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

1976 ◽  
Vol 41 (5) ◽  
pp. 609-611 ◽  
Author(s):  
S. Albersheim ◽  
R. Boychuk ◽  
M. M. Seshia ◽  
D. Cates ◽  
H. Rigatto
Keyword(s):  
Preterm Infants ◽  
Ventilatory Response ◽  
Background Concentrations ◽  
Peripheral Chemoreceptor ◽  
Co2 Response ◽  
Peripheral Chemoreceptors ◽  
Paradoxical Response

We wanted to know wheter the paradoxical response to CO2 under various background concentrations of O2 in preterm infants was mediated at the peripheral chemoreceptors. In five preterm infants we estimated peripheral chemoreceptor activity using the immediate change in ventilation (first 30 s) when 15%, 40%, 60%, or 100% O2 was substituted for 21% O2. Potentiation between O2 and CO2 was assessed by comparing the response with and without 4% CO2. CO2 enhanced the immediate hyperventilation with hypoxia (P less than 0.005) and reduced the immediate hypoventilation with hyperoxia (P less than 0.025 for 40% O2). This effect of CO2 increased from .00% to 15% O2 (P lessthan 0.05). These findings suggest: 1) CO2 interacts with O2 at the peripheral chemoreceptor level, and 2) because this interaction is more pronouncedwith hypoxia, the flatter CO2 response we observed with hypoxia was probably not mediated through the peripheral chemoreceptors and is likely to be central in origin.

PERIODIC BREATHING AND APNEA IN PRETERM INFANTS. I. EVIDENCE FOR HYPOVENTILATION POSSIBLY DUE TO CENTRAL RESPIRATORY DEPRESSION

PEDIATRICS ◽  
1972 ◽  
Vol 50 (2) ◽  
pp. 202-218
Author(s):  
Henrique Rigatto ◽  
June P. Brady
Keyword(s):  
Preterm Infants ◽  
Periodic Breathing ◽  
Significant Shift ◽  
Peripheral Chemoreceptor ◽  
Co2 Response ◽  
Peripheral Chemoreceptors ◽  
Mean Values ◽  
Periodic Groups ◽  
Major Defect ◽  
Alveolar Capillary

We made 84 studies on 20 "healthy" preterm infants during the first 34 days of life to discover whether infants breathing periodically hypoventilate or hyperventilate and whether the major defect is at the central or peripheral chemoreceptors. Six infants breathed periodically (n = 26) and seven regularly (n = 27) at all times; seven infants breathed periodically (n = 15) or regularly (n = 16) in different studies. In these three groups (periodic, regular, and intermediate), we compared respiratory minute volume and frequency, heart rate, alveolar oxygen tension (PAO2) and alveolar carbon dioxide tension (PACO2) and PO2, PCO2 and pH of arterialized capillary blood, alveolar-capillary differences for PO2 and PCO2, peripheral chemoreceptor sensitivity and CO2 responses. We measured ventilation with a nosepiece and a screen flowmeter. The mean values for the intermediate and periodic groups were similar. There were major differences between the periodic and regular groups. The infants breathing periodically (1) hypoventilated, (2) showed a significant shift of the CO2 response curve to the right with a 22% decrease in slope, and (3) had an increased response to O2. However, the two groups had similar alveolar-capillary PO2 and PCO2 differences. These findings suggest that the major defect is not in the lungs or at the peripheral chemoreceptors but at the respiratory center (or central receptors).

