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ANALGESIA

Crystalloid/Colloid Versus Crystalloid Intravascular Volume Administration Before Spinal Anesthesia in Elderly Patients: The Influence on Cardiac Output and Stroke Volume

From the Department of Anesthesiology and Intensive Care Medicine, Klinikum der Stadt Ludwigshafen, Ludwigshafen, Germany.

Address correspondence and reprint requests to André Riesmeier, MD, Department of Anesthesiology and Intensive Care Medicine, BG Unfallklinik Ludwigshafen, Ludwig-Guttmann-Str. 13, D-67071 Ludwigshafen, Germany. Address e-mail to ariesmeier{at}web.de.

Abstract

BACKGROUND: Hypotension is the most common cardiovascular response to spinal anesthesia. We compared the effects of crystalloid/colloid versus crystalloid administration before spinal anesthesia on cardiac output (CO) in elderly patients undergoing transurethral resection of the prostate.

METHODS: Sixty male ASA I–III patients were randomized to one of three groups the control group received no intravascular volume preload, the saline group received 500 mL saline, and the hydroxyethyl starch (HES) group received 500 mL of saline plus 500 mL of 6% HES 130/0.4 within 20 min before spinal anesthesia. Mean arterial blood pressure (MAP) and heart rate, CO, and stroke volume were recorded with a thoracic electrical bioimpedance device.

RESULTS: MAP significantly decreased from baseline in the control group (from 104 ± 20 mm Hg to 88 ± 11 mm Hg [P = 0.005]) and was significantly lower than in the HES group (from 107 ± 13 mm Hg to 97 ± 12 mm Hg [P = 0.001]). In the saline group, MAP decreased (103 ± 14 mm Hg to 92 ± 17 mm Hg) with no significant differences compared with the control and HES groups. CO decreased significantly in the control group (from 4.9 ± 1.6 L/min to 3.8 ± 0.9 L/min [P = 0.002]) and was significantly lower than in the HES patients in whom CO increased significantly after volume preload (from 5.2 ± 1.23 L/min to 6.2 ± 1.43 L/min [P = 0.003]) and remained at baseline level until the end of the study.

CONCLUSION: Intravascular volume preload with saline plus HES prevented a decrease of CO, but did not prevent spinal anesthesia-induced hypotension in elderly patients undergoing transurethral resection of the prostate.

Hypotension is the most common cardiovascular response to spinal anesthesia. More than 30% of patients undergoing spinal anesthesia develop intraoperative spinal-induced hypotension.1,2 Spinal anesthesia-induced hypotension may increase the risk for serious cardiac complications such as myocardial ischemia and acute heart failure.3,4

Discontinuous measurements of mean arterial blood pressure (MAP) and heart rate (HR) are unlikely to demonstrate changes in blood flow in real time.5 In recent years, less invasive or noninvasive methods for continuous measurement of cardiac output (CO) have been introduced. Most methods have been shown to be as accurate as the monitoring CO using the pulmonary artery catheter.6 Thoracic electrical bioimpedance is a promising method as it is a noninvasive technique that may be used in the awake patient. Thoracic electrical bioimpedance relates changes in thoracic electrical conductivity to changes in thoracic aortic blood volume and blood flow and has been proposed as a simple and readily reproducible technique for the determination of stroke volume (SV), contractility, CO, systemic vascular resistance, and thoracic fluid content on a beat-to-beat basis.7,8

The administration of an IV crystalloid or colloid intravascular volume preload to prevent spinal-induced hypotension before spinal anesthesia has become a common practice. The efficacy of volume preload before spinal block has been tested mostly in otherwise healthy obstetric patients.9–12 Only a small number of studies have evaluated the value of crystalloid or colloid administration before spinal block in general surgery patients13,14 or elderly patients.13,15 In this study, we compared the effects of crystalloid/colloid versus crystalloid administration before spinal anesthesia on CO in elderly patients undergoing transurethral resection of the prostate (TURP).

METHODS

Patients and Grouping
After obtaining institutional review board approval and patient’s written informed consent, we included 60 male ASA I–III patients scheduled for TURP with spinal anesthesia in this prospective randomized single-blind study. Patients with a history of severe congestive heart failure (New York Heart Association III/IV) and β-blocker therapy were excluded from the study.

