Relative CO2 Reactivity Research Articles

Effect of dexmedetomidine on dynamic cerebral autoregulation and carbon dioxide reactivity during sevoflurane anesthesia in healthy patients.

BackgroundThere are conflicting opinions on the effect of dexmedetomidine on cerebral autoregulation. This study assessed its effect on dynamic cerebral autoregulation (dCA) using a transcranial Doppler (TCD).MethodsThirty American Society of Anesthesiologists physical status I and II patients between 18 and 60 years, who underwent lumbar spine surgery, received infusions of dexmedetomidine (Group D) or normal saline (Group C), followed by anesthesia with propofol and fentanyl, and maintenance with oxygen, nitrous oxide and sevoflurane. After five minutes of normocapnic ventilation and stable bispectral index value (BIS) of 40–50, the right middle cerebral artery flow velocity (MCAFV) was recorded with TCD. The transient hyperemic response (THR) test was performed by compressing the right common carotid artery for 5–7 seconds. The lungs were hyperventilated to test carbon dioxide (CO2) reactivity. Hemodynamic parameters, arterial CO2 tension, pulse oximetry (SpO2), MCAFV and BIS were measured before and after hyperventilation. Dexmedetomidine infusion was discontinued ten minutes before skin-closure. Time to recovery and extubation, modified Aldrete score, and emergence agitation were recorded.ResultsDemographic parameters, durations of surgery and anesthesia, THR ratio (Group D: 1.26 ± 0.11 vs. Group C: 1.23 ± 0.04; P = 0.357), relative CO2 reactivity (Group D: 1.19 ± 0.34 %/mmHg vs. Group C: 1.23 ± 0.25 %/mmHg; P = 0.547), blood pressure, SpO2, BIS, MCAFV, time to recovery, time to extubation and modified Aldrete scores were comparable.ConclusionsDexmedetomidine administration does not impair dCA and CO2 reactivity in patients undergoing spine surgery under sevoflurane anesthesia.

Steady-state tilt has no effect on cerebrovascular CO2 reactivity in anterior and posterior cerebral circulations.

What is the central question of this study? We investigated the effects of superimposed tilt and hypercapnia-induced cerebral arteriolar dilatation on anterior and posterior cerebrovascular CO2 reactivity using hyperoxic rebreathing in human participants. What is the main finding and its importance? The main findings are threefold: (i) cerebrovascular CO2 reactivity in the anterior and posterior cerebrovasculature is unchanged with tilt; (ii) cerebral autoregulation is unlikely responsible due to unchanging cerebrovascular resistance reactivity between positions; and (iii) cerebral blood flow is not pressure passive during tilt as it is with pharmacological or lower body negative pressure-induced changes in mean arterial pressure, suggesting that sympathetic activation or balanced transmural pressures during head-down tilt regulate cerebral blood flow. Cerebral autoregulation is a protective feature of the cerebrovasculature that maintains relatively constant cerebral perfusion in the face of static and dynamic fluctuations in mean arterial pressure (MAP). However, the extent that the cerebrovasculature can autoregulate in the face of superimposed steady-state orthostasis-induced changes in MAP (e.g. head-up and head-down tilt; HUT and HDT) and CO2 -mediated arteriolar dilatation is unknown. We tested the effects of steady-state tilt on cerebrovascular CO2 reactivity in the middle and and posterior cerebral artery in the following five body positions: 90 deg HUT, 45 deg HUT, supine, 45 deg HDT and 90 deg HDT on a tilt table during a modified hyperoxic rebreathing test. Absolute and relative cerebrovascular CO2 reactivity [cerebral blood velocity (CBV)/CO2 ], cerebrovascular resistance (CVR) reactivity (CVR/CO2 ) and MAP reactivity (MAP/CO2 ) were quantified using linear regression. Mean arterial pressure was significantly elevated in 90 deg HDT compared with other positions during baseline steady-state tilt (P < 0.01). Absolute CBV/CO2 and CVR/CO2 were greater in the middle cerebral artery than the posterior cerebral artery (P < 0.01) in all body positions, but relative measures were not different (P = 0.143 and P = 0.360, respectively), nor was there any interaction with tilt position. In addition, there was no difference in absolute (P = 0.556) and relative MAP/CO2 (P = 0.308) between positions. Our data demonstrate that cerebral blood flow remains well regulated during superimposed steady-state orthostatic stress and dynamic changes in the partial pressure of end-tidal CO2 during rebreathing. Cerebral autoregulation is likely not the mechanism responsible, but rather sympathetic nervous system activation or a balanced cerebrovascular transmural pressure with HDT maintains resting cerebral blood flow and cerebrovascular CO2 reactivity during rebreathing.

