Comparison of variability in cardiorespiratory measurements following desflurane anesthesia at a multiple of the minimum alveolar concentration for each dog versus a multiple of a single predetermined minimum alveolar concentration for all dogs in a group

Bruno H. Pypendop Department of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Jan E. Ilkiw Department of Surgical and Radiological Sciences, School of Veterinary Medicine, University of California, Davis, CA 95616.

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Abstract

Objective—To determine whether the variability of cardiorespiratory measurements is smaller when administering desflurane at a multiple of the individual's minimum alveolar concentration (MAC) or at a predetermined, identical concentration in all subjects.

Animals—10 dogs.

Procedures—Desflurane was administered at 1.5 times the individual's MAC (iMAC) and 1.5 times the group's MAC (gMAC). The order of concentrations was randomly selected. Heart rate, respiratory rate, arterial blood pressure, central venous pressure, mean pulmonary artery pressure, pulmonary artery occlusion pressure, arterial and mixed-venous blood gas tensions and pH, and cardiac output were measured. The desflurane concentration required to achieve a mean arterial pressure (MAP) of 60 mm Hg was then determined. Finally, the desflurane concentration required to achieve an end-tidal PCO2 of 55 mm Hg was measured.

Results—Variances when administering 1.5 iMAC or 1.5 gMAC were not significantly different for any variable studied. Differences between the MAC multiples needed to reach an MAP of 60 mm Hg and the mean of the sample were significantly larger when gMAC was used, compared with iMAC, indicating that a multiple of iMAC better predicted the concentration resulting in a MAP of 60 mm Hg.

Conclusions and Clinical Relevance—Results suggest that, in a small group of dogs, variability in cardiorespiratory measurements among dogs is unlikely to differ whether an inhalant anesthetic is administered at a multiple of the iMAC in each dog or at an identical gMAC in all dogs.

Abstract

Objective—To determine whether the variability of cardiorespiratory measurements is smaller when administering desflurane at a multiple of the individual's minimum alveolar concentration (MAC) or at a predetermined, identical concentration in all subjects.

Animals—10 dogs.

Procedures—Desflurane was administered at 1.5 times the individual's MAC (iMAC) and 1.5 times the group's MAC (gMAC). The order of concentrations was randomly selected. Heart rate, respiratory rate, arterial blood pressure, central venous pressure, mean pulmonary artery pressure, pulmonary artery occlusion pressure, arterial and mixed-venous blood gas tensions and pH, and cardiac output were measured. The desflurane concentration required to achieve a mean arterial pressure (MAP) of 60 mm Hg was then determined. Finally, the desflurane concentration required to achieve an end-tidal PCO2 of 55 mm Hg was measured.

Results—Variances when administering 1.5 iMAC or 1.5 gMAC were not significantly different for any variable studied. Differences between the MAC multiples needed to reach an MAP of 60 mm Hg and the mean of the sample were significantly larger when gMAC was used, compared with iMAC, indicating that a multiple of iMAC better predicted the concentration resulting in a MAP of 60 mm Hg.

Conclusions and Clinical Relevance—Results suggest that, in a small group of dogs, variability in cardiorespiratory measurements among dogs is unlikely to differ whether an inhalant anesthetic is administered at a multiple of the iMAC in each dog or at an identical gMAC in all dogs.

The MAC is an index of potency for inhalant anesthetics. It is defined as the alveolar concentration that prevents gross purposeful movement in response to supramaximal noxious stimulation in 50% of subjects.1–3 The minimum alveolar concentration is reported to vary by 10% to 20% among individuals of the same species.4

The MAC can be determined with the up-and-down, or quantal, method and the bracketing method.3 With the bracketing method, which is most commonly used in animal studies, MAC can be determined in individuals. Group MAC is then defined as the mean of the individual MAC values of this defined group of animals.

