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Departments of *Anesthesiology and Intensive Care Medicine, Neurology, and Pediatric Surgery, Friedrich-Schiller-University Jena, Jena, Germany
Address correspondence and reprint requests to Egbert Hüttemann, MD, DEAA, Klinik für Anästhesiologie und Intensivtherapie, Friedrich-Schiller-Universität Jena, Bachstrasse 18, D-07740 Jena, Germany. Address e-mail to Egbert.Huettemann{at}med.uni-jena.de
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Abstract |
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IMPLICATIONS: Laparoscopic surgery is performed frequently in pediatric patients. Cerebral blood flow velocities increase during insufflation of the intraperitoneal cavity for minimally invasive surgery in children. The vasoreactivity as part of the cerebral autoregulation remains unaffected.
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Introduction |
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Methods |
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All children received a standardized anesthetic. After premedication with midazolam (0.5 mg/kg) per os, anesthesia was induced with thiopental (5 mg/kg), and fentanyl (0.3 µg/kg), and maintained with 0.75 minimum alveolar anesthetic concentration (MAC) of sevoflurane and 67% nitrous oxide in oxygen (2). Intubation was facilitated by rocuronium (0.6 mg/kg). Mechanical ventilation was performed using a pressure-controlled mode (AS3; Datex-Engstroem, Helsinki, Finland) in which I/E ratio was 1:1 and end-expiratory pressure was maintained at 5 cm H2O throughout the procedure. Controlled ventilation was adjusted before CO2 insufflation to keep PETCO2 at 34 mm Hg. After CO2 insufflation, ventilatory frequency was increased to maintain a constant PETCO2. Later, PETCO2 was allowed to increase to a level of 38 mm Hg to allow calculation of the CO2 vasoreactivity. After deflation of the abdomen, ventilatory frequency was reduced to preinsufflation levels.
Noninvasive systolic, diastolic, and mean arterial blood pressure (MAP), heart rate (HR), peripheral oxygen saturation, fraction of inspired oxygen, PETCO2, body temperature, respiratory minute volume, airway pressures, and inspiratory and end-tidal concentrations of nitrous oxide and sevoflurane were continuously monitored throughout the study (AS3; Datex). Because I/E ratio was 1:1, airway pressure (Pmean) was calculated as: Pmean = positive end-expiratory pressure + inspiratory plateau pressure/2.
Blood flow velocity in the middle cerebral artery (MCA) was measured by using a transcranial ultrasonography probe (Multidop T; DWL Medizintechnik, Sipplingen, Germany). The probe was positioned over the temporal bone window (the temporal area just above the zygomatic arch) and was fixed to the patient’s head with an elastic bandage so that the angle of insonation remained constant during the investigation. Doppler signals from the MCA, M1 segment, were identified and measured at a depth of 30–40 mm. Time-averaged MCA blood flow velocity was calculated and monitored continuously. Blood flow velocities were expressed in centimeter/second. The pulsatility index (PI), an index reflecting waveform appearance, was calculated according to the formula PI = (systolic velocity - diastolic velocity)/mean velocity.
After stabilization of respiratory and hemodynamic variables, defined as changes in MAP, HR, PETCO2, and expiratory anesthesia gas concentrations of <10% within 10 min, the blood flow velocity in the MCA was measured after the induction (baseline), and after the insufflation of the abdominal cavity with CO2 at an intraabdominal pressure (IAP) of 12 mm Hg at 2 PETCO2 levels, 34 mm Hg (PP1 12) and 38 mm Hg (PP2 12). The last measurements were obtained 10 min after abdominal deflation at the end of surgery while maintaining anesthesia unchanged (control).
All values were expressed as mean (SD). Statistical analysis was performed by using analysis of variance for repeated measurements and a pairwise multiple comparison procedure (Student-Newman-Keuls method, SigmaStat; SPSS, Chicago, IL). A probability of <0.05 was regarded as statistically significant.
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Discussion |
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Cerebral blood flow (CBF) can be measured by several techniques. Transcranial Doppler ultrasound is a safe, noninvasive method, thus rendering it particularly useful in children. Although CBF cannot be absolutely quantified with this method, a comparison with PET measurements revealed a close correlation between changes in CBF and changes in CBFV during vasomotor reactivity tests (3,4). Consequently, transcranial Doppler sonography is a useful tool in studying hemodynamic changes, e.g., during surgical procedures.
