Estimation of Critical Closing Pressure in the Cerebral Circulation of Newborns

Panerai, R.B.; Kelsall, AW; Rennie, Janet M.; Evans, David H.

doi:10.1055/s-2007-979748

Cited by 39 publications

(40 citation statements)

References 5 publications

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“…Limited data sets report CrCPs in term and preterm newborns ranging from 24 to 33 mm Hg, which is similar to reported values in mature subjects (5,6). Low ABP in premature infants results in a closing margin that is strikingly low (Figure 1).…”

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confidence: 78%

“…Low ABP in premature infants results in a closing margin that is strikingly low (Figure 1). Premature infants are commonly treated for low values of blood pressure based on mean ABP thresholds related to their gestational age (GA) (7)(8)(9), and these thresholds are within the range of published CrCP values (5,6). Moreover, during postnatal transition, a period of time often characterized by shock, premature infants can have CBF limited to the systolic phase of the cardiac cycle (10).…”

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confidence: 99%

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Ontogeny of cerebrovascular critical closing pressure

Rhee

Fraser²,

Kibler

et al. 2015

Pediatr Res

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Background: Premature infants are at risk of vascular neurologic insults. Hypotension and hypertension are considered injurious, but neither condition is defined with consensus. Cerebrovascular critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which cerebral blood flow (CBF) ceases. CrCP may serve to define subject-specific low or high ABP. Our objective was to determine the ontogeny of CrCP. Methods: Premature infants (n = 179) with gestational age (GA) from 23-31 wk had recordings of ABP and middle cerebral artery flow velocity twice daily for 3 d and then daily for the duration of the first week of life. All infants received mechanical ventilation. CrCP was calculated using an impedance-model derivation with Doppler-based estimations of cerebrovascular resistance and compliance. The association between GA and CrCP was determined in a multivariate analysis. results: The median (interquartile range) CrCP for the cohort was 22 mm Hg (19-25 mm Hg). CrCP increased significantly with GA (r = 0.6; slope = 1.4 mm Hg/wk gestation), an association that persisted with multivariate analysis (P < 0.0001). conclusion: CrCP increased significantly from 23 to 31 wk gestation. The low CrCP observed in very premature infants may explain their ability to tolerate low ABP without global cerebral infarct or hemorrhage. c erebrovascular critical closing pressure (CrCP) is the arterial blood pressure (ABP) at which blood flow to the brain ceases due to vascular collapse. Also referred to as collapsing pressure, CrCP can be easily and noninvasively monitored at the bedside using Doppler ultrasound and ABP measurements (1). CrCP is posited to be the sum of vascular wall tension and intracranial pressure (2). CrCP can be conceptualized as a factor for the normalization of ABP to an "effective cerebral perfusion pressure" or "closing margin" (3,4). The "effective cerebral perfusion" or "closing margin" (ABP-CrCP) can be determined for any phase of the cardiac cycle by subtracting the CrCP from systolic, mean, or diastolic ABP.Limited data sets report CrCPs in term and preterm newborns ranging from 24 to 33 mm Hg, which is similar to reported values in mature subjects (5,6). Low ABP in premature infants results in a closing margin that is strikingly low (Figure 1). Premature infants are commonly treated for low values of blood pressure based on mean ABP thresholds related to their gestational age (GA) (7-9), and these thresholds are within the range of published CrCP values (5,6). Moreover, during postnatal transition, a period of time often characterized by shock, premature infants can have CBF limited to the systolic phase of the cardiac cycle (10).Disparity in the definition of hypotension and treatment thresholds for low ABP are likely attributable to a lack of outcome data in premature infants demonstrating a benefit for treating low ABP (11). We propose that an important confounding factor may be the low closing margin relative to the range of CrCP in this population. For example, a difference of 10 mm Hg Cr...

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confidence: 78%

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confidence: 99%

Ontogeny of cerebrovascular critical closing pressure

Rhee

Fraser²,

Kibler

et al. 2015

Pediatr Res

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“…28 CrCP is greater than 0 mm Hg. [37][38][39] In the mature brain, CrCP has been reported to be nearly 30 mmHg, which is above the mean ABP of many infants in this cohort. 36 Thus, inter-subject variability of CrCP could have a profound confounding effect on the assumption that mean ABP is a surrogate for cerebral perfusion pressure in premature infants.…”