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 temperature on central chemical control of ventilation in the alligator Alligator mississippiensis

1993 ◽  
Vol 179 (1) ◽  
pp. 261-272
Author(s):  
L. G. Branco ◽  
S. C. Wood
Keyword(s):  
Fourth Ventricle ◽  
Ventilatory Response ◽  
Pulmonary Ventilation ◽  
Gas Mixtures ◽  
Alligator Mississippiensis ◽  
Effect Of Temperature ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Ph Values ◽  
Arterial Ph

Central chemoreceptor function was assessed in unanesthetized alligators, Alligator mississippiensis, at body temperatures of 15, 25 and 35 degrees C. Two experiments were performed. In the first experiment, the fourth ventricle was perfused with mock cerebrospinal fluid (CSF) solutions of different pH values (7.1-7.9). Changes in pulmonary ventilation were evaluated with a pneumotachograph and arterial pH (pHa) was measured. Perfusion with low-pH solutions increased ventilation and arterial pH. Perfusion with high-pH solutions decreased ventilation and arterial pH. Mock CSF pH had a greater effect at higher temperatures. In the second experiment, the relative contributions of central and peripheral chemoreceptor drive to breathing were evaluated using hypercapnic gas mixtures to stimulate both central and peripheral chemoreceptors. Hypercapnia caused an increase in ventilation which was larger at higher temperatures. To stimulate only the peripheral chemoreceptors, the same hypercapnic gas mixtures were applied while the CSF pH of the fourth ventricle was kept constant by perfusion with a mock CSF solution. This reduced significantly the ventilatory response induced by hypercapnia. These data indicate that, regardless of the temperature, central chemoreceptors play a major role in the ventilatory regulation of the alligator. The change in pHa with temperature is compatible with the alphastat hypothesis.

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.

Ventilatory effects of acetazolamide in cats during hypoxemia

1992 ◽  
Vol 72 (5) ◽  
pp. 1717-1723 ◽  
Author(s):  
L. J. Teppema ◽  
F. Rochette ◽  
M. Demedts
Keyword(s):  
Steady State ◽  
Ventilatory Response ◽  
Significant Rise ◽  
Hypoxic Ventilatory Response ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Relative Contribution ◽  
Ventilatory Effects ◽  
Arterial Po2 ◽  
Mean Alveolar Pco2

In normoxemic cats, acetazolamide (ACTZ) has been shown to cause a large rise in ventilation (VE) but a decrease in peripheral chemoreceptor activity. The relative contribution of the peripheral chemoreceptors to ventilation is higher during hypoxemia than during normoxemia. Therefore, what are the effects of ACTZ during steady-state hypoxemia? The aims of this study in anesthetized cats were 1) to study the effect of ACTZ (50 mg/kg iv) on mean hypoxemic [arterial PO2 (PaO2) approximately 6 kPa] ventilation and 2) to study the effect of ACTZ on the isocapnic hypoxic ventilatory response. In the first study, in six cats with an inspiratory CO2 fraction of 0, ACTZ led to an insignificant rise in mean VE of 119 ml.min-1.kg-1 after 1 h. In five other cats maintained at an inspiratory CO2 fraction of 0.015, ACTZ resulted in a significantly larger response in VE (268 and 373 ml.min-1.kg-1 after 1 and 2 h, respectively). In the second study, before infusion in five cats, an isocapnic fall in mean PaO2 from 13 to 4.7 kPa led to a significant rise in mean VE of 385 ml.min-1.kg-1; 1 h later, the response (at the same mean alveolar PCO2) was reduced to an insignificant rise of 38 ml.min-1.kg-1. Before infusion four other cats showed a significant rise in mean VE of 390 ml.min-1.kg-1 when mean PaO2 was lowered isocapnically from 12.4 to 6.8 kPa; 2 h after infusion, an isocapnic fall in mean PaO2 from 13.9 to 7.2 kPa led to an insignificant rise of 112 ml.min-1.kg-1.(ABSTRACT TRUNCATED AT 250 WORDS)

Ventilatory response in the fetal lamb following peripheral chemodenervation

1977 ◽  
Vol 42 (4) ◽  
pp. 630-635 ◽  
Author(s):  
D. E. Woodrum ◽  
T. A. Standaert ◽  
C. R. Parks ◽  
D. Belenky ◽  
J. Murphy ◽  
...  
Keyword(s):  
Ventilatory Response ◽  
Blood Gases ◽  
System Control ◽  
Fetal Blood ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Marked Variability ◽  
Fetal Lamb ◽  
Before And After ◽  
Chemical Stimuli

