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© 2001 International Anesthesia Research Society
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Abstract |
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Infusions of hyperosmotic-hyperoncotic solutions such as hypertonic saline dextran (HSD) are used in Europe for resuscitation of traumatic shock and perioperative volume support as an adjunct to conventional isotonic crystalloids. Whereas plasma volume expansion of HSD has been measured at single time points after the intravascular volume expansion, the detailed time course of fluid shifts during and after infusions have not been reported. We compared the time course of volume expansion during and after 30-min infusions of 4 mL/kg HSD and 25 mL/kg lactated Ringer’s solution (LR) in normovolemic conscious splenectomized sheep. Peak plasma volume (Evans blue and hemoglobin dilution) expansion was similar for HSD (7.8 ± 0.9 mL/kg) and the larger sixfold volume of LR (7.2 ± 0.5 mL/kg). However, 30 min after the 30-min infusion (T60), plasma expansion remained larger after HSD (5.1 ± 0.9 mL/kg) than after LR (1.7 ± 0.6 mL/kg). Both solutions caused an equivalent diuresis. Intravascular volume expansion efficiency (VEE), defined as milliliter plasma expansion/milliliter fluid infused at 0 (T30), 30 (T60), and 60 (T90) min after infusion ended was 1.8, 1.3, and 0.8, respectively for HSD, whereas LR provided a VEE of only 0.27, 0.07, and 0.07. The relative expansion efficiency of HSD versus LR, calculated as the ratio (VEEHSD/VEELR), was 7-fold that of LR at the end of infusion T30, and 20-fold at T60, but decreased to 9-fold by T120. Intravascular volume dynamic studies of different volume expanders in animals and patients may provide anesthesiologists with a new tool for monitoring the effectiveness of fluid therapy.
IMPLICATIONS: Hypertonic saline dextran (HSD) is a new plasma expander recently approved for clinical use in Europe. We compared the plasma volume expansion of HSD versus lactated Ringers (LR) in normovolemic sheep. After a 30 min infusion, HSD was 7 times as effective at expanding volume as an equal volume of LR, but for the next 90 minutes the relative effectiveness of HSD increased to 10-20 times.
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
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An important goal of perioperative fluid therapy is to maintain normovolemia. This seemingly simple aim is complicated by difficulties in measuring vascular volume and by the different distribution volumes for available plasma substitutes. The effective intravascular volume expansion of isotonic crystalloid solutions is only a fraction of infused volume because such fluids are distributed throughout the extracellular volume and, in addition, they induce diuresis (1,2). Colloid solutions expand vascular volume by an amount approximately equal to their infused volume with slight differences depending on the type of colloid (1,3). Hyperosmotic-hyperoncotic solutions (HHS) have become available for clinical use in Europe and have been used for intraoperative volume support (4–6). Although the volume expansion properties of HHS have been studied after rapid bolus infusions in animals subjected to hemorrhagic shock, little is known about the volume expansion properties of HHS when infused at the slower rates used for intraoperative care such as in cardiac surgery (4).
Hyperosmotic crystalloid solutions, e.g., 7.5% NaCl, expands both the vascular and interstitial volume by borrowing fluid from the intracellular compartment (7,8). The addition of a colloid such as dextran or hetastarch to hypertonic saline (HS) slightly increases and substantially prolongs volume expansion (9). Rapid infusion (4 mL/kg over 2 min) of 7.5% NaCl 6% dextran 70 (HSD) increases intravascular volume by 200%–400% of the infused volume (9,10). In these studies, volume expansion was measured by using dye or radioisotope-labeled albumin. However, these techniques produce only a single time point measure of plasma volume and are difficult to apply in a clinical situation. Serial changes in blood hemoglobin (Hb) concentration as an indicator of vascular dilution are easier to measure. This approach has been used by obtaining multiple samples at short intervals to mathematically model the "volume kinetics" of plasma expanders during and after isotonic and hypertonic infusions (11–13). Volume kinetic modeling provides data on virtual spaces of dilution and distribution, but lacks the ability to define changes in true physiologic spaces because there is no definitive measurement of baseline plasma volume with which to calibrate vascular dilution. Also, these studies did not account for urinary losses, or evaluate shifts in extravascular volume. Urine collection devices are currently available that record urine output in 5-min increments, thus allowing a precise calculation of net fluid balance over time.