The effects of head‐up and head‐down tilt on cerebrovascular CO2 reactivity in anterior and posterior cerebral circulations

Cerebral autoregulation is a protective feature of the cerebrovasculature that maintains relatively constant cerebral perfusion in the face of static and dynamic fluctuations in mean arterial pressure (MAP). However, gravity‐dependent shifts in blood volume distribution during head‐up and head‐down tilt (HUT, HDT) have profound effects on venous return, cardiac output and MAP. Further, cerebral blood flow (CBF) is highly sensitive to the influence of changes in arterial CO2 (PaCO2) on arteriolar diameter. We tested the effects of steady‐state tilt on cerebral blood velocity (CBV) and CO2 reactivity in the middle and posterior cerebral arteries (MCA, PCA) using hyperoxic rebreathing and transcranial Doppler ultrasound in various positions on a tilt table. Following initial testing in supine position, subjects were positioned randomly and tested in each of four positions: 90° HDT, 45° HDT, 45° HUT and 90° HUT. There were no differences in steady‐state MCA or PCA CBV across positions. Absolute and relative CO2 reactivity slopes were calculated for the MCA and PCA using linear regression. Absolute reactivity was greater in the MCA than the PCA in all 5 positions, but there was no interaction between reactivity and tilt. Our data demonstrate that CBF is maintained through cerebral autoregulation in the face of superimposed steady‐state orthostatic stress and dynamic changes in PaCO2.

Evaluation of cerebrovascular carbon dioxide reactivity in patients with diabetes mellitus under sedative doses of propofol

The present study compared cerebrovascular CO2 reactivity in diabetic patients on different treatment modalities under sedative doses of propofol. Fifteen patients with diabetes mellitus (on three different antidiabetic treatment modalities) who required mechanical ventilation during intensive care therapy were studied, sedation during mechanical ventilation being maintained using propofol. As controls, 6 patients without diabetes were monitored. A 2.5-MHz pulsed transcranial Doppler probe was attached to the head of the patient at the right temporal window for continuous measurement of mean blood flow velocity in the middle cerebral artery (Vmca). After establishing baseline values of Vmca and cardiovascular hemodynamics, end-tidal CO2 was decreased by increasing ventilatory frequency by 5-8 breaths.min(-1). Values for absolute and relative CO2 reactivity in insulintreated patients were lower than those in the other three groups (absolute CO2 reactivity [means +/- SD]: control, 3.1 +/- 0.6 cm.s(-1).mmHg(-1), diet, 3.8 +/- 1.4 cm.s(-1) x mmHg(-1); oral antidiabetic drug 3.2 +/- 0.9 cm x s(-1) x mmHg(-1); insulin, 1.1 +/- 0.6 cm x s(-1) x mmHg(-1); P = 0.002).The present study shows that insulin-treated diabetic patients probably have lower cerebrovascular CO2 reactivity under propofol anesthesia than control patients or diabetics treated with dietary therapy or oral hypoglycemics.

The comparative effects of sevoflurane versus isoflurane on cerebrovascular carbon dioxide reactivity in patients with previous stroke

The use of volatile anesthetics is reportedly related to altered cerebrovascular carbon dioxide (CO2) reactivity. We examined the comparative effects of sevoflurane versus isoflurane on cerebrovascular CO2 reactivity in patients with previous stroke. Twenty-four patients with previous stroke and 20 patients without previous stroke (serving as controls) were studied. Anesthesia was maintained with either end-tidal 1.0 minimum alveolar concentration (MAC) sevoflurane or 1.0 MAC isoflurane in 33% oxygen and 67% nitrous oxide. A 2.5-MHz pulsed transcranial Doppler (TCD) probe was attached to the patient's head at the right or left temporal window for continuous measurement of mean blood flow velocity in the middle cerebral artery (Vmca). After establishing baseline values of Vmca and cardiovascular hemodynamics, we increased end-tidal CO2 by decreasing the ventilatory frequency by 2-5 breaths x min(-1). We found that values for absolute and relative CO2 reactivity in the sevoflurane groups were lower than those in the isoflurane groups (absolute CO2 reactivity in the sevoflurane groups: control, 3.3 +/- 0.4*; previous stroke, 3.4 +/- 0.4*; absolute CO2 reactivity in the isoflurane groups: control, 4.2 +/- 0.3; previous stroke, 4.5 +/- 0.4, cm x s(-1) x mmHg(-1); *P < 0.05 compared with isoflurane group). There were no significant differences in the values for absolute and relative CO2 reactivity between the controls and the previous-stroke patients within each of the sevoflurane and isoflurane groups. Our findings suggest that, in patients with previous stroke, cerebrovascular CO2 reactivity under sevoflurane anesthesia was lower than that under isoflurane anesthesia.

