Fuminori Kawahara

Diabetic Patients Have an Impaired Cerebral Vasodilatory Response to Hypercapnia Under Propofol Anesthesia

Background and Purpose— The purpose of this study was to examine the effects of diabetes mellitus and its severity on the cerebral vasodilatory response to hypercapnia. Methods— Thirty diabetic patients consecutively scheduled for elective major surgery were studied. After induction of anesthesia, a 2.5-MHz pulsed transcranial Doppler probe was attached to the patient’s head at the right temporal window, and mean blood flow velocity of the middle cerebral artery (Vmca) was measured continuously. After the baseline Vmca, arterial blood gases, and cardiovascular hemodynamic values were measured, end-tidal CO2 was increased by reducing ventilatory frequency by 2 to 5 breaths per minute. Measurements were repeated when end-tidal CO2 increased and remained stable for 5 to 10 minutes. Results— Significant differences were observed in absolute and relative CO2 reactivity between the diabetes and control groups (absolute CO2 reactivity: control, 2.8±0.7; diabetes mellitus, 2.1±1.3; P <0.01; relative CO2 reactivity: control, 6.3±1.4; diabetes mellitus, 4.5±2.7; P <0.01, Mann-Whitney U test). Significant differences were also found between diabetic patients with retinopathy and those without retinopathy in absolute (P =0.002) and relative (P =0.002) CO2 reactivity, glycosylated hemoglobin (P =0.0034), and fasting blood sugar (P =0.01) (Scheffé’s test, Mann-Whitney U test). There was an inverse correlation between absolute CO2 reactivity and glycosylated hemoglobin (r =0.69, P <0.001). Conclusions— Insulin-dependent diabetic patients have an impaired vasodilatory response to hypercapnia compared with that of the control group, and the present findings suggest that their degree of impairment is related to the severity of diabetes mellitus.

Effects of hypothermic and normothermic cardiopulmonary bypass on brain oxygenation

BACKGROUND In this study, we assessed the effects of normothermia and hypothermia during cardiopulmonary bypass (CPB) both on internal jugular venous oxygen saturation (SjvO2) and the regional cerebral oxygenation state (rSO2) estimated by near infrared spectroscopy (NIRS). METHODS Thirty patients scheduled for elective coronary artery bypass graft surgery (CABG) were randomly divided into two groups. Group 1 (n = 15) underwent surgery for normothermic (> 35 degrees C) CPB, and group 2 (n = 15) underwent surgery for hypothermic (30 degrees C) CPB, and alpha-stat regulation was applied. A 4.0-French fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to continuously monitor the SjvO2 value. To estimate the rSO2 state, a spectrophotometer probe was attached to the mid-forehead. SjvO2 and rSO2 values were then collected simultaneously using a computer. RESULTS Neither the cerebral desaturation time (duration during SjvO2 value below 50%), nor the ratio of the cerebral desaturation time to the total CPB time significantly differed (normothermic group: 18+/-6 min, 15+/-6%; hypothermic group: 17+/-6 min, 13+/-6%, respectively). The rSO2 value in the normothermic group decreased during the CPB period compared with the pre-CPB period. The rSO2 value in the hypothermic group did not change throughout the perioperative period. CONCLUSIONS These findings suggest that near infrared spectroscopy might be sensitive enough to detect subtle changes in regional cerebral oxygenation.

Slow rewarming improves jugular venous oxygen saturation during rewarming

Background: There have been many studies regarding the etiology of postoperative cognitive dysfunction after coronary artery bypass graft (CABG) surgery. Although its etiology remains unresolved, one possible factor related to postoperative cognitive dysfunction is a reduced internal jugular venous oxygen hemoglobin saturation (SjvO2) during the rewarming period. The purpose of this study was to examine the effect of rewarming rates on SjvO2 during rewarming.

Jugular venous bulb oxygen saturation in patients with preexisting diabetes mellitus or stroke during normothermic cardiopulmonary bypass.