Our goal for the present study was to describe and compare the "volume dynamics" during and after an infusion of isotonic crystalloid or HHS. Specifically, we measured preinfusion plasma volume by using Evans blue, serial Hb, and urine outputs to calculate the "volume-dynamics" and intravascular and extravascular fluid volume shifts during and after a 30-min infusion of either 25 mL/kg lactated Ringer’s solution (LR) or 4 mL/kg HSD in conscious normovolemic sheep. The infused volume size (25 mL/kg LR versus 4 mL/kg HSD) was decided based on a theoretical estimate endeavoring to provide similar total intravascular fluid load at the end of infusion (8,14). Further, a 4 mL/kg dose of HSD is often used for perioperative volume support or prehospital resuscitation of trauma (4–6), and a 25 mL/kg dose of LR is a reasonable volume of isotonic crystalloid representative of a clinical infusion to augment blood volume.
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Methods |
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The experimental protocol was reviewed and approved by the Institutional Animal Care and Use Committee of the University of Texas Medical Branch at Galveston, with adherence to the National Institutes of Health Guide for Care and Use of Laboratory Animals.
Preliminary Surgical Treatment
Five adult female Merino sheep weighing 28–40 kg were surgically prepared in a sterile operating environment. The sheep were orotracheally intubated and mechanically ventilated under 1.5%–2.5% halothane anesthesia. Indwelling vascular catheters were placed in the abdominal aorta through the right femoral artery for recording of blood pressure and heart rate and for obtaining arterial blood samples and in the inferior vena cava via the right femoral vein for fluid infusions. A 7-French (F) flow-directed thermodilution pulmonary arterial catheter (Swan-Ganz 131-7F; Baxter Healthcare Corp., Irvine, CA) was introduced through the right jugular vein with its tip positioned in the pulmonary artery. This catheter was used for measurement of pulmonary arterial pressure and pulmonary arterial occlusion pressure (PAOP), and cardiac output by thermodilution. The spleen was surgically removed through a subcostal incision after careful ligature of connecting blood vessels and ligaments. Catheters were exteriorized and the surgical incisions closed by layered suture. All catheters were filled with 1000 U/mL heparin sodium solution and secured to the fleece on the back of the animal. Animals were given postoperative care, including analgesia with buprenorphine (0.3 mg bid) for postoperative pain, and recovered in large metal cages with free access to food and water. Experiments were performed 4–7 days after surgery.
On the day before the study, the vascular catheters were attached to pressure transducers (Baxter Pressure Monitoring kit; Baxter Healthcare) and connected to a Hewlett-Packard Monitor model 78901A (Hewlett-Packard, Andover, MA) for continuous hemodynamic monitoring, and to condition the sheep to the experimental setup. A urinary bladder catheter (Foley 12F) was placed and connected to a calibrated urine collector and volume recorder (CritiCore Urine Output Monitor; Bard, Springfield, IL) for automated urine volume measurement set for 5-min intervals. Sheep were denied free access to water and food beginning 12 h before each experiment. Isotonic saline was infused at 5 mL/h to maintain catheter patency. This infusion was discontinued 2 h before the experiment was started.
