Ventilatory response of the sleeping newborn to CO2 during normoxic rebreathing

1991 ◽  
Vol 71 (1) ◽  
pp. 168-174 ◽  
Author(s):  
G. Cohen ◽  
C. Xu ◽  
D. Henderson-Smart
Keyword(s):  
Rem Sleep ◽  
Ventilatory Response ◽  
Relative Magnitude ◽  
Quiet Sleep ◽  
Volume Response ◽  
The Mean ◽  
Arterial O2 Saturation ◽  
Arterial Po2 ◽  
Rebreathing Method ◽  
Ventilatory Response To Co2

The ventilatory response of the newborn to CO2 was studied using a rebreathing method that minimized changes in arterial PO2 during the test. The aim was to study the variability of the ventilatory response to CO2 and take this into account to assess the relative magnitude of the response to CO2 during rapid-eye-movement (REM) sleep and quiet sleep (QS). Five full-term babies aged 4–6 days were given 5% CO2 in air to rebreathe for 1.5–3 min. O2 was added to the rebreathing circuit to maintain arterial O2 saturation and transcutaneous PO2 (Ptco2) at prerebreathing levels. Tests were repeated four to five times in REM sleep and QS. Mean Ptco2 levels varied between individuals but were similar during REM sleep and QS tests for each subject. The mean coefficient of variability of the ventilatory response was 35% (range 15–77%) during QS and 120% (range 32–220%) during REM sleep. PtcO2 fluctuations during tests [6.0 +/- 3.0 (SD) Torr, range 1–13 Torr] were not correlated with ventilatory response. Overall the ventilatory response was significantly lower in REM sleep than in QS (12.2 +/- 3.0 vs. 38.7 +/- 3.0 ml.min-1.Torr-1.kg-1, P less than 0.001; 2-way analysis of variance) due to a small (nonsignificant) fall in the tidal volume response and a significant fall in breathing rate. In 12 REM sleep tests there was no significant ventilatory response; mean inspiratory flow increased significantly during 8 of these 12 tests. We conclude that there is a significant decrease in the ventilatory response of the newborn to CO2 rebreathing during REM sleep compared with QS.

Maturation of ventilatory response to hypoxia in puppies during sleep

1982 ◽  
Vol 52 (2) ◽  
pp. 309-314 ◽  
Author(s):  
G. G. Haddad ◽  
M. R. Gandhi ◽  
R. B. Mellins
Keyword(s):  
Rem Sleep ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Blood Gases ◽  
Inspiratory Time ◽  
Sleep State ◽  
Quiet Sleep ◽  
Steady Level ◽  
The Mean ◽  
Ventilatory Response To Hypoxia

Using the barometric method, we studied the maturation of the ventilatory response to steady-level hypoxia (FIO2 = 15%O2) during sleep in 37 beagle puppies. In rapid-eye-movement (REM) sleep, instantaneous minute ventilation (VT/Ttot) and mean inspiratory time (VT/TI) increased, and inspiratory time (TI) and expiratory time (TE) were shortened in response to hypoxia at all the ages studied (14, 19, 24, 29 days). In quiet sleep, however, VT/Ttot decreased, and TE and Ttot were prolonged at 14 days in response to the same hypoxic stimulus. There was no change in VT/Ttot at 19 and 24 days of age, but VI/Ttot and VT/TI increased, and TI and TE were shortened at 29 days of age in response to hypoxia in the same sleep state. The mean arterial O2 tension (PaO2) dropped during hypoxia to about 45 Torr, and the mean arterial CO2 tension (PaCO2) decreased, and the mean pH increased at all ages in both REM and quiet sleep. We conclude that in beagles puppies 1) the ventilatory response to hypoxia matures at a slower rate in quiet than in REM sleep and depends primarily on timing rather than volume mechanisms: and 2) in response to hypoxia, the regulation of blood gases in REM sleep may be achieved differently from that in quiet sleep in early life.

