BJA Advance Access published online on June 3, 2008
British Journal of Anaesthesia, doi:10.1093/bja/aen136
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Effects of remifentanil-based general anaesthesia with propofol or sevoflurane on muscle microcirculation as assessed by near-infrared spectroscopy
Department of Anaesthesiology and Intensive Care, University of Rome ‘La Sapienza’, Second Faculty of Medicine, Sant’Andrea Hospital, Rome, Italy
* Corresponding author. E-mail: radbl{at}libero.it
Accepted for publication March 14, 2008.
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Abstract |
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Background: Although anaesthetics are known to alter microcirculation no study has, to our knowledge, documented changes in human skeletal microcirculatory function during general anaesthesia.
Methods: Forty-four patients undergoing maxillofacial surgery at a university hospital were prospectively randomized to receive general anaesthesia with remifentanil combined with propofol or sevoflurane. Muscle microcirculation was investigated with near-infrared spectroscopy (NIRS) before general anaesthesia was induced and 30 min later. An NIRS device (NIMO, Nirox) was used to quantify calf deoxyhaemoglobin [HHb], oxyhaemoglobin [HbO2], and total haemoglobin [HbT] concentrations, coupled to a series of venous and arterial occlusions to measure calf blood flow, muscle oxygen consumption, calf vascular resistance, microvascular compliance, and haemoglobin resaturation rate (RR).
Results: In both the groups, general anaesthesia induced marked changes in muscle microcirculation: the tissue blood volume increased (+33% in remifentanil–sevoflurane and +45% with remifentanil–propofol groups), microvascular resistance decreased (–31% and –38%, respectively), and the post-ischaemic haemoglobin RR decreased (–48% and –36%, respectively). In the remifentanil–propofol group, the muscle blood flow increased (P<0.001), whereas in the remifentanil–sevoflurane group microvascular compliance and muscle oxygen consumption decreased (P<0.01).
Conclusions: Remifentanil-based general anaesthesia with propofol or sevoflurane altered the muscle microcirculation in different ways. Quantitative NIRS, a technique that takes into account the optical tissue properties of the individual subject, can effectively measure these changes non-invasively.
Keywords: anaesthesia, general; anaesthetics volatile, sevoflurane; microcirculation; propofol
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Introduction |
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Microcirculation (small vessels of size <150 µm) regulates tissue blood flow and local tissue oxygen diffusion, and has a key role in the development of numerous diseases and dysfunctions.1 It can be investigated non-invasively with near-infrared spectrophotometry (NIRS).
NIRS is a technique now available as a stand-alone portable device that uses near-infrared light to investigate tissue non-invasively: it differs from all the other devices used to monitor microcirculation because it is the only one able to explore muscle microcirculation in vivo. We have already used NIRS to measure forearm muscle blood flow in healthy subjects2 and critically ill patients,3 brain oxygenation,4 and to highlight microvascular dysfunction during sepsis and septic shock.5 No published study has used quantitative NIRS to analyse changes in the muscle microcirculation during general anaesthesia in healthy subjects. Studying healthy subjects is important because it excludes possible changes in the microcirculation in critically ill patients concomitantly treated with analgesics and hypnotics,6 drugs whose possible effects on the microcirculation remain unclear.7 8 Knowing more about how hypnotic and opioid drugs alter the microcirculation during general anaesthesia would be useful in interpreting data about microcirculatory dysfunction coming from trials on critically ill patients receiving these drugs.
Our aim in this prospective randomized study was to assess changes in skeletal muscle microcirculation (microvascular function, vascular reactivity, regulation and resistance, cell metabolism, and tissue optical properties) non-invasively using NIRS during remifentanil–propofol and remifentanil–sevoflurane general anaesthesia in otherwise healthy patients undergoing maxillofacial surgery.
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Methods |
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The study protocol was approved by the Institutional Review Board of the Anaesthesia and Intensive Care Medicine Department of Sant’ Andrea University Hospital (Rome, Italy), and written informed consent was obtained from all participants.
Forty-four patients, all ASA I, participated in this investigation. We selected the patients who underwent elective maxillofacial surgery, and were not receiving medications, had no disorders likely to influence the microcirculation (diabetes, peripheral vascular disease, or chronic venous insufficiency), and no known contraindications for the anaesthetic agents used.
Patients were sequentially enrolled and randomly allocated, by sealed envelopes to one of the two groups to receive general anaesthesia induced and maintained with either remifentanil–propofol (22 patients) or remifentanil–sevoflurane (22 patients).
