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Brain tissue oxygenation in patients with cerebral occlusive

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					British Journal of Anaesthesia 1997; 78: 169–171




Brain tissue oxygenation in patients with cerebral occlusive disease
and arteriovenous malformations


W. E. HOFFMAN, F. T. CHARBEL, G. EDELMAN AND J. I. AUSMAN



Summary                                                   Patients and methods
It is not clear if ventilation with oxygen increases      The studies were approved by the University of
brain tissue oxygen pressure (PO2) during                 Illinois Institutional Review Board for Clinical
ischaemia. We have measured brain tissue PO2              Research and informed consent was obtained.
carbon dioxide pressure (PCO2) and pH during              Patients in group 1 (n:9) served as controls for the
baseline anaesthesia and oxygen ventilation in            study. None of these patients bled or had clinical
non-ischaemic control patients (n:9), patients            signs of ischaemia before surgery. Neurosurgery was
with cerebral occlusive disease (n:11) and                performed in these patients for clipping of cerebral
patients with arteriovenous malformations (AVM,           aneurysms. Patients in group 2 (n:11) had evidence
n:12). The same anaesthetic treatment was given           of cerebral ischaemia, as determined by neurological
to all groups and anaesthesia was constant during         examination or the presence of transient ischaemic
the study. Arterial pressure, brain temperature and       episodes. Decreased regional cerebral perfusion was
arterial blood-gas tensions were similar between          confirmed in these patients by single photon emis-
groups. Under baseline conditions, brain tissue PO2       sion computed tomography (SPECT) or cerebral
was mean 4.2 (SD 1.4) kPa in the controls and was         angiography. Six of these patients were undergoing
70% lower in patients with ischaemia and AVM.             extracerebral to intracerebral vascular bypass, two
Patients with occlusive disease also had elevated         patients cerebral aneurysm surgery with confirmed
tissue PCO2 and acidosis. During oxygen ventila-          cerebral vasospasm and three patients had a cerebral
tion, PO2 increased to 7.5 (2.9) kPa in controls and      embolism. Patients in group 3 (n:12) were under-
this was 50% greater than the increase in the             going neurosurgery for AVM resection. Nine of
ischaemia and AVM patients. The results showed            these patients had previous neuroradiological AVM
that baseline tissue oxygenation and increases in         embolization procedures performed before AVM
PO2 during hyperoxia were attenuated in patients          resection.
with ischaemia or AVM. (Br. J. Anaesth. 1997; 78:            All patients were anaesthetized with thiopentone
169–171)                                                  3–5 mg kg91 and fentanyl 10–15 g kg91. Tracheal
                                                          intubation was facilitated with vecuronium 0.1 mg
Key words                                                 kg91 and the lungs ventilated with 0.5–1.5% isoflu-
Brain, ischaemia. Brain, carbon dioxide. Complications,   rane and oxygen in room air (inspired oxygen frac-
arteriovenous  malformation.  Carbon   dioxide, partial   tion:0.4). Oesophageal temperature was measured
pressure.                                                 and allowed to decrease to approximately 34 C.
                                                          Arterial carbon dioxide tension ( P aCO 2 ) was adjusted
                                                          to 3.9–4.6 kPa. Monitoring included mean radial
Under normal conditions, brain tissue PO2 is              arterial pressure (MAP) measured by a Marquette
reported to be in the range 3.3–5.2 kPa in animals        Electronics Tramscope (Milwaukee, WI, USA);
and patients.1–3 Tissue oxygenation may be                end-tidal isoflurane and PCO2 were measured with a
inhibited by cerebral occlusive disease or by arterial    Datex Ultima (Helsinki, Finland).
venous malformations (AVM), which attenuate                  After craniotomy, a PO2, PCO2, pH and tempera-
cerebral perfusion pressure by producing a low            ture sensor (Paratrend, Biomedical Sensors,
resistance shunt for blood flow.4–6 It has been           Malvern, PA) was inserted into cortex tissue
reported that the upper limit of tissue oxygenation is    (diameter:0.5 mm). The sensor is a sterile, dispos-
controlled in normal brain tissue during oxygen           able device comprised of two modified optical fibres
ventilation, but that these regulating mechanisms
are missing after head injury.3 Little is known of        WILLIAM E. HOFFMAN*, PHD, GUY EDELMAN, MD (Department of
tissue changes in PO2 during hyperoxia in tissue          Anesthesiology); FADY T. CHARBEL, MD, JAMES I. AUSMAN, MD,
affected by occlusive disease or AVM. The purpose         PHD (Department of Neurosurgery); University of Illinois at
of this study was to evaluate the effect of oxygen        Chicago, Chicago, IL, USA. Accepted for publication: September
                                                          29, 1996.
ventilation in patients with cerebral occlusive             *Address for correspondence: Anesthesiology Department,
disease and AVM compared with non-ischaemic               University of Illinois Hospital, 1740 W Taylor, Suite 3200,
controls.                                                 Chicago, IL 60612, USA.
170                                                                                                      British Journal of Anaesthesia
Table 1 Mean arterial pressure (MAP), arterial oxygen and carbon dioxide partial pressures and pH, tissue carbon dioxide partial
pressure, pH and brain temperature during 40% (baseline) and 100% oxygen ventilation (oxygen) in controls, and in those with cerebral
occlusive disease (COD) and arteriovenous malformations (AVM) (mean SD)). PaO2 :arterial PO2, PaCO2 :arterial PCO2, pHa:arterial
pH, PtCO2 :tissue PCO2, pHt:tissue pH. *P:0.05 compared with baseline, †P:0.05 compared with control

