Cerebral Carbon Dioxide Reactivity Research Articles

Measuring Cerebral Carbon Dioxide Reactivity With Transcranial Doppler and Near-Infrared Spectroscopy in Children With Ventricular Septal Defect

Neurologic impairment is frequently observed in children with congenital heart disease. Impairment in cerebrovascular carbon dioxide reactivity (CO2R) is related with poor neurologic outcomes. The present study examined CO2R measured with transcranial Doppler (TCD) and near-infrared spectroscopy (NIRS) in children with ventricular septal defect undergoing cardiac surgery. Prospective, paired controlled study. Operating room of a tertiary care center. Twenty children with ventricular septal defect and younger than 1 year were enrolled, and 17 children were studied (age: 6.0 ± 2.0 mo, weight 5.9 ± 1.0 kg). After induction of anesthesia and tracheal intubation, the lungs were ventilated and mechanical ventilation was initiated. Partial pressure of end-tidal carbon dioxide (PETCO2) was adjusted at 4 different levels (30, 35, 40, and 45 mmHg). Paired measurements of middle cerebral artery mean blood flow velocity (VMCA) by TCD and tissue oxygen index (TOI) by NIRS were recorded at each level of PETCO2. CO2R was calculated as the percentage change of VMCA and TOI per mmHg change in PETCO2. Systemic hemodynamic parameters were recorded. As PETCO2 rose from 30 to 45 mmHg, VMCA and TOI increased linearly (p < 0.001 for both), and CO2R-TCD and CO2R-NIRS were calculated to be 2.8% ± 0.9%/mmHg and 1.2% ± 0.3 %/mmHg, respectively. CO2R-NIRS was significantly lower compared with CO2R-TCD (p < 0.001). Significant correlations were found between VMCA and TOI (r = 0.487; p < 0.001) and between ΔVMCA and ΔTOI (r = 0.693; p < 0.001), but not between CO2R-TCD and CO2R-NIRS (r = 0.18; p = 0.24). With the increase of PETCO2, cardiac index, systemic vascular resistance index, and mean arterial pressure remained constant (p > 0.05 for all) and the heart rate decreased significantly (p = 0.018). During anesthesia, CO2R remains preserved in children with a ventricular septal defect. Even though there is lack of correlation between CO2R-TCD and CO2R-NIRS, changes in TOI and VMCA were correlated as the PETCO2 changed. NIRS may be used as a surrogate to investigate CO2R when the ultrasound window is poor.

Dynamic cerebral carbon dioxide reactivity at rest and during exercise

The cerebral vasculature is highly sensitive to direct arterial carbon dioxide tension (PaCO2) changes. Hypocapnia causes cerebral vasoconstriction, while hypercapnia causes cerebral vasodilation to maintain the brain tissue PCO2 within narrow limits. The cerebral blood flow (CBF) responses to PaCO2 changes should be quick, but the cerebral vasculature sensitivity as cerebral CO2 is measured during steady‐state vascular responses. Therefore, the CBF time response to PaCO2 changes remains unknown. The purpose of this study was to examine dynamic cerebral CO2 reactivity at rest and during exercise using the frequency domain analysis.Seven healthy young subjects participated in the study. At rest and during exercise (30% VO2max and cycling exercise), the dynamic CO2 reactivity was calculated based on the transfer function analysis between the end‐tidal CO2 (PETCO2) and the middle cerebral artery mean blood velocity (MCAvm), using a binary white‐noise sequence (0%–7% inspired CO2 fraction). Dynamic characteristics of the respiratory controller showed a low‐pass filter characteristic for regulating ventilation, and the dynamic gain was decreased gradually to 0.7 at 0.02 Hz. However, the gain from PETCO2 to MCAvm (dynamic CO2 reactivity) remained reasonably constant up to 0.02 Hz. Moreover, it did not change during exercise.These findings suggest that the dynamic cerebral CO2 reactivity is reflected in slow to fast PaCO2 changes, and does not change during exercise. In terms of CO2 homeostasis, the cerebral CO2 reactivity may be a more important physiological mechanism to adapt to fast CO2 changes than the ventilatory response to PaCO2 changes.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Assessment of dynamic cerebral autoregulation and cerebral carbon dioxide reactivity during normothermic cardiopulmonary bypass.

