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Anesth Analg 2002;95:1200-1206
© 2002 International Anesthesia Research Society

PEDIATRIC ANESTHESIA

Pulmonary-to-Systemic Blood Flow Ratio Effects of Sevoflurane, Isoflurane, Halothane, and Fentanyl/Midazolam with 100% Oxygen in Children with Congenital Heart Disease

Tracy H. Laird, MD*, Stephen A. Stayer, MD{dagger}, Shannon M. Rivenes, MD*, Mark B. Lewin, MD§, E. Dean McKenzie, MD{ddagger}, Charles D. Fraser, MD{ddagger}, and Dean B. Andropoulos, MD{dagger}

Divisions of *Pediatric Cardiology, {dagger}Pediatric Cardiovascular Anesthesiology, and {ddagger}Congential Heart Surgery, Texas Children’s Hospital and Baylor College of Medicine, Houston; and §Division of Pediatric Cardiology, Children’s Hospital and Regional Medical Center and the University of Washington School of Medicine, Seattle, Washington

Address correspondence and reprint requests to Dean B. Andropoulos, MD, Division of Pediatric Cardiovascular Anesthesiology, Texas Children’s Hospital, 6621 Fannin, WT 19345H, Houston, TX 77030-2399. Address e-mail to dra{at}bcm.tmc.edu


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 Appendix
 References
 
The cardiovascular effects of volatile anesthetics in children with congenital heart disease have been studied, but there are limited data on the effects of anesthetics on pulmonary-to-systemic blood flow ratio (Qp:Qs) in patients with intracardiac shunting. In this study, we compared the effects of halothane, isoflurane, sevoflurane, and fentanyl/midazolam on Qp:Qs and myocardial contractility in patients with atrial (ASD) or ventricular (VSD) septal defects. Forty patients younger than 14 yr old scheduled to undergo repair of ASD or VSD were randomized to receive halothane, sevoflurane, isoflurane, or fentanyl/midazolam. Cardiovascular and echocardiographic data were recorded at baseline, randomly ordered 1 and 1.5 mean alveolar anesthetic concentration (MAC) levels, or predicted equivalent fentanyl/midazolam plasma levels. Ejection fraction (using the modified Simpson’s rule) was calculated. Systemic (Qs) and pulmonary (Qp) blood flow was echocardiographically assessed by the velocity-time integral method. Qp:Qs was not significantly affected by any of the four regimens at either anesthetic level. Left ventricular systolic function was mildly depressed by isoflurane and sevoflurane at 1.5 MAC and depressed by halothane at 1 and 1.5 MAC. Sevoflurane, halothane, isoflurane, or fentanyl/midazolam in 1 or 1.5 MAC concentrations or their equivalent do not change Qp:Qs in patients with isolated ASD or VSD.

IMPLICATIONS: Sevoflurane, halothane, isoflurane, and fentanyl/midazolam do not change pulmonary-to-systemic blood flow ratio in children with atrial and ventricular septal defects when administered at standard anesthetic doses with 100% oxygen.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 Appendix
 References
 
Sevoflurane, halothane, isoflurane, and fentanyl/midazolam in combination are all used for patients with congenital heart disease (CHD). Earlier studies have shown that halothane depresses myocardial contractility more than sevoflurane, isoflurane, or fentanyl/midazolam (1–5). There are few studies concerning the effects of these anesthetics on pulmonary (Qp) to systemic (Qs) blood flow ratio (Qp:Qs) or their effects on hemodynamics in patients with intracardiac shunting (6,7). Chronic increases in Qp:Qs lead to pulmonary overcirculation, right heart overload, and congestive heart failure in patients with left to right shunts such as atrial septal defect (ASD) or ventricular septal defect (VSD) (8). This increased workload in an acute setting may be undesirable, particularly before a period of aortic cross-clamping with associated myocardial ischemia. Decreasing the Qp:Qs to <1:1 in the operating room could potentially have beneficial effects on the myocardium.

