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Anesth Analg 2001;92:710-714
© 2001 International Anesthesia Research Society

REGIONAL ANESTHESIA AND PAIN MEDICINE

The Effects of Lactated Ringer’s Solution Infusion on Cardiac Output Changes After Spinal Anesthesia

Mirt Kamenik, MSc, MD*, and Vesna Paver-Erzen, PhD, MD{dagger}

*Department of Anesthesiology, Intensive Care, and Pain Management, Maribor Teaching Hospital, Maribor, Slovenia; and {dagger}Clinical Department of Anesthesiology and Intensive Therapy, University Medical Center of Ljubljana, Ljubljana, Slovenia

Address correspondence and reprint requests to Mirt Kamenik, MD, Department of Anesthesiology, Intensive Care, and Pain Management, Maribor Teaching Hospital, Ljubljanska 5, 2000 Maribor, Slovenia. Address e-mail to mirt.kamenik{at}mf.uni-lj.si


   Abstract
Top
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
We evaluated the effects of an infusion of lactated Ringer’s (LR) solution on changes in cardiac output (CO) after spinal anesthesia. Seventy-five patients scheduled for lower extremity surgery under spinal anesthesia were studied. We measured CO (impedance cardiography method) and blood pressure for 25 min before and 30 min after spinal anesthesia. Patients were randomly assigned to three groups. In the No Infusion group, no LR solution was given during the period of measurements. The LR Before group received 12 mL/kg of LR solution within 20 min before spinal anesthesia. The LR After group received 12 mL/kg of LR solution within 20 min starting immediately after spinal anesthesia. After spinal anesthesia, CO decreased by 13.9% in the No Infusion group. In the LR Before group, CO increased after the infusion by 20% and returned to baseline value 30 min after spinal anesthesia. In the LR After group, CO increased after spinal anesthesia, and 30 min after spinal anesthesia, CO was 11.3% above baseline. We conclude that the decrease in CO after spinal anesthesia can be prevented by the infusion of an LR solution, with CO reaching the highest value while the infusion is running.

Implications: We studied the effects of lactated Ringer’s solution infusion on cardiac output changes after spinal anesthesia. If the patients received no infusion, cardiac output decreased after spinal anesthesia. However, if the patients received lactated Ringer’s solution infusion, cardiac output was maintained.


   Introduction
Top
 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
Several studies have shown that crystalloid preload is not effective in reducing the incidence of hypotension after spinal anesthesia (1–3). Some authors have expressed concern about the current lack of knowledge concerning the influence of crystalloid preload on changes in cardiac output (CO) after spinal anesthesia (4). However, no studies have been done to evaluate the most appropriate time at which the crystalloid infusion should be started with respect to spinal block. Hahn et al. (5) studied the volume kinetics of lactated Ringer’s (LR) solution in volunteers. The results of their study show that during the infusion of LR solution, about 33% of the infused volume is retained in the vascular compartment, and 30 min after stopping the infusion, <20% of the infused volume is retained. This indicates that the effect of LR solution on increasing CO would be the largest while the infusion is running. The aim of our study was to evaluate the effects of LR solution infusion, given either before or immediately after spinal anesthesia, on changes in CO after spinal anesthesia.


   Methods
Top
 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
We studied 75 ASA class I patients scheduled for lower extremity surgery under spinal anesthesia. The study was approved by the National Medical Ethics Committee. Informed consent was obtained from each patient.

The patients were fasted overnight. Oral fluid intake was allowed for up to 6 h before the operation. Premedication consisted of oral diazepam 10 mg 1 h before surgery. Before entering the study, the patients received no IV fluids. Patients were allocated randomly to one of the three treatment groups. The No Infusion group (n = 25) received no IV fluids before or for 30 min after spinal anesthesia. The LR Before group (n = 25) received 12 mL/kg of LR solution within 20 min before spinal anesthesia; immediately after that, the local anesthetic solution was injected, and the patients received no additional IV fluids for the next 30 min. The LR After group (n = 25) received no infusion before spinal anesthesia, but the patients received 12 mL/kg of LR solution within 20 min starting immediately after spinal anesthesia.

CO was measured with the impedance cardiography method (NCCOM3; BoMed Medical Manufacturing, Irvine, CA). Data were recorded continuously and stored in an IBM-compatible computer. For graphic presentation, data were averaged over 1-min intervals. Systolic blood pressure (SBP) and diastolic blood pressure were measured every 3 min with an automated device (BCI 6004 monitor; BCI International, Waukesha, WI).

