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From the *Service d'Anesthésie-Réanimation et Unité Propre de Recherche de l'Enseignement Supérieur-Equipe d'Accueil (UPRES-EA 392); and Service de Réanimation Pédiatrique, Centre Hospitalo-Universitaire de Bicêtre, Assistance Publique-Hôpitaux de Paris (AH-HP), Le Kremlin Bicêtre, France.
Address correspondence and reprint requests to Karim Asehnoune, MD, PhD, Service d'Anesthésie-Réanimation, Hôpital de Bicêtre 94275 Le Kremlin Bicêtre, France. Address e-mail to asehnounekarim{at}hotmail.com.
Abstract
BACKGROUND: It is thought that pediatric epidural anesthesia (EA) provides hemodynamic stability in children. However, when compared with information relating to adults, little is known about the hemodynamic effects of epidural EA on cardiac output (CO) in infants.
METHODS: Using transesophageal Doppler to monitor CO, we prospectively studied 14 infants <10 kg who were scheduled for abdominal surgery. During sevoflurane general anesthesia, CO transesophageal Doppler monitoring was performed before and after lumbar EA with 0.75 mL/kg of 0.25% bupivacaine and 1:200,000 adrenaline. CO, arterial blood pressure, and heart rate were measured before and 5, 15, and 20 min after performance of EA.
RESULTS: In patients anesthetized with sevoflurane and sufentanil, EA resulted in an increase in stroke volume by 29% (P < 0.0001) and a decrease in heart rate by 13% (P < 0.0001). EA also induced a significant decrease in systolic, diastolic, mean arterial blood pressure, and systemic vascular resistance by 11%, 18%, 15%, and 25%, respectively. Conversely, CO remained unchanged.
CONCLUSIONS: The increase in stroke volume observed is probably explained by optimization of afterload because of the sympathetic blockade induced by EA. These results confirm that EA provides hemodynamic stability in infants weighing <10 kg and supports the use of EA in this pediatric population.
It is generally recognized that epidural anesthesia (EA) does not cause significant hemodynamic alteration in children. This technique has been increasingly used in recent years, especially in patients undergoing abdominal surgery (1–4). EA is reliable and safe, even when combined with general anesthesia (5–9). Nevertheless, little is known about its hemodynamic effects in infants and children. Two major concepts may explain the pediatric specificity regarding central block-induced hemodynamic changes. 1) Children have lower basal sympathetic tone as compared to adults (5,10–12). 2) The lower-limb blood volume in children might explain a slower rate of blood pooling in the denervated lower extremities (5,10,11). These concepts have been challenged. Payen et al. suggested that caudal anesthesia induces blood pooling in the denervated lower extremities (blocked areas) and a reflex vasoconstriction in the innervated areas (13). Moreover, Larousse et al. suggested that hemodynamic alterations observed after caudal anesthesia were induced by sympathetic block (8).
At present, the effects of EA on cardiac output (CO) in infants is not known. The recent introduction into clinical practice of a noninvasive measurement of CO for infants, has allowed us to examine the hemodynamic alterations caused by EA in a group of infants weighing <10 kg undergoing abdominal or urologic surgery.
