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From the Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, Yamaguchi, Japan.
Dr. Ryuichi Kawata, Department of Anesthesiology-Resuscitology, Yamaguchi University School of Medicine, 1-1-1 Minami-Kogushi, Ube, Yamaguchi 755-8505, Japan. Phone: 836-22-2291; Fax: 836-22-2292; E-mail: sakabe{at}po.cc.yamaguchi-u.ac.jp
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Abstract |
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Methods: Twenty-one female patients undergoing elective gynecological surgery performed through a lower median abdominal incision were enrolled. After obtaining steady general anesthesia with 1.7% sevoflurane and 60% nitrous oxide, the patients were randomly assigned to three groups, hypocapnia (PaCO2=30 mmHg), normocapnia (PaCO2=38 mmHg), and hypercapnia (PaCO2=44 mmHg) groups. The changes in mean blood flow velocity in the middle cerebral artery (Vmca) were evaluated using transcranial Doppler ultrasonography during nine minutes after surgical incision.
Results: The change in Vmca (
Vmca) with surgical incision during hypercapnia (30–36 cm•sec–1) was significantly greater than during normocapnia (20–22 cm•sec–1) and hypocapnia (13–15 cm•sec–1). The Vmca in the hypocapnia group was significantly smaller than in the normocapnia group. Arterial blood pressure increased with incision but there was no significant difference among the three groups.
Conclusion: Cerebral hemodynamic changes evoked by surgical stimulation are attenuated by hypocapnia and are augmented by hypercapnia, even within a clinically relevant range of PaCO2.
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Introduction |
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The arterial partial pressure of carbon dioxide (PaCO2) is an important regulator of cerebral vascular tone and an alteration of PaCO2 may interact with several physiologic processes in the brain.3 However, little is known whether altering cerebral vascular tone via manipulation of PaCO2 influences the response of CBF to nociceptive stimulation.
We hypothesized that the CBF response elicited by nociceptive stimulation can be attenuated by prior constriction of cerebral vessels through hypocapnia and be augmented by dilatation of them through hypercapnia. We tested this hypothesis in surgical patients by measuring blood flow velocity in the middle cerebral artery using noninvasive transcranial Doppler ultrasonography (TCD).
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Methods |
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General anesthesia was induced with 4 mg•kg–1 thiopentone and 0.15 mg•kg–1 vecuronium administered intravenously and was deepened with inhalation of 3.0% sevoflurane in 60% nitrous oxide and oxygen. After intubation of the trachea, the lungs were ventilated mechanically with 1.7% sevoflurane (end-tidal) in 60% nitrous oxide and oxygen (total 1.6 MAC). The patients were randomly assigned to three groups, a hypocapnia group (PaCO2=30 mmHg), a normocapnia group (PaCO2=38 mmHg) and a hypercapnia group (PaCO2=44 mmHg). Mechanical ventilation was adjusted (tidal volume of 8–10 mL•kg–1 and respiratory rate of 6–10 times•min–1) to maintain a PETCO2 2–3 mmHg lower than target PaCO2 values. After anesthesia induction, attachment of TCD probe was reconfirmed and care was taken to obtain the values continuously throughout the study period. Blood samples for analysis of blood gases, hemoglobin, blood glucose, and electrolyte concentrations were obtained by an arterial puncture. The nasopharyngeal temperature was monitored continuously and was maintained at normothermia (36.0–36.5°C) using a water blanket (Medi-Therm II, Gaymar, New York, NY, USA) and a convective warming blanket (Warm touch, Mallinckrodt Medical, Eden Prairie, MN, USA).
Vmca, arterial blood pressure, HR, and PETCO2 were measured and recorded at the following time points: just before surgical incision and one, three, five, seven, and nine minutes after surgical incision.
The increase in flow velocity ( Vmca) and the increase in mean arterial blood pressure ( MABP) at the different time points were calculated as the difference between preincisional Vmca and postincisional Vmca [ Vmca=(post-Vmca) – (pre-Vmca)] and the difference between preincisional MABP and postincisional MABP [ MABP=(post-MABP) – (pre-MABP)], respectively.
Data analysis
All data are reported as mean ± standard deviation (SD). An analysis of variance was used for intergroup comparisons of patients' clinical data and preincisional blood gases, hemoglobin, glucose, temperature, and Vmca data. A repeated measure analysis of variance was used for intergroup comparisons of Vmca change and MABP change. Fisher's protected least significant difference was used for post hoc test. A P value less than 0.05 was considered to be statistically significant.
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Results |
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shows patients' characteristics. There were no significant differences among the three groups in age, height, weight, awake values of PETCO2, Vmca, MABP, and HR.
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shows the values of preincisional blood gases, hemoglobin, blood glucose, and nasopharyngeal temperature and Vmca. There were no significant differences among the three groups except for PaCO2 and Vmca values. The Vmca in the hypercapnia group was significantly greater than in the normocapnia and hypocapnia groups and the Vmca in the hypocapnia group, though it was numerically smaller, was not significantly different from the normocapnia group.