To determine the pharmacodynamic effects of anesthetic agents, a predefined anesthetic state must be obtained. For injectable anesthetic agents, this is difficult as it requires administration of a drug at predetermined steady-state plasma concentrations or, better still, at predetermined steady-state concentrations within the effect site, for example the brain. For inhalant anesthetics, MAC or a multiple of MAC has become that predefined anesthetic state because, at equilibrium, anesthetic concentration in the CNS will be mirrored by the alveolar (end-tidal) concentration.2 Because MAC is easy to determine, this has allowed not only the determination of the pharmacodynamic effects of inhalant anesthetics in a variety of species but also the comparison of specific effects (eg, cardiovascular and respiratory) of anesthetic agents and across species.5–10 It is also used to determine safety criteria for inhalant agents, such as a determination of the respiratory or cardiac indexes, and thus to establish that in a certain species, 1 inhalant may be safer than another.11,12

When the literature on pharmacodynamic effects of inhalant anesthetics is reviewed, it appears that some investigators have chosen to first determine the individual MAC for each animal enrolled in the study and then collected their data at set multiples of these individual MAC values, for example, 1.5 and 2.0 MAC.9,10,13 Because MAC may vary by ≥ 20% among individuals, the established concentration across individuals in these studies is likely to have that degree of variation. For example, in a study from our laboratory, the range of individual isoflurane MAC values in cats was 1.93% to 2.58%.14 We have also demonstrated that this variation is consistent across inhalant anesthetics, suggesting a genetic basis to variations in anesthetic requirement.15 On the other hand, some investigators have chosen to use a published value of MAC and have then established that concentration or a multiple of that concentration in each animal, so that an identical end-tidal concentration is established in all animals.16–25 Data have then been collected at this concentration. With this latter method, studies are easier and quicker to undertake because a separate experiment to establish individual MAC values for each animal is not required. Some investigators might consider this an inferior method, as individual animals are not considered at equipotent anesthetic concentrations. However, it is not known whether cardiovascular and respiratory effects in an individual are correlated with that individual's anesthetic requirements defined in terms of MAC. Although it would intuitively seem to be the case (ie, an animal requiring high anesthetic concentration to inhibit movement in response to noxious stimulation would also require high anesthetic concentration to reach a given level of cardiovascular or respiratory depression), to our knowledge, this has not been studied.

Indirect evidence actually suggests that individual anesthetic requirements as defined by MAC may not predict effects other than (lack of) movement in that individual. For example, it appears that the slope of the curves describing the distribution of MAC values in a population is different if MAC is defined as the concentration inhibiting movement or as the concentration inhibiting autonomic responses to noxious stimulation.26 This would indicate that the anesthetic requirement defined by the lack of movement is a poor predictor of the anesthetic requirements to block autonomic responses. It is possible that equipotent cardiovascular and respiratory effects of an inhalant anesthetic in a group of animals may be better achieved by administering an identical anesthetic concentration in all animals than by use of individual MAC values.

Knowing whether a multiple of the individual's MAC should be used in each animal or whether an identical anesthetic concentration should be administered to all animals when similar cardiovascular and respiratory effects are desired in a group of animals is of importance for the design of studies on the cardiorespiratory effects of inhalant anesthetics or adjuncts to inhalant anesthesia because lower variability between individuals will improve statistical power and facilitate the interpretation of results.

The purpose of the study reported here was to determine whether the variability of cardiorespiratory measurements is smaller when administering desflurane at a multiple of the individual's MAC or at a predetermined identical concentration in all subjects of the group. We hypothesized that the effects would be less variable between individual dogs when the same anesthetic concentration is administered to all dogs than when a multiple of the individual's MAC is used for each dog.

Materials and Methods

Animals—Ten healthy adult dogs (mean ± SD, weight 24.1 ± 4.1 kg; 5 males and 5 females) were used in the study. Food, but not water, was withheld from dogs for 12 hours before the experiments. The Institutional Animal Care and Use Committee at the University of California–Davis approved the study.

Experimental design—Two studies were conducted. In study 1, the MAC of desflurane was determined in each dog. In study 2, cardiovascular and respiratory measurements were obtained during administration of desflurane at 1.5 times each individual's MAC and 1.5 times the group's MAC (ie, the mean of the individual MAC values). Moreover, the desflurane concentrations needed to produce an MAP of 60 mm Hg and ETCO2 of 55 mm Hg were determined. At least 10 days separated the 2 studies.