Experimental Protocol
Sheep were assigned to receive a 30-min IV infusion of 25 mL/kg LR or 4 mL/kg HSD. The two test solutions at room temperature were infused in each animal during two individual experiments separated by at least 2 days. The order of test solutions was alternated with sequential animals. Before infusing the test solution, the sheep’s plasma volume was measured by using the Evans blue dilution technique (described below). At the same time, 3000 IU of sodium heparin was infused IV to prevent clotting in catheters and test tubes. Beginning at time zero (T0), each study period lasted for 120 min (T0 to T120), including the 30-min test solution infusion starting at T0. Arterial blood samples (3 mL) were carefully collected using a reproducible technique. To assure acquisition of fresh circulating blood without saline dilution from the transducer flush system, withdrawal of 4 mL of blood from the catheter preceded sample collection. After sample collection, this blood was returned to the animal. Preinfusion baseline samples were collected in duplicate at three time points between 5 and 30 min before T0 (start of infusion), every 5 min during the first 60 min, and every 10 min during the next 60 min. At each time point, we measured hemodynamic variables: heart rate, mean arterial pressure, central venous pressure, mean pulmonary arterial pressure, and PAOP. During the experiment, cardiac output was measured before starting the infusion (T0), at end of infusion (T30), 30 min after infusion (T60), and at the end of the experiment (T120). Urine output was measured at 5-min intervals during the first 60 min and every 10 min during the second 60 min.
Blood Analyses
At each time point, Hb concentration of sampled blood was measured in triplicate by using a CO-Oximeter, IL-482 (Instrumentation Laboratory System, Lexington, MA) and the mean value was used in subsequent calculations. From the same sample, blood was centrifuged for 10 min and hematocrit (Hct) was measured in duplicate and the mean value recorded. Plasma and urine Na+, K+, and Cl- were measured with a Lablyte System 810 plasma electrolyte analyzer (Beckman, Brea, CA).
Evans Blue Measurements
In each experiment, 1 h before the test fluid infusion, a 40-mL blood sample was drawn to provide plasma for preparing the Evans blue standards and calibrating an absorption-versus-dye concentration calibration curve. The baseline plasma volume (PV0) of each animal was measured at baseline by using Evans blue dilution (15). Exactly 4 mL of Evans blue dye at a concentration of 4.5 mg/mL (The New World Trading Corporation, FL) was mixed with the animal’s blood and rapidly injected. A stopwatch was started at the time of injection. The dye was thoroughly washed into the vein using 15 mL of heparinized saline. Next, four samples of fresh circulating blood were withdrawn from an arterial catheter and timed so that the midpoint of withdrawal was exactly 2, 4, 6, and 8 min after injection. A log fit to the plasma decay of Evans blue concentration was extrapolated to the time of injection. The calculated plasma concentration of Evans blue at injection time was used to determine the plasma volume (milliliters) calculated as Evans blue dose (milligrams) divided by plasma concentration (milligrams/milliliter).
Fluid Volume Calculations
Arterial Hct and measured PV0 were used to calculate baseline blood volume (BV0) and red blood cell volume (RBCV0). The baseline BV0 and RBCV0 calculations were corrected for the difference in whole body and large vessel Hct by using an F-cell ratio of 0.9 (16,17). The sample volume (SV) of all blood samples and all IV fluid infused were included in our calculations. At the first measurement after start of infusion, the sheep’s blood volume at T5 (BV5) can be expressed as:
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Plasma volume at T5 (PV5) can be expressed as:
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Subsequent blood volume and plasma volume determinations were made from sequential iterations of these formulas for each 5- or 10-min sampling period. The intravascular loss or gain of fluid at each time point was calculated as the difference between infused volume (IV) and changes in plasma volume. Fluid losses are attributed to urine volume (UV) and net transcapillary filtration, whereas fluid gain is attributed to reabsorption and lymphatic return to the circulation. The net change in extravascular fluid volume (EVV) between T0 and T5 was calculated as:
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Volume changes for blood, extravascular fluid, and cumulative urinary output were calculated at every sample time point. The change in blood volume divided by the volume of test fluid infused was calculated as an indicator of the volume expansion efficiency (VEE) of the infused fluid. Infused volume minus vascular expansion and urine loss was used as an indicator of extravascular expansion or contraction. All volumes were expressed as milliliter/kilogram.
