Analysis of cerebral blood flow autoregulation in neonates

Panerai, Ronney B.; Kelsall, AW; Rennie, Janet M.; Evans, D.H.

doi:10.1109/10.508541

Cited by 79 publications

(67 citation statements)

References 36 publications

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“…This question warrants further study. Surprisingly, we found no association between acid-base status, oxygen or carbon dioxide levels, and cerebral pressurepassivity, given the known cerebral vasoreactive effects of blood gases, particularly carbon dioxide (10,20,21). However, this lack of association is likely related to the fact that blood gases were measured intermittently as opposed to our continuous and prolonged hemodynamic measurements.…”

Section: Discussioncontrasting

confidence: 52%

Fluctuating Pressure-Passivity Is Common in the Cerebral Circulation of Sick Premature Infants

et al. 2007

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Cerebral blood flow pressure-passivity results when pressure autoregulation is impaired, or overwhelmed, and is thought to underlie cerebrovascular injury in the premature infant. Earlier bedside observations suggested that transient periods of cerebral pressure-passivity occurred in premature infants. However, these transient events cannot be detected reliably by intermittent static measurements of pressure autoregulation. We therefore used continuous bedside recordings of mean arterial pressure (MAP; from an indwelling arterial catheter) and cerebral perfusion [using the nearinfrared spectroscopy (NIRS) Hb difference (HbD) signal) to detect cerebral pressure-passivity in the first 5 d after birth in infants with birth weight Ͻ1500 g. Because the Hb difference (HbD) signal [HbD ϭ oxyhemoglobin (HbO2) Ϫ Hb] correlates with cerebral blood flow (CBF), we used coherence between MAP and HbD to define pressure-passivity. We measured the prevalence of pressurepassivity using a pressure-passive index (PPI), defined as the percentage of 10-min epochs with significant low-frequency coherence between the MAP and HbD signals. Pressure-passivity occurred in 87 of 90 premature infants, with a mean PPI of 20.3%. Cerebral pressure-passivity was significantly associated with low gestational age and birth weight, systemic hypotension, and maternal hemodynamic factors, but not with markers of maternal infection. Future studies using consistent serial brain imaging are needed to define the relationship between PPI and cerebrovascular injury in the sick premature infant. C erebral pressure autoregulation maintains CBF relatively constant despite changes over a range of systemic blood pressures known as the autoregulatory plateau (1). Conversely, when changes in blood pressure result in concordant changes in CBF, the cerebral circulation is deemed "pressure passive." Current understanding is that cerebral pressurepassivity develops when changes in blood pressure exceed the capacity of the intact cerebral autoregulatory system or when the system is impaired by illness, injury, or vasoactive medications. Cerebral pressure-passivity is considered a risk factor for cerebrovascular injury in the sick premature infant (2-4). The current study extends our earlier work (3) using bedside NIRS to measure continuously cerebrovascular responses to spontaneous fluctuations in blood pressure. In our previous studies, we observed that cerebral pressure-passivity may wax and wane over relatively short periods in premature infants. To study the fluctuating nature of cerebral pressure-passivity and quantify its prevalence over time, we developed a continuous recording and analysis system because previously described techniques using intermittent static measurements (5-7) would be unable to measure the prevalence of fluctuating cerebral pressure-passivity over the highest risk for brain injury in premature infants. The principal aim of this technique is to make quantitative measurements of the prevalence of cerebral pressure-passivity rather...

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Section: Discussioncontrasting

confidence: 52%

Fluctuating Pressure-Passivity Is Common in the Cerebral Circulation of Sick Premature Infants

et al. 2007

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“…1). In other words, the model reflects myogenic regulatory mechanisms but not regulation of metabolic origin (26,34). To take the possibility of myogenic regulation into account, it would be necessary to extend the model represented by Fig.…”

Section: Discussionmentioning

confidence: 99%

Multiple coherence of cerebral blood flow velocity in humans

Panerai¹,

Eames²,

Potter³

2006

American Journal of Physiology-Heart and Circulatory Physiology

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The coherence function has been used in transfer function analysis of dynamic cerebral autoregulation to assess the statistical significance of spectral estimates of gain and phase frequency response. Interpretation of the coherence function and choice of confidence limits has not taken into account the intrinsic nonlinearity represented by changes in cerebrovascular resistance due to vasomotor activity. For small spontaneous changes in arterial blood pressure (ABP), the relationship between ABP and cerebral blood flow velocity (CBFV) can be linearized, showing that corresponding changes in cerebrovascular resistance should be included as a second input variable. In this case, the standard univariate coherence function needs to be replaced by the multiple coherence, which takes into account the contribution of both inputs to explain CBFV variability. With the use of two different indicators of cerebrovascular resistance index [CVRI ϭ ABP/CBFV and the resistance-area product (RAP)], multiple coherences were calculated for 42 healthy control subjects, aged 20 to 40 yr (28 Ϯ 4.6 yr, mean Ϯ SD), at rest in the supine position. CBFV was measured in both middle cerebral arteries, and ABP was recorded noninvasively by finger photoplethysmography. Results for the ABP ϩ RAP inputs show that the multiple coherence of CBFV for frequencies Ͻ0.05 Hz is significantly higher than the corresponding values obtained for univariate coherence (P Ͻ 10 Ϫ5 ). Corresponding results for the ABP ϩ CVRI inputs confirm the principle of multiple coherence but are less useful due to the interdependence between CVRI, ABP, and CBFV. The main conclusion is that values of univariate coherence between ABP and CBFV should not be used to reject spectral estimates of gain and phase, derived from small fluctuations in ABP, because the true explained power of CBFV in healthy subjects is much higher than what has been usually predicted by the univariate coherence functions. cerebral autoregulation; coherence function; transfer function analysis; multivariate modeling; transcranial Doppler ultrasound TRANSFER FUNCTION ANALYSIS (TFA) is a useful technique to study physiological systems whose properties are characterized by linear or quasi-linear dynamic relationships between two or more physiological time series (6, 36). One area that has benefited from this approach is the study of dynamic cerebral blood flow (CBF) autoregulation in humans (27,28,40). Aaslid et al. (2) have extended the classical concept of "static" autoregulation (20) by showing that a sudden change in arterial blood pressure (ABP) leads to a relatively fast recovery of CBF to its original level. This transient response of the autoregulatory mechanisms is what is now termed "dynamic" cerebral autoregulation (CA) (2). TFA of dynamic CA was initially proposed by Giller (13), who modeled CA as an input-output relationship between beat-to-beat values of ABP and CBF, as estimated by transcranial Doppler ultrasound (TCD) recordings of CBF velocity (CBFV). The many contributions that followed...