Mean arterial pressure (MAP) (mm Hg) was calculated as:

equation


Systemic vascular resistance (SVR) (in dynes · s · cm-5) was calculated as:

equation


After arrival in the operating room, an IV line was placed in the patient’s left arm, and the electrodes for impedance cardiography measurement were placed at the appropriate position as previously described (6). Then the patient was placed in the left lateral position. The measurements were started 5 min after the patient was placed in the lateral position and were recorded for 25 min before and 30 min after spinal anesthesia. In the LR Before group, the infusion of LR solution was started 5 min after the beginning of the hemodynamic measurements. Fifteen minutes after the beginning of measurements, the spinal block procedure was begun without interrupting the measurements. Subarachnoid puncture was done with a 25-gauge Sprotte needle at the L2-3 interspace, by using the left paramedial approach. Exactly 25 min after the beginning of measurements, 3 mL (15 mg) of 0.5% plain bupivacaine (Marcaine 0.5% plain; Astra, Sodertalje, Sweden) was injected into the subarachnoid space.

The dermatome level of sensory blockade was assessed by a blinded observer by use of an ice-cold alcohol-immersed sponge 30 min after injection of local anesthetic.

Hypotension was defined as a decrease in SBP to <90 mm Hg or <70% of baseline. Hypotension was treated with IV boluses of ephedrine 5 mg repeated every 3 min and additional infusion of LR solution. Bradycardia was defined as heart rate <55 bpm and was treated with atropine 1 mg.

Data were analyzed with the Statistica 5.1 statistical package (StatSoft, Tulsa, OK). Demographic data and baseline values were compared with one-way analysis of variance, the Kruskal-Wallis test, and {chi}2 where appropriate. Analysis of variance for repeated measurements with Bonferroni correction was done to compare the hemodynamic effects among the three groups. Analysis of variance for repeated measurements was used to compare the hemodynamic data after spinal anesthesia with baseline values. P < 0.05 was considered statistically significant.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Eight patients developed complications. Their data were excluded from analysis and are described separately. The groups were similar with respect to age, sex, height, and weight ( Table 1). No statistically significant differences were found among the groups with respect to baseline values (defined as the average of the first 5 min of measurements) of MAP, CO, and SVR (Table 1). Although the median block level was two segments higher in the LR After group (Table 1), differences among the groups were not statistically significant (P = 0.19).


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  		Table 1. Demographic Data, Baseline Hemodynamic Measurements, and the Sensory Block Level in Three Groups of Patients
 
A mild statistically significant increase in MAP immediately before spinal anesthesia with respect to baseline value was found in the LR Before (P = 0.002) and the LR After (P = 0.001) groups ( Table 2), but the differences in MAP among the three groups were not statistically significant (Table 2). After spinal anesthesia, MAP decreased significantly in all three groups (P < 0.001), but no differences were found among the groups (Table 2).


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  		Table 2. The Change in Mean Arterial Pressure (MAP), Cardiac Output (CO), and Systemic Vascular Resistance (SVR) Immediately Before Spinal Anesthesia (21–25 min), 20 Min After Spinal Anesthesia (41–45 min), and 30 Min After Spinal Anesthesia (51–55 min) in Three Groups of Patients
 
CO increased significantly in the period before spinal anesthesia with respect to baseline values in the LR Before group (P < 0.001), but not in the other two groups (Table 2). This increase in CO in the LR Before group was statistically significant with respect to the No Infusion (P < 0.001) and the LR After (P = 0.002) groups (Table 2). In the No Infusion group, CO decreased statistically significantly after spinal anesthesia (P = 0.001) (Table 2). After spinal anesthesia, CO decreased significantly in the LR Before group with respect to the value immediately before spinal anesthesia (P < 0.001) but did not change with respect to baseline (Table 2). In the LR After group, after spinal anesthesia CO increased significantly (Table 2). The increase in CO at the end of measurements was statistically significant with respect to the No Infusion group (P = 0.001), but not with respect to the LR Before group (Table 2).

SVR decreased significantly before spinal anesthesia with respect to baseline in the LR Before group (P < 0.001), but not in the two other groups (Table 2). After spinal anesthesia, a statistically significant decrease in SVR was measured in the LR After group (P < 0.001). In the last 5 min of measurements, the decrease in SVR in the LR After group was statistically significant with respect to the No Infusion group (P < 0.001), but not with respect to the LR Before group (Table 2).

