Does Maturity Affect Cephalic Perfusion and T/QRS Ratio during Prolonged Umbilical Cord Occlusion in Fetal Sheep?

Guido Wassink,Eleanor R Gunn,Laura Bennet,Alistair J Gunn,Paul P Drury,Robert Galinsky

doi:10.1155/2014/314159

Guido Wassink, Eleanor R Gunn + Show 4 more

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https://doi.org/10.1155/2014/314159

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Abstract

T/QRS ratio monitoring is used to help identify fetal asphyxia. However, immature animals have greater capacity to maintain blood pressure during severe asphyxia, raising the possibility that they may show an attenuated T/QRS increase during asphyxia. Chronically instrumented fetal sheep at 0.6 of gestation (0.6 GA; n = 12), 0.7 GA (n = 12), and 0.8 GA (n = 8) underwent complete umbilical cord occlusion for 30 min, 25 min, or 15 min, respectively. Cord occlusion was associated with progressive metabolic acidosis and initial hypertension followed by severe hypotension, with a more rapid fall in mean arterial blood pressure (MAP) and carotid blood flow (CaBF) with advancing gestation. T/QRS ratio rose after occlusion more rapidly at 0.8 GA than in immature fetuses, to a similar final peak at all ages, followed by a progressive fall that was slower at 0.8 GA than in the immature fetuses. The increase in T/QRS ratio correlated with initial hypertension at 0.8 GA (P < 0.05, R 2 = 0.38), and conversely, its fall correlated closely with falling MAP in all gestational groups (P < 0.01, R 2 = 0.67). In conclusion, elevation of the T/QRS ratio is an index of onset of severe asphyxia in the last third of gestation, but not of fetal compromise.

Highlights

Brain injury from perinatal asphyxia remains a significant cause of mortality and long-term morbidity in newborn infants [1, 2]
Previous evidence suggests that cerebrovascular autoregulation is relatively immature in fetal sheep at 0.6 and 0.7 of gestational age (GA) [7, 8], with cerebral blood flow falling in parallel with development of hypotension [9]
Baseline T/QRS ratio and fetal heart rate (FHR) was significantly lower at 0.8 GA, while mean arterial blood pressure (MAP) and carotid blood flow (CaBF) increased significantly with advancing gestation

Summary

Introduction

Brain injury from perinatal asphyxia remains a significant cause of mortality and long-term morbidity in newborn infants [1, 2]. The development of hypoxicischemic neural injury is broadly associated with the degree and duration of exposure to systemic hypotension and cerebral hypoperfusion [3,4,5,6]. Previous evidence suggests that cerebrovascular autoregulation is relatively immature in fetal sheep at 0.6 and 0.7 of gestational age (GA) [7, 8], with cerebral blood flow falling in parallel with development of hypotension [9]. Isolated hypercarbia can impair regional cerebral autoregulation in healthy, normotensive newborn piglets [12]. We have previously shown that the immature fetus at 0.6 and 0.7 GA can maintain its arterial blood pressure for much longer during prolonged asphyxia than at 0.8 GA [13], suggesting later impairment of cerebral perfusion in immature fetuses

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