The purpose of this study was to compare pulmonary and systemic hemodynamics as well as the effects on myocardial contractility of these four anesthetic regimens in patients undergoing surgery for ASD or VSD using transthoracic echocardiography. Change in Qp:Qs was our primary outcome variable, and we hypothesized that there would be a significant increase in Qp:Qs when these anesthetics were administered with 100% oxygen.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 Appendix
 References
 
After IRB approval and informed consent from a parent, patients aged 13 yr or younger undergoing congenital heart surgery were enrolled. All patients had two ventricles and a primary diagnosis of either VSD or secundum ASD. Patients were excluded from the study if they had a patent ductus arteriosus because of its additive effects on pulmonary blood flow and alterations in echocardiographic assessment of Qp:Qs. Patients were also excluded if they had aortic or pulmonary stenosis or aortic or pulmonary regurgitation because these conditions would affect the accuracy of the flow measurements in the respective great arteries.

Patients were randomized to one of four groups by selecting the first of a lot of prelabeled cards representing each group. They were thoroughly mixed to ensure randomization and maintained so that the group assignment of the next patient was not known until the card was actually drawn. The four groups were halothane, isoflurane, sevoflurane, or fentanyl/midazolam. All patients received premedication with oral midazolam 0.75 mg/kg or IV midazolam 0.05–0.2 mg/kg to achieve a sedated but responsive state. After the application of standard monitors and recording of heart rate (HR), oscillometric blood pressure, and SpO2, a baseline transthoracic echocardiogram was performed with the patient breathing room air. Anesthesia was then induced with either an inhaled anesthetic using calibrated vaporizers, with 10 L/min of oxygen, or a fentanyl/midazolam infusion for 1 min. Muscle relaxation was facilitated with vecuronium 0.3–0.4 mg/kg, and the trachea was intubated. Fractional inspired oxygen was maintained at 1.0 and the ETCO2 at 30–40 mm Hg. The lowest possible mean airway pressure was maintained, and peak inspiratory pressure remained <25 cm H2O; a positive end-expiratory pressure of 2 cm H2O and an I:E ratio of 1:2 to 1:3 were used. In random order (according to the second to last digit of the seven-digit medical record number, with even numbered patients receiving 1 mean alveolar anesthetic concentration [MAC] first and odd numbers 1.5 MAC first), an age-adjusted MAC of 1 or 1.5 was achieved for the inhaled anesthetics (9–11) using the technique of overpressure (12) to achieve the target end-tidal concentration as rapidly as possible. The randomization scheme, both for anesthetic and MAC level, was known only to the single investigator (DBA) actually administering the anesthetic. ETCO2 and fraction of inspired O2 concentrations (FIO2) were measured at a side port on the elbow connector attached to the patient’s endotracheal tube with an infrared sidestream device calibrated weekly with standard gas mixtures. For patients randomized to fentanyl/midazolam infusion and maintenance, infusion rates were calculated based on published pediatric pharmacokinetic data to predict two different plasma levels: 4 and 6 ng/mL for fentanyl and 100 and 200 ng/mL for midazolam (see Appendix for doses). These levels are associated with sedation, hypnosis, and analgesia for surgery and approximate 1 and 1.5 MAC levels of the volatile anesthetics (13–18). The order of predicted plasma levels was always 1 MAC first because of the lack of time available to allow for the plasma levels of the drugs to decrease if the 1.5 MAC level were achieved first. The inhaled anesthetics or the fentanyl/midazolam infusion were maintained at a constant end-tidal concentration or infusion rate for 10 min. A second echocardiogram was performed, and vital signs were again recorded. The inhaled anesthetics were then adjusted to the second MAC level and allowed to equilibrate for 10 min; the fentanyl/midazolam patients were given a second infusion equal to 50% of the first, and the maintenance rate was increased by 50% for 10 min. A final echocardiogram was performed, and vital signs were repeated.

