Analysis of Intracranial Pressure Pulse-Pressure Relationship: Experimental Validation.

The slope of linear relationship between the amplitude of pulsations in intracranial pressure (ICP) versus mean ICP has recently been suggested as a useful guide for selecting patients for shunt surgery in normal pressure hydrocephalus (NPH). To better understand how the pathophysiology of cerebral circulation influences this parameter, we aimed to study the relationship between mean pressure and pulsation amplitude in a wide range of conditions affecting cerebrovascular tone and ICP in experimental conditions.We retrospectively analysed experimental material collected previously. Three physiological manoeuvres were studied in 29 New Zealand white rabbits: lumbar infusion with an infusion rate ≤0.2 mL/min to induce mild intracranial hypertension (n = 43), sympathetic blockade to induce arterial hypotension (n = 19), and modulation of the ventilator tidal volume, simultaneously influencing arterial carbon dioxide partial pressure (PaCO2) to induce hypocapnia or hypercapnia (n = 17). We investigated whether the slope of the pulse amplitude (AMP)-ICP line depended on PaCO2 and arterial blood pressure (ABP) changes.We found a linear correlation between AMP-ICP and ICP with positive slope. Regression of slope against mean ABP showed a negative dependence (p = 0.03). In contrast, the relationship between slope and PaCO2 was positive, although not reaching statistical significance (p = 0.18).The slope of amplitude-pressure line is strongly modulated by systemic vascular variables and therefore should be taken as a descriptor of cerebrospinal fluid dynamics with great care.

A comparison of the time constant of the cerebral arterial bed using invasive and non-invasive arterial blood pressure measurements.

OBJECTIVE: The time constant of the cerebral arterial bed (τ), which is an index of brain haemodynamics, can be estimated in patients using continuous monitoring of arterial blood pressure (ABP), transcranial Doppler cerebral blood flow velocity (CBFV) and intracranial pressure (ICP) if these measures are available. But, in some clinical scenarios invasive measurement of ABP is not feasible. Therefore, in this study we aimed to investigate whether invasive ABP can be replaced with non-invasive ABP, monitored using the Finapres photoplethysmograph (fABP). APPROACH: Forty-six recordings of ICP, ABP, fABP, and CBFV in the right and left middle cerebral arteries were performed daily for approximately 30 min in 10 head injury patients. Two modelling approaches (constant flow forward [CFF, pulsatile blood inflow and steady blood outflow] and pulsatile flow forward [PFF, where both blood inflow and outflow are pulsatile]) were applied to estimate τ using either invasive ABP (τCFF, τPFF) or non-invasive ABP (fτCFF, fτPFF). MAIN RESULTS: Bland-Altman analysis showed quite poor agreement between the fτ and τ methods of estimation. The fτ method produced significantly higher values than the τ method when calculated using both the CFF and PFF models (p < .001 for both). The correlation between fτCFF and τCFF was moderately high (r s = 0.63; p < .001), whereas that between fτPFF and τPFF was weaker (r s = 0.40; p = .009). SIGNIFICANCE: Our results suggest that using non-invasive ABP for estimation of τ is inaccurate in head injury patients.

Critical closing pressure during experimental intracranial hypertension: comparison of three calculation methods.

Objectives: The critical closing pressure (CrCP) defines arterial blood pressure below which cerebral arteries collapse. It represents a clinically relevant parameter for the estimation of cerebrovascular tone. Although there are few methods to assess CrCP, there is no consensus which of them estimates this parameter most accurately. The aim of present retrospective, experimental study was to compare three methods of CrCP estimation: conventional Aaslid's formula and methods based on the cerebrovascular impedance: the established continuous flow forward (CFF) and a new pulsatile flow forward (PFF) model.Methods: The effects of the following physiological manoeuvres on the CrCP were studied in New Zealand white rabbits: lumbar infusion of Hartmann's solution to induce mild intracranial hypertension, sympathetic blockade to induce arterial hypotension, and modulation of respiratory tidal volume to induce hypocapnia or hypercapnia.Results: During intracranial hypertension, all CrCP estimates were significantly higher than at baseline, decreased with decreasing ABP and increased with gradual hypocapnia. During hypercapnia, all CrCP estimates were significantly decreased but only in the case of CrCPA the negative, non-physiological values were observed (16% of the cases). The Bland-Altman analysis revealed that a good agreement between each impedance method and Aaslid's method deteriorated significantly in the low range of the average numerical value of the estimates.Discussion: Our results confirm the limited usage of Aaslid's formula for the calculation of CrCP. Although both impedance methods seem to be equivalent, the fact that PFF model better describes cerebrovascular hemodynamic allows the recommendation of this model for the calculation of CrCP.

Assessment of cerebral hemodynamic parameters using pulsatile versus non-pulsatile cerebral blood outflow models.