Despite increased risk of neurological complications after cardiac surgery, monitoring of cerebral hemodynamics during cardiopulmonary bypass (CPB) is still not a common practice. Therefore, a technique to evaluate dynamic cerebral autoregulation and cerebral carbon dioxide reactivity (CO2R) during normothermic nonpulsatile CPB is presented. The technique uses continuous recording of invasive arterial blood pressure, middle cerebral artery blood flow velocity, absolute cerebral tissue oxygenation, in-line arterial carbon dioxide levels, and pump flow measurement in 37 adult male patients undergoing elective CPB. Cerebral autoregulation is estimated by transfer function analysis and the autoregulation index, based on the response to blood pressure variation induced by cyclic 6/min changes of indexed pump flow from 2.0 to 2.4 up to 2.8 L/min/m(2). CO2R was calculated from recordings of both cerebral blood flow velocity and cerebral tissue oxygenation. Cerebral autoregulation and CO2R were estimated at hypocapnia, normocapnia, and hypercapnia. CO2R was preserved during CPB, but significantly lower for hypocapnia compared with hypercapnia (p < 0.01). Conversely, cerebral autoregulation parameters such as gain, phase, and autoregulation index were significantly higher (p < 0.01) during hypocapnia compared with both normocapnia and hypercapnia. Assessing cerebral autoregulation and CO2R during CPB, by cyclic alteration of pump flow, showed an impaired cerebral autoregulation during hypercapnia.

Identification of posttraumatic ischemia and hyperperfusion by determination of the effect of induced arterial hypertension on carbon dioxide reactivity.

Both ischemia and hyperperfusion are known phenomena that follow traumatic brain injury. Cerebral carbon dioxide reactivity is diminished in both conditions. Differentiation is important because ischemia is thought to be a major factor of secondary neuronal loss and is potentially amenable to therapy by manipulation of cerebral perfusion pressure. The response of transcranial Doppler-based carbon dioxide reactivity to pharmacologically induced hypertension was studied sequentially in 29 patients with severe to moderate head injury to identify ischemia and luxury perfusion. After simultaneous baseline registration of the carbon dioxide reactivity of both middle cerebral arteries by two-channel transcranial Doppler, systolic arterial pressure was raised approximately 20 mm Hg by means of phenylephrine (Neosynephrine) infusion, and the carbon dioxide reactivity test was repeated. A significant improvement of impaired (< 2%/mm Hg) carbon dioxide reactivity after arterial pressure was raised by 20 mm Hg (signaling ischemia) was found in 32 of 124 evaluated middle cerebral arteries. Further deterioration of impaired reactivity occurred in only four tested hemispheres. While ischemic conditions were identified during the entire study period, hyperperfusion was encountered only after day 3. Ischemia after traumatic brain injury is a frequent phenomenon, whereas hyperperfusion is rare. Whether therapeutic optimization of carbon dioxide reactivity can improve the outcome of head-injury patients needs to be evaluated in further studies.

Sepsis-induced vasoparalysis does not involve the cerebral vasculature: indirect evidence from autoregulation and carbon dioxide reactivity studies

We have studied cerebral autoregulation and vasoreactivity to carbon dioxide in 10 patients with the sepsis syndrome receiving intensive therapy. All patients were sedated with infusions of midazolam and fentanyl, and their lungs were ventilated mechanically with oxygen-air to maintain normoxia and normocapnia. Inotropic support and antibiotics were administered as necessary. During a period of constant level of sedation and stable haemodynamics, cerebral autoregulation was tested by increasing mean arterial pressure (MAP) by 23 (SD 2) mm Hg from baseline with an infusion of phenylephrine and simultaneously recording middle cerebral artery blood flow velocity (vmca) using transcranial Doppler ultrasonography. Carbon dioxide reactivity was tested by varying PaCO2 between 3.0 and 7.0 kPa and simultaneously recording vmca. There was no significant change in vmca (57 (22) and 59 (23) cm s-1) during the increase in MAP (75 (11) to 98 (10) mm Hg). The mean index of autoregulation (IOR) was 0.92 (SEM 0.03), which was not significantly different from 1, indicating near perfect autoregulation. Although absolute carbon dioxide reactivity was lower than reported previously in awake subjects, relative carbon dioxide reactivity was within normal limits for all patients (11.6 (SEM 0.8) cm s-1 and 20.3 (3) % kPa-1, respectively). We conclude that cerebral carbon dioxide reactivity and pressure autoregulation remained intact in patients with the sepsis syndrome, providing indirect evidence that at least in the early stages of the syndrome, the widespread sepsis-induced vasoparalysis does not involve the cerebral vasculature.