All patients either received maintenance IV fluids until the time of the induction or if no IV catheter was present, were allowed to ingest clear liquids until 2 h before the induction. Only maintenance IV fluids were administered during the study period. No vasoactive drugs were given aside from the anesthetics. Each patient had a right internal jugular vein catheter inserted immediately after tracheal intubation to measure central venous pressure for calculation of systemic vascular resistance (SVR). A radial artery catheter was placed as soon as possible, and an arterial blood gas was sampled during steady-state ventilation and hemodynamics. Any hemodynamic response perceived to be due to these procedures was allowed to subside before echocardiographic assessment; all measurements were made during periods of steady-state hemodynamics.

Two-dimensional and pulsed Doppler transthoracic echocardiography was performed by a pediatric cardiologist using an Acuson 128XP/10 or Acuson Sequoia ultrasonic imaging system. The pediatric echocardiographer was blinded to the type of anesthetic administered and to the MAC randomization. Studies at baseline, 1 MAC, and 1.5 MAC were each obtained over 3–5 min during a period of unchanging HR and blood pressure. Each study was performed in the same manner, according to the recommendations of the American Society of Echocardiography Committee on Standards (19), and all analyses were performed offline. All measurements were obtained over three consecutive cardiac cycles, and the average of the values was recorded. Orthogonal left ventricular end-diastolic volume and left ventricular end-systolic volume were traced; ejection fraction (EF) was calculated according to the modified Simpson’s biplane method. Aortic and pulmonary artery velocity time integrals were traced, and the aortic and pulmonary valve annuli were measured. The following variables were measured or calculated at the three time periods: HR, mean arterial blood pressure, EF, stroke volume index, left ventricular end-diastolic volume index, Qs (equal to the systemic cardiac output), Qp, and SVR index (20,21). The anesthetic and MAC order was unknown to the echocardiographers during the analyses. See Appendix for hemodynamic and echocardiographic calculations.

Data are reported as mean ± SD. Statistical calculations and analyses were performed using Sigma Stat version 2.03 (SPSS Inc, Chicago, IL). Analysis of variance for repeated measures was used to compare variables at the three MAC levels within the same group. To compare variables between the four groups at each MAC level, a two-way analysis of variance with repeated measures was used. The Tukey test was used for post hoc pair-wise comparisons of the mean responses to the different treatment groups. {chi}2 analysis was used to compare the number of patients in each group with an increase in Qp:Qs at the 1.5 MAC level of more than 50% from baseline. P < 0.05 was considered significant for all tests.


   Results
Top
 Abstract
 Introduction
 Methods
 Results
Discussion
 Appendix
 References
 
Forty patients were studied. Patient characteristics and cardiac diagnoses are presented in Table 1. Of the 40 patients, 23 had a VSD as the primary cardiac diagnosis, and 17 had a secundum ASD. All patients were acyanotic with left-to-right intracardiac shunting through all defects. All patients had some degree of right atrial and right ventricular dilation, and all had normal baseline left ventricular systolic function as measured by EF. All patients had preoperative evidence of either clinical congestive heart failure or normal pulmonary pressures by echocardiography, suggesting the lack of abnormal pulmonary vascular resistance (PVR). There were no significant differences in patient age or weight among the four groups. There were no clinically significant differences in SpO2 and ETCO2 within or between groups. The blood gas values were not different between groups and reflected the lack of any right-to-left intracardiac shunting. The changes in measured and calculated hemodynamic variables are presented in Table 2.


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  		Table 1. Patient Characteristics
 

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  		Table 2. Measured and Calculated Hemodynamic and Echocardiographic Variables
 
The baseline values at 0 MAC for the hemodynamic variables were compared and were similar between groups for all comparisons. For each of the variables, interactions were sought between the anesthetic and the MAC level of the anesthetic and were found for the following: HR, mean arterial blood pressure, EF, and SVR index. No interactions were found for Qp, Qs, Qp:Qs, Qp + Qs, stroke volume index, and left ventricular end-diastolic volume index.

