Critical closing pressure determined with a model of cerebrovascular impedance.
Ontology highlight
ABSTRACT:
SUBMITTER: Varsos GV
PROVIDER: S-EPMC3564193 | biostudies-other | 2013 Feb
REPOSITORIES: biostudies-other
Similar Datasets
Project description:The effect of cerebral vasospasm (CVS) after aneurysmal subarachnoid hemorrhage (SAH) on critical closing pressure (CrCP) has not been fully delineated. Using cerebral impedance methodology, we sought to assess the behavior of CrCP during CVS. As CrCP expresses the sum of intracranial pressure (ICP) and vascular wall tension, we also explored its role in reflecting changes in vascular tone occurring in small vessels distal to spasm. This retrospective analysis was performed using recordings from 52 patients, diagnosed with CVS through transcranial Doppler measurements. Critical closing pressure was calculated noninvasively using arterial blood pressure and blood flow velocity. Outcome was assessed at both discharge and 3 months after ictus with the Glasgow Outcome Scale. The onset of CVS caused significant decreases in CrCP (P=0.025), without any observed significant changes in ICP (P=0.134). Vasospasm induced asymmetry, with CrCP ipsilateral to CVS becoming significantly lower than contralateral (P=0.025). Unfavorable outcomes were associated with a significantly lower CrCP after the onset of CVS (discharge: P=0.014; 3 months after SAH: P=0.020). Critical closing pressure is reduced in the presence of CVS in both temporal and spatial assessments. As ICP remained unchanged during CVS, reduced CrCP most probably reflects a lower wall tension in dilated small vessels distal to spasm.
| S-EPMC4814058 | biostudies-other
Project description:OBJECTIVES:The lower limit of cerebral blood flow autoregulation is the critical cerebral perfusion pressure at which cerebral blood flow begins to fall. It is important that cerebral perfusion pressure be maintained above this level to ensure adequate cerebral blood flow, especially in patients with high intracranial pressure. However, the critical cerebral perfusion pressure of 50 mm Hg, obtained by decreasing mean arterial pressure, differs from the value of 30 mm Hg, obtained by increasing intracranial pressure, which we previously showed was due to microvascular shunt flow maintenance of a falsely high cerebral blood flow. The present study shows that the critical cerebral perfusion pressure, measured by increasing intracranial pressure to decrease cerebral perfusion pressure, is inaccurate but accurately determined by dopamine-induced dynamic intracranial pressure reactivity and cerebrovascular reactivity. DESIGN:Cerebral perfusion pressure was decreased either by increasing intracranial pressure or decreasing mean arterial pressure and the critical cerebral perfusion pressure by both methods compared. Cortical Doppler flux, intracranial pressure, and mean arterial pressure were monitored throughout the study. At each cerebral perfusion pressure, we measured microvascular RBC flow velocity, blood-brain barrier integrity (transcapillary dye extravasation), and tissue oxygenation (reduced nicotinamide adenine dinucleotide) in the cerebral cortex of rats using in vivo two-photon laser scanning microscopy. SETTING:University laboratory. SUBJECTS:Male Sprague-Dawley rats. INTERVENTIONS:At each cerebral perfusion pressure, dopamine-induced arterial pressure transients (~10 mm Hg, ~45 s duration) were used to measure induced intracranial pressure reactivity (? intracranial pressure/? mean arterial pressure) and induced cerebrovascular reactivity (? cerebral blood flow/? mean arterial pressure). MEASUREMENTS AND MAIN RESULTS:At a normal cerebral perfusion pressure of 70 mm Hg, 10 mm Hg mean arterial pressure pulses had no effect on intracranial pressure or cerebral blood flow (induced intracranial pressure reactivity = -0.03 ± 0.07 and induced cerebrovascular reactivity = -0.02 ± 0.09), reflecting intact autoregulation. Decreasing cerebral perfusion pressure to 50 mm Hg by increasing intracranial pressure increased induced intracranial pressure reactivity and induced cerebrovascular reactivity to 0.24 ± 0.09 and 0.31 ± 0.13, respectively, reflecting impaired autoregulation (p < 0.05). By static cerebral blood flow, the first significant decrease in cerebral blood flow occurred at a cerebral perfusion pressure of 30 mm Hg (0.71 ± 0.08, p < 0.05). CONCLUSIONS:Critical cerebral perfusion pressure of 50 mm Hg was accurately determined by induced intracranial pressure reactivity and induced cerebrovascular reactivity, whereas the static method failed.