Background The authors hypothesized that patients with cerebrovascular abnormalities or metabolic disorders may experience abnormality in cerebral circulation more frequently than patients without these risks. The current study attempted to assess jugular venous bulb oxygen saturation (SjvO2) in patients with preexisting diabetes mellitus or stroke undergoing normothermic cardiopulmonary bypass. Methods Thirty-nine patients undergoing elective coronary artery bypass graft surgery were studied, including 19 age-matched control patients, 10 diabetic patients, and 9 patients with preexisting stroke A 4.0-French fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to continuously monitor internal SjvO2. Hemodynamic parameters and arterial and jugular venous blood gases were measured at seven time points: (1) after the induction of anesthesia and before the start of surgery, (2) just after the beginning of cardiopulmonary bypass, (3) 20 min after the beginning of bypass, (4) 40 min after the beginning of bypass, (5) 60 min after the beginning of bypass, (6) just after the cessation of bypass, and (7) at the end of the operation. Results No significant differences were seen in mean arterial pressure, arterial carbon dioxide tension (PaCO2), or hemoglobin concentration among the three groups during the study. The SjvO2 value did not differ among the three groups after anesthesia induction and before surgery, just after the beginning of cardiopulmonary bypass, 60 min after the beginning of bypass, just after the end of bypass, or at the end of the operation. Significant differences between the control group and the diabetic and stroke groups were observed, however, at 20 min and 40 min after the beginning of bypass (at 20 min: control group 62.2 ± 6.8%, diabetes group 48.4 ± 5.1%, stroke group 45.9 ± 6.3%; at 40 min: control group 62.6 ± 5.2%, diabetes group 47.1 ± 5.2%, stroke group 48.8 ± 4.1% [values expressed as the mean ± SD];P < 0.05). Also, values in the diabetes and stroke groups were decreased at 20 min and 40 min after the beginning of bypass compared with before the start of surgery. Conclusions A reduced SjvO2 value was observed more frequently in patients with preexisting diabetes mellitus or stroke during normothermic cardiopulmonary bypass. It is possible that cerebral circulation during normothermic bypass is altered in patients with risk factors for cerebrovascular disorder.

Balloon pump–induced pulsatile perfusion during cardiopulmonary bypass does not improve brain oxygenation☆☆☆★

BACKGROUND Whether pulsatile flow offers substantial advantages for brain protection during cardiopulmonary bypass is controversial. The purpose of this study is to determine whether differences exist between pulsatile and nonpulsatile bypass concerning the effects on internal jugular venous saturation and on the state of regional cerebral oxygenation during normothermia. METHODS Twenty-two patients undergoing elective coronary artery bypass grafting were randomly divided into 2 groups: group 1 (n = 11) received nonpulsatile perfusion during cardiopulmonary bypass and group 2 (n = 11) received pulsatile perfusion during bypass. We used an intra-aortic balloon pump to generate pulsatility. A spectrophotometric probe (INVOS 3100R, Somanetics, Troy, Mich) was used to assess the state of regional cerebral oxygenation. A 4F fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to monitor jugular venous oxygen saturation. Hemodynamic variables, arterial and jugular venous blood gases, and regional cerebral oxygenation were measured at 7 times points. RESULTS In both groups, jugular venous oxygen saturation decreased at the early stage of the cardiopulmonary bypass (P =.03). Five patients in group 1 and 6 in group 2 had a jugular venous oxygen saturation of less than 50%. In both groups, the regional cerebral oxygenation value decreased during cardiopulmonary bypass (P =.04). CONCLUSIONS The present results showed that pulsatility generated through the use of intra-aortic balloon pumping did not produce any beneficial effects on jugular venous oxygen saturation and regional cerebral oxygenation at normothermia.