Patients were allocated randomly to one of the three groups using a closed envelope system. The control group (n = 20) received no IV fluids before or for 30 min after spinal anesthesia, the saline group (n = 20) received 500 mL of saline solution within 20 min before spinal anesthesia, and the hydroxyethyl starch (HES) group (n = 20) received 500 mL of saline plus 500 mL of HES (6% HES 130/0.4; Voluven®, Fresenius Kabi, Bad Homburg, Germany) within 20 min before spinal anesthesia. Patients were not blinded to the study groups. During surgery, lactated Ringer’s solution was given at a rate of 2 mL/kg per hour in all patients.

Anesthesia
One hour before surgery, all patients were premedicated with oral midazolam 3.75 mg. Spinal anesthesia and data recording were performed by an anesthesiologist blinded to the type of fluid group. The patient was placed in sitting position and spinal anesthesia was performed at the L3–4 or L4–5 intervertebral space with a 25-gauge pencil-point needle with the aperture directed cephalad. Hyperbaric bupivacaine 15 mg was injected into the subarachnoid space. The level of spinal blockade was evaluated with ice and pinprick. Immediately after injection of the local anesthetic, the patient was placed in the supine position.

Hypotension was defined as a decrease in MAP to <60 mm Hg or <70% of the baseline measurement. Hypotension was treated with 5-µg IV boluses of norepinephrine (Arterenol, Sanofi Aventis, Frankfurt, Germany) to establish a MAP >60 mm Hg. Bradycardia was defined as a HR <50 bpm and was treated with atropine 0.5 mg IV.

Hemodynamic Monitoring
Perioperative hemodynamic monitoring included the noninvasive measurement of MAP, HR, noninvasive measurement of CO, cardiac index (CI) and SV. CO was measured with a thoracic electrical bioimpedance device. Two pairs of standard electric cardiogram surface electrodes, located side-by-side in vertical direction, were placed at the base of the neck and at the lower thorax in the midaxillary line, at the level of the xiphoid process. These electrodes were connected to the thoracic electrical impedance cardiograph (Aesculon^TM; Osypka Medical; Berlin, Germany). The Aesculon uses Electrical Velocimetry^TM, which interprets the maximum rate of change of thoracic electrical bioimpedance as the ohmic equivalent of mean aortic flow acceleration.16 Electrical Velocimetry extracts the conductivity change because of change in blood conductivity to determine SV and CO according to the Bernstein–Osypka equation.16 CO derived from thoracic electrical bioimpedance was recorded continuously online and data were saved to a computer.

Measurements
Measurements were started 5 min after the patient arrived in the operating room and were continued until the end of the surgery. Data points were recorded before fluid administration (T1), after fluid administration (T2), in the upright position (T3), after spinal anesthesia reached a peak sensory block of Th9 (T4), after elevating the legs to lithotomy position in the operating room (T5), 15 min (T6), 45 min (T7), 75 min (T8) thereafter, and after lowering the legs (T9).

Statistical Analysis
The primary outcome variable was CI after spinal blockade. Secondary outcome variables were systemic hemodynamics (MAP, HR) and the incidence of spinal-induced hypotension.

A sample size of 17 patients in each group was calculated to be sufficient to detect a difference in CI of 0.5 L · min^–1 · m^–2 assuming a standard deviation (sd) of approximately 0.25 L · min^–1 · m^–2, a power of 80%, and a significance level of 5%. To allow for potential dropouts from treatment, 20 patients in each group were included. A MedCalc 4.30 (MedCalc Software, Mariakerke, Belgium) software package was used for statistical analyses. Data were presented as either mean ± sd or median (25th percentile; 75th percentile). The assumption of normality was checked using the Kolmogorov-Smirnov test. Continuous, normally distributed data were compared using paired and unpaired Student’s t-test or analysis of variance for repeated measures. When multiple comparisons were made, the Bonferroni correction was applied. P < 0.05 was defined to be statistically significant.

RESULTS

There were no significant differences among groups in patients’ demographics (Table 1). One patient from the saline group was excluded from the study because of inadequate spinal anesthesia.

Four patients in the saline group, one patient in the control group, and one patient in the HES group developed spinal-induced hypotension (P > 0.05). In the control group, one patient developed bradycardia (P > 0.05).