Anesthesia and instrumentation—Anesthesia was induced with desflurane in O2 by use of a face mask. The trachea was then intubated with a cuffed endotracheal tube, and anesthesia was maintained with desflurane in O2 delivered via a circle circuit with a fresh gas flow of 1 to 2 L/min. Ventilation was spontaneous throughout the study. A catheter was passed through the lumen of the endotracheal tube so that its tip was positioned at the end of the tube. This catheter was connected to a Raman spectrometera for continuous measurement of ETCO2 and inspired and end-tidal O2 and desflurane concentrations. The spectrometer was calibrated with room air and 2 (study 1) or 3 (study 2) calibration gasesb of known desflurane concentrations (4.90%, 9.66%, and 14.90 %) every 80 minutes, corresponding to its internal calibration interval. Dogs were placed in left lateral recumbency. A 20-gauge, 4.7-cm catheter was inserted in a cephalic vein, and lactated Ringer's solution was administered at 3 mL/kg/h. A 20-gauge, 4.7-cm catheter was inserted in a dorsal pedal artery for continuous measurement of SAP, MAP, and DAP and for arterial blood sample collection. This catheter was connected to a transducer and physiograph.c The transducer was zeroed at the level of the sternum and calibrated against a mercury manometer prior to each experiment. A pulse oximeterd probe was placed on the tongue for SpO2 measurement. A thermistor,e calibrated prior to each experiment against a certified thermometer, was placed in the esophagus, at the level of the midthorax, and connected to the physiograph for continuous temperature monitoring. External heat (warm water and forced-air blankets) was supplied as needed to maintain body temperature between 38° and 39°C. An ECG (lead II) was continuously monitored with the physiograph.

In addition, for study 2, an 8-F, 10-cm introducerf was placed in a jugular vein. A 7-F, 110-cm thermodilution catheterg was inserted through the introducer and positioned with its distal port and thermistor in the pulmonary artery by use of fluoroscopic observation; this catheter was used for measurement of cardiac output, mean pulmonary arterial pressure, pulmonary artery occlusion pressure, central venous pressure, and core body temperature and for collection of mixed-venous blood samples (ie, samples from the pulmonary artery). Blood pH, PCO2, PO2, and hemoglobin concentration and SpO2 were determined in blood samples by use of a blood gas analyzerh and hemoximeter,i respectively.

End-tidal desflurane concentration determination—For each determination, 50 mL of end-tidal gas was collected by hand in a glass syringe throughout 7 to 12 breaths. Desflurane concentration in these samples was measured with the Raman spectrometer. Three samples were obtained for each determination, and the desflurane concentrations were averaged.

Study 1—For each MAC determination, end-tidal desflurane concentration was kept constant for ≥ 20 minutes. End-tidal desflurane concentration was determined as described. Heart rate, respiratory rate, SAP, MAP, DAP, body temperature, SpO2, and ETCO2 were recorded. An arterial blood sample (1 mL) was collected and immediately analyzed. A 20-cm Martin forceps was positioned on the tail and closed to the first ratchet until gross purposeful movement was observed or 1 minute had elapsed, whichever occurred first. Desflurane concentration was increased or decreased by 10%, following a positive (gross purposeful movement) or negative response to tail clamping, respectively. The new concentration was kept constant for ≥ 20 minutes, and the measurements repeated. The MAC of desflurane was defined as the mean of 2 successive desflurane concentrations, 1 allowing and 1 preventing gross purposeful movement in response to tail clamping. The MAC was determined in triplicate (ie, minimum of 4 tail-clamping procedures), and the mean was recorded.

Study 2—Sixty minutes after induction of anesthesia (ie, after instrumentation was completed), desflurane was administered to each dog at 1.5 times the individual's MAC and 1.5 times the group's MAC. The order of concentrations was randomly selected according to a computer-generated list. End-tidal desflurane concentration was kept constant for 30 minutes. End-tidal desflurane concentration was determined as described. Heart rate, respiratory rate, SAP, MAP, DAP, central venous pressure, mean pulmonary arterial pressure, pulmonary artery occlusion pressure, body temperature, SpO2, and ETCO2 were recorded. Arterial and mixed-venous samples (1 mL) were obtained and immediately analyzed. Cardiac output was determined in triplicate by use of a thermodilution technique and a cardiac output computer.j Five milliliters of iced 5% dextrose was injected through the proximal port of the thermodilution catheter at the end of expiration for each determination. The mean value of the 3 measurements was then calculated. Cardiac index, stroke index, rate-pressure product, systemic vascular resistance index, pulmonary vascular resistance index, left ventricular stroke work index, right ventricular stroke work index, arterial O2 concentration, mixed-venous O2 concentration, O2 delivery, O2 consumption, O2 extraction ratio, alveolar-to-arterial difference in PO2, and venous admixture were calculated by use of standard equations.27–29

Desflurane concentration was then adjusted to achieve an MAP of 60 mm Hg. After 15 minutes of stable end-tidal desflurane concentration at that blood pressure, desflurane concentration was determined as described. Finally, desflurane concentration was adjusted to achieve an ETCO2 of 55 mm Hg. After 15 minutes of stable end-tidal desflurane concentration at that ETCO2, desflurane concentration was determined as described.