Comparative effects of propofol vs dexmedetomidine on cerebrovascular carbon dioxide reactivity in patients with septic shock

The use of sedative drugs is reportedly related to altered cerebrovascular CO2 reactivity. The present study examined the comparative effects of propofol vs dexmedetomidine on cerebrovascular CO2 reactivity in patients with septic shock. A total of 20 patients with septic shock who required mechanical ventilation were included in this study. Sedation during mechanical ventilation was maintained using either propofol or dexmedetomidine. A 2.5 MHz pulsed transcranial Doppler probe was attached to the head of the patient at the right temporal window for continuous measurement of mean blood flow velocity in the middle cerebral artery (V(mca)). After establishing baseline values of V(mca) and cardiovascular haemodynamics, end-tidal CO2 was increased by decreasing ventilatory frequency by 5-8 bpm. The absolute and relative CO2 reactivity values in patients with septic shock were lower for both propofol and dexmedetomidine than those for control groups, with significant differences between these values in the two septic shock groups (absolute CO2 reactivity in septic shock under propofol: 2.6 (sd 0.3) cm s(-1) mm Hg(-1); absolute CO2 reactivity in septic shock under dexmedetomidine: 2.0 (0.3) cm s(-1) mm Hg(-1); P<0.01). This study showed that cerebrovascular CO2 reactivity was lower under dexmedetomidine sedation than under propofol sedation during almost identical sedation in patients with septic shock.

The comparative effects of sevoflurane vs. isoflurane on cerebrovascular carbon dioxide reactivity in patients with hypertension

Sevoflurane has been shown to have different effects on cerebrovascular CO(2) reactivity in comparison with isoflurane. In this study, the comparative effects of sevoflurane vs. isoflurane on cerebrovascular CO(2) reactivity were examined in patients with hypertension. Fifty patients, 30 hypertensive and 20 normotensive, were included in this study. The 30 hypertensive patients were divided into two groups: sevoflurane and isoflurane. Patients with controlled hypertension (n= 9 in each of the two groups) were those with normal blood pressure levels (systolic blood pressure below 139 mmHg). Patients with uncontrolled hypertension (n= 6 in each of the two groups) were those with high blood pressure levels despite medication (systolic blood pressure above 160 mmHg). Anesthesia was maintained with either 1.0 minimum alveolar concentration (MAC) of sevoflurane or 1.0 MAC of isoflurane in 33% oxygen and 67% nitrous oxide. A 2.5-MHz pulsed transcranial Doppler probe was attached to the patient's head at the right temporal window for continuous measurement of the mean blood flow velocity in the middle cerebral artery (V(mca)). After establishing baseline values of V(mca) and cardiovascular hemodynamics, the end-tidal CO(2) was increased by decreasing the ventilatory frequency by 2-5 breaths per minute. Values of the absolute and relative CO(2) reactivity in the sevoflurane groups were lower than those in the isoflurane groups. There were no significant intra-group differences in the absolute and relative CO(2) reactivity within the sevoflurane and isoflurane groups. Our findings suggest that, in hypertensive patients, the control of cerebral blood flow by altering the pressure of arterial CO(2) (P(a)co(2)) can be more effectively achieved during isoflurane rather than sevoflurane anesthesia.

Effects of nicardipine-induced hypotension on cerebrovascular carbon dioxide reactivity in patients with diabetes mellitus under sevoflurane anesthesia