Cerebral Pressure Autoregulation and Carbon Dioxide Reactivity During Propofol-Induced EEG Suppression

We studied cerebral pressure autoregulation and carbon dioxide reactivity during propofol-induced electrical silence of the electroencephalogram (EEG) in 10 patients. Anaesthesia was induced with propofol 2.5 mg kg−1, fentanyl 3 μg kg−1 and vecuronium 0.1 mg kg−1, and a propofol infusion of 250–300 μg kg−1 min−1 was used to induce EEG silence. Cerebral pressure autoregulation was tested by increasing mean arterial pressure (MAP) by 24 (SEM 5) mm Hg from baseline with an infusion of phenylephrine and simultaneously recording middle cerebral artery blood flow velocity (vmca) using transcranial Doppler. Carbon dioxide reactivity was tested by varying Paco2 between 4.0 and 7.0 kPa and recording vmca simultaneously. Although absolute carbon dioxide reactivity was reduced, relative carbon dioxide reactivity was within normal limits for all patients studied (mean 8.5 (SEM 0.8) cm s−1 kPa−1 and 22 (2)% kPa−1, respectively). No significant change in vmca (34 (2) and 35 (2) cm s−1) was observed with the increase in MAP (77 (4) to 101 (4) mm Hg) during autoregulation testing. We conclude that cerebral carbon dioxide reactivity and pressure autoregulation remain intact during propofol-induced isoelectric EEG.

Cerebral pressure autoregulation and carbon dioxide reactivity during propofol-induced EEG suppression

We studied cerebral pressure autoregulation and carbon dioxide reactivity during propofol-induced electrical silence of the electroencephalogram (EEG) in 10 patients. Anaesthesia was induced with propofol 2.5 mg kg-1, fentanyl 3 micrograms kg-1 and vecuronium 0.1 mg kg-1, and a propofol infusion of 250-300 micrograms kg-1 min-1 was used to induce EEG silence. Cerebral pressure autoregulation was tested by increasing mean arterial pressure (MAP) by 24 (SEM 5) mm Hg from baseline with an infusion of phenylephrine and simultaneously recording middle cerebral artery blood flow velocity (vmca) using transcranial Doppler. Carbon dioxide reactivity was tested by varying PaCO2 between 4.0 and 7.0 kPa and recording vmca simultaneously. Although absolute carbon dioxide reactivity was reduced, relative carbon dioxide reactivity was within normal limits for all patients studied (mean 8.5 (SEM 0.8) cm s-1 kPa-1 and 22 (2)% kPa-1, respectively). No significant change in vmca (34 (2) and 35 (2) cm s-1) was observed with the increase in MAP (77 (4) to 101 (4) mm Hg) during autoregulation testing. We conclude that cerebral carbon dioxide reactivity and pressure autoregulation remain intact during propofol-induced isoelectric EEG.

Local cerebral blood flow measured by stable xenon CT during fentanyl-diazepam anesthesia.

We assessed the local cerebral blood flow (LCBF) in 40 patients under fentanyl-diazepam anesthesia. The measurement of LCBF was made using 50%-70% stable xenon with 20 min of inhalation interval and a shuttle method for computed tomography imaging. All patients were anesthetized with 5.95±1.76 μg·kg-1 fentanyl and 0.22±0.07 mg·kg-1 diazepam under mechanical ventilation during CBF measurement. The values and distribution of LCBF on non-affected hemisphere appeared to be unaltered by fentanyldiazepam anesthesia. We also assessed the cerebral carbon dioxide reactivity in 6 patients. The cerebral carbon dioxide reactivity, expressed as percentage change in LCBF per unit change in arterial carbon dioxide partial pressure, was 5.39±1.07, and there were no significant differences of reactivity among regions studied. In conclusion, we showed reference values of LCBF and carbon dioxide reactivity, measured by stable xenon-enhanced computed tomography, in patients under fentanyl-diazepam anesthesia. Carbon dioxide reactivity was preserved in all regions including gray matter, white matter, and basal ganglia.

The clinical role of the cerebral collateral circulation in carotid occlusion

Abstract The occurrence and severity of ischemic cerebral symptoms after carotid occlusion depends on the interdependency of cerebral collateral blood supply. Only those with the "fittest" collateral capacity survive this process of natural selection. Using the transcranial Doppler method in 55 patients with unilateral carotid occlusion, we tested the dependency of each cerebral hemisphere on the remaining patent carotid artery by digital carotid compression, and in 41 of these patients we also tested the carbon dioxide reactivity in each hemisphere. Both hemispheric dependency and carbon dioxide reactivity were compared to 15 healthy controls. Mean blood flow velocities in the middle cerebral artery were lower on the occluded side than on the patent side ( p p r = −0.63). Tests of cerebral collateral reserve in patients with unilateral carotid occlusion evaluated by carotid compression and cerebral carbon dioxide reactivity may discriminate between survivors and potential nonsurvivors before the patent carotid artery occludes. (J VASC SURG 1990;12:113-8.)

