Correlations among critical closing pressure, pulsatility index and cerebrovascular resistance

Section of Neurology, Department of Internal Medicine, Veterans General Hospital-Taichung, Taichung Taiwan and the Institute of Clinical Medicine, National Yang-Ming University, Taipei 11217, Taiwan.
Ultrasound in Medicine & Biology (Impact Factor: 2.21). 11/2004; 30(10):1329-35. DOI: 10.1016/j.ultrasmedbio.2004.08.006
Source: PubMed


We attempted to explore the relationships among critical closing pressure (CrCP), resistance-area product (RAP) and traditional resistance indices of cerebral hemodynamics. Twenty healthy volunteers were studied. Blood pressure was obtained with servo-controlled plethysmography. Cerebral blood flow velocity (CBFV) was monitored by transcranial Doppler. Hemodynamic changes were induced by hyperventilation and by 5% CO 2 inhalation. Beat-to-beat CrCP and RAP values were extracted by linear regression analysis of instantaneous arterial blood pressure (ABP) and CBFV tracings. Gosling's pulsatility index (PI) and cerebrovascular resistance (CVR) were calculated. RAP correlated well with CVR at rest and during provocative tests (p = 0.006 ∼ <0.001). There was no correlation among CrCP, CVR and PI. The changes in CVR correlated with those in RAP (p = 0.008 for the 5% CO 2 test and p = 0.014 for the hyperventilation test). The changes in PI and CrCP showed significant correlation (p = 0.004 for the 5% CO 2 test and p = 0.003 for the hyperventilation test). RAP reliably reflected cerebrovascular resistance. The changes in CrCP were valuable in assessing cerebrovascular regulation. Estimating changes in CrCP and RAP provided better understanding of the nature of cerebrovascular regulation. ([email protected]
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    • "This study focuses on correlating changes in CBFV and RAP after cuff inflation/deflation with those in CBFV latency extracted by different methods. In the future study, several existing cerebral vascular indices, including cerebral CCP, RAP, CBFV pulsatility index (PI), should be studied more thoroughly, together with CBFV latency because there exists a large body of literature pertaining to their role as cerebrovascular indices (Czosnyka et al, 1999; Hsu et al, 2004; Michel et al, 1997; Panerai et al, 1993, 1999; Panerai, 2003), which would provide additional corroboration needed for further illustrating whether CBFV (or ICP) latency may be useful for characterizing pathologic cerebral vascular changes. "
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    ABSTRACT: Changes in cerebral blood flow velocity (CBFV) pulse latency reflect pathophysiological changes of the cerebral vasculature based on the theory of pulse wave propagation. Timing CBFV pulse onset relative to electrocardiogram QRS is practical. However, it introduces confounding factors of extracranial origins for characterizing the cerebral vasculature. This study introduces an approach to reducing confounding influences on CBFV latency. This correction approach is based on modeling the relationship between CBFV latency and systemic arterial blood pressure (ABP) pulse latency. It is tested using an existing data set of CBFV and ABP from 14 normal subjects undergoing pressure cuff tests under both normoxic and acute hypoxic states. The results show that the proposed CBFV latency correction approach produces a more accurate measure of cerebral vascular changes, with an improved positive correlation between beat-to-beat CBFV and the CBFV latency time series, for example, correlation coefficient increased from 0.643 to 0.836 for group-averaged cuff deflation traces at normoxia. In conclusion, this study suggests that subtraction of systemic ABP latency improves CBFV latency measurements, which in turn improve the characterization of cerebral vascular changes.
    Journal of cerebral blood flow and metabolism: official journal of the International Society of Cerebral Blood Flow and Metabolism 01/2009; 29(4):688-97. DOI:10.1038/jcbfm.2008.160 · 5.41 Impact Factor
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    ABSTRACT: Estimating changes in critical closing pressure (CrCP) and resistance area product (RAP) provided better understanding of the nature of cerebrovascular regulation (arterial stiffening or narrowing). The critical closing pressure of the cerebral circulation indicates the value of the arterial blood pressure (ABP) at which cerebral blood flow (CBF) approaches zero. Measurements in animals and in humans have shown that the CrCP is significantly greater than zero. Studies of the cerebral circulation need to take CrCP and RAP into account, to obtain more accurate estimates of cerebrovascular resistance changes, and to reflect the correct dynamic relationship between instantaneous ABP and CBF. This analysis was performed on 48 healthy subjects and 11 hypertensive subjects. Due to the non-linear shape of the complete ABP-CBF curve, most methods proposed for estimation of CrCP and RAP can only represent the linear range of the pressure-flow (or velocity) relationship.
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    ABSTRACT: The passive relationship between arterial blood pressure (ABP) and cerebral blood flow velocity (CBFV) has been expressed by a single parameter [cerebrovascular resistance (CVR)] or, alternatively, by a two-parameter model, comprising a resistance element [resistance-area product (RAP)] and a critical closing pressure (CrCP). We tested the hypothesis that the RAP+CrCP model can provide a more consistent interpretation to CBFV responses induced by mental activation tasks than the CVR model. Continuous recordings of CBFV [bilateral, middle cerebral artery (MCA)], ABP, ECG, and end-tidal CO(2) (EtCO(2)) were performed in 13 right-handed healthy subjects (aged 21-43 yr), in the seated position, at rest and during 10 repeated presentations of a word generation and a constructional puzzle paradigm that are known to induce differential cortical activation. Due to its small relative change, the CBFV response can be broken down into standardized subcomponents describing the relative contributions of ABP, CVR, RAP, and CrCP. At rest and during activation, the RAP+CrCP model suggested that RAP might reflect myogenic activity in response to the ABP transient, whereas CrCP was more indicative of metabolic control. These different influences were not reflected by the CVR model, which indicated a predominantly metabolic response. Repeated-measures multi-way ANOVA showed that CrCP (P = 0.025), RAP (P = 0.046), and CVR (P = 0.002) changed significantly during activation. CrCP also had a significant effect of paradigm (P = 0.045) but not hemispheric dominance. Both RAP (P = 0.039) and CVR (P = 0.0008) had significant effects of hemispheric dominance but were not sensitive to the different paradigms. Subcomponent analysis can help with the interpretation of CBFV responses to mental activation, which were found to be dependent on the underlying model of the passive ABP-CBFV relationship.
    Journal of Applied Physiology 01/2006; 99(6):2352-62. DOI:10.1152/japplphysiol.00631.2005 · 3.06 Impact Factor
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