Statistical analysis—All data were log transformed before analysis. Equality of variances for each measured or calculated variable when administering desflurane at 1.5 times the individual's MAC or 1.5 times the group's MAC was examined with a Levene ANOVA.30 Absolute differences between the log-transformed individual or group MAC multiples needed to reach an MAP of 60 mm Hg and an ETCO2 of 55 mm Hg, and the sample mean of the log-transformed MAC multiples were calculated and compared by use of a Fisher sign test. Significance was set at a value of P < 0.05. Data are presented as mean ± SD.

Results

The MAC of desflurane in this group of dogs was 7.64 ± 0.62% and ranged from 6.94% to 8.98%. Variances of the effects of 1.5 times the individuals' MACs of desflurane and 1.5 times the group's MAC of desflurane on measured and calculated variables were determined (Tables 1 and 2). Variances were not significantly different in the 2 groups for any variable.

Table 1—

Mean and variance of cardiovascular variables during administration of desflurane at 1.5 times the individual's MAC and 1.5 times the group's MAC (mean of the iMACs) in 10 dogs.

Variable1.5 iMAC1.5 gMAC
MeanVarianceMeanVariance
Heart rate (beats/min)116249114222
SAP (mm Hg)108399104128
MAP (mm Hg)69866955
DAP (mm Hg)57735743
CVP (mm Hg)74.763.2
MPAP (mm Hg)146.9148.7
PAOP (mm Hg)118.5105.3
Cardiac index (L/min/m2)2.70.52.60.6
Stroke index (mL/beats/m2)23.010.322.625.3
SVRI ([{dynes × s}/cm5]/m2)1,88981,5342,025142,839
PVRI ([{dynes × s}/cm5]/m2)1127581261,270
RPP (beats × mm Hg)12,64517,026,79011,9136,616,943
LVSWI ([g × m]/m2)18.528.818.640.5
RVSWI ([g × m]/m2)2.52.52.52.3

iMAC = Individual MAC. gMAC = Group MAC. CVP = Central venous pressure. MPAP = Mean pulmonary arterial pressure. PAOP = Pulmonary artery occlusion pressure. SVRI = Systemic vascular resistance index. PVRI = Pulmonary vascular resistance index. RPP = Rate-pressure product. LVSWI = Left ventricular stroke work index. RVSWI = Right ventricular stroke work index.

Table 2—

Mean and variance of selected respiratory variables during administration of desflurane at 1.5 times individual MAC and 1.5 times group MAC in 10 dogs.

Variable1.5 iMAC1.5 gMAC
MeanVarianceMeanVariance
Arterial pH7.320.0027.320.002
PaCO2 (mm Hg)45.174.846.479.4
PaO2 (mm Hg)481.41,763.8477.1681.2
Arterial HCO3(mmol/L)22.44.722.24.8
Arterial Hb (g/dL)12.92.812.62.0
Mixed-venous pH7.290.0027.280.002
PvCO2 (mm Hg)53.1114.155.4113.8
PvO2 (mm Hg)65.049.864.467.4
Mixed-venous HCO3(mmol/L)23.95.724.46.3
Mixed-venous Hb (g/dL)12.92.912.72.5
CaO2 (mL/dL)18.34.718.03.2
CvO2 (mL/dL)15.14.614.94.9
O2 delivery (mL/min)413.432,447391.931,274
O2 consumption (mL/min)67.9256.462.1181.1
O2 extraction ratio0.170.0010.170.003
PAo2–PaO2 (mm Hg)1821,727.5185470.6
QS/QT0.150.0020.160.001

Hb = Hemoglobin. CaO2 = Arterial O2 concentration. CvO2 = Mixed-venous O2 concentration. PAO2–PaO2 Alveolar-to-arterial difference in PO2. QS/QT = Venous admixture.

See Table 1 for remainder of key.

Because apnea occurred in 3 dogs at MAPs of > 60 mm Hg, and because the administration of intermittent positive pressure ventilation would likely have affected the cardiovascular effects of desflurane, the desflurane concentration required to reach an MAP of 60 mm Hg was determined in 7 dogs only. That concentration was 13.57 ± 1.49%, which represented 1.79 ± 0.10 times the individuals' MACs or 1.78 ± 0.20 times the group's MAC. The Fisher sign test result was significant, indicating that the individual's MAC multiple better reflected the desflurane concentration resulting in an MAP of 60 mm Hg than did a group MAC multiple.