Blood pressure, cardiac output (CO), body temperature, intrathoracic pressure, and depth of anesthesia may influence CBF (5). In the present investigation, temperature remained constant during the study. There was a slight, but not significant, increase in mean airway pressure, likely reflecting an increase in intrathoracic pressure. Whereas halothane tends to increase CBF (6), neither isoflurane nor sevoflurane (0.5–1.5 MAC) produce significant dose-related changes of blood flow velocities (7). Furthermore, CBF autoregulation remains intact during 0.5 and 1.5 MAC sevoflurane anesthesia (8). In this study, the end-tidal concentration of sevoflurane was kept constant at 0.75 MAC. Nitrous oxide causes a mild increase in CBFV (9,10) but it does not affect the dynamic cerebrovascular reactivity in acute arterial CO2 changes (9,10). Thus, because the anesthetic concentrations remained constant throughout the study period, our results cannot be explained by cerebral vasodilation caused by anesthetics or by impaired autoregulation.
Our finding of an increased CBFV during PP indicates either an increase in CBF or a constriction of the insonated vessel. CBF remains constant if cerebral perfusion pressure is varied between 60 and 130 mm Hg of MAP (11). However, the increase in MAP occurring in the setting during PP is mediated by catecholamines and vasopressin (12–15). Several investigations have demonstrated that norepinephrine may lead to significant increases in CBFV (16–18). Indirect evidence for vasopressor (norepinephrine and/or vasopressin) related MCA vasoconstriction is provided by the decrease in PI. Investigators studying the hemodynamic effects of PP in infants reported a decrease in cardiac index after insufflation. In one study using noninvasive continuous esophageal aortic blood flow echo-Doppler, a decrease in aortic blood flow and stroke index of 33% and 32%, respectively, has been described at an IAP of 10 mm Hg (19). Another study using transesophageal echocardiography found a decrease in cardiac index and stroke index of 13% and 5%, respectively, at an IAP of 12 mm Hg (20). Given these data, there is no evidence that the increase in CBFV during PP is related to an increase in stroke volume or CO. However, we cannot exclude a redistribution of CO during PP leading to an increase in CBF.
In an investigation of adult patients undergoing laparoscopic cholecystectomy, CO2 insufflation up to an IAP of 10 mm Hg was shown to lead to an increase of CBFV of approximately 30% (1). Ventilation was kept constant and arterial CO2 concentration (PaCO2) increased from 36 to 39 mm Hg. However, this increase in PaCO2 does not fully explain the observed increase of CBFV. Given the CO2 vasoreactivity of 3%–4% per mm Hg change in PaCO2 measured in that study, an increase in PETCO2 of 3 mm Hg would only account for an increase of approximately 9% in the CBFV (about one-third of the total 30% increase). Thus, approximately 60%–70% of the increase in CBFV was directly related to the PP and not to hypercapnia. Thus, an additional cause for the increase in CBFV is supported by data in adults as well.
Because PaCO2 profoundly influences CBF and hypercapnia causes intense cerebral vasodilation and increases CBF (8), PETCO2 was kept constant by adjustment of minute volume. We did not routinely measure PaCO2 because this would have required placement of an arterial line. Data from adult studies indicate that the difference between PaCO2 and PETCO2 (alveolo-arterial gradient) remains constant during the creation of a PP in adults over a wide range of values (21–23). In two cases (two and three years of age) independent of this study, in which the PaCO2 was measured, the alveolo-arterial gradient did not change. If a change of the alveolo-arterial gradient is to occur during a PP, one might at the earliest expect an increase of the alveolo-arterial gradient. Given a constant PETCO2, this would lead to an underestimation of the increase of CBFV, because a decrease in PaCO2 would, in part, counteract the PP-induced increase in CBFV. Thus, the increase in CBFV cannot be explained by an increase in PaCO2.
An important finding of this study is the preserved CO2 reactivity during PP. The CO2 reactivity slope (relative change of CBFV in relation to a defined change of PETCO2) value of 4.0% ± 1.9%/mm Hg in this study was almost in the same range as that described for the awake state (3.2%) (24).
There are two major limitations of our study. First, we did not determine baseline CBFV-CO2 reactivity to compare with CBFV-CO2 reactivity during PP. Thus, it remains open whether CBFV-CO2 reactivity, though being in the normal range, is altered during PP. Second, we did not investigate CBFV-CO2 reactivity to hypocapnia in order to evaluate that hyperventilation could overcome the effects of PP on CBFV. These issues need to be studied.
In summary, the major findings of this study are that the induction of PP leads to an increase in MCA blood flow velocity in young children independent from changes in PETCO2, and that CO2 reactivity is preserved.
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This article has been cited by other articles:
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  J. L. Zitsman Current Concepts in Minimal Access Surgery for Children Pediatrics, June 1, 2003; 111(6): 1239 - 1252. [Abstract] [Full Text] [PDF]
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