| S-EPMC6395276 | biostudies-literature
Project description:The critical closing pressure ( CrCP) of the cerebral circulation depends on both tissue intracranial pressure and vasomotor tone. CrCP defines the arterial blood pressure ( ABP) at which cerebral blood flow approaches zero, and their difference ( ABP?-? CrCP) is an accurate estimate of cerebral perfusion pressure. Here we demonstrate a novel non-invasive technique for continuous monitoring of CrCP at the bedside. The methodology combines optical diffuse correlation spectroscopy (DCS) measurements of pulsatile cerebral blood flow in arterioles with concurrent ABP data during the cardiac cycle. Together, the two waveforms permit calculation of CrCP via the two-compartment Windkessel model for flow in the cerebral arterioles. Measurements of CrCP by optics (DCS) and transcranial Doppler ultrasound (TCD) were carried out in 18 healthy adults; they demonstrated good agreement (R?=?0.66, slope?=?1.14?±?0.23) with means of 11.1?±?5.0 and 13.0?±?7.5?mmHg, respectively. Additionally, a potentially useful and rarely measured arteriole compliance parameter was derived from the phase difference between ABP and DCS arteriole blood flow waveforms. The measurements provide evidence that DCS signals originate predominantly from arteriole blood flow and are well suited for long-term continuous monitoring of CrCP and assessment of arteriole compliance in the clinic.
| S-EPMC5536813 | biostudies-other
Project description:PurposeTo investigate cerebrovascular hemodynamics, including critical closing pressure (CrCP) and pulsatility index (PI), and their independent relationship with cerebral small vessel disease (CSVD) burden in patients with small-vessel occlusion (SVO).MethodsWe recruited consecutive patients with SVO of acute cerebral infarction who underwent brain magnetic resonance imaging (MRI), transcranial Doppler (TCD) and CrCP during admission. Cerebrovascular hemodynamics were assessed using TCD. We used the CSVD score to rate the total MRI burden of CSVD. Multiple regression analysis was used to determine parameters related to CSVD burden or CrCP.ResultsNinety-seven of 120 patients (mean age, 64.51 ± 9.99 years; 76% male) completed the full evaluations in this study. We observed that CrCP was an independent determinant of CSVD burden in four models [odds ratio, 1.41; 95% confidence interval (CI), 1.17-1.71; P < 0.001] and correlated with CSVD burden [β (95% CI): 0.05 (0.04-0.06); P < 0.001]. In ROC analysis, CrCP was considered as a predictor of CSVD burden, and AUC was 86.2% (95% CI, 78.6-93.9%; P < 0.001). Multiple linear regression analysis showed that CrCP was significantly correlated with age [β (95% CI): 0.27 (0.06 to 0.47); P = 0.012], BMI [β (95% CI): 0.61 (0.00-1.22)] and systolic BP [β (95% CI): 0.16 (0.09-0.23); P < 0.001].ConclusionsCrCP representing cerebrovascular tension is an independent determinant and predictor of CSVD burden. It was significantly correlated with age, BMI and systolic blood pressure. These results provide new insights in the mechanism of CSVD development.
| S-EPMC10071665 | biostudies-literature
Project description:In obstructive sleep apnea (OSA), there are various pathophysiological factors affecting the upper airway during sleep. Two prominent factors contributing to OSA are site and pattern of upper airway collapse and degree of pharyngeal collapsibility. In a clinical setting, drug-induced sleep endoscopy (DISE) is used to visualize the structures of the upper airway. Critical closing pressure (Pcrit) is the gold standard measure of pharyngeal collapsibility. This prospective clinical study aimed to investigate the feasibility and protocol of Pcrit measurements during DISE. Thirteen patients with OSA were included. Pcrit was calculated using peak inspiratory airflow and inspiratory ventilation. The proposed protocol was successful in Pcrit measurement during DISE in all subjects [median[Q1;Q3] Pcrit for "peak inspiratory method" (n = 12): -0.84[-2.07;0.69] cmH2O, "ventilation method" (n = 13): -1.32[2.32;0.47] cmH2O], highlighting the feasibility of the approach. There was no significant difference (P = 0.67) between calculated Pcrit with either of the calculation methods, indicating high reliability. Correlation analysis showed Pcrit as an independent parameter of any of the anthropometric or polysomnographic parameters. The ventilation method proved to be more successful in assessment of Pcrit in subjects with epiglottic collapse (e.g., with high negative effort dependence). Subjects with palatal complete concentric collapse during DISE had a wide Pcrit range ([-2.86;2.51]cmH2O), suggesting no close correlation between Pcrit and this DISE pattern (P = 0.38). Incorporation of Pcrit measurements into DISE assessments is feasible and may yield valuable additional information for OSA management. Combining Pcrit and DISE provides information on both the site and degree of upper airway collapse and the degree of pharyngeal collapsibility.NEW & NOTEWORTHY The protocol of this study was successful in concomitant measurement of Pcrit during routine clinical endoscopy. Comparison of two calculation methods for Pcrit showed that the inspiratory ventilation method was more successful in assessment of Pcrit in subjects with epiglottic collapse who have high negative effort dependence. Subjects with palatal complete concentric collapse during DISE had a wide Pcrit range and did not have a greater Pcrit than patients in other site of collapse categories.