The purpose of this study was to examine the effects of nicardipine-induced hypotension on cerebrovascular CO2 reactivity in patients with diabetes mellitus under sevoflurane anesthesia. Nineteen diabetic patients, and 11 nondiabetic patients (serving as controls), undergoing elective orthopedic, cardiovascular, or thoracic surgery were included in the study. The diabetic patients were divided into three groups according to the antidiabetic therapy they were receiving, i.e., diet therapy (n = 6), oral antidiabetic drugs (n = 7), and insulin (n = 6). Anesthesia was maintained with 1.0 minimum alveolar concentration of sevoflurane. Absolute and relative cerebrovascular CO2 reactivity was calculated using a 2.5-MHz pulsed transcranial Doppler (TCD) probe for the continuous measurement of mean blood flow velocity in the middle cerebral artery (Vmca). The cerebrovascular CO2 reactivity was measured both at baseline and during hypotension by increasing the ventilatory frequency by 4 to 7 breaths.min(-1). Nicardipine was used to induce hypotension. We found that values for the Bispectral index (BSI), baseline mean blood pressure, endtidal CO2 (Pet(CO2)), and Vmca were essentially identical in all patients, irrespective of the type of antidiabetic treatment being taken. Values for absolute and relative CO2 reactivity in insulin-dependent patients, at both baseline blood pressure and during hypotension, were lower than those in patients in the antidiabetic drug, diet, and control groups (during hypotension, absolute CO2 reactivity: diet group: 3.2 +/- 0.9; oral antidiabetic drug group: 3.2 +/- 0.7; insulin group: 1.5 +/- 0.6; control group: 3.4 +/- 0.8 cm.s(-1).mmHg(-1), [P < 0.05 insulin group vs the other groups]; relative CO2 reactivity: diet group, 6.3 +/- 1.0; oral antidiabetic drug group, 6.5 +/- 0.8; insulin group, 3.5 +/- 0.8; control group, 6.5 +/- 0.7%.mmHg(-1), [P < 0.05 insulin group vs the other groups]. We concluded that cerebrovascular CO2 reactivity in insulin-dependent patients is impaired during nicardipine-induced hypotension under sevoflurane anesthesia.

The Comparative Effects of Sevoflurane Versus Isoflurane on Cerebrovascular Carbon Dioxide Reactivity in Patients with Diabetes Mellitus

The use of volatile anesthetics has been reported to alter cerebrovascular carbon dioxide (CO2) reactivity. We examined the comparative effects of sevoflurane versus isoflurane on cerebrovascular CO2 reactivity in 40 patients with diabetes mellitus. Anesthesia was maintained with either 1.0 minimum alveolar anesthetic concentration of sevoflurane or 1.0 minimum alveolar anesthetic concentration of isoflurane in 33% oxygen and 67% nitrous oxide. A 2.5-MHz pulsed transcranial Doppler probe was attached to the patient's head at the right temporal window for continuous measurement of mean blood flow velocity in the middle cerebral artery. After establishing baseline middle cerebral artery velocity values and cardiovascular hemodynamics, we increased end-tidal CO2 by decreasing ventilatory frequency by 2-5 breaths/min and repeated the measurements. These were then used to calculate absolute and relative CO2 reactivity. Absolute CO2 reactivity was less in insulin-treated patients with either sevoflurane or isoflurane compared with those patients on oral antidiabetic drugs or dietary therapy (sevoflurane group: diet = 2.6 +/- 0.6; oral antidiabetic drug = 2.5 +/- 0.8; insulin = 1.6 +/- 0.8*; isoflurane group: diet = 3.3 +/- i0.7; oral antidiabetic drug = 3.4 +/- 0.7; insulin = 1.9 +/- 0.7* cm.s(-1).mm Hg(-1); *P < 0.05, respectively). Relative CO2 reactivity showed a similar pattern in the diet-controlled and oral antidiabetic groups, absolute and relative CO2 reactivities were lower with sevoflurane versus isoflurane. Hence, we conclude that cerebrovascular CO2 reactivity in insulin-dependent patients is impaired under both sevoflurane and isoflurane anesthesia.

Dynamic cardiorespiratory interaction during head-up tilt-mediated presyncope.

In 28 healthy adults, we compared the dynamic interaction between respiration and cerebral autoregulation in 2 groups of subjects: those who did and did not develop presyncopal symptoms during 70 degrees passive head-up tilt (HUT), i.e., nonpresyncopal (23 subjects) and presyncopal (5 subjects). Airflow, CO2, cerebral blood flow velocity (CBF), ECG, and blood pressure (BP) were recorded. To determine whether influences of mean BP (MBP) and systolic SP (SBP) on CBF were altered in presyncopal subjects, coherencies and transfer functions between these variables and mean and peak CBF (CBFm and CBFp) were estimated. To determine the influence of end-tidal CO2 (ETco2) on CBF, the relative CO2 reactivity (%change in CBFm per mmHg change in ETco2) was calculated. We found that in presyncopal subjects before symptoms during HUT, coherence between SBP and CBFp was higher (P=0.02) and gains of transfer functions between BP (MBP and SBP) and CBFm were larger (MBP, P=0.01; SBP, P=0.01) in the respiratory frequency region. In the last 3 min before presyncope, presyncopals had a reduced relative CO2 reactivity (P=0.005), likely a consequence of the larger decrease in ETco2. We hypothesize that the CO2-mediated increase in resistance attenuates autoregulation such that the relationship between systemic and cerebral hemodynamics is enhanced. Our results suggest that an altered cardiorespiratory interaction involving cerebral hemodynamics may contribute in the cascade of events during tilt that culminate in unexplained syncope.