The time course of CO change in the three groups is shown in Figure 1. In the No Infusion group, after spinal anesthesia CO started to decrease and decreased up to 14% at the end of measurements (Fig. 1). In the LR Before group, CO started to increase soon after starting the infusion of LR solution (in the sixth minute), and the highest CO was measured at the time of local anesthetic injection (25th minute), when the infusion of LR solution was terminated (Fig. 1). After that, CO started to decrease, and at the end of measurements CO was approximately at baseline value. In the LR After group, the time course of CO before spinal anesthesia was similar to the No Infusion group. After spinal anesthesia, CO started to increase and reached the highest value in the 45th minute (at the end of infusion of LR solution). After that, CO started to decrease but was still 11% above baseline at the end of measurements.



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  		Figure 1. Time course of percentage of change (mean ± SD) in cardiac output (CO) before and after spinal anesthesia in the three groups of patients. Data of patients developing complications are excluded from analysis.

 
Eight patients developed complications. Four patients were in the No Infusion group; two developed bradycardia, one developed hypotension, and one developed both complications. In the LR Before group, two patients developed bradycardia, and in the LR After group, one patient developed hypotension and one developed bradycardia. The difference in the incidence of complications among groups was not statistically significant. All complications were successfully treated with appropriate medication according to the study protocol.


   Discussion
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
In our study we used the impedance cardiography method for CO measurement. This method is noninvasive and, although the absolute value of CO mea-sured with this method is controversial, its value for monitoring the trend of CO change has been accepted by most investigators (7,8). The measurement of CO with the impedance cardiography method is not accurate when the patient is moving because of the occurrence of interferences caused by changes in electrode position. For this reason, we did not want to move the patients during the measurement period. In our previous study, we showed that the trend of CO change can be measured with the impedance cardiography method with the patient in the left lateral position (6). Placing the patient in the left lateral position before the beginning of measurements enabled us to measure CO without interruption during the performance of the spinal block. This was very important because our results show (Fig. 1) that the influence of LR solution infusion on CO is very rapid and that the time when the infusion is given is critical.

After spinal anesthesia, MAP decreased in all three groups, but only three patients (4%) developed hypotension, with no statistically significant differences between the groups. One reason for the infrequent incidence of hypotension is that we studied middle-aged ASA class I patients known to have an infrequent incidence of side effects after spinal anesthesia (9). The second reason for the decreased incidence of hypotension is the low limit set in our study (SBP <90 mm Hg or <70% below baseline). If we had set the limit of hypotension to SBP <100 mm Hg or <80% below baseline, as in some other studies (10,11), 11 patients (14%) would have developed hypotension, with no differences among the groups (four patients in the No Infusion group, three patients in the LR Before group, and four patients in the LR After group). This indicates that with the infusion of LR solution we cannot influence the decrease in blood pressure and the incidence of hypotension after spinal anesthesia. This is in agreement with other studies. Coe and Revanäs (12) showed that the incidence of hypotension after spinal anesthesia cannot be decreased by crystalloid preload in the elderly patient. Park et al. (13) showed in parturients scheduled for Cesarean delivery that a preload with LR solution as large as 30 mL/kg cannot significantly decrease the incidence of hypotension.

However, the infusion of LR solution does affect the time course of CO change after spinal anesthesia. The decrease in CO after spinal anesthesia in the No Infusion group (Fig. 1) was caused by venodilation caused by the sympathetic block. In the LR Before group, CO started to increase immediately after the beginning of the infusion of LR solution and was increasing while the infusion was running (Fig. 1). This increase in CO was caused by the increase in blood volume, caused by the infusion. After spinal anesthesia, CO started to decrease because of the development of the sympathetic block (Fig. 1). But the effect of LR solution infusion on CO was still present at the end of measurements, when CO in the LR Before group reached approximately the baseline value. In the LR After group, CO started to increase immediately after spinal anesthesia when we started the infusion of LR solution and reached the highest value in the 45th minute, when the infusion was stopped (Fig. 1). This indicates that while the infusion was running, the effects of the blood volume increasing CO outweighed the effects of the sympathetic block decreasing CO. Immediately after we stopped the infusion, CO started to decrease. But at the end of measurements, CO in the LR After group was still about 11% above the baseline value. Our results show that the infusion of a crystalloid solution can also increase CO in patients under spinal anesthesia, with CO reaching the highest value while the infusion is running.

