Cerebral Vascular Responses to Changes in Carbon Dioxide Tension in Term and Preterm Infants with Apnea

Abstract

Carbon dioxide (CO₂) plays important roles in regulating both respiratory drive and cerebral blood flow. These effects are mediated, in part, by activity of the sympathetic nervous system. We hypothesized that the presence of acute life-threatening events or apnea in term or preterm infants, respectively, would serve as a marker for immaturity of cerebral autonomic innervation and that such infants would display a reduced cerebral vascular response to elevated pCO₂. Therefore, we evaluated the cerebral vascular response during CO₂ challenge tests in groups of term and preterm infants with primary apnea. In term infants (39 ± 2 weeks gestation) with acute life-threatening events, elevated pCO₂ was accompanied by decreasing pulsatility index and increasing mean anterior cerebral blood flow velocity. However, in preterm infants (29 ± 2 weeks’ gestation) with apnea, pulsatility index and anterior cerebral artery flow velocity did not significantly change in response to CO₂ supplementation. We conclude that preterm, but not term, infants with apnea exhibit impaired vascular responses to hypercarbia.

Anoxic Injury-Associated Cerebral Hyperperfusion Identified with Arterial Spin-Labeled MR Imaging

“…Previous studies have shown up to a 200% increase in CBF as PCO 2 increases to values similar to case 6 (PCO 2 , 54). [18][19][20][21][22][23][24][25][26] We believe that the global hyperperfusion in case 6 is a result of hypercapnia rather than anoxia.…”

Assessment of fetal cerebral arterial and venous blood flow before and after vaginal delivery or Cesarean section

“…Secondly, the rapid decrease of pCO 2 and increase of pO 2 occurring during the first minutes of life could play a role in the reduction of cerebral blood flow observed in the neonates in the first hours of life4. Increase in arterial pCO 2 causes cerebral vasodilatation18, 19. Hypoxemia is also a strong vasodilator, while an increase in oxygen tension correlates with decreased cerebral blood flow velocities20, 21.…”

Hypercapnia-Induced Cerebral Hyperperfusion: An Underrecognized Clinical Entity

“…2,7,8 Previous human studies demonstrated up to a 200% increase in CBF as pCO 2 was raised experimentally. 3,4,[8][9][10][11][12][13]35 However, a blunted hypercapnic response in elderly subjects has been shown during experimentally induced hypercapnia. 11,36,[40][41][42][43][44] The impaired vasodilatory response with aging may be related to sclerotic changes in the arterial wall or baseline oxyhemoglobin concentrations.…”

“…2,7,8 Even small increases in the partial pressure of CO 2 (pCO 2 ) on the order of 5 to 6 mm Hg are capable of generating appreciable changes on perfusion imaging. 3,4,[7][8][9][10][11][12][13] Techniques such as transcranial Doppler, nuclear medicine positronemission tomography (PET) and single-photon emission CT, angiography, phase-contrast MR imaging, and arterial spinlabeled (ASL) MR perfusion have been used to evaluate the experimental hypercapnic effect on cerebral perfusion. 4,7,[11][12][13][14][15][16][17][18][19][20][21][22][23] It is not uncommon that hospitalized patients can have marked increases in pCO 2 in excess of 30 mm Hg from baseline, both on an acute or on a chronic basis.…”