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.

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.

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.

Effect of a single breath of 100% oxygen on respiration in neonates during sleep

1984 ◽  
Vol 57 (5) ◽  
pp. 1531-1535 ◽  
Author(s):  
T. Aizad ◽  
J. Bodani ◽  
D. Cates ◽  
L. Horvath ◽  
H. Rigatto
Keyword(s):  
Gestational Age ◽  
Minute Ventilation ◽  
Control Period ◽  
Full Term ◽  
Preterm Neonates ◽  
Sleep State ◽  
Quiet Sleep ◽  
Peripheral Chemoreceptor ◽  
Term Infants ◽  
Single Breath

To determine the effect of a single breath of 100% O2 on ventilation, 10 full-term [body wt 3,360 +/- 110 (SE) g, gestational age 39 +/- 0.4 wk, postnatal age 3 +/- 0.6 days] and 10 preterm neonates (body wt 2,020 +/- 60 g, gestational age 34 +/- 2 wk, postnatal age 9 +/- 2 days) were studied during active and quiet sleep states. The single-breath method was used to measure peripheral chemoreceptor response. To enhance response and standardize the control period for all infants, fractional inspired O2 concentration was adjusted to 16 +/- 0.6% for a control O2 saturation of 83 +/- 1%. After 1 min of control in each sleep state, each infant was given a single breath of O2 followed by 21% O2. Minute ventilation (VE), tidal volume (VT), breathing frequency (f), alveolar O2 and CO2 tension, O2 saturation (ear oximeter), and transcutaneous O2 tension were measured. VE always decreased with inhalation of O2 (P less than 0.01). In quiet sleep, the decrease in VE was less in full-term (14%) than in preterm (40%) infants (P less than 0.001). Decrease in VE was due primarily to a drop in VT in full-term infants as opposed to a fall in f and VT in preterm infants (P less than 0.05). Apnea, as part of the response, was more prevalent in preterm than in full-term infants. In active sleep the decrease in VE was similar both among full-term (19%) and preterm (21%) infants (P greater than 0.5). These results suggest greater peripheral chemoreceptor response in preterm than in full-term infants, reflected by a more pronounced decrease in VE with O2. The results are compatible with a more powerful peripheral chemoreceptor contribution to breathing in preterm than in full-term infants.

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.

Response to hypercapnia and exercise hyperpnea in graded anesthesia

1984 ◽  
Vol 57 (6) ◽  
pp. 1796-1802 ◽  
Author(s):  
T. Chonan ◽  
Y. Kikuchi ◽  
W. Hida ◽  
C. Shindoh ◽  
H. Inoue ◽  
...  
Keyword(s):  
Steady State ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Exercise Hyperpnea ◽  
Sciatic Nerves ◽  
End Tidal ◽  
Response To Exercise ◽  
The Relationship ◽  
End Tidal Co2 ◽  
Rebreathing Method

We examined the relationship between response to hypercapnia and ventilatory response to exercise under graded anesthesia in eight dogs. The response to hypercapnia was measured by the CO2 rebreathing method under three grades of chloralose-urethan anesthesia. The degrees of response to hypercapnia (delta VE/delta PETCO2, 1 X min-1 X Torr-1) in light (L), moderate (M), and deep (D) anesthesia were 0.40 +/- 0.05 (mean +/- SE), 0.24 +/- 0.03, and 0.10 +/- 0.02, respectively, and were significantly different from each other. Under each grade of anesthesia, exercise was performed by electrically stimulating the bilateral femoral and sciatic nerves for 4 min. The time to reach 63% of full response of the increase in ventilation (tauVE) after beginning of exercise was 28.3 +/- 1.5, 38.1 +/- 5.2, and 56.0 +/- 6.1 s in L, M, and D, respectively. During steady-state exercise, minute ventilation (VE) in L, M, and D significantly increased to 6.17 +/- 0.39, 5.14 +/- 0.30, and 3.41 +/- 0.16 1 X min-1, from resting values of 3.93 +/- 0.34, 2.97 +/- 0.17, and 1.69 +/- 0.14 1 X min-1, respectively, while end-tidal CO2 tension (PETCO2) in L decreased significantly to 34.8 +/- 0.9 from 35.7 +/- 0.9, did not change in M (38.9 +/- 1.1 from 38.9 +/- 0.8), and increased significantly in D to 47.3 +/- 1.9 from 45.1 +/- 1.7 Torr.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory sensitivity to CO2 in hyperoxia and hypoxia in older aged humans