We found no study evaluating the effects of a crystalloid infusion on the time course of hemodynamic changes after spinal anesthesia when the infusion is given after the spinal block. Cassati et al. (14) studied the changes in blood pressure and cardiac index (CI) in patients receiving either no preload or a preload of 10 mL/kg LR solution over 20 minutes before unilateral spinal anesthesia for lower extremity surgery. After spinal anesthesia, the authors measured a decrease in CI of 15% in the group of patients not receiving preload, whereas CI was at about baseline value 30 minutes after spinal anesthesia in the group receiving crystalloid preload. An analysis of the temporal relationship between the time of infusion and the change in CI in this study is not possible, because they did not measure the CI during the infusion of LR solution, and the time between the end of infusion and the injection of local anesthetic solution was not standardized.

Our study showed that with the infusion of LR solution, we cannot influence the change in blood pressure and the incidence of hypotension after spinal anesthesia in middle-aged patients without concurrent disease. However, the change in CO after spinal anesthesia is highly influenced by the infusion of LR solution, with CO reaching the highest value while the infusion is running. Therefore, every patient scheduled for spinal anesthesia should receive an infusion of a crystalloid solution to prevent the decrease in CO. If despite that, blood pressure decreases below the desired level, a vasopressor should be given because the most probable cause for hypotension is a decrease in SVR. Only middle-aged ASA I patients were analyzed in our study. Whether the infusion of a crystalloid solution also maintains CO after spinal anesthesia in patients with high risk of developing hypotension (parturients undergoing Cesarean delivery or elderly patients) and whether this management of spinal anesthesia is also appropriate in patients with cardiac disease needs to be investigated by further studies.


   Acknowledgments
 
The authors wish to thank Marijana Gajsek-Marchetti, translator, from the Medical Research Department of Maribor Teaching Hospital, for her contribution in preparing the manuscript.


   References
Top
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 

  1. Buggy D, Higgins P, Moran C, et al. Prevention of spinal anesthesia-induced hypotension in the elderly: comparison between preanesthetic administration of crystalloids, colloids, and no prehydration. Anesth Analg 1997; 84: 106–10.[Abstract]
  2. Husaini SW, Russell IF. Volume preload: lack of effect in the prevention of spinal-induced hypotension at caesarean section. Int J Obstet Anesth 1998; 7: 76–81.[Web of Science][Medline]
  3. Rout CC, Rocke DA, Levin J, et al. A reevaluation of the role of crystalloid preload in the prevention of hypotension associated with spinal anesthesia for elective cesarean section. Anesthesiology 1993; 79: 262–9.[Web of Science][Medline]
  4. Lawes EG. Volume preloading, spinal anaesthesia, and Caesarean section. Br J Anaesth 1996; 76: 334–5.[Free Full Text]
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  6. Kamenik M. The influence of left lateral position on cardiac output changes after head up tilt measured by impedance cardiography. J Clin Monit Comput 1999; 15: 519–23.[Web of Science][Medline]
  7. Critchley LAH. Electrical bioimpedance for noninvasive cardiac measurement [letter; comment]. Crit Care Med 1998; 26: 1460–1.[Web of Science][Medline]
  8. Olschewski H, Bruck K. Cardiac responses to the Valsalva manoeuvre in different body positions. Eur J Appl Physiol 1990; 61: 20–5.
  9. Carpenter RL, Caplan RA, Brown DL, et al. Incidence and risk factors for side effects of spinal anesthesia. Anesthesiology 1992; 76: 906–16.[Web of Science][Medline]
  10. Riley ET, Cohen SE, Rubenstein AJ, Flanagan B. Prevention of hypotension after spinal anesthesia for Cesarean section: six percent hetastarch versus lactated Ringer’s solution. Anesth Analg 1995; 81: 838–42.[Abstract]
  11. Ueyama H, He YL, Tanigami H, et al. Effects of crystalloid and colloid preload on blood volume in the parturient undergoing spinal anesthesia for elective Cesarean section. Anesthesiology 1999; 91: 1571–6.[Web of Science][Medline]
  12. Coe AJ, Revanäs B. Is crystalloid preloading useful in spinal anesthesia in the elderly? Anaesthesia 1990; 45: 241–3.[Web of Science][Medline]
  13. Park GE, Hauch MA, Curlin F, et al. The effects of varying volumes of crystalloid administration before cesarean delivery on maternal hemodynamics and colloid osmotic pressure. Obstet Anesth 1996; 83: 299–303.
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Accepted for publication October 31, 2000.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press