Ventilatory Patterns During Hypoxia, Hypercapnia, and Exercise in Adolescents With Mild Scoliosis

PEDIATRICS ◽  
1986 ◽  
Vol 77 (5) ◽  
pp. 692-697
Author(s):  
R. J. Smyth ◽  
K. R. Chapman ◽  
T. A. Wright ◽  
J. S. Crawford ◽  
A. S. Rebuck
Keyword(s):  
Tidal Volume ◽  
Vital Capacity ◽  
Severe Disease ◽  
Pulmonary Mechanics ◽  
Normal Range ◽  
Ventilatory Responses ◽  
Volume Response ◽  
The Mean ◽  
Arterial O2 Saturation ◽  
Maximal Voluntary Ventilation

Adolescents with mild, asymptomatic scoliosis (thoracic curvature <35°) may have little or no impairment of resting lung volumes. Progression to more severe disease may, however, be accompanied by lung restriction, impaired exercise tolerance, and respiratory failure with CO2 retention. We wished to see whether adolescents with mild scoliosis and minimally abnormal resting pulmonary mechanics had impairment of their responses to hypercapnia, hypoxia, and progressive cycle exercise. Forty-four adolescents with idiopathic scoliosis were studied. The mean forced vital capacity (FVC), expressed as a percentage of the predicted value, was 94.3 ± 2.2 (SE). The mean ventilatory response to hypercapnia (2.57 ± 0.24 L/min/mm Hg) was within the normal range but was achieved with a tidal volume response (1.87 ± .17% vital capacity [VC]/mm Hg) that was significantly lower than that previously reported in healthy young adults. Ventilatory responses to exercise were also within the normal range, the mean dyspnea index (VE-max/maximal voluntary ventilation) = 0.92 ± 0.04. However, at a ventilation of 30 L/min, the tidal volume was 0.38 ± 0.01% FVC, which was considerably lower than predicted. The tidal volume response to hypoxia was also abnormally low, the mean response being 0.52 ± 0.059% VC/% decrease in arterial O2 saturation. These findings indicated that, even when scoliosis is asymptomatic and associated with minimal impairment of resting pulmonary function, abnormal patterns of ventilation occur during exercise or in response to chemical stimuli.

Augmentation of ventilatory response to asphyxia by prochlorperazine in humans

1982 ◽  
Vol 53 (3) ◽  
pp. 637-643 ◽  
Author(s):  
L. G. Olson ◽  
M. J. Hensley ◽  
N. A. Saunders
Keyword(s):  
Ventilatory Response ◽  
Blocking Agent ◽  
Control Value ◽  
Before And After ◽  
Venous Pco2 ◽  
Hypercapnic Hypoxia ◽  
Dopamine Hydrochloride ◽  
Response Line ◽  
Arterial O2 Saturation ◽  
Ventilatory Response To Co2

The effect of the dopamine-receptor blocking agent prochlorperazine on the ventilatory response to hypercapnic hypoxia was studied in six healthy adults. Repeated episodes of transient hypoxia were induced at the mixed venous PCO2 level by a nonrebreathing technique in five males and one female before and after an intravenous bolus injection of prochlorperazine mesylate (12.5 mg = 10 mg base). The ventilatory response to CO2 was also studied before and after drug administration. Prochlorperazine produced a modest (15%) increase in resting ventilation (P less than 0.05) but a marked increase in the ventilatory response to asphyxia such that the group mean response was double the control value [2.0 +/- 0.7 vs. 4.2 +/- 1.5 l . min-1 . % arterial O2 saturation (%SaO2); P less than 0.001]. Two-thirds of this change in ventilatory response was due to an increase in frequency response to hypoxia (0.34 +/- 0.20 vs. 0.81 +/- 0.52 breaths . min-1 . %SaO2; P less than 0.001). The position of the ventilatory response line, as judged by the computed ventilation at 95% SaO2, was increased by prochlorperazine (22.2 +/- 9.6 vs. 35.9 +/- 10.9 l . min-1; P less than 0.01) due to an increase in both tidal volume (P less than 0.05) and frequency of breathing (P less than 0.0125). The ventilatory response to CO2 was unchanged by drug injection. In separate experiments prochlorperazine was shown to 1) increase the ventilatory response to steady-state eucapnic hypoxia (P less than 0.01) demonstrating that the drug effect was not dependent on either the presence of hypercapnia or rapidly changing states of arterial oxygenation; and 2) reverse the depressant effect of intravenously infused dopamine hydrochloride (5 micrograms . kg-1 . min-1) on the ventilatory response to transient asphyxia (P less than 0.01). We conclude that prochlorperazine augments hypoxic responsiveness in humans. The mechanism may be blockade of dopaminergic receptors that modulate carotid body discharge.