The clinical role of the cerebral collateral circulation in carotid occlusion

The occurrence and severity of ischemic cerebral symptoms after carotid occlusion depends on the interdependency of cerebral collateral blood supply. Only those with the "fittest" collateral capacity survive this process of natural selection. Using the transcranial Doppler method in 55 patients with unilateral carotid occlusion, we tested the dependency of each cerebral hemisphere on the remaining patent carotid artery by digital carotid compression, and in 41 of these patients we also tested the carbon dioxide reactivity in each hemisphere. Both hemispheric dependency and carbon dioxide reactivity were compared to 15 healthy controls. Mean blood flow velocities in the middle cerebral artery were lower on the occluded side than on the patent side (p less than 0.003). When the patent carotid artery was compressed middle cerebral artery blood flow velocities on the occluded side were mainly independent of the patent carotid artery, but on the patent side there was a high degree of dependency (p less than 0.0001). Carbon dioxide reactivity did not differ between the hemispheres, but in hemispheres with total dependency, carbon dioxide reactivity was inversely proportional to the severity of stenosis (r = -0.63). Tests of cerebral collateral reserve in patients with unilateral carotid occlusion evaluated by carotid compression and cerebral carbon dioxide reactivity may discriminate between survivors and potential nonsurvivors before the patent carotid artery occludes.

The clinical role of the cerebral collateral circulation in carotid occlusion

The occurrence and severity of ischemic cerebral symptoms after carotid occlusion depends on the interdependency of cerebral collateral blood supply. Only those with the “fittest” collateral capacity survive this process of natural selection. Using the transcranial Doppler method in 55 patients with unilateral carotid occlusion, we tested the dependency of each cerebral hemisphere on the remaining patent carotid artery by digital carotid compression, and in 41 of these patients we also tested the carbon dioxide reactivity in each hemisphere. Both hemispheric dependency and carbon dioxide reactivity were compared to 15 healthy controls. Mean blood flow velocities in the middle cerebral artery were lower on the occluded side than on the patent side (p < 0.003). When the patent carotid artery was compressed middle cerebral artery blood flow velocities on the occluded side were mainly independent of the patent carotid artery, but on the patent side there was a high degree of dependency (p < 0.0001). Carbon dioxide reactivity did not differ between the hemispheres, but in hemispheres with total dependency, carbon dioxide reactivity was inversely proportional to the severity of stenosis (r = −0.63). Tests of cerebral collateral reserve in patients with unilateral carotid occlusion evaluated by carotid compression and cerebral carbon dioxide reactivity may discriminate between survivors and potential nonsurvivors before the patent carotid artery occludes.

Cerebral Carbon Dioxide Reactivity during Nonpulsatile Cardiopulmonary Bypass

Five patients undergoing extensive cerebral monitoring during cardiopulmonary bypass (CPB) procedures were subjected to studies on cerebral CO 2 reactivity during nonpulsatile CPB. The cerebral monitoring included recording of arterial blood pressure (BP), central venous pressure (CVP), epidural intracranial pressure (EDP), cerebral electrical activity by a cerebral function monitor (CFM), and middle cerebral artery (MCA) flow velocity by transcranial Doppler technique. The cerebral perfusion pressure (CPP) was thus continuously recorded (CPP = BP - EDP). During steady-state CPB with constant hematocrit, temperature, and arterial carbon dioxide tension (PaCO 2), MCA flow velocity varied with changing CPP in a pressure-passive manner, indicating that the cerebral autoregulation was not operative. During moderately hypothermic (28 to 32°C), nonpulsatile CPB, with steady-state hematocrit, temperature, and pump flow, we deliberately and rapidly changed PaCO 2 for periods of 1 or 2 minutes by increasing gas flow to the membrane oxygenator, thereby testing the cerebral CO 2 reactivity. Nineteen CO 2 reactivity tests, performed at CPP levels ranging from 17 to 75 mm Hg, disclosed that the cerebral CO 2 reactivity decreased with CPP, especially with CPP levels below 35 mm Hg. In these patients, concomitant changes in CPP during the CO 2 reactivity test could be compensated for by adjusting the observed change in MCA flow velocity. The corrected CO 2 reactivity values obtained in this way ranged from below 1.0 (observed at CPP levels below 20 mm Hg) to a 3.0 to 4.5% · mm Hg −1 change in PaCO 2 (observed at CPP levels above 35 mm Hg). Four CO 2 reactivity tests performed after rewarming was completed revealed corrected CO 2 reactivity values in the range from 1.3 to 1.9% · mm Hg −1 change in PaCO 2, observed at CPP in the range of 41 to 50 mm Hg. Cerebral CO 2 reactivity seems to be partially retained down to CPP levels of 20 mm Hg during moderately hypothermic, nonpulsatile CPB.