Dataset Information

Rapid chest compression effects on intracranial pressure in patients with acute cerebral injury.

ABSTRACT:

Background

Patients with acute brain injury often require invasive mechanical ventilation, increasing the risk of developing complications such as respiratory secretions retention. Rapid chest compression is a manual chest physiotherapy technique that aims to improve clearance of secretions in these patients. However, the rapid chest compression technique has been suggested to be associated with increased intracranial pressure in patients with acute brain injury. The aim of this work is to elucidate the effects of the technique on intracranial pressure in mechanically ventilated patients with acute brain injury. Furthermore, the effects of the technique in different volumes and flows recorded by the ventilator and the relationship between the pressure applied in the intervention group and the different variables will also be studied.

Methods

Randomized clinical trial, double-blinded. Patients with acute brain injury on invasive mechanical ventilation > 48 h will be included and randomized in two groups. In the control group, a technique of passive hallux mobilization will be applied, and in the intervention group, it will be performed using the rapid chest compression technique. Intracranial pressure (main variable) will be collected with an intracranial pressure monitoring system placed at the lateral ventricles (Integra Camino).

Discussion

The safety of chest physiotherapy techniques in patients at risk of intracranial hyperpressure is still uncertain. The aim of this study is to identify if the rapid manual chest compression technique is safe in ventilated patients with acute brain injury.

Trial registration

NCT03609866 . Registered on 08/01/2018.

SUBMITTER: Rodrigues-Gomes RM

PROVIDER: S-EPMC9012060 | biostudies-literature | 2022 Apr

REPOSITORIES: biostudies-literature

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Publications

Rapid chest compression effects on intracranial pressure in patients with acute cerebral injury.

Rodrigues-Gomes Ricardo Miguel RM Martí Joan-Daniel JD Rolán Rosa Martínez RM Gelabert-González Miguel M

Trials 20220415 1

<h4>Background</h4>Patients with acute brain injury often require invasive mechanical ventilation, increasing the risk of developing complications such as respiratory secretions retention. Rapid chest compression is a manual chest physiotherapy technique that aims to improve clearance of secretions in these patients. However, the rapid chest compression technique has been suggested to be associated with increased intracranial pressure in patients with acute brain injury. The aim of this work is ...[more]

PMID: 35428364

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Project description:BackgroundCerebral autoregulation is a robust regulatory mechanism that stabilizes cerebral blood flow in response to reduced blood pressure, thereby preventing cerebral ischaemia. Scientists have long believed that cerebral autoregulation also stabilizes cerebral blood flow against increases in intracranial pressure, which is another component that determines cerebral perfusion pressure. However, this idea was inconsistent with the complex pathogenesis of normal pressure hydrocephalus, which includes components of chronic cerebral ischaemia due to mild increases in intracranial pressure.MethodsTwenty-one patients who underwent ventriculoperitoneal shunt surgery for normal pressure hydrocephalus were included in this study. To determine the pressure setting of the Codman-Hakim programmable valve, intracranial pressure was measured after shunt surgery by puncturing the Ommaya reservoir, which formed a closed circuit with the needle and the syringe. Then, intracranial pressure was continuously measured with intermittent infusion of cerebrospinal fluid from the same closed circuit. We also continuously measured oximetry data, such as regional cerebral oxygen saturation derived from near-infrared spectroscopy monitoring. These data were digitized, recorded, and used for calculating intracranial compliance and the relationship between cerebrospinal fluid volume loading and intracranial pressure.ResultsThis study demonstrates that in patients with normal pressure hydrocephalus, cerebral venous vascular bed compression induces mild cerebral ischaemia when intracranial pressure is slightly higher than physiological venous pressure. Cerebral venous compression impairs cerebral blood flow by quadratically increasing circulatory resistance according to Poiseuille's law. Furthermore, chronic cerebral ischaemia occurred even at low or normal intracranial pressures when deep and subcortical white matter hyperintensities (DSWMHs) were severe.ConclusionThe fact that cerebral blood flow impairment begins at very low intracranial pressures indicates that cerebral autoregulation to compensate for reduced venous blood flow is not functioning adequately in NPH. These processes provide a link between impaired cerebrospinal fluid circulation, cerebral autoregulation, and neurological dysfunction, which has been missing in patients with NPH involving small vessel arteriosclerosis. These findings may provide insight into similar conditions, such as normal-tension glaucoma and chronic kidney disease, in which a mild increase in local compartment pressure leads to chronic ischemia in organs protected by autoregulatory mechanisms.

Project description:PurposeTo evaluate the alteration of pressure characteristics in the cerebral venous sinuses before and after venous sinus stenting (VSS) using mean sinus pressures (MSPs), sinus pressure gradient (SPG), and sinus pressure pulsatility (SPP) parameters among the idiopathic intracranial hypertension (IIH) patients.Materials and methodsProspective evaluation of 45 consecutive IIH patients who underwent VSS at our institution. A written informed consent approved by the Weill Cornell Institutional Review Board was signed by the study participants. All patients (n = 45) were evaluated for MSPs and SPG. In a subgroup of 12 (n = 12) consecutive patients, SPP was measured. MSP was measured using microcatheter at superior sagittal sinus (SSS), transverse sinus (TS), and sigmoid sinus (SS). SPG was measured as trans-stenotic gradient and trans-torcular gradient. SPP was recorded in the dominant TS with a six French intermediate catheter. Statistical analysis was performed using paired student t-test and two sample t-tests tested for both equal and unequal variances. P values below 0.05 were considered significant.ResultsThe mean age of the study population was 30.6 ± 10 years (7-59 years) and 43 out of 45 are female patients. The mean weight and BMI of the study population were 96 ± 24.7 kg (30.8-144 kg) and 35.6 ± 8.3 kg/M2 (16.4-51.4 kg/M2), respectively. VSS in IIH patients resulted in immediate reduction of MSP in the SSS {Δ Mean: -8.1 mm Hg [95% confidence interval (CI): -5.0-11.7 mm Hg], p < 0.001} and TS [Δ Mean: -11.8 mm Hg (95% CI: -7.5 to 13.4 mm Hg), p < 0.001] and increase of MSP in SS [Δ Mean: 7.5 mm Hg (95% CI: 6-10.1 mm Hg), p < 0.001]. Significant reduction of trans-stenotic SPG reduction [Δ Mean: -15.7 mm Hg (95% CI: -13.6-17.8 mm Hg), p < 0.001] and SPP [Δ Mean: -8 mm Hg (95% CI: -2.5-13.4 mm Hg), p < 0.05] was observed following VSS.ConclusionVSS resulted in immediate alteration of the cerebral venous sinus pressure measurements in patients with IIH.

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.

Dataset Information

Rapid chest compression effects on intracranial pressure in patients with acute cerebral injury.

Background

Methods

Discussion

Trial registration

Publications

Rapid chest compression effects on intracranial pressure in patients with acute cerebral injury.

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