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shows the changes in flow velocity and MABP after surgical incision calculated as Vmca and MABP. The Vmca in the hypercapnia group was significantly greater than in the normocapnia and hypocapnia groups. The Vmca in the hypocapnia group was significantly smaller than in the normocapnia group. The MABP significantly increased with incision in all three groups but there was no significant difference among the groups.
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Discussion |
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We found that changing the basal cerebral vascular tone by PaCO2 manipulation influenced the increase in Vmca elicited by surgical stimulation: the increase in Vmca elicited by surgical incision was attenuated by prior constriction of cerebral vessels through hypocapnia (PaCO2=30 mmHg) and was augmented by dilatation of cerebral vessels through hypercapnia (PaCO2=44 mmHg). This observation may be important in the management of patients with a decreased intracranial compliance because PaCO2 elevation, even if it is mild, would not only increase steady state CBF but also augment CBF response to surgical stimulation and hence increase ICP, whereas hypocapnia provides an opposite effect, which is favourable for these patients.
The aim of anesthesia is to attenuate the undesirable response to various nociceptive stimuli. However, 1.6 MAC anesthesia used in the present study did not prevent an increase in Vmca induced by surgical incision. Many, but not all, stressful events are accompanied by increases in CBF and/or cerebral metabolism.5 Although we did not measure cerebral metabolism in the present study, it is possible that increases in Vmca elicited by surgical stimulation might be due in part to the activation of cerebral metabolism. In awake humans, somatosensory stimulation has been reported to increase CBF but not cerebral metabolic rate for oxygen (CMRO2) in the sensorimotor cortex,6 and visual stimulation raised CBF and cerebral metabolic rate for glucose with little change in CMRO2.7 It is uncertain whether normal functional activation in the brain is supported by energy derived from aerobic or anaerobic metabolism. Assuming aerobic metabolism is the case, CBF increases in excess of O2 demand. Indeed, in humans, Inada et al. reported a decrease in cerebral arteriovenous oxygen content difference from 6.5 vol% to 5.3 vol% with surgical incision under 1.2% sevoflurane and 65% nitrous oxide anesthesia.8 This suggests that stimulation altered the flow-metabolism coupling balance to a state of relative hyperemia in this anesthetic condition. Thus, it seems acceptable to attenuate the increase in CBF elicited by nociceptive stimulation without decreasing cerebral metabolism.
Kuramoto et al. reported in dogs that, under deep halothane anesthesia, CBF increased significantly after stimulation of the sciatic nerve, while CMRO2 did not increase.9 Thus, increases in CBF elicited by stimulation may not always be associated with an increase in cerebral metabolism or the magnitude of increases in CBF and metabolism may not always be parallel. With morphine given with nitrous oxide, the increase in CBF induced by stimulation was augmented.9 At a plasma thiopentone concentration over 37 µg•mL–1, responses of CBF, CMRO2 and electroencephalography to stimulation were completely abolished.10 Taken together, these results suggest that the increase in CBF is more pronounced when subjects are anesthetized with drugs possessing vasodilatory properties than when anesthetized with drugs having vasoconstrictive properties. In the present study, hypocapnia, which induces cerebral vasoconstriction, attenuated CBF response to surgical stimulation and hypercapnia, which induces vasodilation, augmented the response. It might therefore be possible to control the CBF response to surgical stimulation by prior regulation of cerebral vascular tone, either chemically or pharmacologically.
To block the sympathoadrenal response to stimuli, more than 1.5 MAC is required (MAC BAR).11 In the present study, while patients were anesthetized at 1.6 MAC, surgical incision increased arterial blood pressure and HR and the observed increase in Vmca may be due, in part, to increased arterial blood pressure. von Knobelsdorff et al. investigated the effects of surgical stimulation on blood flow velocity using TCD in isoflurane anesthetized patients.12 They reported that noradrenaline-induced increases in arterial blood pressure, which were greater than those induced by surgery, did not change blood flow velocity significantly. They concluded that increases in blood flow velocity with surgical stimulation were not a function of changes in arterial blood pressure.12 However, if the increase in arterial blood pressure elicited by surgical stimulation is abrupt, it will cause a transient increase in CBF because cerebral autoregulation is not instantaneous. PaCO2 also modifies cerebral autoregulation. Hypocapnia maintains autoregulation better, while hypercapnia tends to cause dysautoregulation.13,14 Thus, the increase in CBF may be more pronounced in hypercapnia than in hypocapnia, even if the increases in arterial blood pressure are almost the same. In this context, though the magnitude of arterial blood pressure elevation elicited by surgical stimulation in the present study was very similar in the three groups, the possibility that the differences in Vmca responses may be related, in part, to the change in arterial blood pressure cannot be excluded.