Cerebral oxygénation during prostaglandin E1 induced hypotension

PurposeTo evaluate the cerebral oxygenation effects of hypotension induced by prostaglandin E1(PGE1) during fentanyl-oxygen anaesthesia.MethodsTen patients who underwent elective cardiac surgery received infusion of PGE1. After measuring the baseline arterial, mixed venous and internal jugular vein blood gases, systemic haemodynamics, and regional cerebral oxygen saturation (rSO2) estimated by INVOS 3l00R, PGE1 was continuously infused at 0.25-0.65 μg·kg−1·min−1 (mean dosage: 410 ± 41.4 mg·kg−1·min−1) intravenously. Ten, 20 and 30 minutes after the start of drug infusions, blood gases described above were obtained simultaneously with the measurement of systemic haemodynamics and rSO2. Thirty minutes from the start of drug infusions, administration of PGE1 was stopped. The same parameters were measured again 10, 30 minutes after the stop of drug infusion.ResultsPGE1 decreased mean arterial pressure (MAP) to approximately 70% of the baseline value (P < 0.05). PGE1 increased mixed venous saturation, but in contrast did not effect internal jugular pressure, internal jugular oxygen saturation and rSO2.ConclusionsThese results suggest that PGE1 is a suitable drug for induced hypotension because flow/metabolism coupling of brain and regional cerebral oxygenation were well maintained during hypotension.RésuméObjectifÉvaluer les effets de l’hypotension, induite par la prostaglandine E1(PGE1), sur l’oxygénation cérébrale pendant l’anesthésie avec fentanyl et oxygène.MéthodesDix patients qui devaient subir une chirurgie cardiaque élective ont reçu une perfusion de PGE1. Après avoir procédé à la gazométrie artérielle de base, à celle du sang veineux mêlé et à celle de la veine jugulaire interne, évalué l’hémodynamie systémique et la saturation en oxygène cérébral régional (SO2r) par INVOS 3100R, la PGE1 a été administrée en perfusion intraveineuse continue à 0,25-0,65 μg·kg−1·min−1 (dosage moyen: 410 ± 41,4 μg·min−1). Dix, 20 et 30 minutes après le début des perfusions de médicaments, les gaz du sang déjà cités ont été obtenus simultanément avec la mesure de l’hémodynamie systémique et la SO2r. Trente minutes après le début des perfusions, l’administration de la PGE1 a été arrêtée. Les mêmes paramètres ont été mesurés encore après 10 et 30 minutes après l’arrêt de la perfusion de médicament.RésultatsLa PGE1 abaisse la tension artérielle moyenne (TAM) à 70 % de sa valeur de base environ (P < 0,05). La PGE1 augmente la saturation en oxygène du sang veineux mêlé mais, au contraire, n’a pas d’effet sur la tension de la veine jugulaire interne, sur la saturation en oxygène de cette veine et sur la SO2r.ConclusionCes résultats montrent que la PGE, est un médicament approprié pour induire de l’hypotension parce que le couplage débit/métabolisme du cerveau et l’oxygénation cérébrale régionale ont été maintenus pendant l’hypotension.

Anesthetic management for clipping a giant basilar artery aneurysm with moderate hypothermia, extracorporeal circulation assistance, and propofol infusion.

&NA; A 65‐year‐old female patient underwent surgery to clip a giant basilar artery aneurysm with closed‐chest extracorporeal circulation using femorofemoral bypass. Moderate hypothermia (27°C‐30°C), retention of spontaneous circulation, and propofol infusion (3–5 mg • kg‐1 • h‐1) were used under general anesthesia. Blood outflow via femoral vein was sufficient to maintain cardiopulmonary bypass and to induce hypothermia. Hemodynamics were controlled with dopamine and noradrenaline. In this case, extracorporeal circulation under moderate hypothermia was used to assist rather than substitute for spontaneous circulation, and spontaneous circulation was maintained at all times. We think that this method had advantages over deep hypothermic circulatory arrest with regard to intraoperative risks and postoperative complications.