1993 ◽  
Vol 75 (5) ◽  
pp. 2209-2216 ◽  
Author(s):  
M. J. Poulin ◽  
D. A. Cunningham ◽  
D. H. Paterson ◽  
J. M. Kowalchuk ◽  
W. D. Smith
Keyword(s):  
Linear Equation ◽  
Response Curve ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Ventilatory Responses ◽  
Co2 Sensitivity ◽  
End Tidal ◽  
Effects Of Aging ◽  
Peripheral Chemoreflex ◽  
Ventilatory Response To Co2

Findings from studies of the effects of aging on the human respiratory controller are equivocal. This study assessed the ventilatory response to CO2 in hyperoxia and hypoxia in groups of younger (YS) and older (OS) humans. Two protocols were used. In the first, end-tidal PCO2 (PETCO2) was clamped at 1–2 Torr above rest (eucapnia), and, in the second, PETCO2 was clamped at 7–8 torr above resting PETCO2 (moderate hypercapnia). End-tidal PO2 was clamped at 100 Torr throughout except for two 2-min periods at 500 and 50 Torr. The ventilatory responses for each subject at each PO2 were fitted to the linear equation, VE = S(PETCO2 - B), where VE is minute ventilation, S is the response curve slope, and B is the response curve threshold. In eucapnia, there were no differences in hypoxic and hyperoxic VE between YS and OS. In hypercapnia, hypoxic VE was 24% lower in OS [39.93 +/- 2.71 (SE) l/min] than in YS (52.16 +/- 3.17 l/min). In hypoxia, S was significantly lower in OS (3.25 +/- 0.38 l.min-1.Torr-1) than in YS (4.76 +/- 0.37 l.min-1.Torr-1). We conclude that, in older humans, VE is lower in hypoxia during moderate hypercapnia, resulting mainly from a decreased peripheral chemoreflex CO2 sensitivity.

Effects of airway anesthesia on ventilatory responses to graded dead spaces and CO2

1988 ◽  
Vol 64 (5) ◽  
pp. 1885-1892 ◽  
Author(s):  
C. Shindoh ◽  
W. Hida ◽  
Y. Kikuchi ◽  
T. Chonan ◽  
H. Inoue ◽  
...  
Keyword(s):  
Steady State ◽  
Dead Space ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Co2 Response ◽  
Co2 Gas ◽  
Ventilatory Responses ◽  
Before And After ◽  
End Tidal ◽  
And Control

Ventilatory response to graded external dead space (0.5, 1.0, 2.0, and 2.5 liters) with hyperoxia and CO2 steady-state inhalation (3, 5, 7, and 8% CO2 in O2) was studied before and after 4% lidocaine aerosol inhalation in nine healthy males. The mean ventilatory response (delta VE/delta PETCO2, where VE is minute ventilation and PETCO2 is end-tidal PCO2) to graded dead space before airway anesthesia was 10.2 +/- 4.6 (SD) l.min-1.Torr-1, which was significantly greater than the steady-state CO2 response (1.4 +/- 0.6 l.min-1.Torr-1, P less than 0.001). Dead-space loading produced greater oscillation in airway PCO2 than did CO2 gas loading. After airway anesthesia, ventilatory response to graded dead space decreased significantly, to 2.1 +/- 0.6 l.min-1.Torr-1 (P less than 0.01) but was still greater than that to CO2. The response to CO2 did not significantly differ (1.3 +/- 0.5 l.min-1.Torr-1). Tidal volume, mean inspiratory flow, respiratory frequency, inspiratory time, and expiratory time during dead-space breathing were also depressed after airway anesthesia, particularly during large dead-space loading. On the other hand, during CO2 inhalation, these respiratory variables did not significantly differ before and after airway anesthesia. These results suggest that in conscious humans vagal airway receptors play a role in the ventilatory response to graded dead space and control of the breathing pattern during dead-space loading by detecting the oscillation in airway PCO2. These receptors do not appear to contribute to the ventilatory response to inhaled CO2.

The Auditory Steady-State Response: Full-Term and Premature Neonates

2002 ◽  
Vol 13 (05) ◽  
pp. 260-269 ◽  
Author(s):  
Barbara Cone-Wesson ◽  
John Parker ◽  
Nina Swiderski ◽  
Field Rickards
Keyword(s):  
Steady State ◽  
Premature Infants ◽  
Modulation Frequency ◽  
Otoacoustic Emission ◽  
Full Term ◽  
Steady State Response ◽  
Pass Rates ◽  
Term Infants ◽  
State Response ◽  
Auditory Steady State Response

Two studies were aimed at developing the auditory steady-state response (ASSR) for universal newborn hearing screening. First, neonates who had passed auditory brainstem response, transient evoked otoacoustic emission, and distortion-product otoacoustic emission tests were also tested with ASSRs using modulated tones that varied in frequency and level. Pass rates were highest (> 90%) for amplitude-modulated tones presented at levels ≥ 69 dB SPL. The effect of modulation frequency on ASSR for 500- and 2000-Hz tones was evaluated in full-term and premature infants in the second study. Full-term infants had higher pass rates for 2000-Hz tones amplitude modulated at 74 to 106 Hz compared with pass rates for a 500-Hz tone modulated at 58 to 90 Hz. Premature infants had lower pass rates than full-term infants for both carrier frequencies. Systematic investigation of ASSR threshold and the effect of modulation frequency in neonates is needed to adapt the technique for screening.