Carotid infusions of sodium cyanide solution and perfusions of hypoxemic or hypercapnic fetal blood were done before and after peripheral chemoreceptor denervation. Step changes in PaO2 ranged from -11 to -22 Torr; step changes in PaCO2 ranged from +17 to +42 Torr. The cyanide dose was 0.2 mg/kg per loop system. Control perfusions consisted of 25 ml of fetal blood without changes in pH and blood gases. A ventilatory response occurred in the majority of all experimental perfusions regardless of innervation status of the peripheral chemoreceptors. No response occurred with control perfusions. There was a marked variability in the time of onset of ventilatory activity with a delay of greater than 10 s occurring following most perfusions. These studies demonstrate that the fetus has an attenuated ventilatory response to chemical stimuli and that hypoxia stimulates ventilation in the absence of peripheral chemoreceptors.

Effect of Continuous Positive Airway Pressure on the Ventilatory Response to CO2 in Preterm Infants

PEDIATRICS ◽  
1983 ◽  
Vol 71 (4) ◽  
pp. 634-638
Author(s):  
Manuel Durand ◽  
Ellen McCann ◽  
June P. Brady
Keyword(s):  
Tidal Volume ◽  
Preterm Infants ◽  
Airway Pressure ◽  
Positive Airway Pressure ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Co2 Response ◽  
Expiratory Time ◽  
Ventilatory Response To Co2

The effect of continuous positive airway pressure (CPAP) on the ventilatory response to CO2 in newborn infants is unknown. The CO2 response to 4% CO2 in air was studied in nine preterm infants without lung disease before and during administration of CPAP (4 to 5 cm H2O) delivered by face mask. Minute ventilation, tidal volume, respiratory frequency, and end-tidal Pco2 were measured, and the slope and intercept of the CO2 response were calculated. Respiratory pattern and changes in oxygenation were also analyzed by measuring inspiratory and expiratory time, mean inspiratory flow, mean expiratory flow, effective respiratory timing, endtidal Po2, and transcutaneous Po2. CPAP significantly decreased minute ventilation from 278.7 to 197.6 mL/mm/kg (P &lt; .001). Tidal volume and respiratory frequency were also significantly decreased. The slope of the CO2 response during CPAP was not significantly different from the slope before CPAP (36 v 33 mL/min/kg/mm Hg, P &gt; .1), but the intercept was shifted to the right (P &lt; .001). The decrease in respiratory frequency was primarily due to a prolongation of expiratory time (P &lt; .05). In addition, transcutaneous Po2 increased during administration of CPAP (P &lt; .001). These findings indicate that: (1) CPAP significantly decreases ventilation in preterm infants without lung disease, affecting both tidal volume and respiratory frequency; (2) CPAP does not appreciably alter the ventilatory response to CO2; (3) the changes in respiratory frequency are primarily accounted for by a prolongation of expiratory time; (4) CPAP improves oxygenation.

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.

The Hypoxic Drive to Breathing in Chronic Bronchitis and Emphysema

1970 ◽  
Vol 38 (4) ◽  
pp. 503-518 ◽  
Author(s):  
D. C. Flenley ◽  
D. H. Franklin ◽  
J. S. Millar
Keyword(s):  
Cerebrospinal Fluid ◽  
Chronic Hypoxia ◽  
Ventilatory Response ◽  
Whole Body ◽  
Chronic Obstructive ◽  
Peripheral Chemoreceptor ◽  
Co2 Response ◽  
Lumbar Cerebrospinal Fluid ◽  
Normal Men ◽  
Ventilatory Response To Co2

