Correlations among critical closing pressure, pulsatility index and cerebrovascular resistance.
ABSTRACT 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 approximately <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.
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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: Static cerebral autoregulation (sCA) is believed to be resistant to aging and hypertensive pathology. However, methods to characterize autoregulation commonly rely on beat-by-beat mean hemodynamic measures, and do not consider within-beat pulse wave characteristics that are impacted by arterial stiffening. We examined the role of critical closing pressure (CrCP) and resistance area product (RAP) - two measures derived from the pulse wave - across supine lying, sitting, and standing postures in young adults, normotensive older adults, and older adults with controlled and uncontrolled hypertension (N = 80). Traditional measures of sCA, using both intracranial and extracranial methods, indicated similar efficiency across all groups, but within-beat measures suggested different mechanisms of regulation. At rest, RAP was increased in hypertension compared to young adults (p < 0.001), but CrCP was similar. In contrast, the drop in CrCP was the primary regulator of change in cerebrovascular resistance upon adopting an upright posture. Both CrCP and RAP demonstrated group-by-posture interaction effects (p < 0.05), with older hypertensive adults exhibiting a rise in RAP that was absent in other groups. The posture-related swings in CrCP and RAP were related to changes in both the pulsatile and mean components of arterial pressure, independent of age, cardiac output and carbon dioxide. Group-by-posture differences in pulse pressure were mediated in part by an attenuated heart rate response in older hypertensive adults (p = 0.002). Examination of pulsatile measures in young, elderly and hypertensive adults identified unique differences in how cerebral blood flow is regulated in upright posture.AJP Heart and Circulatory Physiology 05/2014; 307(2). DOI:10.1152/ajpheart.00086.2014 · 4.01 Impact Factor
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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 · 5.34 Impact Factor