Section: Critical Closing Pressurementioning

confidence: 65%

The Ontogeny of Cerebrovascular Pressure Autoregulation in Premature Infants

Rhee

Fraser²,

Kibler

et al. 2016

Acta Neurochirurgica Supplement

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Objective-To quantify cerebrovascular autoregulation as a function of gestational age (GA) and across the phases of the cardiac cycle.Study design-The present study is a hypothesis-generating re-analysis of previously published data. Premature infants (n=179), with a GA range of 23 to 33 weeks were monitored with umbilical artery catheters and transcranial Doppler insonation of the middle cerebral artery for 1-hour sessions over the first week of life. Autoregulation was quantified by three methods, as a moving correlation coefficient between: 1) systolic arterial blood pressure (ABP) and systolic cerebral blood flow (CBF) velocity (Sx); 2) mean ABP and mean CBF velocity (Mx); and 3) diastolic ABP and diastolic CBF velocity (Dx). Comparisons of individual and cohort cerebrovascular pressure autoregulation were made across GA for each aspect of the cardiac cycle.Results-Systolic, mean and diastolic ABP increased with GA (r=0.3, 0.4, and 0.4; p<0.0001). Systolic CBF velocity was pressure-passive in infants with the lowest GA, and Sx decreased with advancing GA (r=−0.3; p<0.001), indicating increased capacity for cerebral autoregulation during systole during development. By contrast, Dx was elevated, indicating dysautoregulation, in all subjects and showed minimal change with advancing GA (r=−0.06; p=0.05). Multivariate analysis confirmed that both GA (p<0.001) and "effective cerebral perfusion pressure" (ABP minus critical closing pressure; p<0.01) were associated with Sx. HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptConclusion-Premature infants have low and usually pressure-passive diastolic CBF velocity. By contrast, the regulation of systolic CBF velocity by pressure autoregulation developed in this cohort between 23 and 33 weeks GA. Elevated effective cerebral perfusion pressure derived from the critical closing pressure was associated with dysautoregulation.

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“…The slope can be defined as the inverse cerebrovascular resistance or the inverse of the resistance area product. 11 Similar to the coronary circulation, 19 flow in the cerebral vascular bed seems to be regulated by 2 factors: CCP (back pressure) and slope ("resistance proper"). We should, however, caution that in a normal physiological state the relative contribution of each factor could be different than for the present data.…”

Section: Discussionmentioning

confidence: 99%

Dynamic Pressure–Flow Velocity Relationships in the Human Cerebral Circulation

Aaslid

Lash

Bardy

et al. 2003

Stroke

111

133

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Background and Purpose-The pressure-flow velocity relationship in the cerebral circulation is characterized by the critical closing pressure (CCP), which is the pressure at which flow ceases, and the linear slope of a plot between pressure and flow velocity. It has been suggested, but not validated, that CCP can be determined from arterial blood pressure (ABP) and transcranial Doppler (TCD) recordings during the cardiac cycle. We studied a group of patients in whom ventricular fibrillation (VF) was induced. The time interval before defibrillation enabled calculation of CCP from data in which flow approached zero. These estimates were compared with values calculated before and after fibrillation and during regular heartbeats. Methods-TCD velocities and ABP in the radial artery were recorded before, during, and after 28 episodes of VF in 13 patients. CCPs were calculated by 3 different methods: (1) linear extrapolation from data during VF (gold standard); (2) linear extrapolation from normal heartbeat data; and (3) first harmonic Fourier filtering of normal heartbeat data. Results-The CCP during VF calculated from long diastoles was 32.9Ϯ11 mm Hg (meanϮSD). The regular heartbeat estimate was 6.0Ϯ4.3 mm Hg lower (PϽ0.05). The CCP estimate with the use of a Fourier filter was 1.4Ϯ3.9 mm Hg (PϭNS) lower than during VF. During hyperemia after defibrillation, the CCP decreased by 13.3 mm Hg, while velocity increased by 63%. The decrease in CCP could explain half of the increase in flow velocity during hyperemia. Conclusions-CCP can be accurately estimated from regular heartbeat data and is an important factor in regulation of the cerebral circulation. Key Words: cerebrovascular circulation Ⅲ ultrasonography, Doppler, transcranial Ⅲ vasoreactivity T he classic concept defining cerebrovascular tone is cerebral vascular resistance. This concept was developed from cerebral blood flow (CBF) determinations with the use of indicator methods such as nitrous oxide or 133 Xe. Basically this concept assumes that perfusion pressure and flow are linearly and proportionally related. It follows that flow stops only when the perfusion pressure is zero. However, when dynamic measurement techniques are used, such as electromagnetic flowmetry or ultrasound Doppler, the limitations of this concept become manifest. 1,2 Dynamically, flow may stop at pressure levels significantly higher than zero. The arterial blood pressure (ABP) level at which flow stops is defined as the critical closing pressure (CCP) 1-3 or, in cardiac literature, the zero-flow pressure (P fϭ0 ). 4 Above the CCP, an approximately linear slope, sometimes referred to as the inverse flow resistance, defines the relation between pressure and flow, when these variables are plotted as an x-y function 1,2 ( Figure 1). It follows that flow is linearly (but not proportionally) related to pressure and that it can be regulated by changes in both CCP (the x intercept) and slope. The pressure-flow relation is mainly a function of the peripheral resistance cerebral vascular bed. It...

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Estimation of Critical Closing Pressure in the Cerebral Circulation of Newborns

Cited by 39 publications

References 5 publications

Ontogeny of cerebrovascular critical closing pressure

Ontogeny of cerebrovascular critical closing pressure

The Ontogeny of Cerebrovascular Pressure Autoregulation in Premature Infants

Dynamic Pressure–Flow Velocity Relationships in the Human Cerebral Circulation

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