Cerebral blood flow, cerebral metabolic rate of oxygen and relative CO2 reactivity during neurolept anaesthesia in patients subjected to craniotomy for supratentorial cerebral tumours.

In 10 patients subjected to craniotomy for supratentorial cerebral tumours in neurolept anaesthesia, cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured twice peroperatively by a modification of the Kety & Schmidt technique, using 133Xe. The relative CO2 reactivity was assessed indirectly as the % change of the arteriovenous oxygen difference (AVDO2) per mm change in PaCO2. The patients were premedicated with diazepam 10-15 mg perorally. For induction, thiopentone 4-6 mg/kg, droperidol 0.2 mg/kg and fentanyl 5 micrograms/kg were used, and for maintenance N2O 67% and fentanyl 4 micrograms/kg/h. During the first flow measurement the median and range of CBF was 30 ml/100 g/min (range 17-45), of AVDO2 8.0 vol % (range 4.1-9.5), and of CMRO2 2.28 ml O2/100 g/min (range 1.57-2.84). During the second CBF study, AVDO2 increased to 9.3 vol % (range 3.4-11) (P less than 0.05), and CMRO2 increased to 2.51 ml O2/100 g/min (range 1.88-3.00) P less than 0.05, while CBF was unchanged. The CO2 reactivity was present in all studies, median 1.8%/mmHg (range 0.5-15.1). The correlation coefficients between jugular venous oxygen tension/saturation, respectively, and CBF were high at tensions/saturations exceeding 4.0 kPa and 55%, indicating that hyperperfusion is easily unveiled by venous samples from the jugular vein during this anaesthesia.

The relationship between cerebral metabolic rate of oxygen and cerebral blood flow in the acute phase of head injury.

In 20 comatose patients (Glasgow coma scale less than or equal to 6 at admission) with severe head injury, the cerebral metabolic rate of oxygen (CMRO2) was calculated as the product of the hemispheric cerebral blood flow (CBF) and the arterio-venous oxygen content difference (AVDO2). The hemispheric CBF was calculated by the intracarotid 133xenon washout method by stochastic analysis as the average of 16 regions, and the measurements were performed within 3 weeks after the acute trauma. Generally no significant correlation (P less than 0.05) between CMRO2 and CBF was found, either in the total number of paired observations, in studies of hyperaemia defined as CBF greater than or equal to 30 ml 100 g-1 min-1; or in studies with reduced flow (CBF less than 30 ml 100 g-1 min-1). However, in about 50% of patients subjected to repeated studies within days, CBF was positively correlated to CMRO2, and this correlation was observed independently of the CBF value. Hyperaemia was associated with a significant decrease in AVDO2, a significant increase in both absolute and relative CO2 reactivity, and a significant increase in ventricular fluid pH; but not to an increase in intraventricular pressure, mean arterial blood pressure or significant changes in ventricular fluid lactate or lactate/pyruvate ratio.

Local vascular response to change in carbon dioxide tension. Long term observation in the cat's brain by means of the hydrogen clearance technique.

Thirty six small hydrogen sensitive electrodes were inserted into the brains of 6 cats to evaluate the local vascular response to change in PaCO2, of cortex, subcortical white matter, and caudate nucleus. Repeated measurements (617) of local cerebral blood flow (ICBF) were performed over a period of 12 weeks. Within a PaCO2 range from 19 to 96 mmHg the local response of CBF was linear in most of the regions measured. The absolute local CO2 reactivity (CO2-R) showed a positive correlation to ICBF at PaCO2 = 40 mmHg (ICBF40) with the regression line: absolute CO2-R = 0.02 ICBF40 + 0.22, r = 0.71 (p less than 0.01). Therefore relative ICBF change was calculated in relation to ICBF40 to make comparisons between the CO2 response of different measuring days and of different regions examined. No significant change in relative CO2-R was observed during the 12 weeks interval. Differences of relative CO2-R between investigated regions were insignificant. The uniformity of relative CO2 response might support the hypothesis of a direct effect of PaCO2 or pH on the vessel wall. For comparison of CBF, the individual determination of CBF40 and relative CO2-R would be necessary.