Another concern is that CO2 itself has effects on central nervous system function. Extreme hypocapnia (respiratory alkalosis pH >7.50) and hypercapnia (PaCO2 
245 mmHg) can cause narcosis,15 and can likely influence anesthetic depth. Recently, Zhou et al. reported that hypercapnia and hypocapnia at more clinically relevant levels (PETCO2 of 25 and 45 mmHg) affected spinal motor neuron excitability during isoflurane anesthesia.16 Spinal cord neuron excitability was determined by measuring the posterior tibial nerve H-reflex amplitude and F-wave persistence. Not only hypercapnia, but also hypocapnia decreased H-reflex amplitude and F-wave persistence, which may affect motor response to surgical stimulation. It is uncertain whether cerebral cortical neuronal excitability was affected and hence the functional/metabolic response to surgical stimulation were influenced at the PaCO2 levels (30–44 mmHg) examined in the present study.
The subjects of the present study were female patients with no brain pathology. Extrapolation of these findings to a mixed population of patients with intracranial pathology deserves consideration. A recent report has demonstrated that regional CBF during visual stimulation increased more in women than in men.17 Therefore, it is possible that the magnitude of response to nociceptive stimulation could be less in men than women. In patients with various intracranial pathologies, it would be difficult to perform a study like ours. We suggest that our results may be applicable to diseased brain, provided the cerebrovascular response to CO2 is preserved.
In conclusion, increases in Vmca evoked by surgical stimulation were attenuated by hypocapnia and were augmented by hypercapnia, even within a clinically relevant range of PaCO2. Our findings suggest that hypocapnia should be achieved prior to nociceptive stimulation in patients at risk of complications from increased CBF.
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Footnotes |
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Received for publication July 27, 2001. Accepted for publication May 16, 2001.
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References |
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2
Ngai AC, Ko KR, Morii S, Winn HR. Effect of sciatic nerve stimulation on pial arterioles in rats. Am J Physiol 1988; 254: H133–9.
3 Brian JE Jr. Carbon dioxide and the cerebral circulation. Anesthesiology 1998; 88: 1365–86.[Medline]
4
Bishop CCR, Powell S, Rutt D, Browse NL. Transcranial Doppler measurement of middle cerebral artery blood flow velocity: a validation study. Stroke 1986; 17: 913–5.
5
Bryan RM Jr. Cerebral blood flow and energy metabolism during stress. Am J Physiol 1990; 259: H269–80.
6
Fox PT, Raichle ME. Focal physiological uncoupling of cerebral blood flow and oxidative metabolism during somatosensory stimulation in human subjects. Proc Natl Acad Sci USA 1986; 83: 1140–4.
7
Fox PT, Raichle ME, Mintun MA, Dence C. Nonoxidative glucose consumption during focal physiologic neural activity. Science 1988; 241: 462–4.
8
Inada T, Shingu K, Uchida M, Kawachi S, Tsushima K, Niitsu T. Changes in the cerebral arteriovenous oxygen content difference by surgical incision are similar during sevoflurane and isoflurane anaesthesia. Can J Anaesth 1996; 43: 1019–24.
9 Kuramoto T, Oshita S , Takeshita H, Ishikawa T. Modification of the relationship between cerebral metabolism, blood flow, and electroencephalogram by stimulation during anesthesia in the dog. Anesthesiology 1979; 51: 211–7.[Medline]
10 Miyauchi Y, Sakabe T, Maekawa T, Ishikawa T, Takeshita H. Responses of EEG, cerebral oxygen consumption and blood flow to peripheral nerve stimulation during thiopentone anaesthesia in the dog. Can Anaesth Soc J 1985; 32: 491–8.[Medline]
11 Roizen MF, Horrigan RW, Frazer BM. Anesthetic doses blocking adrenergic (stress) and cardiovascular responses to incision-MAC BAR. Anesthesiology 1981; 54: 390–8.[Medline]
12 von Knobelsdorff G, Kusagaya H, Werner C, Kochs E, am Esch JS. The effects of surgical stimulation on intracranial hemodynamics. J Neurosurg Anesthesiol 1996; 8: 9–14.[Medline]
13
Paulson OB, Olesen J, Christensen MS. Restoration of autoregulation of cerebral blood flow by hypocapnia. Neurology 1972; 22: 286–93.
14 Raichle ME, Stone HL. Cerebral blood flow autoregulation and graded hypercapnia. Eur Neurol 1972; 6: 1–5.
15 Eisele JH, Eger II EI, Muallem M. Narcotic properties of carbon dioxide in the dog. Anesthesiology 1967; 28: 856–65.[Medline]
16
Zhou HH, Turndorf H. Hyper- and hypoventilation affects spinal motor neuron excitability during isoflurane anesthesia. Anesth Analg 1998; 87: 407–10.
17 Kastrup A, Li T-Q, Glover GH, Krüger G, Moseley ME. Gender differences in cerebral blood flow and oxygenation response during focal physiologic neural activity. J Cereb Blood Flow Metab 1999; 19: 1066–71.[Medline]
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