CBF Reactivity in Hypotensive and Normotensive Preterm Infants

Abstract

Perinatal distress in the preterm neonate, and the consequent loss of cerebrovascular autoregulation, has been implicated in the pathogenesis of neonatal cerebral lesions. A component of this distress is thought to be hypotension. We examined the autoregulatory capacity of hypotensive and normotensive infants using the 133 Xe technique to measure cerebral blood flow. Global CBF was measured during only normotension in 5 infants, and during both hypotension and normotension in 11 infants. All the infants were ventilated and blood pressure was measured using an intra-arterial catheter. Fourteen CBF measurements were made on the normotensive infants. Forty-seven CBF measurements were made on the hypotensive infants, 34 measurements during hypotension and 13 during normotension. The global CBF of the normotensive and hypotensive infants were 13.3 and 13.6 mL/ 100 g/min, respectively. The mean arterial blood pressure (MABP)-CBF reactivity (95% CI) of the normotensive and hypotensive infants were 1.9% (Ϫ0.8% to 4.7%)/mm Hg and 1.9% (0.8% to 3.0%)/mm Hg, respectively. The CO 2 -CBF reactivity (95%CI) of the normotensive and hypotensive infants was 11.1% (6.8% to 15.5%)/KPa ⌬PaCO 2 and 4.1% (Ϫ5.0% to 14.1%)/KPa ⌬PaCO 2 . The implications of these calculated CBF reactivities is that normotensive infants may have intact autoregulation but with a diminished response to fluctuations in PaCO 2 . Hypotension in the sick preterm infant has been implicated as one causative factor in the pathogenesis of a number of serious conditions including intraventricular hemorrhage (IVH) (1), periventricular leukomalacia (PVL) (2), necrotizing enterocolitis (3), and developmental delay in preterm infants (4).It is thought that perinatal asphyxia combined with hypotension leads to a loss of cerebrovascular autoregulation, which may lead to a pressure passive cerebral circulation (5). In this state, abrupt elevations in systemic blood pressure may be transmitted to the fragile vessels of the germinal matrix, possibly resulting in intraventricular hemorrhage. Historically, systemic hypotension was thought to lead to under perfusion of watershed areas, which then underwent infarction and cystic necrosis, resulting in PVL (6). Thus, absent autoregulation may be central to many causes of perinatal CNS pathology.The work of Tyszczuk et al. among others, has led to the re-evaluation of the absent autoregulation hypothesis (7). They found no significant difference between the cerebral blood flow (CBF) of normotensive infants and that of hypotensive infants. Furthermore, a number of studies have found no association between hypotension and PVL (2, 8, 9). More recently, it was found that 53% of ventilated preterm infants had evidence of impaired autoregulation (10) and Boylan et al. have identified abnormalities in the autoregulatory capacity of preterm infants (11). Only in the work of Tyszczuk was the influence of hypotension analyzed in the etiology of impaired autoregulation.Changes in arterial carbon dioxide are a major mediator of CBF variatio...

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Measuring cerebrovascular autoregulation in preterm infants using near-infrared spectroscopy: an overview of the literature

“…Experience was initially gained by data from animal models like preterm lambs [11,12]. Early techniques that were used to study static autoregulation in preterm infants are the xenon clearance ( 133 Xe) technique or the oxyhemoglobin (HbO 2 ) method by NIRS [13][14][15].…”

Correspondence

“…Their letter raises a number of points primarily concerning the methodology of our study (1). The first question they raise is how CO 2 reactivity was examined.…”

“…The first question they raise is how CO 2 reactivity was examined. The multiple-regression model used paired values of blood pressure and PaCO 2 measured contemporaneously with CBF measurements (1). In this way, we hoped to determine the individual effects of these predictor variables on our outcome variable (CBF).…”