Because excessive cardiovascular depression, judged as potentially life threatening, occurred in 5 dogs before an ETCO2 of 55 mm Hg was reached, the desflurane concentration required to reach an ETCO2 of 55 mm Hg was determined in 5 dogs only. That concentration was 13.42 ± 3.12%, which represented 1.70 ± 0.41 times the individuals' MACs or 1.76 ± 0.41 times the group's MAC. The Fisher sign test result was not significant for this measurement.

Discussion

In our study, we examined the question of whether it is important to use individual MAC values when studying the cardiovascular and respiratory effects of inhalant anesthetics (or those of adjuncts to inhalant anesthesia) or whether a predetermined anesthetic concentration (eg, a multiple or fraction of a published MAC value) could be administered to all dogs instead. This question was addressed in terms of interindividual variability in a group of dogs, assuming that it is important to reduce this variability to maximize statistical power and to reach equipotent inhalant-induced cardiovascular and respiratory effects in all dogs of the group.

Two approaches were used to investigate our study question. In the first part of study 2, the anesthetic concentration was fixed by the protocol and the variability of the cardiovascular and respiratory effects was examined when desflurane was administered at a multiple of the individual's MAC in each dog or at an identical concentration in all dogs.

In the second part of study 2, the opposite approach was taken in which the cardiovascular (represented by MAP) and respiratory (ETCO2) effects were fixed by the protocol and the desflurane concentration needed to produce these effects was studied. We then examined whether the interindividual variability of that desflurane concentration would be lower if the concentration is expressed as a multiple of the individual's MAC or as a multiple of the group's MAC (the latter indicating that a fixed effect is better achieved by administering an identical anesthetic concentration to all dogs). This approach answers the same question as the first approach because it determines whether consistent cardiovascular and respiratory effects are best achieved with a multiple of the individual's MAC in each dog or an identical anesthetic concentration in all dogs. This second approach could be considered as the ultimate way of examining how to obtain consistent cardiovascular and respiratory effects because the effect was fixed and identical in all individuals. It was used as a complement to the more global study of variances in cardiorespiratory variables when administering the agent at a multiple of the individual's MAC or at an identical concentration in all dogs. However, fixing the effect was only possible for selected variables because of time and technical constraints (ie, the need for an accurate and continuous measurement allowing the titration of the anesthetic agent to a specific effect).

Desflurane was selected as the inhalant anesthetic for our study because information in the literature suggests that the relative variation in MAC between individual dogs is slightly larger for desflurance than that of other inhalant anesthetics.7,31–34 Larger differences in MAC in individual dogs will indeed maximize the likelihood of detecting a difference in variability of the effects when the agent is administered at a multiple of the individual's MAC in each dog or at an identical concentration in all dogs (in the extreme situation where all individuals have the same MAC, administering the agent at a multiple of the individual's MAC in each dog is equivalent to administering an identical concentration in all dogs).

A high MAC multiple was desirable to maximize the likelihood of detecting a difference in variability because it amplifies the absolute difference in anesthetic requirements between dogs (eg, the lowest and highest individual MACs in our study were 6.94% and 8.98%; at 1 MAC, the difference is 2.04%; at 1.5 MAC, the difference is 3.06%). However, at high concentrations, desflurane may induce excessive cardiorespiratory depression, which was not desirable in our study. Excessive respiratory depression would indeed be characterized by apnea, requiring mechanical ventilation and preventing the assessment of respiratory variability. For these reasons, and also because it is relevant to studies on clinical concentrations of inhalant anesthetics, 1.5 MAC was used in our study.

For the part of our study on fixed cardiovascular and respiratory effects, an MAP of 60 mm Hg and an ETCO2 of 55 mm Hg were selected. These values were chosen because they were caused by moderately high desflurane concentrations, maximizing the likelihood of detecting differences in variability between the concentrations indexed to the individual's or the group's MAC. The MAP and ETCO2 were used as indices of cardiovascular and respiratory effects, respectively, first because of their relevance to cardiovascular and respiratory functions and second because they can be accurately and continuously measured, making the titration of the anesthetic agent to fixed values possible.