In the operating room, an i.v. catheter was inserted but no drugs or fluids were given before the anaesthesia was induced. Routine monitoring included an ECG, pulse oximetry, non-invasive arterial pressure, and capnography. In the remifentanil–propofol group, anaesthesia was induced with 2 mg kg–1 of propofol and a bolus injection of 1 µg kg–1 of remifentanil, and in the remifentanil–sevoflurane group with 5% of inhaled sevoflurane and an i.v. 1 µg kg–1 of remifentanil bolus; all the remifentanil boluses were administered over at least 30 s to prevent chest rigidity. Anaesthesia was maintained with either a continuous infusion of 5.5 mg kg–1 h–1 of propofol and 0.3 µg kg–1 min–1 of remifentanil (remifentanil–propofol group) or 1.8% end-tidal sevoflurane with a continuous infusion of 0.3 µg kg–1min–1 of remifentanil (remifentanil–sevoflurane group).
All patients received 0.1 mg kg–1 of vecuronium bromide for muscle relaxation after loss of consciousness to facilitate tracheal intubation and intermittent positive-pressure ventilation using a mixture of O2 and air (equal measures), a tidal volume of 8 ml kg–1, and a ventilatory frequency adjusted to maintain end-tidal CO2 between 4.7 and 5.3 kPa.
Until intraoperative NIRS data collection ended, patients received only 0.9% saline (<500 ml). Intraoperative changes in mean arterial pressure (MAP) or heart rate of more than 25% from baseline values measured before anaesthesia induction were immediately treated and the patient was excluded from the study.
A warming blanket kept all the patients normothermic during intraoperative NIRS measurements.
Before induction of anaesthesia, an NIRS probe (NIMO-4 Tissue probe, Nirox srl, Brescia, Italy) was placed and secured with an elastic band along the lateral side of the calf (lateral gastrocnemius muscle) avoiding the course of visible veins. To avoid hampering venous return, the foot was raised by about 10 cm. Two pneumatic cuffs were attached around the thigh and the ankle and connected to an automatic inflation system (Hokanson E20 Rapid Cuff Inflator, AG101 Cuff Inflator Air Source) capable of reaching a predefined pressure in <0.5 s. To avoid the possible interference of ambient light on NIRS measurements, the whole leg was wrapped in a black cloth. Before the probe was applied, the calf skin-fold thickness was measured using a skinfold caliper (Gima SpA, Milan, Italy).
Two sets of measures were recorded: one just before the induction of anaesthesia and the other 30 min after tracheal intubation; for each set, NIRS data were collected at baseline and during two different types of pneumatic compression. First, three different pneumatic cuff inflation pressures, 30, 40, and 50 mm Hg, or in patients with diastolic pressures of <50 mm Hg, a maximum value equal to the diastolic pressure minus 10 mm Hg, were maintained for about 50 s (venous occlusion). To yield good reproducibility, a 60 s rest was allowed between each compression.9 Secondly, when compressions ended, subjects rested for 10 min and ischaemia was then induced at a cuff pressure equal to the systolic arterial pressure+100 mm Hg and maintained for 5 min (arterial occlusion). Then the occlusion was released and reactive hyperaemia (overshoot) was recorded for at least 3 min.
Deoxyhaemoglobin [HHb], oxyhaemoglobin [HbO2], and total haemoglobin [HbT] concentrations were quantified with a continuous-wave tissue oximeter (NIMO, Nirox srl, Brescia, Italy) as detailed elsewhere.10 11
Assuming that the water absorption coefficient at 975 nm is dominant over other chromophores (i.e. HbO2 and HHb) and that the tissue scattering properties vary linearly with wavelength, NIMO exploits a precise absorption measurement close to the absorption peak of the water to measure the scattering coefficient at this wavelength and to calculate its spectrum. Once the scattering spectrum is known, the absorption coefficient and differential pathlength factors (DPFs) can be estimated at other wavelengths (685 and 830 nm), thus yielding the absolute HbO2 and HHb tissue concentrations.
To account for the possible influence of the s.c. fat layer on NIRS,12 we also applied a real-time correction using an algorithm included in the software program v2.0 supplied with the spectrometer (Nimo Data Analysis v2.0). The correlation coefficients (used for the algorithm) were obtained by applying a two-layered analytical model13 using published absorption and scattering coefficients of the fat layer for wavelengths of interest.14
The spectrophotometer directly measured [HbO2] and [HHb]; two different DPF values (DPF685 and DPF830, one for each studied wavelength) were measured, in each of the two measurement sets, before serial venous and arterial occlusions.