Qp decreased at both 1 and 1.5 MAC with halothane, but there was no change in the other groups. Qs (systemic cardiac index) decreased at 1.5 MAC with halothane and at both 1 and 1.5 MAC with sevoflurane and fentanyl/midazolam. Qp:Qs did not change statistically from baseline within any of the four anesthetic groups, nor was there a difference between groups. The 32% increase in Qp:Qs from baseline with fentanyl/midazolam at the 1.5 MAC equivalent did not reach statistical significance (P = 0.069). Three of 9 fentanyl/midazolam patients had an increase in Qp:Qs of more than 50% from baseline at 1.5 MAC. One of 10 patients in the isoflurane and halothane groups and none of the 11 patients in the sevoflurane group increased Qp:Qs by more than 50% from baseline at 1.5 MAC. This difference between groups was also not significant (P = 0.28; {chi}2 analysis). In addition, when Qp + Qs, representing total volume of blood pumped through the heart per minute, was assessed, this also reflected no change from baseline with any regimen at either concentration. The Qp:Qs for each individual patient is presented in Figure 1.



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  		Figure 1. Individual patient pulmonary-to-systemic blood flow ratio (Qp:Qs) data for each anesthetic (halothane, n = 10; sevoflurane, n = 11; isoflurane, n = 10; and fentanyl/midazolam, n = 9). Heavy black line indicates mean value at each anesthetic concentration.

 

   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
Appendix
 References
 
This study demonstrates that there is no change in Qp:Qs in response to 1 or 1.5 MAC sevoflurane, halothane, or isoflurane, or an equivalent dose of fentanyl/midazolam when patients receive normocapneic ventilation with FIO2 of 1.0. Qs decreased with both halothane and sevoflurane, but a concomitant decrease in Qp with halothane and a small nonstatistically significant decrease in Qp with sevoflurane maintained Qp:Qs at baseline. Qs also decreased with fentanyl/midazolam, solely because of the decrease in HR, and Qp was maintained at baseline levels, resulting in an increase in Qp:Qs that did not reach statistically significant levels. Isoflurane decreased EF at 1.5 MAC, but Qp, Qs, and Qp:Qs remained unchanged. The hemodynamic effects of isoflurane were because of a decrease in SVR and maintenance of Qs from decreased stroke volume but increased HR.

An FIO2 of 1.0 was chosen for this study to replicate common clinical conditions and would be expected to increase Qp and thus Qp:Qs (8). In patients with reactive pulmonary vasculature, oxygen relaxes tone in the pulmonary arterial system. This decreased tone will lower PVR and lead to an increased Qp in patients with intracardiac shunting. However, we did not observe increased Qp from oxygen therapy. One possible explanation is that positive-pressure ventilation decreased Qp. In this study, the peak and mean airway pressures were maintained as low as possible; however, this pressure is transmitted to the pulmonary capillary bed, increasing resistance in the pulmonary vasculature and possibly offsetting the vasodilating effect of oxygen.

Direct studies of Qp:Qs changes in response to these anesthetic regimens in children with unrepaired CHD have not been reported. Glenski et al. (6) reported that fentanyl, halothane, and isoflurane did not change right ventricular preejection period, an indirect echocardiographic M-mode measure that estimates PVR. They studied a group of 48 infants and children with CHD, most of whom had left-to-right intracardiac shunt like the patients in our study. Hickey et al. (7) reported that 25 µg/kg of fentanyl did not change cardiac index or SVR or PVR in the immediate postoperative period in 12 patients with repaired CHD, of which 10 previously had left-to-right cardiac shunts. This study was performed using thermodilution measurement of cardiac index, with direct measurements of left atrial, right atrial, and pulmonary artery pressures.

