PEDIATRICS Vol. 115 No. 4 April 2005, pp. 1115-1116 (doi:10.1542/peds.2005-0148)
Preterm Circulatory Support Is More Complex Than Just Blood Pressure: In Reply
Michael J. Munro, MBChB, MRCP, MRCPCHAdrian M. Walker, BSc, MSc, PhD
Charles P. Barfield, MBBS, FRACP
Ritchie Centre for Baby Health Research
Monash Institute of Reproduction and Development
Monash University and Newborn Services
Monash Medical Centre
Victoria 3168, Australia
Prompted by our study,1 Evans et al raise several issues, the central one being the usefulness of maintaining arterial blood pressure as a means of ensuring adequate cerebral blood flow (CBF).
First, they "disagree that this can be ensured solely on the basis of a mean blood pressure (MBP) of >30 mm Hg." In response, we would wholeheartedly agree, because the complexity of CBF regulation and the range of clinical conditions influencing the circulation of sick preterm infants would make such an approach clinically simplistic. Recognizing this, we have been at pains to avoid leading readers to the view that there is a single point (30 mm Hg) above which CBF will be normal and below which there will be hypoperfusion; the uncertainty of the estimate along with the many possible confounding factors does not allow such precision. In clarification, we reiterate our view that the data provide support for the widespread use of 30 mm Hg as a benchmark for clinical decision, adding to the information that lower pressure increases the risk for cerebral hypoperfusion and brain injury. We also cautioned that raising MBP in hypotensive infants with a pressure-passive cerebral circulation may raise CBF above normal levels.
Evans et al also propose that additional cardiovascular measurements are needed to define the cause of low CBF and hypotension; we agree. They suggest systemic blood flow (SBF) as the additional measurement, one that they have promoted for assessment of cerebral perfusion in NICUs.2 SBF could aid in understanding the basis of hypotension to the extent that it might reflect cardiac output, because arterial pressure is the product of cardiac output and systemic vascular resistance. However, SBF is not likely to represent cerebral perfusion reliably, because it includes a large component of venous return from noncerebral vascular beds, the physiologic responses of which are opposite to those of the brain. In compensating for hypotension, nonvital systemic vascular beds such as skin vasoconstrict (to restore arterial pressure) while the brain vasodilates (to preserve CBF). Because systemic vasoconstriction (and hence lower SBF) is a fundamental physiologic response for restoring arterial blood pressure, it is not surprising that Evans et al found "many infants with a MBP of <30 mm Hg have normal SBF" and "infants with normal MBP who have low SBF."
Evans et al claim that "Other workers[3] using near-infrared spectroscopy have found the same phenomenon" (low SBF with normal arterial pressure). The statement is inaccurate because Tyszczuk et al3 measured CBF, not SBF. Nevertheless, as we noted, Tyszczuk et al found CBF to be independent of MBP, in contrast to our findings. An explanation for these seemingly disparate results may be found in the different outcomes of the study groups. It is notable that all infants in our study were neurologically normal, whereas significant numbers (8 of 30) of those in the Tyszczuk study died or were brain injured.
We agree that autoregulation being lost "seems to be a problem in some infants," and understanding the mechanisms of this process is clearly an important issue. Although this problem of pressure-passive cerebral circulation persists, maintenance of MBP remains a vital clinical objective. Furthermore, new methods of clinical monitoring need to focus on the primary protection against brain injury, namely ensuring adequate perfusion to meet the oxygen requirements of the brain. Here near-infrared spectroscopy offers promise for bedside assessments of cerebral autoregulation,4 intravascular oxygenation,5 tissue oxygenation,6 and oxygen utilization.7
That ischemic brain injury is still a major problem in NICUs is unquestioned. The inference that persisting rates of injury reflect a failure of a "30 mm Hg" policy is not. Although many units may attempt to maintain a MAP of >30 mm Hg, how many are actually successful? There are no reliable data available to inform NICUs on this or on the associated neurologic outcomes. Without new data, the suggestion from Miall-Allen et al8 that brain injury is more likely in infants with a MAP consistently <30 mm Hg remains a useful clinical benchmark.
REFERENCES
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6. Buchvald FF, Kesje K, Greisen G. Measurement of cerebral oxyhaemoglobin saturation and jugular blood flow in term healthy newborn infants by near-infrared spectroscopy and jugular venous occlusion. Biol Neonate. 1999;75 :97 –103[CrossRef][Web of Science][Medline]
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PEDIATRICS (ISSN 1098-4275). ©2005 by the American Academy of Pediatrics
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- Preterm Circulatory Support Is More Complex Than Just Blood Pressure
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