All recorded tracks were visually inspected: a venous occlusion was considered satisfactory for further analysis if the baseline track remained steady before occlusion, oxy- and deoxyhaemoglobin rose during the occlusion and returned to a similar baseline value after the occlusion was released. Similarly, an arterial occlusion was considered satisfactory and analysed only if the baseline track remained steady before occlusion, [HbT] remained completely or almost unchanged during the ischaemic occlusion, while [HbO2] decreased and [HHb] increased, and releasing the occlusion induced a classic reperfusion pattern.
Data were analysed off-line with the software program supplied with the NIMO oximeter. Microvascular function was evaluated by considering tissue blood volume (TBV), microvascular compliance, and vascular reactivity from the post-ischaemic haemoglobin resaturation rate (RR); microvascular regulation analysis included calf haemoglobin flow (CHF), calf blood flow (CBF), and calf microvascular resistance (CVR); cell metabolism was assessed by muscle oxygen consumption (VO2) and tissue oxygen saturation (StO2).
TBV (in ml of blood per 100 ml of tissue) was determined from [HbT] in relation to the endovascular haemoglobin content.5 Microvascular compliance (expressed in ml per mm Hg per litre of tissue) was calculated at each inflation pressure as the change in [HbT] per change in occlusion pressure (mm Hg), as previously described.5 [HbT] values were collected approximately 30–40 s after each cuff inflation, when superficial, deep, and other small vessels were assumed to be fully distended. Compliance curves were obtained by plotting the relationship between cuff pressure and [HbT]. After the arterial occlusion was released, the haemoglobin RR was calculated from the haemoglobin resaturation slope during the first 10 s of post-ischaemic reperfusion.
CBF and CHF were calculated by evaluating the linear increase in [HbT], expressed in µmol s–1, within the first seconds of venous occlusion.2 For CBF, changes in [HbT] were then converted to ml (of blood) per 100 ml (of tissue) per minute using the individual Hb content obtained from preoperative blood samples, taking into account the molecular weight of Hb and the molecular ratio between Hb and O2. CVR (expressed in mm Hg ml–1 min–1 per 100 ml tissue) was calculated as MAP/CBF.
Muscle oxygen consumption (VO2) was measured during venous occlusion as the initial linear increase in [Hb], after subtracting the [HHb] increase from arterial blood (3%);2 tissue saturation (StO2) was obtained from the ratio of [HbO2] to [HbT].
All values are expressed as mean (SD). Data were analysed with SPSS 13.0 for Windows (SPSS Inc., Chicago, IL, USA) and SigmaStat 3.1 for Windows (Systat Software, San Jose, CA, USA). To test for the statistical significance of differences we used non-parametric tests, including Mann–Whitney U-test (independent samples) to detect the baseline differences between the groups and Wilcoxon signed rank test (paired samples) to highlight the effects of anaesthesia on the variables in each group. Spearman's rank correlation test was used to determine the possible linear relationship between the studied variables. Based on our previous studies5 and a pilot study in the same setting, we determined that a sample size of 20 patients in each group would have at least 80% power to detect at least an intraoperative difference of 35% in [HbT], [HbO2], StO2, HBF, and VO2 between groups at 
=0.05. Differences with a two-tailed P-value <0.05 were considered statistically significant.
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Results |
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We enrolled 44 patients and randomized 22 to each group to receive general anaesthesia with remifentanil–sevoflurane or remifentanil–propofol. Both the groups had similar characteristics (Table 1). Of the 44 traces obtained, four (two from each group) were excluded from the analysis: three because [HbO2] failed to increase significantly during arterial occlusion and one because [HbT] failed to increase significantly when the pneumatic cuff was inflated during venous occlusion.
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The changes in calf muscle microcirculation after general anaesthesia differed in the two groups (Table 2). In both the groups, although StO2 remained unchanged from baseline during induction and maintenance of anaesthesia, [HbO2] increased significantly (+25% in the remifentanil–sevoflurane group and +43% in the remifentanil–propofol group) and so did [HHb] (+22% and +39%, respectively). The deoxygenated [HHb] during general anaesthesia was significantly higher in the remifentanil–propofol group than in the remifentanil–sevoflurane group. During general anaesthesia, the quantity of blood within the tissue increased: [HbT] increased (+27% in the remifentanil–sevoflurane and +39% in the remifentanil–propofol group) and so did TBV (+33% and +45%, respectively).