It is common practice to reduce the oxygen concentration in patients with left-to-right shunts to avoid overcirculation of blood to the lungs and steal from the systemic circulation. Data from this study would indicate that such a practice is unnecessary because the four anesthetic regimens evaluated did not significantly change the Qp:Qs, despite the use of 100% oxygen and positive-pressure ventilation. We do not know how Qp:Qs might be affected by anesthetics in patients with left-to-right shunts if FIO2 was maintained at 0.21; it is certainly possible that changes in Qp, Qs, or Qp:Qs might in this case be elicited.

The results of this study cannot be applied to all patients with CHD or to all patients with left-to-right shunting. We studied only patients with two ventricles and isolated VSD or ASD as the source of intracardiac shunting. Patients with a more critical dependence on relative SVR and PVR and blood flows, such as single ventricle patients with a large patent ductus arteriosus or systemic-to-pulmonary artery shunt as their major source of communication between pulmonary and systemic circulations (22), or patients with unrepaired truncus arteriosus (23), were not studied. Also, only three infants younger than six months were studied. These patients demonstrate more profound myocardial depressant responses to the volatile anesthetics and increased hemodynamic compromise with large concentrations of inspired oxygen, as relatively more blood is shunted into their reactive pulmonary vascular bed (24). We also did not study patients with right-to-left intracardiac shunting and cyanosis.

With only 9–11 patients in each group, the statistical power of the negative findings, with a type I error protection of 0.05, was less than the desired level of 0.80 for most tests. This is of particular importance for the main outcome variable Qp:Qs, which is subject to a type II statistical error, i.e., a falsely negative statistical outcome.

In conclusion, sevoflurane, halothane, isoflurane, or fentanyl/midazolam in 1 or 1.5 MAC concentrations or their equivalent do not change Qp:Qs in patients with isolated ASD or VSD when positive-pressure ventilation and FIO2 of 1.0 are used.


   Appendix
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Appendix
References
 
Drug Dosage Calculations
For fentanyl and midazolam, the dose calculations were as follows: (13–18)

equation


where Vd = volume of distribution

Infusion rate (µg · kg-1 · h-1) = desired plasma level (ng/mL) x CL (L · kg-1 · min-1) x 60,

where CL = drug clearance

Appendix
Go


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  		Table 3. Fentanyl.
 
The second bolus was 50% of the first dose, and the maintenance infusion rates then increased by 50% for the second measurement.

Midazolam. Because of the reported variability in pharmacokinetic data of midazolam in children, the same initial and maintenance infusion was chosen for all ages (20–22). Calculations were based on a CL of 0.009 L · kg · -1min-1, and a Vd of 1.9 L/kg. A dose of 0.29 mg/kg was followed by an infusion of 139 µg · kg · -1h-1. The second dose was 0.15 mg/kg followed by an infusion of 208 µg · kg · -1h-1.

Echocardiographic Calculations (19–23)

equation


EF = ejection fraction; LVEDV = left ventricular end-diastolic volume; LVESV = left ventricular end-systolic volume

equation


CO = systemic cardiac output; Da = aortic diameter; VTIa = aortic velocity time integral.

equation


equation


SV = stroke volume, HR = heart rate

equation


SVR = systemic vascular resistance, MAP = mean arterial blood pressure, CVP = central venous pressure. SV, LVEDV, and CO were divided by the patient’s body surface area to calculate an index to account for the different patient sizes. The SVR was multiplied by the body surface area to calculate an SVR index.


   Acknowledgments
 
Financial support provided by the Divisions of Pediatric Cardiology, Department of Anesthesiology, and Division of Congenital Heart Surgery, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030.

The authors thank Barbara Skjonsby, R.N. for technical assistance, and Anna Frolov, M.S. for statistical consultation.


   Footnotes
 
Presented, in part, at the Society for Cardiovascular Anesthesia 22nd Annual Meeting & Workshops, Orlando, FL, May 9, 2000; and at the American Society of Echocardiography 11th Annual Scientific Sessions, June 11, 2000.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 Appendix
 References
 

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Accepted for publication June 17, 2002.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2002 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press