METHODS
After approval by our Human Studies Committee, and parental written informed consent were obtained, 14 consecutive ASA I-II children weighing <10 kg, were enrolled. Patients with known cardiovascular or esophageal abnormalities, and those with conditions contraindicating EA were excluded from the study. Fasting time was 6 h for solids and all infants received an oral intake of 15 mL/kg of 15% glucose 2 h before surgery. Midazolam 0.5 mg/kg per os was administered 45 min before surgery. On arrival in the operating room, heart rate (HR) was continuously recorded, and noninvasive arterial blood pressure was measured by an automated blood pressure cuff every 5 min. After denitrogenation, general anesthesia was induced by inhalation of 100% oxygen and 8% sevoflurane until the patient lost conciousness and then the sevoflurane concentration was decreased to 4%. An IV cannula was inserted and sufentanil (0.2 µg/kg) and atracurium (0.5 mg/kg) were administered to facilitate tracheal intubation. Anesthesia was then maintained with 50% nitrous oxide, oxygen, and sevoflurane (1 MAC end-tidal concentration, according to age). Mechanical ventilation was adjusted to ensure end-tidal CO2 (ETco2) to 30–35 mm Hg. One percent dextrose in lactated Ringer's solution was infused for intraoperative fluid maintenance using standard maintenance guidelines for infants weighing <10 kg (4 mL·kg–1·h–1). Rectal temperature was monitored and maintained in a normal range with a forced-air warmer. The following measurements were collected: HR, systolic (SAP), diastolic (DAP) and mean arterial pressure (MAP), ETCO2, and body temperature. The following calculated variables: CO, stroke volume (SV), and systemic vascular resistances (SVR) were also collected.
CO was evaluated with a transesophageal Doppler (TED) device, the CardioQP® (Deltex Medical, Chichester, UK). As recommended by the manufacturer, the pediatric probe is for use in patients >3 kg. The probe was inserted orally while the patient was under general anesthesia. The probe was connected to a monitor displaying the blood flow velocity wave form after spectral analysis of the reflected Doppler-shift signal. The probe was located with its tip positioned in the midesophagus (T5–6) and rotated so that a characteristic aortic blood flow (ABF) signal was obtained. Probe position was optimized by slow rotation and alteration of the depth of insertion to generate a clear signal. Both an audible, maximal pitch and a visual signal that produced a sharply defined velocity wave form with minimal spectral dispersion defined the correct probe position. Gain setting was adjusted to obtain the best outline of the aortic velocity wave form. Before each measurement, the probe position was adjusted to ensure optimal acquisition of the maximal velocity signal. The monitor was preset to calculate CO by averaging five consecutive measurements. CO is calculated from the product of HR and stroke volume (SV). SV was calculated as the product of stroke distance (SD) and De, where De is the calibration constant derived from the pediatric nomogram based on the patient's age, weight, and height.
The children were positioned on their left sides and the lumbar epidural block was performed with a 29-gauge Tuohy needle. A catheter was advanced 3–4 cm into the epidural space and patients were then repositioned in the supine position. Adequate placement of the catheter was verified with an aspiration test and a test dose of 0.25% bupivacaine with 1:200,000 epinephrine (10% of the induction dose). One minute after the epidural test dose, injection of 0.25% bupivacaine with 1:200,000 epinephrine (0.75 mL/kg) was administered. Four sets of data were recorded. Each set included: HR, SAP, DAP, MAP, ETCO2, SV, SVR, and CO. The first set of measurements (baseline value: T0) occurred after a 10-min steady-state period under general anesthesia and before EA performance. The second, third, and fourth set of measurements were performed 5, 15, and 20 min after the end of the epidural injection, respectively. Surgery began after completion of the study.
Results are reported as means and 95% confidence interval. Data were compared using a variance analysis for repeated measurement, followed by Student-Newman-Keuls test. Differences were considered statistically significant at the 5% level (P < 0.05).
RESULTS
The procedure was proposed and accepted by the parents of 16 patients but an epidural technique failure occurred in two patients. No significant hemodynamic alteration was observed in these two patients compared with baseline values, except HR, which increased by 12% maximally, 20 min after induction of general anesthesia. Fourteen patients, aged 4.4 (±5.2) mo and weighing 5.5 (±2.3) kg, were therefore included in our analysis. Demographic data, surgical procedures, and patient's characteristics are summarized in Table 1. No complications occurred using the TED.
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The mean CO at the different times were: 0.9 (0.8–1.1) L/min, 1.1 (0.9–1.2) L/min, 1.0 (0.9–1.1) L/min, 1.1 (0.9–1.2) L/min. There was no statistical difference in CO after EA when compared with general anesthesia alone (Fig. 1). SV significantly increased at 29% from baseline (from 7.3 to 9.1 mL; P < 0.0001) (Fig. 2). HR significantly decreased from 138 (120–146) bpm to 121 (111–130) bpm (P < 0.0001).