MAP decreased significantly in the control group (from 104 ± 20 mm Hg to 88 ± 11 mm Hg [P = 0.005]) and was significantly lower than in the HES group (from 107 ± 13 mm Hg to 97 ± 12 mm Hg [P = 0.001]). In the saline group, MAP decreased (103 ± 14 mm Hg to 92 ± 17 mm Hg) with no significant differences compared with the control and HES group (Fig. 1). HR remained unchanged in the control and HES group with no significant differences. In the saline group, HR decreased (from 72 ± 11 L/min to 62 ± 8 L/min) without significant differences compared with the control patients (Fig. 2).

View larger version (11K): [in this window] [in a new window]   Figure 1. Mean arterial blood pressure (MAP) before and after spinal anesthesia in three groups. Mean ± sd; *P < 0.05 compared with the control group; P < 0.05 compared with saline group; P < 0.05 compared with baseline. (T1) Before fluid administration, (T2) after fluid administration, (T3) in the upright position, (T4) after spinal anesthesia, (T5) after elevating the legs to lithotomy position, (T6) 15 min, (T7) 45 min, (T8) 75 min, (T9) after lowering the legs.

View larger version (11K): [in this window] [in a new window]   Figure 2. Heart rate (HR) before and after spinal anesthesia in three groups. Mean ± sd; *P < 0.05 compared with control group; P < 0.05 compared with saline group; P < 0.05 compared with baseline. (T1) Before fluid administration, (T2) after fluid administration, (T3) in the upright position, (T4) after spinal anesthesia, (T5) after elevating the legs to lithotomy position, (T6) 15 min, (T7) 45 min, (T8) 75 min, (T9) after lowering the legs.

CO decreased significantly in the control group 75 min after fluid administration (from 4.9 ± 1.6 L/min to 3.8 ± 0.9 L/min [P = 0.002]) and was significantly lower than in the HES patients in whom CO increased significantly after preload (from 5.2 ± 1.23 L/min to 6.2 ± 1.43 L/min [P = 0.003]) and remained at baseline level until the end of the study (Fig. 3). In the saline group, CO decreased (from 4.9 ± 0.9 L/min to 4.0 ± 0.8 L/min) with no significant differences compared with control patients (Fig. 4).

View larger version (12K): [in this window] [in a new window]   Figure 3. Cardiac output (CO) before and after spinal anesthesia in three groups. Mean ± sd; *P < 0.05 compared with the control group; P < 0.05 compared with saline group; P < 0.05 compared with baseline. (T1) Before fluid administration, (T2) after fluid administration, (T3) in the upright position, (T4) after spinal anesthesia, (T5) after elevating the legs to lithotomy position, (T6) 15 min, (T7) 45 min, (T8) 75 min, (T9) after lowering the legs.

View larger version (12K): [in this window] [in a new window]   Figure 4. Stroke volume (SV) before and after spinal anesthesia in three groups. Mean ± sd; *P < 0.05 compared with the control group; P < 0.05 compared with saline group; P < 0.05 compared with baseline. (T1) Before fluid administration, (T2) after fluid administration, (T3) in the upright position, (T4) after spinal anesthesia, (T5) after elevating the legs to lithotomy position, (T6) 15 min, (T7) 45 min, (T8) 75 min, (T9) after lowering the legs.

SV significantly decreased in the control group 75 min after fluid administration (from 71.8 ± 12.2 mL to 63.9 ± 10.6 mL [P = 0.005]) and was significantly lower than in the HES group (Fig. 4). In the HES group, SV increased significantly after preloading (from 74.7 ± 14.8 mL to 86.0 ± 14.5 mL [P = 0.001]) and remained at baseline until the end. In the saline group, SV remained unchanged (from 68.8 ± 11.6 mL to 65.9 ± 3.9 mL) but was significantly lower than in the HES group (P = 0.003) (Fig. 4).

DISCUSSION

Because elderly patients undergoing surgery are likely to have an increased risk for cardiovascular complications, traditional monitoring of spinal anesthesia using HR and MAP might not be adequate to optimize hemodynamics in these patients. There is increasing evidence that an inadequate CO results in reduced organ perfusion and an impaired microcirculation, subsequently leading to organ dysfunction or cardiovascular complications.17 Organ perfusion is highly dependent on blood flow and, to a lesser extent, on MAP. Optimizing cardiac preload may be fundamental to prevent hypoperfusion (not hypotension) and thus organ dysfunction, especially in elderly patients.18–20 The main finding of our study was that only a combined crystalloid/colloid preload with saline plus HES prevented a decrease of CO after spinal blockade in elderly patients undergoing TURP.