BACKGROUND: Prior methods evaluating the changes in cerebral arterial blood volume (∆CaBV) assumed that brain blood transport distal to big cerebral arteries can be approximated with a non-pulsatile flow (CFF) model. In this study, a modified ∆CaBV calculation that accounts for pulsatile blood flow forward (PFF) from large cerebral arteries to resistive arterioles was investigated. The aim was to assess cerebral hemodynamic indices estimated by both CFF and PFF models while changing arterial blood carbon dioxide concentration (EtCO2) in healthy volunteers. MATERIALS AND METHODS: Continuous recordings of non-invasive arterial blood pressure (ABP), transcranial Doppler blood flow velocity (CBFVa), and EtCO2 were performed in 53 young volunteers at baseline and during both hypo- and hypercapnia. The time constant of the cerebral arterial bed (τ) and critical closing pressure (CrCP) were estimated using mathematical transformations of the pulse waveforms of ABP and CBFVa, and with both pulsatile and non-pulsatile models of ∆CaBV estimation. Results are presented as median values ± interquartile range. RESULTS: Both CrCP and τ gave significantly lower values with the PFF model when compared with the CFF model (p ≪ 0.001 for both). In comparison to normocapnia, both CrCP and τ determined with the PFF model increased during hypocapnia [CrCPPFF (mm Hg): 5.52 ± 8.78 vs. 14.36 ± 14.47, p = 0.00006; τPFF (ms): 47.4 ± 53.9 vs. 72.8 ± 45.7, p = 0.002] and decreased during hypercapnia [CrCPPFF (mm Hg): 5.52 ± 8.78 vs. 2.36 ± 7.05, p = 0.0001; τPFF (ms): 47.4 ± 53.9 vs. 29.0 ± 31.3, p = 0.0003]. When the CFF model was applied, no changes were found for CrCP during hypercapnia or in τ during hypocapnia. CONCLUSION: Our results suggest that the pulsatile flow forward model better reflects changes in CrCP and in τ induced by controlled alterations in EtCO2.

Cerebral arterial time constant calculated from the middle and posterior cerebral arteries in healthy subjects.

The cerebral arterial blood volume changes (∆CaBV) during a single cardiac cycle can be estimated using transcranial Doppler ultrasonography (TCD) by assuming pulsatile blood inflow, constant, and pulsatile flow forward from large cerebral arteries to resistive arterioles [continuous flow forward (CFF) and pulsatile flow forward (PFF)]. In this way, two alternative methods of cerebral arterial compliance (Ca) estimation are possible. Recently, we proposed a TCD-derived index, named the time constant of the cerebral arterial bed (τ), which is a product of Ca and cerebrovascular resistance and is independent of the diameter of the insonated vessel. In this study, we aim to examine whether the τ estimated by either the CFF or the PFF model differs when calculated from the middle cerebral artery (MCA) and the posterior cerebral artery (PCA). The arterial blood pressure and TCD cerebral blood flow velocity (CBFVa) in the MCA and in the PCA were non-invasively measured in 32 young, healthy volunteers (median age: 24, minimum age: 18, maximum age: 31). The τ was calculated using both the PFF and CFF models from the MCA and the PCA and compared using a non-parametric Wilcoxon signed-rank test. Results are presented as medians (25th-75th percentiles). The cerebrovascular time constant estimated in both arteries using the PFF model was shorter than when using the CFF model (ms): [64.83 (41.22-104.93) vs. 178.60 (160.40-216.70), p < 0.001 in the MCA, and 44.04 (17.15-81.17) vs. 183.50 (153.65-204.10), p < 0.001 in the PCA, respectively]. The τ obtained using the PFF model was significantly longer from the MCA than from the PCA, p = 0.004. No difference was found in the τ when calculated using the CFF model. Longer τ from the MCA might be related to the higher Ca of the MCA than that of the PCA. Our results demonstrate MCA-PCA differences in the τ, but only when the PFF model was applied.

Critical Closing Pressure During a Controlled Increase in Intracranial Pressure.

OBJECTIVES: The objectives were to compare three methods of estimating critical closing pressure (CrCP) in a scenario of a controlled increase in intracranial pressure (ICP) induced during an infusion test in patients with suspected normal pressure hydrocephalus (NPH). METHODS: We retrospectively analyzed data from 37 NPH patients who underwent infusion tests. Computer recordings of directly measured intracranial pressure (ICP), arterial blood pressure (ABP) and transcranial Doppler cerebral blood flow velocity (CBFV) were used. The CrCP was calculated using three methods: first harmonics ratio of the pulse waveforms of ABP and CBFV (CrCPA) and two methods based on a model of cerebrovascular impedance, as a function of cerebral perfusion pressure (CrCPinv), and as a function of ABP (CrCPninv). RESULTS: There is good agreement among the three methods of CrCP calculation, with correlation coefficients being greater than 0.8 (p < 0.0001). For the CrCPA method, negative values were found for about 20% of all results. Negative values of CrCP were not observed in estimators based on cerebrovascular impedance. During the controlled rise of ICP, all three estimators of CrCP increased significantly (p < 0.05). The strongest correlation between ICP and CrCP was found for CrCPinv (median R = 0.41). CONCLUSION: Invasive CrCP is most sensitive to variations in ICP and can be used as an indicator of the status of the cerebrovascular system during infusion tests.

Critical Closing Pressure During Controlled Increase in Intracranial Pressure-Comparison of Three Methods.

GOAL: Critical closing pressure (CrCP) is the arterial blood pressure (ABP) threshold, below which small arterial vessels collapse and cerebral blood flow ceases. Here, we aim to compare three methods for CrCP estimation in scenario of a controlled increase in intracranial pressure (ICP), induced by infusion tests performed in patients with suspected normal pressure hydrocephalus (NPH). METHODS: Computer recordings of directly-measured ICP, ABP, and transcranial Doppler cerebral blood flow velocity (CBFV), from 37 NPH patients undergoing infusion tests, were retrospectively analyzed. The CrCP was calculated with three methods: one with the first harmonics ratio of the pulse waveforms of ABP and CBFV (CrCPA) and two methods based on a model of cerebrovascular impedance, as functions of both cerebral perfusion pressure (CrCPinv), and of ABP (CrCPninv). CONCLUSION: All methods give similar results in response to ICP changes. In the case of individual CrCP measurements for each patient, CrCPA may provide negative, nonphysiological values. Invasive critical closing pressure is most sensitive to variations in ICP and CPP and can be used as an indicator of the cerebrospinal and the cerebrovascular system status during infusion tests.