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MAP significantly decreased from 48 (41–55) mm Hg to 41 (35–48) mm Hg (P = 0.01), SAP significantly decreased from 72 (62.5–81.2) mm Hg to 64 (56–71) mm Hg (P = 0.001), DAP significantly decreased from 39 (34–43) mm Hg to 32 (27–37) mm Hg (P = 0.003). Finally, SVR significantly decreased from 4117.4 (3265–4969) dyn s/cm5 to 3078.2 (2622; 3534) dyn sec/cm5 (P = 0.001) after EA.(Table 2).
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DISCUSSION
In this study of infants anesthetized with sevoflurane and sufentanil, the lumbar epidural injection of bupivacaine with adrenaline resulted in a decrease of HR and SVR and an increase of SV. CO remained unchanged during the procedure.
The Doppler technique is widely used to measure CO and studies have demonstrated good agreement with thermodilution (14). The esophageal approach provides an excellent signal and avoids positional artifact (15). In adults, the clinical usefulness of TED monitoring has been demonstrated in numerous anesthetic situations, such as vascular surgery, orthopedic surgery (16), and laparoscopic surgery (17). A pediatric esophageal probe has been available since 1996, and provides a valuable noninvasive tool for evaluating hemodynamic changes during anesthesia. Studies in children have demonstrated that correct probe positioning and excellent recording quality are easy to obtain. Whatever the operative position, no adverse effects have been reported, and TED is accurate to estimate CO changes across the entire pediatric age range (18–21). However, training is required to ensure accurate measurements when using the transesophageal probe (22). In our study, the same trained investigator performed all measurements.
It was demonstrated, in adults, that CO may decrease as much as 20% after EA (23). The most likely explanation for EA-induced CO change is dilation of venous vessels by sympathetic blockade that provokes blood pooling, which may explain a decrease in venous return and a decrease in CO (23,24). In supine humans, EA and spinal anesthesia lead to sympathetic block, which leads to blood pooling in the denervated lower extremities (25) with a reflex vasoconstriction in the innervated arms (26). Moreover, general anesthesia combined with EA can lead to a large decrease in CO, associated with bradycardia and substantial hypotension (27). Few studies have reported the impact of central blocks on CO in children. First, Payen et al., using pulsed Doppler, suggested that caudal anesthesia induced blood pooling in the denervated lower extremities with a reflex vasoconstriction of the innervated areas which did not change CO (13). We (8), and others (9), using TED, described CO changes that occur after central blocks in children. Using the transesophageal pulse Doppler approach, coupled with echographic monitoring of aortic diameter, we demonstrated that adrenaline added to caudal anesthesia induced a significant increase in ABF and aortic SV after caudal injection with a probable increase in CO. The significant increase in ABF and the decrease in lower body vascular resistance suggest that vasodilation was induced by sympathetic block. Raux et al., using the transesophageal continuous Doppler technique, have shown that CO was increased after EA only when a local anesthetic solution with adrenaline was used (9). There are several possible explanations for these conflicting results. First, in the study of Payen et al., general anesthesia was induced and maintained with halothane, an anesthetic with negative inotropic effects, and the caudal was performed with a plain bupivacaine solution without adrenaline. Second, the assumption that the cross-sectional area of the descending aorta (CSAao) and descending-aortic to total-blood flow ratio remained constant with time in each patient with a sympathetic blockade is questionable. Indeed, our team, using a TED probe coupled with echographic monitoring of the aortic diameter in children, showed an increase in the aortic diameter by 15% after adrenaline was added to caudal anesthesia (8). Finally, the heterogeneity of the populations studied in terms of age, and the different methods used to monitor CO, can explain the discrepancies among the studies cited above (8,9,13). For this reason, and because at present there is a lack of information concerning CO changes in infants, we chose to study a homogeneous population of infants <10 kg in weight using an easily available system for noninvasive measurement of CO (TED approach).