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CVR diminished in both the groups (–31% in the remifentanil–sevoflurane group and –38% in the remifentanil–propofol group), and both CBF and CHF increased significantly only in the remifentanil–propofol group (+46%). In patients randomized to receive remifentanil–propofol anaesthesia, the induced changes in CBF correlated with the changes in [HbT] (P<0.01, Spearman's R=0.73) and [HbO2] (P=0.02, Spearman's R=0.59) (Fig. 1). No correlation was found between MAP and CBF in either group either before or during general anaesthesia.
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VO2 diminished significantly during general anaesthesia only in patients randomized to receive remifentanil–sevoflurane and the reduction correlated significantly with the increased [HbO2] (P<0.01, Spearman's R=–0.69) (Fig. 2).
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Microvascular compliance diminished significantly only in the remifentanil–sevoflurane group, whereas it remained unchanged in the remifentanil–propofol group. Conversely, the post-ischaemic haemoglobin RR diminished markedly during general anaesthesia in both the groups (–48% in the remifentanil–sevoflurane group and –36% in the remifentanil–propofol group).
Under baseline conditions (before anaesthesia and pre-occlusion), DPF685 was 4.59 (0.77) and DPF830 was 4.08 (0.45). Before and after general anaesthesia, regardless of cuff occlusions, these values remained statistically unchanged (mean reduction <2% and <6%, respectively). During general anaesthesia, in the remifentanil–propofol group DPF values remained statistically unchanged from baseline (mean reduction DPF685 –2.29%, P=0.49; DPF830 –2.59%, P=0.24), whereas in the remifentanil–sevoflurane group both measures decreased slightly but significantly (mean DPF685 –4.58%, P=0.02; DPF830 –2.62%, P=0.04).
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Discussion |
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Our study using NIRS showed that general anaesthesia with remifentanil–propofol or remifentanil–sevoflurane induced marked changes in skeletal muscle microcirculation in healthy adults undergoing maxillofacial surgery. In both the groups, general anaesthesia increased TBV, reduced CVR, and reduced the post-ischaemic haemoglobin RR. In patients who received general anaesthesia with remifentanil–propofol muscle blood flow increased, whereas in those who received remifentanil–sevoflurane microvascular compliance and muscle oxygen consumption (VO2) diminished.
To interpret the changes we observed in muscle microcirculation during general anaesthesia, we recall that NIRS quantifies the tissue haemoglobin concentration in the microcirculation, thus estimating the extent of the tissue microvascular bed. The marked increase in [HbT] and TBV in both the groups provided evidence that general anaesthesia markedly increased the vascular bed. Although small arterioles and venules appear sensitive to the vasodilator effects of propofol15 16 and sevoflurane,17 whether this vasodilatation reflects direct vascular relaxation or inhibition of tonic sympathetic vasoconstrictor outflow remains controversial.18
In our study, during general anaesthesia the deoxygenated haemoglobin concentration was significantly larger in the remifentanil–propofol than in the remifentanil–sevoflurane group. Brookes and colleagues15 noted that although small arterioles and venules appear sensitive to propofol-induced vasodilation, the most significant difference in vasodilatation involved the V3 venules (
40 µm). Moreover, Ahn and colleagues19 showed that propofol–remifentanil anaesthesia, compared with the sevoflurane–remifentanil association, improves surgical field conditions and intranasal bleeding during endoscopic sinus surgery. These studies imply that the anaesthesia-induced vasodilatation we detected might predominantly involve venules. Our study design precludes us from stating whether this vasodilatation arises from the hypnotic drug or the opioid.
In the remifentanil–propofol group, the increased CBF during general anaesthesia correlated with the increase in [HbO2] and [HbT] (Fig. 1). The increased arteriolar inflow was therefore confirmed by the increased ‘arteriolar’ component of blood present within the tissue, associated with a generic increase in the muscle vascular bed probably linked to recruiting of some normally non-perfused muscle capillaries.20 Conversely, in the remifentanil–sevoflurane group, the increased [HbO2] during general anaesthesia cannot reflect CBF (a variable that remained unchanged) but might be linked to reduced cell metabolism (VO2). Reduced cell metabolism receives support from the reduced oxygen consumption (
VO2) that correlated with the increased oxygenated haemoglobin ([HbO2]) (Fig. 2) and the deoxygenated haemoglobin concentration that was significantly lower in patients who received remifentanil–sevoflurane than in those who received remifentanil–propofol, in whom muscle VO2 remained unchanged. Similar sevoflurane changes in blood flow and oxygen consumption have been documented in the human brain,21 and sevoflurane attenuates cell respiration in a dose-dependent manner.22
The NIRS data we obtained on skeletal muscle blood flow are in contrast with those reported in a similar study that used plethysmography7 to measure changes in forearm blood flow during general anaesthesia with remifentanil–propofol and remifentanil–sevoflurane but found no significant differences in the changes induced by the two anaesthetic combinations. They nevertheless gave the two anaesthetics in markedly lower doses than we did and the technique used yields a mean blood flow value that fails to distinguish between the flow components coming from muscle microcirculation or from other structures (large vessels, bone, connective tissue).
