Chemoreceptor Reflexes in Preterm Infants: II. The Effect of Gestational and Postnatal Age on the Ventilatory Response to Inhaled Carbon Dioxide

PEDIATRICS ◽  
1975 ◽  
Vol 55 (5) ◽  
pp. 614-620 ◽  
Author(s):  
Henrique Rigatto ◽  
June P. Brady ◽  
Rafael de la Torre Verduzco
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Preterm Infants ◽  
Dead Space ◽  
Ventilatory Response ◽  
Gas Mixtures ◽  
Postnatal Life ◽  
Constant Flow ◽  
Flow Through ◽  
Carbon Dioxide Response

We studied nine "healthy" preterm infants (birthweight, 1,000 to 2,000 gm) 58 times during postnatal life to define the effects of gestational and postnatal age on the ventilatory response to carbon dioxide. The infants were given air and 2% and 4% carbon dioxide in air to breathe for five minutes each. We determined respiratory minute and tidal volumes, frequency, heart rate, and alveolar Pco2 and Po2. We measured ventilation with a nosepiece and a screen flowmeter, using a constant flow-through to eliminate valves and reduce dead space. Analyses were made during the fifth minute while the baby breathed the various gas mixtures. The slope of the carbon dioxide response increased 42% from 32 to 37 weeks gestation (P < .05) and 62% from 2 to 27 days of age (P < .025). However, the intercept at .3 liter/mm/kg was the same at different gestational ages, but significantly greater at 2 compared with 27 days of age (P < .05). We suggest that the unresponsiveness with increasing prematurity is primarily central and that after birth is primarily dependent on the mechanical abnormalities of the lung.

Chemoreceptor Reflexes in Preterm Infants: I. The Effect of Gestational and Postnatal Age on the Ventilatory Response to Inhalation of 100% and 15% Oxygen

PEDIATRICS ◽  
1975 ◽  
Vol 55 (5) ◽  
pp. 604-613
Author(s):  
Henrique Rigatto ◽  
June P. Brady ◽  
Rafael de la Torre Verduzco
Keyword(s):  
Heart Rate ◽  
Preterm Infant ◽  
Preterm Infants ◽  
Ventilatory Response ◽  
Periodic Breathing ◽  
Postnatal Life ◽  
Low Oxygen ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Oxygen Breathing

We studied 16 "healthy" preterm infants (birthweight, 1,000 to 2,000 gm) 94 times during postnatal life to define the effect of gestational and postnatal age on the ventilatory response to 100% and 15% oxygen. They were given air, then 100% oxygen for two and five minutes respectively (No. = 63) or 21%, 15%, and then 21% oxygen for five minutes each (No. = 31). We measured respiratory minute and tidal volumes, frequency, heart rate, and alveolar Pco2 and Po2. We used the magnitude of the immediate change in ventilation during 100% and 15% oxygen breathing to test peripheral chemoreceptor function. The immediate decrease in ventilation with 100% oxygen and the immediate increase in ventilation with 15% oxygen were statistically similar at different gestational and postnatal ages. The late increase in ventilation (five minutes) with 100% oxygen was also similar at different ages. However, the late decrease in ventilation with 15% oxygen was not present at 18 days of age. These findings suggest that: (1) the peripheral chemoreceptors are active at least from 28 weeks of gestation and are probably not important in triggering periodic breathing or apnea in preterm infants; and (2) the preterm infant matures his response to hypoxia and is able to sustain hyperventilation with low oxygen by 18 days of age.

Effect of baseline oxygenation on the ventilatory response to inhaled 100% oxygen in preterm infants

1995 ◽  
Vol 79 (6) ◽  
pp. 2101-2105 ◽  
Author(s):  
A. Z. Haider ◽  
V. Rehan ◽  
S. Al-Saedi ◽  
R. Alvaro ◽  
K. Kwiatkowski ◽  
...  
Keyword(s):  
Preterm Infants ◽  
Ventilatory Response ◽  
Recovery Period ◽  
Control Period ◽  
Periodic Breathing ◽  
Quiet Sleep ◽  
Peripheral Chemoreceptor ◽  
Lower Baseline ◽  
O2 Concentration ◽  
Flow Through