Congenital Central Hypoventilation and Sleep State

PEDIATRICS ◽  
1980 ◽  
Vol 66 (3) ◽  
pp. 425-428
Author(s):  
Peter J. Fleming ◽  
Darlene Cade ◽  
M. Heather Bryan ◽  
A. Charles Bryan
Keyword(s):  
Metabolic Control ◽  
Eye Movement ◽  
Rem Sleep ◽  
Ventilatory Response ◽  
Respiratory Control ◽  
Rapid Eye Movement ◽  
Sleep State ◽  
Quiet Sleep ◽  
Awake State ◽  
Central Hypoventilation

Congenital central hypoventilation (Ondine's curse) is described in an infant with persistant symptoms throughout the first nine months of life. Respiratory control was most severely affected in quiet sleep, although abnormalities were present in rapid eye movement (REM) sleep and while awake. Failure of metabolic control in quiet sleep led to profound hypoventilation. Behavioral or "behavioral-like" inputs in the awake state and REM sleep increased ventilation, but not to expected normal levels. The ventilatory response to inhaled 4% CO2 was markedly depressed in all states.

Ventilatory responses of newborn calves to progressive hypoxia in quiet and active sleep

1980 ◽  
Vol 48 (5) ◽  
pp. 892-895 ◽  
Author(s):  
H. E. Jeffery ◽  
D. J. Read
Keyword(s):  
Ventilatory Response ◽  
Active Sleep ◽  
Sleep State ◽  
Quiet Sleep ◽  
Ventilatory Responses ◽  
Progressive Hypoxia ◽  
Newborn Calves ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
And Behavior

Isocapnic progressive hypoxia was produced by rebreathing 8-10% oxygen in replicate tests during quiet and active sleep, in five full-term calves aged 1-8 days. Airflow through a tightly fitting mask was digitized at 50-ms intervals to calculate breath-by-breath ventilation and rate. Using a cuvette oximeter, arterial O2 saturation (SaO2) was recorded continuously. A mass-spectrometer record of end-tidal PO2 and PCO2 confirmed the mask seal and the constancy of PCO2. Sleep state was characterized by EEG, EOG, neck EMG, and behavior. In quiet sleep the ratio of ventilation to its normoxic control (VR) increased linearly as SaO2 fell; reflex arousal occurred at SaO2 84.9 ± 4.3% (SD) with VR 1.4 ± 0.39 (SD). In contrast, during active sleep, hypoxemia progressed without any ventilatory response to a very low SaO2; a reflex arousal occurred at SaO2 59.2 ±11.0%, often with a ventilatory response developing abruptly just prior to arousal. The slope of the VR/SaO2 regression lines for the overlapping range of SaO2 differed significantly with state in each animal (P < 0.001); the pooled VR values at SaO2 75% were 1.73± 0.15 (SD) and 0.91 ± 0.18 for quiet and active sleep respectively. The depression of the ventilatory response to hypoxia in active sleep differs from previous reports on adult dogs. The basis for this difference needs to be evaluated in relation to species and age, in particular in relation to both the mechanics of breathing and to chemoreceptor reflexes.