Previously, a rapid infusion of large volumes of crystalloids was commonly used to maintain stable hemodynamics and as prophylaxis for spinal-induced hypotension. However, this practice is not advisable in elderly patients with impaired cardiac function because of the short intravascular half-life of crystalloids and the increased risk of heart failure and pulmonary edema. Adding a colloid to crystalloid intravascular volume preload appears to be a reasonable approach because colloids remain longer in the vascular space.21,22

Baraka et al.23 found that volume preload with polymerized gelatin reduced the incidence of hypotension and maintained systolic arterial blood pressure compared with crystalloid preloading in elderly men undergoing TURP. Buggy et al.13 demonstrated in elderly patients receiving elective total hip replacement that volume preload with polymerized gelatin sustained systolic arterial blood pressure at higher levels but did not reduce spinal-induced hypotension or ephedrine requirements compared with crystalloid or no prehydration. However, these investigators did not assess CO. These results are similar to our data showing that colloid preload sustained MAP, CO, and SV at higher levels after the induction of spinal anesthesia.

We did not report that a volume preload using saline plus HES did not reduce the incidence of spinal-induced hypotension or vasopressor requirements compared with a pure saline preload group and a group without preload. After spinal anesthesia, MAP decreased in all three groups, but only six patients (9%) developed hypotension. Other studies showed a rate of spinal-induced hypotension up to 30%.1 The reported incidence of hypotension varies widely, depending on the definition of hypotension used. One reason for the low incidence of hypotension in our study may have been the use of MAP instead of systolic blood pressure. We defined a MAP <60 mm Hg or <70% of the baseline measurement as spinal-induced hypotension. Another reason for the decreased incidence of hypotension may have been the low sensory block level in our patients or the lithotomy position after the spinal anesthesia. Carpenter et al. reported an increase in the incidence of spinal-induced hypotension for each increment of one segment in peak sensory block height in their study. They presumed that higher levels of sensory block correlate with higher sympathetic blockade, greater decrease in venous return and CO, and increased risk of spinal-induced hypotension.1,14,24

In our study, we used thoracic electrical impedance cardiography for CO and SV measurements. CO measurements obtained with bioimpedance correlate with those obtained by thermodilution.8,25 Pitfalls with the cardiac bioimpedance technique may be caused by incorrect placement of the electrodes, thoracotomy wounds, sternal wires, and chest drains. The use of thoracic bioimpedance measurements is also limited by uncooperative, moving patients and disturbances through the surgeon’s electrical knife. There have been several previous studies that compared CO measurements obtained by thoracic electrical bioimpedance and the clinical "gold standard" pulmonary artery thermodilution across a broad range of CI data.8,26 Although most of those studies were performed in cardiac surgery patients under continuous sedation in the intensive care unit, these studies reported a good agreement between CO measured by thoracic electrical bioimpedance and the thermodilution technique.

There are two important limitations to the present study. Although we could demonstrate that intravascular volume preload with saline plus HES prevented a decrease of CO, this volume preload regimen did not prevent spinal anesthesia-induced hypotension. This might be explained by the fact that our study was only designed with sufficient power to detect differences in CO but not differences in spinal anesthesia-induced hypotension or other adverse outcomes. Another limitation of the study is that the differences in CI and SV could have resulted from the fact that the patients in the HES group received a larger fluid volume (500 mL saline plus 500 mL HES) than the patients in the saline group (500 mL saline).

In conclusion, noninvasive, continuous monitoring of CO by thoracic electrical bioimpedance demonstrated that only intravascular volume preload with saline plus HES prevented a decrease of CO after spinal blockade in elderly patients undergoing TURP. This intervention, however, did not reduce the incidence of spinal anesthesia-induced hypotension. Large studies with many patients must be undertaken to fully elucidate the value of volume preload in the prevention of spinal anesthesia-induced hypotension and associated complications in the general surgical population.

Footnotes

Accepted for publication October 2, 2008.

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a colleague Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Riesmeier, A. Articles by Suttner, S. Search for Related Content PubMed PubMed Citation Articles by Riesmeier, A. Articles by Suttner, S. Related Collections Physiology Regional Anesthesia