                                  MAP            PaO2            PaCO2                           PtCO2                        Brain temp
Group       Treatment      n      (mm Hg)       (kPa)           (kPa)          pHa              (kPa)          pHt            (ºC)

Control     Baseline       9      86 (15)       24.9 (7.3)      4.3 (0.4)      7.47 (0.04)      6.4 (0.8)      7.14 (0.15)    35.6 (1.3)
            Oxygen                87 (15)       54.0 (7.6)*     4.3 (0.6)      7.43 (0.07)      6.3 (0.8)      7.18 (0.10)    35.6 (1.3)
COD         Baseline       11     88 (12)       29.2 (4.1)      4.5 (0.4)      7.42 (0.06)      9.2 (4.9)†     6.85 (0.25)†   35.0 (0.6)
            Oxygen                88 (12)       58.7 (3.3)*     4.8 (0.3)      7.38 (0.03)      9.1 (3.7)†     6.88 (0.25)†   34.9 (0.6)
AVM         Baseline       12     80 (8)        23.3 (4.7)      4.3 (0.7)      7.43 (0.07)      6.7 (1.2)      7.09 (0.20)    35.2 (0.9)
            Oxygen                81 (8)        52.3 (8.4)*     4.3 (0.5)      7.44 (0.05)      6.5 (1.2)      7.17 (0.17)    35.2 (0.9)


for measurement of PCO2 and pH, a miniaturized
Clark electrode for PO2 measurement and a thermo-
couple for measurement of temperature. The sensor
was calibrated with three precision gases supplied
with the monitor before insertion into the patient.
The gases are: 1:2% carbon dioxide, 15% oxygen,
balance nitrogen; 2:5% carbon dioxide, 15%
oxygen, balance nitrogen; 3:10% carbon dioxide,
15% oxygen, balance nitrogen. The calibration
range and 95% confidence limits for each sensor
have been determined in in vitro testing: oxygen
(range 0–15.7 kPa, 95% confidence limits ;0.1
kPa); carbon dioxide (range 1.3–10.5 kPa, 95% con-
fidence limits ;0.4 kPa); pH (range 6.80–7.80, 95%
confidence limits ;0.03). The 0% to 90% response
time for each sensor is: oxygen:70 s, carbon
dioxide:143 s, pH:78 s.7 All monitored variables
were collected by computer using Labview (National                       Figure 1 Changes in PO2, PCO2 and pH during oxygen
Instruments, Austin, TX) every 10 s.                                     ventilation in a non-ischaemic patient. The scale for PO2 and
   When the sensor was inserted, baseline tissue gas                     PCO2 (kPa) is shown on the left and that for pH on the right.
tensions, pH and temperature, MAP and blood-gas                          Oxygen ventilation produced an increase in PO2 with no change
                                                                         in PCO2 or pH.
tensions were measured after a 30-min equilibration
period. Inspired oxygen fraction was increased from
0.4 to 1.0 for 10 min and then returned to baseline
levels. Samples for arterial blood-gas measurements
were obtained under baseline conditions and during
oxygen ventilation.
   Data are reported as mean (SD). Differences in
mean values between the three groups were analysed
by analysis of variance with post hoc testing if a signif-
icant F value was found. Differences between base-
line and oxygen administration were analysed using
paired t tests. If data distribution failed the underly-
ing assumptions for normality and equal variance,
non-parametric analyses using Kruskal–Wallis or
Wilcoxon tests were performed.

Results
Under baseline conditions, the physiological vari-
ables in table 1 were similar in control, ischaemic                      Figure 2 Tissue PO2 during baseline measurements (Base) and
                                                                         oxygen ventilation (O2). Baseline PO2 was greater in controls
and AVM patients. With administration of 100%                            compared with those with cerebral occlusive disease and AVM.
oxygen in the inspired gases, PaO increased in all
                                            2
                                                                         The increase in PO2 during hypoxia was attenuated in cerebral
three groups to a similar degree. The response to                        occlusive disease and AVM compared with controls. *P:0.05
oxygen ventilation in a normal patient is shown in                       compared with baseline; †P:0.05 compared with control.
figure 1. Tissue PO2 increased in these patients
during the increase in PaO but there was no
                                    2
change in tissue PCO2 or pH. Figure 2 show mean                          attenuated in ischaemic and AVM patients
tissue PO2 data for all patients. Under baseline                         during hyperoxia. Tissue PCO2 increased and
conditions, tissue PO2 decreased in ischaemic and                        pH decreased in ischaemic patients during the
AVM patients compared with controls, and the                             baseline period but neither variable changed
increase in PO2 during oxygen administration was                         during oxygen ventilation (table 1).
Brain tissue oxygen                                                                                                      171

                                                            and AVM were different but that inadequate
Discussion
                                                            tissue oxygenation was a consistent problem in
In non-ischaemic patients, we found a baseline              both groups.
tissue PO2 of 4.2 kPa. This is consistent with pre-
vious reports.1–3 8 During hyperoxia, tissue PO2
increased to 7.5 kPa in non-ischaemic patients. This
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