1. We measured the ventilatory response to CO2 at two levels of arterial Po2 in twelve patients who suffered from chronic obstructive bronchitis. We also determined the lumbar cerebrospinal fluid bicarbonate in ten of these patients. 2. The CO2 response was depressed in nine patients who suffered from hypoxia and CO2 retention when breathing air. The hypoxic drive to breathing was normal in six cases, increased in one and absent in two cases who had severe chronic hypoxia and secondary polycythaemia. 3. The slope of the acute on chronic whole body CO2 titration line expressed in terms of arterial H+ and arterial Pco2 was the same in the hypercapnic patients as in normal men. This relationship allows predictions of the duration of hypercapnia in clinical practice. 4. Increased buffering in cerebrospinal fluid does not account for the depressed ventilatory response to CO2 in these patients. 5. By calculating the probable rise in jugular venous Pco2 which will follow correction of chronic hypoxia in these patients, we conclude that the administration of oxygen will remove a peripheral chemoreceptor stimulus to breathing but increase the central stimulus by a rise in cerebrospinal fluid acidity.

scholarly journals Influence of arterial O2 on the susceptibility to posthyperventilation apnea during sleep

2006 ◽  
Vol 100 (1) ◽  
pp. 171-177 ◽  
Author(s):  
Ailiang Xie ◽  
James B. Skatrud ◽  
Dominic S. Puleo ◽  
Jerome A. Dempsey
Keyword(s):  
Mechanical Ventilation ◽  
Time Course ◽  
Pressure Support ◽  
Ventilatory Response ◽  
Relative Activity ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
The Difference ◽  
End Tidal ◽  
Different Levels

To investigate the contribution of the peripheral chemoreceptors to the susceptibility to posthyperventilation apnea, we evaluated the time course and magnitude of hypocapnia required to produce apnea at different levels of peripheral chemoreceptor activation produced by exposure to three levels of inspired Po2. We measured the apneic threshold and the apnea latency in nine normal sleeping subjects in response to augmented breaths during normoxia (room air), hypoxia (arterial O2 saturation = 78–80%), and hyperoxia (inspired O2 fraction = 50–52%). Pressure support mechanical ventilation in the assist mode was employed to introduce a single or multiple numbers of consecutive, sighlike breaths to cause apnea. The apnea latency was measured from the end inspiration of the first augmented breath to the onset of apnea. It was 12.2 ± 1.1 s during normoxia, which was similar to the lung-to-ear circulation delay of 11.7 s in these subjects. Hypoxia shortened the apnea latency (6.3 ± 0.8 s; P < 0.05), whereas hyperoxia prolonged it (71.5 ± 13.8 s; P < 0.01). The apneic threshold end-tidal Pco2 (PetCO2) was defined as the PetCO2 at the onset of apnea. During hypoxia, the apneic threshold PetCO2 was higher (38.9 ± 1.7 Torr; P < 0.01) compared with normoxia (35.8 ± 1.1; Torr); during hyperoxia, it was lower (33.0 ± 0.8 Torr; P < 0.05). Furthermore, the difference between the eupneic PetCO2 and apneic threshold PetCO2 was smaller during hypoxia (3.0 ± 1.0 Torr P < 001) and greater during hyperoxia (10.6 ± 0.8 Torr; P < 0.05) compared with normoxia (8.0 ± 0.6 Torr). Correspondingly, the hypocapnic ventilatory response to CO2 below the eupneic PetCO2 was increased by hypoxia (3.44 ± 0.63 l·min−1·Torr−1; P < 0.05) and decreased by hyperoxia (0.63 ± 0.04 l·min−1·Torr−1; P < 0.05) compared with normoxia (0.79 ± 0.05 l·min−1·Torr−1). These findings indicate that posthyperventilation apnea is initiated by the peripheral chemoreceptors and that the varying susceptibility to apnea during hypoxia vs. hyperoxia is influenced by the relative activity of these receptors.

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