We tested the hypothesis that the immediate (< 1 min) ventilatory response to 100% O2 in preterm infants, a test of peripheral chemoreceptor activity characterized by a decrease in ventilation due to apnea, is more pronounced at lower baseline O2 concentrations. We studied 12 healthy preterm infants [birth weight 1,425 +/- 103 (SE) g; study weight 1,670 +/- 93 g; gestational age 30 +/- 1 wk; postnatal age 27 +/- 7 days] during quiet sleep. The infants inhaled 15, 21, 25, 30, 35, 40, and 45% O2 for 5 min in a randomized manner (control period), followed by 100% O2 for 2 min, and then the same initial O2 concentration again for 2 min (recovery period). A nose piece and a flow-through system were used to measure ventilation. The immediate decrease in ventilation with 100% O2 was 46% on 15% O2, 24% on 21% O2, 11% on 25% O2, 8% on 30% O2, 12% on 35% O2, and 8% on 40% O2; there was no decrease on 45% O2 (P < 0.01). The corresponding mean duration of apnea was 29 s during 15% O2, 18 s during 21% O2, 8 s during 25% O2, 9 s during 30 and 35% O2, and 3 s during 40% O2; only one infant developed a 5-s apnea during 45% O2 (P < 0.001). The findings suggest that 1) the ventilatory decrease in response to 100% O2 is dependent on the baseline oxygenation, being more pronounced the lower the baseline O2 concentration; and 2) this ventilatory decrease is entirely related to more prolonged apneas observed with lower baseline O2 concentrations. We speculate that the peripheral chemoreceptors, being so active in the small preterm infant with relatively low arterial PO2, are highly susceptible to changes in PO2, and this makes them prone to irregular or periodic breathing, especially during sleep.

Hypoxic-hypercapnic interaction in subjects with bilateral cerebral dysfunction

1963 ◽  
Vol 18 (6) ◽  
pp. 1139-1145 ◽  
Author(s):  
Fred Plum ◽  
Harold W. Brown
Keyword(s):  
Carbon Dioxide ◽  
Brain Damage ◽  
Pyramidal Tract ◽  
Ventilatory Response ◽  
Cerebral Dysfunction ◽  
Tract Disease ◽  
The Brain ◽  
Carbon Dioxide Response ◽  
Ventilatory Response To Hypoxia ◽  
Respiratory Responses

To analyze cerebral influences modifying autonomic respiratory responses, we compared normals and patients with bilateral pyramidal tract disease for their ventilatory response to hypoxia and hypoxia-hypercapnia. During eucapnia, the two groups showed similar hypoxic responses. During hypercapnia, the ventilatory response to hypoxia was greater in the brain-damaged subjects. This apparent augmentation, however, was due entirely to anoxia interacting with an abnormally facilitated carbon dioxide sensitivity: compared with normals, brain-damaged patients at PaOO2 90–100 mm Hg showed an 85% greater CO2 response, and at PaOO2 50 mm Hg showed a 79% greater CO2 response. Since cerebral dysfunction facilitated the ventilatory response to hypoxia-hypercapnia combined but not the response to hypoxia alone, the results imply that the two respiratory stimuli interact centrally rather than peripherally. respiration; brain damage; interaction; carbon dioxide response; forebrain effects; ventilation with CNS disease Submitted on February 18, 1963

Cardiopulmonary reponse to exercise after the Fontan Operation—a cross-sectional and longitudinal evaluation

1996 ◽  
Vol 6 (2) ◽  
pp. 136-142 ◽  
Author(s):  
Luc Mertens ◽  
Ralph Rogers ◽  
Tony Reybrouck ◽  
Monique Dumoulin ◽  
Luc Vanhees ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Heart Rate ◽  
Dead Space ◽  
Ventilatory Threshold ◽  
Fontan Operation ◽  
Aerobic Performance ◽  
Medium Term ◽  
Physiological Dead Space ◽  
End Tidal

AbstractThe purpose of this study was to assess cardiorespiratory responses to submaximal exercise in patients with univentricular atrioventricular connection after the Fontan operation, and to evaluate whether changes occur during medium-term follow-up. Eighteen patients (age 12.1±5.5 years) underwent graded exercise test on a treadmill 2.3±1.4 year after the Fontan repair. Ventilatory gases were measured using breath-by-breath analysis. Results were compared to gender/age-matched controls. Twelve patients (age 14.2±5.4 years) were reevaluated 2.4±2.1 years after the first test. Aerobic exercise performance was subnormal in all patients during the first test. At the lowest level of exercise, the ventilatory threshold was already surpassed in 6/18 patients, while it was reduced in all other patients (p<0.001). All patients were in stable sinus rhythm throughout the test. Heart rate at all exercise levels was ±10% below normal (p<0.05). The respiratory frequency was increased at all exercise levels (p<0.001). The ventilatory equivalent for oxygen was increased (p<0.001), and the end-tidal tension of carbon dioxide was decreased (p<0.001). The ratio of physiological dead space/tidal volume was increased in all patients (p<0.001), while the normal decrease of this ratio during exercise was not observed. Upon reevaluation heart rate, respiratory rate, oxygen uptake, venti latory equivalent for oxygen, end-tidal carbon dioxide tension and physiological dead space did not change signifi cantly. Only a slight further decrease in ventilatory threshold was observed. Aerobic performance after the Fontan procedure ranges widely from just above resting metabolic rate to the lower limit of normal. Dyspnea during exercise is exacerbated by a decreased ventilatory threshold, increased physiological dead space, and decreased respir-atory efficiency. Cardiorespiratory response to exercise, nonetheless, remains relatively stable during medium-term follow-up.