Effects of O2 on the ventilatory response to CO2 in preterm infants

1975 ◽  
Vol 39 (6) ◽  
pp. 896-899 ◽  
Author(s):  
H. Rigatto ◽  
R. De La Torre Verduzco ◽  
D. B. Gates
Keyword(s):  
Preterm Infants ◽  
Gestational Age ◽  
Ventilatory Response ◽  
Respiratory Center ◽  
Response Curves ◽  
Co2 Response ◽  
O2 Concentration ◽  
The Mean ◽  
Ventilatory Response To Co2

To measure the effects of O2 on the ventilatory response to CO2 in preterm infants, we studied eight babies (birth wt 1–2 kg; gestational age 32–36 wk) 10 times during the first 11 days of life. After breathing 21% O2 for 3 min, they were given 15%, 21%, 40%, or 100% O2 for 4 min and then 2% CO2 plus the various concentrations of O2 for 4 min each. The mean slopes of the CO2 response curves were 0.013, 0.027, 0.034, and 0.056 1/(min-kg-mmHg PACO2) with 15%, 21%, 40%, and 100% inspired O2, respectively. Thus, the more hypoxic the infant, the flatter was the response to CO2. These findings suggest that in preterm infants 1) the response to inhaled CO2 is the reverse of that seen in adult man where the higher the inspired O2 concentration, the flatter the response, and 2) the respiratory center is depressed during hypoxia.

Contribution of rib cage and abdomen-diaphragm to tidal volume during CO2 rebreathing

1979 ◽  
Vol 46 (4) ◽  
pp. 709-715 ◽  
Author(s):  
L. D. Pengelly ◽  
A. M. Tarshis ◽  
A. S. Rebuck
Keyword(s):  
Tidal Volume ◽  
Ventilatory Response ◽  
Phase Lag ◽  
Effective Coupling ◽  
Rib Cage ◽  
Volume Response ◽  
The Subject ◽  
Pressure Generator ◽  
Abdominal Compartment ◽  
Ventilatory Response To Co2

In man, there is wide interindividual range in the tidal volume response to CO2. To determine which (rib cage or abdomen-diaphragm) compartment had a greater influence on this range, ventilatory response to CO2 was measured, using Read's method, in eight men and two women seated in a constant-pressure body plethysmograph. Rib cage and abdominal tidal volume was simultaneously measured using magnetometers. Correcting for body size, the tidal volume response of the abdominal compartment was similar in all subjects, whereas that of the rib cage was larger in subjects with high tidal volume response to CO2; a significant correlation was found (P less than 0.01). Rib cage volume displacement lagged behind abdominal in all subjects; phase lag was greatest in the subject with the lowest ventilatory response to CO2. These results suggest that, at high levels of ventilation, a larger volume displacement of the rib cage may reflect a more effective coupling of the diaphragm pressure generator to it or alternatively a reduction in its impedance relative to the abdominal compartment.

Gain of the ventilatory exercise stimulus: definition and meaning

1988 ◽  
Vol 65 (5) ◽  
pp. 2011-2017 ◽  
Author(s):  
F. M. Bennett ◽  
W. E. Fordyce
Keyword(s):  
Ventilatory Response ◽  
Fundamental Property ◽  
Co2 Production ◽  
Nonlinear Properties ◽  
Exchange Processes ◽  
The Mean ◽  
Response To Exercise ◽  
The Relationship ◽  
Exercise Stimulus ◽  
Arterial Po2

The ratio G = delta VE/delta VCO2 where delta VA is change in ventilation and delta VCO2 is change in CO2 production, is often used to quantitate the ventilatory response to exercise and is the overall system gain (G). However, the actual variable of interest often is the gain for the exercise stimulus (GEX). Exercise stimulus refers to a stimulus or group of stimuli other than the mean levels of arterial PO2 (PaCO2), PCO2 (PaCO2), and pH (pHa) that act to increase ventilation during exercise. GEX will be equal to G only if the response to exercise is precisely isocapnic, normoxic, and without metabolic acidosis. A mathematical model was used to examine the relationship between G and GEX when 1) the response to exercise is not strictly isocapnic and 2) when the resting PaCO2 is shifted away from its normal value. It was found that 1) when the exercise response was not strictly isocapnic, G was a poor estimate of GEX and 2) when resting PaCO2 was changed while GEX wa assumed to remain constant, G was a function of the resting PaCO2. However, this dependence of G on resting PaCO2 is a system property that was caused by the nonlinear properties of the gas exchange processes and was not a fundamental property of the controller. It is concluded that G may not always be a good estimate of GEX and may lead to incorrect conclusions concerning the nature of the exercise stimulus.

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