An interesting finding in our study is that even though TBV increased after general anaesthesia in both the randomized groups, in the remifentanil–sevoflurane group microvascular compliance concomitantly diminished. As we proposed in an earlier study,9 microvascular compliance could diminish because vasodilatation increases the vascular bed, thus further limiting the distension induced by the cuff-induced increased backward pressure; it might also diminish owing to microvessel stiffness, in turn dependent on conditions that are intrinsic (e.g. increased muscular tone) or extrinsic to the microcirculation itself (e.g. tissue oedema). Given that general anaesthesia caused the vascular bed to increase in both the groups, the diminished microvascular compliance in the remifentanil–sevoflurane group presumably did not arise from the vasodilatation-induced increase in the vascular bed. Other studies have already investigated compliance of various vascular territories including the large thoracic vessels23 and the upper limb.24 25 The contrasting results cannot be compared with ours because they come from a variety of techniques that did not specifically investigate the skeletal muscle microcirculation.
In both the groups we studied, during general anaesthesia the RR decreased during the phase of reactive hyperaemia that usually follows an ischaemic occlusion. Reactive hyperaemia tests organ maximal ability to increase flow on demand, when demand has been maximally stimulated by a zero flow. Reactive hyperaemia encompasses several phenomena including a myogenic phase followed by a metabolic phase. We measured RR during the first 10 s after reperfusion, namely during the myogenic phase corresponding to the initial upward portion of the hyperaemia peak.26 The decreased RR shows that both combinations of anaesthetic drugs we used alter flow-mediated, endothelium-independent microvessel relaxation. Again, our study leaves unanswered the question of which anaesthetic drug induces this effect although recent evidence shows that opioids such as sufentanil increase the slope of the reperfusion flow-curve assessed by laser Doppler flowmetry in the skin microcirculation.27
An equally interesting technical point is that StO2, a variable simply reflecting the relationship between tissue [HbO2] and [HbT] concentrations, approximates neither microcirculatory perfusion nor the extent of the microcirculatory vascular bed nor even SvO2. During general anaesthesia, even though blood volume within the microcirculation increased, microvascular resistance diminished, muscle blood flow increased (remifentanil–propofol group), VO2 diminished (remifentanil–sevoflurane group), and StO2 remained unchanged. StO2 is widely influenced by the tissue vascular bed (arterioles, capillaries, and small veins) whose volumes can change rapidly under healthy and pathological conditions, between subjects and even within the same subject. To interpret microcirculation function properly, StO2 should be combined with measures that can quantify the various forms of haemoglobin really present within the tissue examined.
Our study has limitations. First, notwithstanding our efforts to standardize the anaesthetic technique by giving the hypnotic agents propofol and sevoflurane at commonly used doses we did not monitor our subjects’ state of consciousness, hence we cannot be sure that in some patients hypnotic drugs were not overdosed or underdosed. Secondly, although the NIRS device we used in this study can correct for signal interference normally caused by the state of s.c. fat,12 this algorithm has not yet been validated. Some observations in this study nonetheless suggest that it can correct the measured values for interference from adipose tissue. For example, we found no difference in tissue optical properties (i.e. DPF) in women and men even though others have reported gender-related changes28 and attributed them to differences in the s.c. fat layers.
The NIRS method we used derives DPF values from the absorption of infrared light due to tissue water, assuming that the tissue water concentration remains almost unchanged throughout the measurements.10 11 We consider this assumption valid under our experimental conditions because general anaesthesia lasting 30 min is unlikely to induce changes in calf muscle water concentrations large enough to affect DPF values.
In conclusion, our study suggests that general anaesthesia alters human skeletal muscle microcirculation. The two hypnotic agents propofol and sevoflurane alter the microcirculation in distinctly different ways. A quantitative NIRS device that assesses optical tissue properties (DPF) in individual subjects can effectively measure these changes non-invasively.
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