Results of our study suggest that in a small group of dogs, administration of individual MAC values or an identical anesthetic concentration to all dogs is unlikely to affect the interindividual variability of cardiovascular and respiratory measurements. However, the fact that the anesthetic concentration resulting in a given MAP is less variable when expressed as a multiple of the individual's MAC values than as a multiple of the group's MAC (ie, the anesthetic concentration) indicates that if similar arterial pressures are desirable in several dogs, a multiple of their individual MAC may be preferable. This was, however, shown for 1 cardiovascular variable (MAP) only and at 1 level of effect (60 mm Hg). It is unknown whether different results would be obtained if another variable or level of effect had been selected. The apparent contradiction with the lack of significance of the difference in variances of MAP when desflurane is administered at 1.5 times the individual's MAC in each dog or 1.5 times the group's MAC in all dogs is likely related to the differences in methods and statistical analysis used to obtain and interpret these results.

The lack of similar results for the ETCO2 end point may be related to a low statistical power. Retrospective power analysis reveals that with a power of 0.8, 10 dogs are needed to determine whether 1 method (ie, individual MAC or group MAC) is significantly better in predicting the anesthetic concentration needed to reach the end point 90% of the time. The target ETCO2 was only reached in 5 dogs, obviously limiting the ability to detect whether an individual or group MAC is likely a better predictor of the anesthetic concentration that results in the selected level of respiratory depression.

Lack of statistical power may also be involved in the failure to detect a significant difference in variance for any cardiovascular or respiratory variable between when a multiple of the individual's MAC is administered or when the same anesthetic concentration is administered to all dogs. However, most veterinary anesthesia studies are conducted on a small number of animals, and the similarity observed in the variances indicates that if a difference in variability exists, it would likely be detected only if a large number of subjects were used. Moreover, mathematic coupling between the 2 concentrations used in our study may have obscured potential differences. The group MAC is indeed calculated as the mean of the individual MAC values. Nevertheless, it was deemed important to examine the variability of the measurements obtained at equipotent concentrations in the 2 groups; therefore, a random concentration could not be selected instead of the multiple of the group MAC.

The range of MAC values measured in our study confirms that interindividual MAC variability is large for desflurane (there was a 23% difference between the highest and lowest value). The mean MAC in our study is comparable to a previously published value.34 Only desflurane was studied, and whether the results can be extrapolated to other inhalant anesthetics remains to be demonstrated. Similarly, our study was conducted in dogs, and it cannot be determined whether the results apply to other species.

An incidental finding of interest was the fact that in 5 of 10 dogs, an ETCO2 of 55 mm Hg could not be reached without excessive cardiovascular depression (ie, severe hypotension and small pulse pressure). The target ETCO2 was considered to reflect mild to moderate respiratory depression. Inhalant anesthetics, including desflurane, have been reported to cause apnea at concentrations significantly lower than those causing cardiovascular collapse.11,12,31,32,35 Although the procedure was aborted, and cardiovascular collapse was therefore not observed, the degree of cardiovascular depression observed with only mild respiratory depression may suggest that the difference in concentrations causing apnea and cardiovascular collapse may be small for desflurane in some dogs or even that cardiovascular collapse might occur at concentrations that do not cause respiratory arrest.

In conclusion, results of our study suggest that, in a small group of dogs, it is unlikely that the variability in cardiorespiratory measurements between dogs would differ if an inhalant anesthetic is administered at a multiple of the individual's MAC in each dog or at an identical concentration in all dogs. Limited evidence was found that a consistent MAP of 60 mm Hg might be best achieved with individual MAC values. Use of multiples or fractions of a published MAC value, instead of measuring MAC in each individual, is unlikely to affect statistical power in studies on the cardiorespiratory effects of inhalant anesthetics or adjuncts to inhalant anesthesia.

ABBREVIATIONS

MAC

Minimum alveolar concentration

MAP

Mean arterial pressure

ETCO2

End-tidal CO2 concentration

SAP

Systolic arterial pressure

DAP

Diastolic arterial pressure

SpO2

Arterial hemoglobin O2 saturation

a.

Rascal II, Ohmeda, Salt Lake City, Utah.

b.

Scott Medical Products, Plumsteadville, Pa.

c.

Gould Instrument Systems, Valley View, Ohio.

d.

Rascal II, Ohmeda, Salt Lake City, Utah.

e.

YSI 701 temperature probe, Yellow Springs Instruments, Yellow Springs, Ohio.

f.

Introducer kit, Arrow International, Reading, Pa.

g.

Thermodilution balloon catheter, Arrow International, Reading, Pa.

h.

ABL 505, Radiometer, Copenhagen, Denmark.

i.

OSM 3, Radiometer, Copenhagen, Denmark.

j.

COM-1, American Edwards Laboratories, Irvine, Calif.

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