| S-EPMC8993534 | biostudies-literature
Project description:Intracranial pressure (ICP), variability in perfusion, and resulting ischemia are leading causes of secondary brain injury in patients treated in the neurointensive care unit. Continuous, accurate monitoring of cerebral blood flow (CBF) and ICP guide intervention and ultimately reduce morbidity and mortality. Currently, only invasive tools are used to monitor patients at high risk for intracranial hypertension. Diffuse correlation spectroscopy (DCS), a noninvasive near-infrared optical technique, is emerging as a possible method for continuous monitoring of CBF and critical closing pressure (CrCP or zero-flow pressure), a parameter directly related to ICP. We optimized DCS hardware and algorithms for the quantification of CrCP. Toward its clinical translation, we validated the DCS estimates of cerebral blood flow index (CBFi) and CrCP in ischemic stroke patients with respect to simultaneously acquired transcranial Doppler ultrasound (TCD) cerebral blood flow velocity (CBFV) and CrCP. We found CrCP derived from DCS and TCD were highly linearly correlated (ipsilateral R2 = 0.77, p = 9 × 10 - 7; contralateral R2 = 0.83, p = 7 × 10 - 8). We found weaker correlations between CBFi and CBFV (ipsilateral R2 = 0.25, p = 0.03; contralateral R2 = 0.48, p = 1 × 10 - 3) probably due to the different vasculature measured. Our results suggest DCS is a valid alternative to TCD for continuous monitoring of CrCP.
| S-EPMC7998065 | biostudies-literature
Project description:Cerebral blood flow (CBF) becomes pulsatile in response to the pulsatile change in perfusion pressure that is regulated by cerebrovascular impedance. In this study, we aimed to characterize age-related differences in cerebrovascular impedance across the adult lifespan. Carotid artery pressure [(CAP), via applanation tonometry] and CBF velocity (CBFV) in the middle cerebral artery (via transcranial Doppler) were measured in 148 healthy adults (21-79 yr, 62% women). Cerebrovascular impedance was quantified using transfer function analysis. Coherence between changes in CBFV and CAP was >0.90 in the frequency range of 0.78-2.73 Hz, suggesting a linear dynamic relationship between these two variables. Impedance modulus at the first harmonics (0.78-1.56 Hz) of CBFV and CAP oscillations (Z1), reflecting mainly heart rate frequency, was 20% higher in the old (>64 yr, P = 0.002) and 13% higher in the middle-aged (45-64 yr, P = 0.08) than in young individuals (<45 yr). In addition, Z1 was 24% higher in men than in women (P < 0.001). Multiple linear regression analysis revealed that Z1 is negatively associated with systolic (β = -0.470), diastolic (β = -0.418), pulsatile (β = -0.374), and mean CBFV (β = -0.473; P < 0.001 for all) after adjustment for age, sex, and body mass index (BMI). These results suggest that older age and male sex are associated with higher cerebrovascular impedance than young individuals, which may contribute to brain hypoperfusion.NEW & NOTEWORTHY Impedance modulus at the first harmonics of cerebral blood flow velocity (CBFV) and carotid artery pressure oscillations (Z1) was higher in the old (>64 yr) than in the young individuals (<45 yr), and it was higher in men than in women. Z1 is negatively associated with CBFV after adjustment for age, sex, and body mass index. Increases in cerebrovascular impedance with age may buffer systemic arterial pressure fluctuations at the cost of increased brain hypoperfusion risk.
