Michael J Munro1, Adrian M Walker, Charles P Barfield. 1. Ritchie Centre for Baby Health Research, Monash Institute of Reproduction and Development, Monash University and Newborn Services, Monash Medical Centre, Victoria, Australia.
Abstract
OBJECTIVES: Whether extremely low birth weight (ELBW) infants are at risk of cerebral hypoperfusion is uncertain because key issues concerning their cerebral blood flow (CBF) and mean arterial pressure (MAP) are unresolved: (1) whether CBF is pressure-passive or autoregulated; (2) the normal level of MAP; and (3) whether inotropic drugs used to increase MAP might inadvertently impair CBF. We addressed these issues in ELBW infants undergoing intensive care. METHODS: CBF (measured by near-infrared spectroscopy) and MAP were measured in 17 infants aged 1.5 to 40.5 hours. RESULTS: Five infants remained normotensive (MAP 37 +/- 2 mm Hg, [mean +/- SEM]); twelve became hypotensive (MAP 25 +/- 1 mm Hg) and were treated with dopamine (10-30 mug x kg(-1) per min). CBF of hypotensive infants (14 +/- 1 mL x 100 g(-1) per min) was lower than the CBF of normotensive infants (19 +/- mL x 100 g(-1) per min). After commencement of dopamine in hypotensive infants, MAP increased (29 +/- 1 mm Hg) and CBF also increased (18 +/- 1 mL x 100g(-1) per min). CBF was correlated with MAP in hypotensive infants before (R = 0.62) and during (R = 0.67) dopamine, but not in normotensive infants. A breakpoint was identified in the CBF versus MAP autoregulation curve of untreated infants at MAP = 29 mm Hg; no breakpoint was evident in dopamine-treated infants. CONCLUSIONS: In ELBW infants (1) cerebral autoregulation is functional in normotensive but not hypotensive infants; (2) a breakpoint exists at approximately 30 mm Hg in the CBF-MAP autoregulation curve; and (3) dopamine improves both MAP and CBF.
OBJECTIVES: Whether extremely low birth weight (ELBW) infants are at risk of cerebral hypoperfusion is uncertain because key issues concerning their cerebral blood flow (CBF) and mean arterial pressure (MAP) are unresolved: (1) whether CBF is pressure-passive or autoregulated; (2) the normal level of MAP; and (3) whether inotropic drugs used to increase MAP might inadvertently impair CBF. We addressed these issues in ELBW infants undergoing intensive care. METHODS: CBF (measured by near-infrared spectroscopy) and MAP were measured in 17 infants aged 1.5 to 40.5 hours. RESULTS: Five infants remained normotensive (MAP 37 +/- 2 mm Hg, [mean +/- SEM]); twelve became hypotensive (MAP 25 +/- 1 mm Hg) and were treated with dopamine (10-30 mug x kg(-1) per min). CBF of hypotensiveinfants (14 +/- 1 mL x 100 g(-1) per min) was lower than the CBF of normotensive infants (19 +/- mL x 100 g(-1) per min). After commencement of dopamine in hypotensiveinfants, MAP increased (29 +/- 1 mm Hg) and CBF also increased (18 +/- 1 mL x 100g(-1) per min). CBF was correlated with MAP in hypotensiveinfants before (R = 0.62) and during (R = 0.67) dopamine, but not in normotensive infants. A breakpoint was identified in the CBF versus MAP autoregulation curve of untreated infants at MAP = 29 mm Hg; no breakpoint was evident in dopamine-treated infants. CONCLUSIONS: In ELBW infants (1) cerebral autoregulation is functional in normotensive but not hypotensiveinfants; (2) a breakpoint exists at approximately 30 mm Hg in the CBF-MAP autoregulation curve; and (3) dopamine improves both MAP and CBF.
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