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“…However, another study of healthy adult subjects exposed to both acute and long-term elevation of environmental carbon dioxide found that static autoregulation was impaired initially, but, after 3 days of exposure, autoregulation was unaffected (24). Clinical studies of neonates, which used the static autoregulatory index, have concluded that hypercapnia impairs autoregulatory reactivity in these patients (13,18). Finally, laboratory studies of acute hypercapnia in the newborn piglet and rat and the adult cat also have reported that hypercapnia impairs autoregulation (19,21,25).…”

Section: Discussionmentioning

confidence: 99%

Influence of hypercapnic vasodilation on cerebrovascular autoregulation and pial arteriolar bed resistance in piglets

Narayanan

Leffler²,

Daley

2008

Journal of Applied Physiology

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Narayanan N, Leffler CW, Daley ML. Influence of hypercapnic vasodilation on cerebrovascular autoregulation and pial arteriolar bed resistance in piglets. J Appl Physiol 105: 152-157, 2008. First published April 24, 2008 doi:10.1152/japplphysiol.00988.2007.-Changes in both pial arteriolar resistance (PAR) and simulated arterial-arteriolar bed resistance (SimR) of a physiologically based biomechanical model of cerebrovascular pressure transmission, the dynamic relationship between arterial blood pressure and intracranial pressure, are used to test the hypothesis that hypercapnia disrupts autoregulatory reactivity. To evaluate pressure reactivity, vasopressininduced acute hypertension was administered to normocapnic and hypercapnic (N ϭ 12) piglets equipped with closed cranial windows. Pial arteriolar diameters were used to compute arteriolar resistance. Percent change of PAR (%⌬PAR) and percent change of SimR (%⌬SimR) in response to vasopressin-induced acute hypertension were computed and compared. Hypercapnia decreased cerebrovascular resistance. Indicative of active autoregulatory reactivity, vasopressin-induced hypertensive challenge resulted in an increase of both %⌬PAR and %⌬SimR for all normocapnic piglets. The hypercapnic piglets formed two statistically distinct populations. One-half of the hypercapnic piglets demonstrated a measured decrease of both %⌬PAR and %⌬SimR to pressure challenge, indicative of being pressure passive, whereas the other one-half demonstrated an increase in these percentages, indicative of active autoregulation. No other differences in measured variables were detectable between regulating and pressure-passive piglets. Changes in resistance calculated from using the model mirrored those calculated from arteriolar diameter measurements. In conclusion, vasodilation induced by hypercapnia has the potential to disrupt autoregulatory reactivity. Our physiologically based biomechanical model of cerebrovascular pressure transmission accurately estimates the changes in arteriolar resistance during conditions of active and passive cerebrovascular reactivity. cerebrovascular pressure transmission; cerebrovascular resistance HYPOVENTILATION WITH SUPPLEMENTAL oxygen ("permissive hypercapnia") is used as a therapeutic intensive care management technique to reduce ventilator-induced lung injury (4, 14, 16). Hypercapnia causes cerebrovascular vasodilation. However, the effect of hypercapnia on cerebrovascular autoregulation is poorly understood. One recent neonatal critical care study suggests that use of levels of the partial pressure of arterial blood carbon dioxide (PCO 2 ) above 45 Torr may abolish autoregulatory reactivity (13). Because an awareness of whether pressure regulation is intact during therapeutic hypercapnia is critical to patient management, this laboratory study was designed to examine the influence of hypercapnia on autoregulatory reactivity.A second aim of this study was to examine the validity of a two-step modeling procedure of cerebrovascular pressure transmission to estima...

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Analysis of cerebral blood flow autoregulation in neonates

Cited by 79 publications

References 36 publications

Fluctuating Pressure-Passivity Is Common in the Cerebral Circulation of Sick Premature Infants

Fluctuating Pressure-Passivity Is Common in the Cerebral Circulation of Sick Premature Infants

Multiple coherence of cerebral blood flow velocity in humans

Influence of hypercapnic vasodilation on cerebrovascular autoregulation and pial arteriolar bed resistance in piglets

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