The results of our study show that EA in infants results in a significant decrease in HR, a significant increase in SV, and an unchanged CO. Compared with our results, other pediatric studies reported no decrease in HR. As previously noted, the heterogeneity of the populations studied may explain the differences in studies. Another explanation is the lack of sensory block measurement. Hence, a difference in the spread of the block may explain the discrepancy between our study and others. Finally, it should be noted that a decrease in HR associated with lumbar EA has been reported in children and adults even when the cardiac sympathetic fibers were not blocked (5,24,28,29). The most likely explanation for the increase in SV concomitant with a decrease in SVR in our study, could be related to an unchanged preload associated with a decrease in afterload because of the arterial vasodilation induced by EA. Indeed, the SV in pediatric patients, especially in newborns, is afterload-dependent because of low myocardial weight. Moreover, different studies found a decrease in SVR after EA (8,9). However, for Raux et al. (9), the main cause of the increase of SV after EA was the adrenaline added to the local anesthetic. We cannot exclude in the current results that the increase in SV relied on epinephrine absorption through an increase of inotropism. Thus, the effects of the epinephrine on chronotropy may have been blunted by general anesthesia, the physiologic changes of EA, or bupivacaine absorption.
Our study has several limitations. The dermatomal spread of the block could not be assessed. This could prove important because EA-induced hemodynamic effects are related to the intensity of the sympathetic block, which is related to the spread of the block. Our results do, therefore, apply to infants receiving epidural administration of 0.75 mL/kg of 0.25% bupivacaine with adrenaline, and require validation in different clinical conditions. Moreover, drugs used for general anesthesia can cause sympathetic block, and basal hemodynamic values obtained before epidural injection should be interpreted with this in mind. In addition, we did not have a control group which would have controlled for the effects of time. Thus, time-related effects of sevoflurane and sufentanil cannot be separated from the effects of the EA. Also, some limitations of the TED must be emphasized. Our esophageal Doppler device (CardioQP) did not provide an echographic CSAao measurement. CO is derived using a nomogram based on the patient's age, weight, and height, validated against cold thermodilution (21). Comparing estimated CSAao by normograms with computerized axial tomography in 100 patients, Muchada et al. (17) found unsatisfactory reliability using age, weight, and height normogramms. Moreover, the descending aortic to total-blood flow ratio has been suggested to be <70% in children (8,30). Although these studies are not directly related to the CardioQP, the absolute values of CO reported in Figure 1 as SV are approximate, and must not be considered as exact. Because these factors are constant in the calculation of CO, this does not influence the changes in CO of each subject over the course of time. Indeed, TED has been favorably correlated to thermodilution monitoring of trends in CO in critically-ill adults and children (21,31). In addition, a noninvasive technique would be highly acceptable to patients and would be more likely to be routinely used. A further limitation is the small number of patients studied. However, hemodynamic changes were consistently obtained, suggesting that our results can be generalized to the whole population of children <10 kg who were studied in similar conditions.
In conclusion, even with limitations of TED monitoring, our study demonstrated alterations in hemodynamic status of EA in infants weighing <10 kg under general anesthesia. Indeed, a decrease in HR with a concomitant increase in SV was observed. This last effect is probably explained by an optimization of the afterload conditions because of the sympathetic blockade induced by EA. However, the increase in SV with an unchanged CO confirms that EA is well tolerated in infants weighing <10 kg, and that these results support the current practice of EA in this pediatric population. Other studies with echocardiographic monitoring are required to better understand the consequences of EA on CO and on regional blood flow in infants.
Footnotes
Accepted for publication March 19, 2007.
REFERENCES
This article has been cited by other articles:
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  D. Galante Transesophageal Doppler Probe and Proseal Laryngeal Mask Airway. A New Technique for Probe Insertion in Pediatric Anesthesia Anesth. Analg., July 1, 2008; 107(1): 348 - 348. [Full Text] [PDF]
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