Time constant of the cerebral arterial bed.
ABSTRACT We have defined a novel cerebral hemodynamic index, a time constant of the cerebral arterial bed (τ), the product of arterial compliance (C(a)) and cerebrovascular resistance (CVR). C(a) and CVR were calculated based on the relationship between pulsatile arterial blood pressure (ABP) and transcranial Doppler cerebral blood flow velocity. This new parameter theoretically estimates how fast the cerebral arterial bed is filled by blood volume after a sudden change in ABP during one cardiac cycle. We have explored this concept in 11 volunteers and in 25 patients with severe stenosis of the internal carotid artery (ICA). An additional group of 15 subjects with non-vascular dementia was studied to assess potential age dependency of τ. The τ was shorter (p = 0.011) in ICA stenosis, both unilateral (τ = 0.18 ± 0.04 s) and bilateral (τ = 0.16 ± 0.03 s), than in controls (τ = 0.22 ± 0.0 s). The τ correlated with the degree of stenosis (R = -0.62, p = 0.001). In controls, τ was independent of age. Further study during cerebrovascular reactivity tests is needed to establish the usefulness of τ for quantitative estimation of haemodynamics in cerebrovascular disease.
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ABSTRACT: Critical closing pressure (CCP) is the arterial blood pressure (ABP) at which brain vessels collapse and cerebral blood flow (CBF) ceases. Using the concept of impedance to CBF, CCP can be expressed with brain-monitoring parameters: cerebral perfusion pressure (CPP), ABP, blood flow velocity (FV), and heart rate. The novel multiparameter method (CCPm) was compared with traditional transcranial Doppler (TCD) calculations of CCP (CCP1). Digital recordings of ABP, intracranial pressure (ICP), and TCD-based FV from previously published studies of 29 New Zealand White rabbits were reanalyzed. Overall, CCP1 and CCPm showed correlation across wide ranges of ABP, ICP, and PaCO2 (R=0.93, P<0.001). Three physiological perturbations were studied: increase in ICP (n=29) causing both CCP1 and CCPm to increase (P<0.001 for both); reduction of ABP (n=10) resulting in decrease of CCP1 (P=0.006) and CCPm (P=0.002); and controlled increase of PaCO2 (n=8) to hypercapnic levels, which decreased CCP1 and CCPm, albeit insignificantly (P=0.123 and P=0.306 respectively), caused by a spontaneous significant increase in ABP (P=0.025). Multiparameter mathematical model of critical closing pressure explains the relationship of CCP on brain-monitoring variables, allowing the estimation of CCP during cases such as hypercapnia-induced hyperemia, where traditional calculations, like CCP1, often reach negative non-physiological values.Journal of Cerebral Blood Flow & Metabolism advance online publication, 14 November 2012; doi:10.1038/jcbfm.2012.161.Journal of cerebral blood flow and metabolism: official journal of the International Society of Cerebral Blood Flow and Metabolism 11/2012; · 5.46 Impact Factor
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ABSTRACT: Cerebrovascular time constant (τ) estimates how fast cerebral blood arrives in cerebral arterial bed after each heart stroke. We investigate the pattern of changes in τ following subarachnoid hemorrhage (SAH), with specific emphasis on the temporal profile of changes in relation to the development of cerebral vasospasm. Simultaneous recordings of arterial blood pressure (ABP) and transcranial Doppler (TCD) blood flow velocity (CBFV) in MCA were performed daily in patients after SAH. In 22 patients (10 males and 12 females; median age: 48 years, range: 34-84 years) recordings done before spasm were compared to those done during spasm. Vasospasm was confirmed with TCD (mean CBFV in MCA > 120 cm/s and Lindegaard ratio > 3). τ was estimated as a product of compliance of cerebral arteries (C (a)) and cerebrovascular resistance (CVR). C (a) and CVR were estimated using mathematical transformations of ABP and CBFV waveforms. Vasospasm caused shortening of τ on both the spastic (before: 0.20 ± 0.05 s vs. spasm: 0.14 ± 0.04 s, P < 0.0008) and contralateral side (before: 0.22 ± 0.05 s vs. spasm: 0.16 ± 0.04 s, P < 0.0008). Before TCD signs of vasospasm were detected, τ demonstrated asymmetry with lower values on ipsilateral side to aneurysm, in comparison to contralateral side (P < 0.009), Cerebral vasospasm causes shortening of τ. Shorter τ at the side of aneurysm can be observed before formal TCD signs of vasospasm are observed, therefore, potentially reducing time to escalation of treatment.Neurocritical Care 11/2011; 16(2):213-8. · 3.04 Impact Factor
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ABSTRACT: Understanding the dynamic relationship between cerebral blood flow (CBF) and the circulation of cerebrospinal fluid (CSF) can facilitate management of cerebral pathologies. For this reason, various hydrodynamic models have been introduced in order to simulate the phenomena governing the interaction between CBF and CSF. The identification of hydrodynamic models requires an array of signals as input, with the most common of them being arterial blood pressure, intracranial pressure, and cerebral blood flow velocity; monitoring all of them is considered as a standard practice in neurointensive care. Based on these signals, physiological parameters like cerebrovascular resistance, compliances of cerebrovascular bed, and CSF space could then be estimated. Various secondary model-based indices describing cerebrovascular dynamics have been introduced, like the cerebral arterial time constant or critical closing pressure. This review presents model-derived indices that describe cerebrovascular phenomena, the nature of which is both physiological (carbon dioxide reactivity and arterial hypotension) and pathological (cerebral artery stenosis, intracranial hypertension, and cerebral vasospasm). In a neurointensive environment, real-time monitoring of a patient with these indices may be able to provide a detection of the onset of a cerebrovascular phenomenon, which could have otherwise been missed. This potentially "early warning" indicator may then prove to be important for the therapeutic management of the patient.Neurocritical Care 10/2013; · 3.04 Impact Factor