| S-EPMC7944933 | biostudies-literature
Project description:Electrical impedance myography (EIM) technology is finding application in neuromuscular disease research as a tool to assess muscle health. Correlations between EIM outcomes, functional, imaging and histological data have been established in a variety of neuromuscular disorders; however, an analytical discussion of EIM is lacking. This review presents an explanation for clinicians and others who are applying EIM and interpreting impedance outcomes. The background of EIM is presented, including the relation between EIM, volume conduction properties, tissue structure, electrode configuration and conductor volume. Also discussed are technical considerations to guide the reader to critically evaluate EIM and understand its limitations and strengths.
| S-EPMC7880888 | biostudies-literature
Project description:BackgroundThe provision of guidance in ventilator therapy by continuous monitoring of regional lung ventilation, aeration and respiratory system mechanics is the main clinical benefit of electrical impedance tomography (EIT). A new application was recently described in critically ill patients undergoing diagnostic bronchoalveolar lavage (BAL) with the intention of using EIT to identify the region where sampling was performed. Increased electrical bioimpedance was reported after fluid instillation. To verify the accuracy of these findings, contradicting the current EIT knowledge, we have systematically analysed chest EIT data acquired under controlled experimental conditions in animals undergoing a large number of BAL procedures.MethodsOne hundred thirteen BAL procedures were performed in 13 newborn piglets positioned both supine and prone. EIT data was obtained at 13 images before, during and after each BAL. The data was analysed at three time points: (1) after disconnection from the ventilator before the fluid instillation and by the ends of fluid (2) instillation and (3) recovery by suction and compared with the baseline measurements before the procedure. Functional EIT images were generated, and changes in pixel electrical bioimpedance were calculated relative to baseline. The data was examined in the whole image and in three (ventral, middle, dorsal) regions-of-interest per lung.ResultsCompared with the baseline phase, chest electrical bioimpedance fell after the disconnection from the ventilator in all animals in both postures during all procedures. The fluid instillation further decreased electrical bioimpedance. During fluid recovery, electrical bioimpedance increased, but not to baseline values. All effects were highly significant (p < 0.001). The fractional changes in individual regions-of-interest were posture-dependent. The regional fall in electrical bioimpedance was smaller in the ventral and larger in the dorsal regions after the fluid instillation than after the initial disconnection to ambient pressure in supine animals (p < 0.001) whereas these changes were of comparable amplitude in prone position.ConclusionsThe results of this study show a regionally dissimilar initial fall in electrical bioimpedance caused by non-uniform aeration loss at the beginning of the BAL procedure. They also confirm a further pronounced fall in bioimpedance during fluid instillation, incomplete recovery after suction and a posture-dependent distribution pattern of these effects.
| S-EPMC6377686 | biostudies-literature
Project description:Arterial blood pressure is oscillatory; whether pulse pressure (PP) regulates cerebral artery myogenic tone (MT) and endothelial function is currently unknown. To test the impact of PP on MT and dilation to flow (FMD) or to acetylcholine (Ach), isolated pressurized mouse posterior cerebral arteries were subjected to either static pressure (SP) or a physiological PP (amplitude: 30 mm Hg; frequency: 550 bpm). Under PP, MT was significantly higher than in SP conditions ( p < 0.05) and was not affected by eNOS inhibition. In contrast, under SP, eNOS inhibition increased ( p < 0.05) MT to levels observed under PP, suggesting that PP may inhibit eNOS. At a shear stress of 20 dyn/cm2, FMD was lower ( p < 0.05) under SP than PP. Under SP, eNOS-dependent [Formula: see text] production contributed to FMD, while under PP, eNOS-dependent NO was responsible for FMD, indicating that PP favours eNOS coupling. Differences in FMD between pressure conditions were abolished after NOX2 inhibition. In contrast to FMD, Ach-induced dilations were higher ( p < 0.05) under SP than PP. Reactive oxygen species scavenging reduced ( p < 0.05) Ach-dependent dilations under SP, but increased ( p < 0.05) them under PP; hence, under PP, Ach promotes ROS production and limits eNOS-derived NO activity. In conclusion, PP finely regulates eNOS, controlling cerebral artery reactivity.
| S-EPMC5381440 | biostudies-literature