Factors Determining the Ventilatory Response to Carbon Dioxide in Chronic Obstructive Airways Disease

1970 ◽  
Vol 39 (5) ◽  
pp. 653-662 ◽  
Author(s):  
T. K. C. King ◽  
D. Yu
Keyword(s):  
Carbon Dioxide ◽  
Response Curve ◽  
Ventilatory Response ◽  
Chronic Obstructive ◽  
Co2 Response ◽  
Arterial Pco2 ◽  
Obstructive Airways Disease ◽  
End Tidal ◽  
Chronic Obstructive Airways Disease ◽  
Carbon Dioxide Response

1. The ventilatory response to carbon dioxide was measured in a group of patients with chronic obstructive airways disease using a rebreathing method. 2. The slope of the carbon dioxide response curve was obtained by plotting the ventilation at successive half minutes against the corresponding mean end tidal Pco2. 3. The slope of the carbon dioxide response curve was positively correlated with (a) the FEV1 and (b) the reciprocal of the resting arterial Pco2, both these correlations being statistically significant. 4. Reference to FEV1 alone could explain more than 80% of the variation in the slope of the CO2 response curve. This explained variation was not significantly improved by the additional consideration of the resting arterial Pco2. 5. It was suggested that whatever the underlying complex mechanisms that determine the response to CO2, the FEV1 can be used as an empirical factor for the prediction of this response in patients with chronic obstructive airways disease.

The Pharmacodynamic Effect of a Remifentanil Bolus on Ventilatory Control

2000 ◽  
Vol 92 (2) ◽  
pp. 393-393 ◽  
Author(s):  
H. Daniel Babenco ◽  
Pattilyn F. Conard ◽  
Jeffrey B. Gross
Keyword(s):  
Carbon Dioxide ◽  
Respiratory Depression ◽  
Response Curve ◽  
Time Course ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Effect Site ◽  
Ventilatory Drive ◽  
Ventilatory Depression ◽  
Carbon Dioxide Response

Background In doses typically administered during conscious sedation, remifentanil may be associated with ventilatory depression. However, the time course of ventilatory depression after an initial dose of remifentanil has not been determined previously. Methods In eight healthy volunteers, the authors determined the time course of the ventilatory response to carbon dioxide using the dual isohypercapnic technique. Subjects breathed via mask from a to-and-fro circuit with variable carbon dioxide absorption, allowing the authors to maintain end-tidal pressure of carbon dioxide (PET(CO2)) at approximately 46 or 56 mm Hg (alternate subjects). After 6 min of equilibration, subjects received 0.5 microg/kg remifentanil over 5 s, and minute ventilation (V(E)) was recorded during the next 20 min. Two hours later, the study was repeated using the other carbon dioxide tension (56 or 46 mm Hg). The V(E) data were used to construct two-point carbon dioxide response curves at 30-s intervals after remifentanil administration. Using published pharmacokinetic values for remifentanil and the method of collapsing hysteresis loops, the authors estimated the effect-site equilibration rate constant (k(eo)), the effect-site concentration producing 50% respiratory depression (EC50), and the shape parameter of the concentration-response curve (gamma). Results The slope of the carbon dioxide response decreased from 0.99 [95% confidence limits 0.72 to 1.26] to a nadir of 0.27 l x min(-1) x mm Hg(-1) [-0.12 to 0.66] 2 min after remifentanil (P&lt;0.001); within 5 min, it recovered to approximately 0.6 l x min(-1) x mm Hg(-1), and within 15 min of injection, slope returned to baseline. The computed ventilation at PET = 50 mm Hg (VE50) decreased from 12.9 [9.8 to 15.9] to 6.1 l/min [4.8 to 7.4] 2.5 min after remifentanil injection (P&lt;0.001). This was caused primarily by a decrease in tidal volume rather than in respiratory rate. Estimated pharmacodynamic parameters based on computed mean values of VE50 included k(eo) = 0.24 min(-1) (T1/2 = 2.9 min), EC50 = 1.12 ng/ml, and gamma = 1.74. Conclusions After administration of 0.5 microg/kg remifentanil, there was a decrease in slope and downward shift of the carbon dioxide ventilatory response curve. This reached its nadir approximately 2.5 min after injection, consistent with the computed onset half-time of 2.9 min. The onset of respiratory depression appears to be somewhat slower than previously reported for the onset of remifentanil-induced electroencephalographic slowing. Recovery of ventilatory drive after a small dose essentially was complete within 15 min.

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