Sexual influence on the control of breathing

1983 ◽  
Vol 54 (4) ◽  
pp. 874-879 ◽  
Author(s):  
D. P. White ◽  
N. J. Douglas ◽  
C. K. Pickett ◽  
J. V. Weil ◽  
C. W. Zwillich
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Premenopausal Women ◽  
Co2 Production ◽  
Menstrual Phase ◽  
Co2 Partial Pressure ◽  
Ventilatory Responses ◽  
Chemical Stimuli ◽  
Low Levels ◽  
Normal Women

Previous investigation has demonstrated that progesterone, a hormone found in premenopausal women, is a ventilatory stimulant. However, fragmentary data suggest that normal women may have lower ventilatory responses to chemical stimuli than men, in whom progesterone is found at low levels. As male-female differences have not been carefully studied, we undertook a systematic comparison of resting ventilation and ventilatory responses to chemical stimuli in men and women. Resting ventilation was found to correlate closely with CO2 production in all subjects (r = 0.71, P less than 0.001), but women tended to have a greater minute ventilation per milliliter of CO2 produced (P less than 0.05) and consequently a lower CO2 partial pressure (PCO2) (men 35.1 +/- 0.5 Torr, women 33.2 +/- 0.5 Torr; P less than 0.02). Women were also found to have lower tidal volumes, even when corrected from body surface area (BSA), and greater respiratory frequency than comparable males. The hypoxic ventilatory response (HVR) quantitated by the shape parameter A was significantly greater in men [167 +/- 22 (SE)] than in women (109 +/- 13; P less than 0.05). In men this hypoxic response was found to correlate closely with O2 consumption (r = 0.75, P less than 0.001) but with no measure of size or metabolic rate in women. The hypercapnic ventilatory response, expressed as the slope of ventilation vs. PCO2, was also greater in men (2.30 +/- 0.23) than in women (1.58 +/- 0.19, P less than 0.05). Finally women tended to have higher ventilatory responses in the luteal than in the follicular menstrual phase, but this was significant only for HVR (P less than 0.05). Women, with relatively higher resting ventilation, have lower responses to hypoxia and hypercapnia.

Effects of sleep state on ventilatory acclimatization to hypoxia in humans

1984 ◽  
Vol 57 (4) ◽  
pp. 1089-1096 ◽  
Author(s):  
A. D. Berssenbrugge ◽  
J. A. Dempsey ◽  
J. B. Skatrud
Keyword(s):  
Eye Movement ◽  
Chronic Hypoxia ◽  
Minute Ventilation ◽  
Barometric Pressure ◽  
Nrem Sleep ◽  
Hypoxic Exposure ◽  
Adult Males ◽  
Sleep State ◽  
Co2 Partial Pressure ◽  
Arterial O2 Saturation

We assessed the influence of sleep state on ventilatory acclimatization to hypoxia. Ventilation, arterial O2 saturation (SaO2), and arterial acid-base status were monitored in healthy adult males during wakefulness, nonrapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep in normoxia [barometric pressure (PB) = 740 Torr] and over 4 continuous days of hypobaric hypoxia (PB = 455 Torr). The relative hypoventilation observed during sleep compared with wakefulness in normoxia was also observed during all stages of hypoxic acclimatization. The characteristic time-dependent changes associated with acclimatization to chronic hypoxia were similar during wakefulness and all sleep states: 1) arterial CO2 partial pressure (PaCO2) decreased 27–31% by night 4 with approximately half of this fall occurring acutely (0.3–3 h hypoxia); 2) minute ventilation increased progressively with duration of hypoxic exposure including increased levels of hyperventilation throughout the initial night of sleep in hypoxia; 3) SaO2 was lowest acutely and gradually increased coincident with the progressive hyperventilation; and 4) pHa increased acutely and remained unchanged despite additional hyperventilation due to a compensatory reduction in [HCO3-]a. In addition, in the acclimatized subject hyperventilation persisted following acute restoration of normoxia, and this continued hyperventilation was similar in magnitude during both wakefulness and NREM sleep. These results indicate that suprapontine influences on ventilatory control associated with the state of wakefulness are not required in the process of ventilatory acclimatization to chronic hypoxia.

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