Effect of CO2 and 100% O2 on cerebral blood flow in preterm infants

Abstract

To determine 1) the effect of arterial CO2 change on the neonatal cerebral circulation and 2) whether 100% O2 would produce significant decrease in cerebral blood flow (CBF), we studied 24 preterm infants to explain the late (5 min) hyperventilation observed in them during hyperoxia. Of these, 12 were studied before and during inhalation of 2-3% CO2 and 12 before and during the inhalation of 100% O2. We measured CBF by a modification of the venous occlusion plethysmography technique and found that CBF increased 7.8% per Torr alveolar carbon dioxide pressure change and that it decreased 15% with 100% O2. These findings suggest that 1) CO2 is an important regulator of CBF in the perterm infant, 2) CBF-CO2 sensitivity in these infants may be greater than in adult subjects, 3) 100% O2 reduced CBF significantly, and 4) a decrease in CBF during administration of 100% O2 may be at least partially responsible for the increase in ventilation with hyperoxia.

Tracheal suctioning is associated with prolonged disturbances of cerebral hemodynamics in very low birth weight infants

“…25 Others have also observed in premature infants that PaCO 2 is an important regulator of CBF. [26][27][28] Acute changes in MABP may also affect CBF, especially if premature infants have impaired cerebral autoregulation. 29,33 In contrast to Perlman et al, 1 in our infant sample, MABP did not significantly influence mean CBFv, suggesting that cerebral autoregulation was probably intact in a majority of our sample group.…”

Cerebral Fractional Oxygen Extraction is Inversely Correlated with Oxygen Delivery in the Sick, Newborn, Preterm Infant

“…In addition, use of high concentrations of oxygen at delivery may increase cerebrovascular resistance, which may remain high for several hours (Leahy et al, 1980;Lundstrom et al, 1995;Rahilly, 1980a). There were no significant changes in PaCO 2 or PaO 2 in the course of this study so it is unlikely that the increase in CBF shown was the result of cerebral vasodilatation caused by a change in blood gases over the first 3 days.…”

“…As discussed above, this is probably a result of low CBF, possibly because of low LVO, possibly in combination with inappropriate cerebral vasoconstriction for other reasons such as hypocarbia or hyperoxia. The latter is known to reflect resuscitation practices (Leahy et al, 1980;Lundstrom et al, 1995;Rahilly, 1980a), but abnormal blood gases relating to lung disease and ventilatory practices may also play a role. If this interpretation is true then at least this infant, and possibly others, may be in a deliverydependent state of cerebral oxygen consumption on day 1.…”

Response of Cerebral Blood Volume to Changes in Arterial Carbon Dioxide Tension in Preterm and Term Infants

“…Quantitative data on the response of cerebral blood flow to changes in Pacer were initially obtained by Kety and Schmidt (2) using the nitrous oxide clearance method. Since then, numerous studies in adults (3,4), newborn infants (5,6), and experimental animals (7)(8)(9)(10) have confirmed the positive relationship between cerebral blood flow and Pacoz in normal individuals. Information on the response of CBV to changing Pacoz is more limited ( I 1-14), and only one report has been published involving newborn infants (1 5).…”