Cerebral CO2 reactivity in severe head injury. A transcranial Doppler study.

BACKGROUND: Cerebral circulation is profoundly affected by changes in PaCO2. CO2 manipulation plays a basic role in the management of intracranial hypertension; CO2 reactivity (CO2R) defines the changes in CBF in response to changes in PaCO2. Transcranial Doppler has allowed exploring its effects "on line". MATERIALS AND METHODS: We conducted a prospective clinical trial, with the objective of studying CO2R in severe head injury patients. Sixteen severe traumatic brain injury patients, mechanically ventilated, were included. Monitoring of MAP, ICP, CPP, SjO2, ETCO2, and cerebral blood flow velocity (CBFV) was performed. Taking into account basal cerebral hemodynamic pattern, minute ventilation was modified to attain a negative ("A") or positive ("B") deltaPCO2. CO2R was calculated as: CO2R = % deltaCBFV/deltaETCO2 in mmHg (normal value 3.7 +/- 1%/mmHg). CO2R was compared with deltaICP/ deltaPCO2 in each patient. FINDINGS: Three patients were excluded because the change in ETCO2 was too low (deltaETCO2 < 3 mmHg). The median value of CO2R in the total group of 13 patients was 3.38. In "A" the values tended to be lower than in "B". There were four low CO2R values in "A" and none in "B". There was no significant correlation between CO2R and deltaICP/deltaPCO2. CONCLUSIONS: The different "A" and "B" behavior might be due to dissimilar mechanisms involved in the basis of vasodilatation and vasoconstriction. Changes in ventilation must be performed with caution, avoiding sudden increases in CO2 that may increase ICP. The absence of correlation between CO2R and deltaICP/deltaPCO2 is explained, at least partially, by different cranio-cerebral compliance in each patient. Therefore, induced blood volume changes are not directly transmitted to ICP, but their effects depend on the shape of the pressure-volume curve and the position on the curve in which each situation is working.

Indomethacin and cerebral autoregulation in severe head injured patients: a transcranial Doppler study.

OBJECTIVE: To assess the effect of indomethacin on cerebral autoregulation, systemic and cerebral haemodynamics, in severe head trauma patients. DESIGN: Prospective, controlled clinical trial, with repeated measurements. SETTINGS: A 12-bed adult general intensive care unit in a third level referral university hospital. PATIENTS: 16 severely head injured patients, 14 males, age range 17-60. INTERVENTIONS: Indomethacin was administrated as a load plus continuous infusion. Indomethacin reactivity was assessed as the estimated cerebral blood flow change elicited by the load. Dynamic and static cerebral autoregulation tests were performed before indomethacin administration, and during its infusion. MEASUREMENTS AND MAIN RESULTS: Systemic and cerebral haemodynamic changes were assessed through continuous monitoring of mean arterial pressure, transcranial Doppler cerebral blood flow velocity, intracranial pressure, cerebral perfusion pressure, and jugular venous oxygen saturation. Indomethacin loading dose was immediately followed by a cerebral blood flow median decrease of 36 or 29% (p = ns) evaluated by two different methods, by an ICP decrease and by an AVDO(2) increase from 3.52 to 6.15 mL/dL (p = 0.002). Dynamic autoregulation increased from a median of 28 to 57% (p<0.05) during indomethacin infusion; static autoregulation also increased, from a median of 72 to 89% (p = ns). CONCLUSIONS: Indomethacin decreased intracranial pressure and cerebral blood flow, and increased cerebral perfusion pressure, while maintaining tissue properties of further extracting O(2). The increase in both autoregulatory values reveals an enhancement of cerebral microvasculature reactivity under indomethacin, during hypertensive and--especially--during hypotensive situations.

Comparison between two static autoregulation evaluation methods.

Cerebral static autoregulation (AR) was evaluated at bedside in 14 severely head injured patients. 16 investigations were performed. Cerebral perfusion pressure (CPP) was increased by infusing vasopressors during one hour, and registered every 2-5 minutes. CBF was simultaneously estimated by: 1) middle cerebral artery mean flow velocity (FV) monitoring with Transcranial Doppler (TDC), and 2) the reciprocal of arteriovenous oxygen content difference, calculated from basal and hypertensive arterial and jugular bulb blood samples. AR assessment: For TCD results, linear regression method was used, studying two pairs of variables: a) %FV-CPP (the regression slope was the main AR value adopted) and b) % cerebrovascular resistance (CVR)-%CPP. For the AVDO2 method, autoregulation was considered preserved if estimated % delta CBF/delta PPE < 1%/mm Hg. TCD method clearly defined three groups. Group 1 and 2 (8 and 5 investigations) were considered as two grades of preserved AR, and the third one (3 cases) as impaired AR. AVDO2 method: 12 studies were evaluated. 10 showed preserved AR, and 2 impaired AR. There was coincidence of results from both methods in 10 out of 12 studies. (0.83).

Gastric intramucosal pH and intraluminal PCO2 during weaning from mechanical ventilation.

OBJECTIVE: To study the value of gastric intramucosal pH and gastric intraluminal PCO2 measurements to predict weaning outcome from mechanical ventilation. DESIGN: Prospective clinical study. SETTING: Intensive care medicine department of a university hospital. PATIENTS: Nineteen adult critically ill patients who were mechanically ventilated because of acute respiratory failure and were considered ready to be weaned. INTERVENTIONS: The patients were weaned with: synchronized intermittent mandatory ventilation plus positive end-expiratory pressure (SIMV+PEEP) or continuous positive airway pressure with pressure support ventilation (CPAP+PSV). A gastric tonometer was placed in all the patients. Tonometric, respiratory, and hemodynamic variables were measured during the weaning process. MEASUREMENTS: Hemodynamic variables, respiratory mechanics, pulmonary gas exchange, respiratory muscle force, spontaneous pattern of breathing, and the central control of breathing were recorded. Simultaneously, the intramucosal pH and gastric intraluminal PCO2 were measured. MAIN RESULTS: Eleven patients were successfully extubated and eight failed. The patients who failed showed higher values of mouth occlusion pressure, respiratory rate, and effective inspiratory impedance (mouth occlusion pressure/mean inspiratory flow). The intramucosal pH was initially 7.19 +/- 0.22 and decreased to 7.10 +/- 0.16 during the weaning process in patients who failed (p < .05). At the same time, the intramucosal pH showed a nonsignificant change from 7.36 +/- 0.07 to 7.32 +/- 0.07 in the patients who were successfully extubated. The intramucosal pH was statistically different when both groups were compared during the initial and the final evaluations (p < .05). For the initial evaluation, the sensitivity and specificity to predict weaning failure when the intramucosal pH was < or =7.30 were 0.88 (95% confidence interval [CI], 0.66-1) and 0.82 (95% CI, 0.59-1), respectively. The gastric intraluminal PCO2 was higher in patients who failed (p < .05). When gastric intraluminal PCO2 was . or =40 torr during the initial evaluation, weaning failure occurred with a sensitivity of 1 (95% CI, 0.31-1) and a specificity of 0.55 (95% CI, 0.26-0.84). CONCLUSIONS: Weaning failure was associated with gastric intramucosal acidosis. The intramucosal pH and gastric intraluminal PCO2 may be helpful to predict weaning outcome. Further controlled clinical trials in a larger group of patients are needed.