the exposures. We found a significant increase in the slopes ofV˙e-[Formula: see text]relationship after both hypoxic exposures compared with control (IH vs. C, P < 0.01; PH vs. C, P < 0.001; analysis of covariance with pairwise comparisons). This increase was not significantly different between protocols IH and PH. No significant changes in the intercept were detected. We conclude that 8 h of hypoxia, whether isocapnic or poikilocapnic, increases the sensitivity of the hyperoxic chemoreflex response to CO2.

Effect of ketamine on control of breathing in cats

1983 ◽  
Vol 55 (3) ◽  
pp. 851-859 ◽  
Author(s):  
N. Jaspar ◽  
M. Mazzarelli ◽  
C. Tessier ◽  
J. Milic-Emili
Keyword(s):  
Breathing Pattern ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Time Profile ◽  
Occlusion Pressure ◽  
Tracheal Occlusion ◽  
Co2 Partial Pressure ◽  
Convex Upward ◽  
End Tidal ◽  
Ventilatory Response To Co2

We studied minute ventilation, breathing pattern, end-tidal CO2 partial pressure (PACO2), and tracheal occlusion pressure in cats anesthetized with ketamine (40 and 80 mg/kg) before and after CO2 inhalation. Before CO2 administration ventilation was reduced and PACO2 increased relative to unanesthetized cats at both ketamine doses. Breathing pattern was of the “apneustic” type, being characterized by 1) prolonged inspiratory duration and relatively short expiratory time and 2) markedly curvilinear (convex upward) inspiratory volume-time profile. The latter reflected a similar curvilinearity in the tracheal occlusion pressure waveform. During CO2 inhalation, the ventilatory response to CO2 was similar to that in unanesthetized cats in spite of a depressed tracheal occlusion pressure response. This discrepancy was due to the fact that in the presence of a convex upward inspiratory volume-time profile, the shortening of inspiratory duration with increasing CO2 results in a marked increase of mean inspiratory flow, and hence the ventilatory response to CO2 remains high.

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.

Ventilatory responses to CO2 and hypoxia after sustained hypoxia in awake cats

1994 ◽  
Vol 76 (6) ◽  
pp. 2262-2266 ◽  
Author(s):  
W. Long ◽  
D. Lobchuk ◽  
N. R. Anthonisen
Keyword(s):  
Initial Response ◽  
Hypoxic Exposure ◽  
Initial Increase ◽  
Hypoxic Response ◽  
Air Breathing ◽  
Ventilatory Responses ◽  
Before And After ◽  
End Tidal ◽  
Awake Cats ◽  
Sustained Hypoxia

In humans and cats the ventilatory response to 30 min of isocapnic hypoxia is biphasic with an initial increase followed by a decrease, termed “hypoxic depression.” In humans, 30 min of hypoxia reduces the initial response to a subsequent hypoxic exposure. These experiments were to determine whether the same occurred in cats. Cats were studied while awake. End-tidal Po2 and Pco2 were measured by sampling tracheal gas, and ventilation was measured plethysmographically. In seven cats we measured ventilatory responses to two 30-min periods of isocapnic hypoxia (end-tidal Po2 = 60–65 Torr) separated by 5 min of room air breathing. The first hypoxic response was biphasic, with ventilation increasing to 149% of control at 5 min and decreasing to 117% of control at 25 min. During the second exposure, ventilation was 119% of control at 5 min and 113% of control at 25 min; 30 min of hypoxia depressed the subsequent hypoxic response. Hypoxic depression outlasted the hypoxia, suggesting that it was mediated by relatively slow neurochemical events. In five cats ventilatory responses to 5% CO2 were measured before and 5 min after 30 min of isocapnic hypoxia and before and after 30 min of room air breathing. Hypoxia did not affect CO2 responses. Thus the neurochemical events that cause hypoxic depression appear not to involve the neurons generating the response to CO2 and may be specific to those involved in the hypoxic response.

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