Data were expressed as mean ± SEM. One way repeated measures analysis of variance was used to detect significant within-group changes before and after treatment, and Student’s t-tests for comparison between LR and HSD were performed at T30, T60, T90, and T120. The Bonferroni procedure was used to correct for multiple comparison. P < 0.05 was considered statistically significant.
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Results |
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During the experiment, the sheep remained calm and exhibited no behavioral response to infusion of either of the two test solutions. The mean weight of the sheep was 35.9 ± 3.1 kg, resulting in test fluid infusion volumes of 147 ± 8 mL for HSD and 918 ± 40 mL for LR.
Hemodilution
Despite a sixfold difference in infusion volume between LR and HSD, both induced similar hemodilution with an average decrease in Hb of 
1.5 g/dL (P < 0.05) that did not return to the preinfusion level during the observation period (Fig. 1). During the LR infusion, the lowest Hb level was reached at T25, i.e., 5 min before the end of infusion, whereas HSD induced the lowest Hb value at T35, i.e., 5 min after the infusion ended. The amount of sampled blood in each sheep totaled 54 mL from the start of infusion.
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Diuresis
The two solutions induced similar urinary output during the 120-min observation period. The total UV through the 2-h observation period was 448 ± 62 mL in the LR group and 474 ± 86 mL in the HSD group (12–13 mL/kg) (Fig. 2). This represents a UV 3 times larger than IV for the HSD group and about half of the IV for the LR group. After infusion, the rate of urinary output continued to increase 15 min after the infusion ended in both groups, after which it declined.
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Time Course of Blood Volume Expansion
Figure 3A shows the time course of volume expansion produced by HSD and LR infusions.
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LR
At all time points during the 30-min infusion period, LR increased vascular volume by an amount less than IV. During the first 5 min of LR infusion, the VEE, calculated as volume expansion/IV, was 0.6 ± 0.04; thereafter, it declined (Fig. 3B). Volume expansion peaked at 25 min into the LR infusion; at that time, the cumulative volume expansion was 7.2 ± 0.5 mL/kg, whereas VEE was 0.3 ± 0.02. During the last 5 min of infusion, the net blood volume change was negative (Fig. 3A), both in the mean data and in the data in four of five individual LR experiments. Immediately after infusion of the entire 25 mL/kg (T30), VEE was 0.27 ± 0.03. Thirty minutes after the LR infusion ended, volume expansion declined and stabilized; during the next hour, VEE was equal to only about 0.07.
HSD
During the HSD infusion, VEE was the highest during the early part of the infusion with a maximum VEE of 2.2 ± 0.5 at T10 and thereafter a gradual decline in VEE occurred. Maximum volume expansion in the HSD group was seen at T35, 5 min after the infusion ended, and was equal to 7.8 ± 0.7 mL/kg with a VEE of 2.0 ± 0.2. At the end of the observation period, T120, the VEE of HSD was approximately 0.7 ± 0.2 of IV. Although both LR and HSD resulted in a similar volume expansion during the infusion, thereafter, HSD produced a more sustained volume expansion compared with LR during the postinfusion observation period (Fig. 3A).
The relative VEE of HSD to that of LR is calculated as a ratio (VEEHSD/VEELR) of the mean data, and is plotted in Figure 4. The VEEHSD/VEELR ratio shows that the relative efficiency of HSD increases from about 5-fold that of LR during infusion to over 10-fold at 15 min postinfusion. The relative VEE for HSD peaked at 20-fold of that of LR at 30 min postinfusion and remained 9-fold or better through the end of the observation period.
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Extravascular Volume Changes
Peak extravascular volume expansion occurred at the end of the LR infusion as shown in Figure 5. This extravascular expansion was 60% of the infused LR volume and decreased only slightly to 43% ± 6% of the IV, by the end of the observation period. Conversely, the HSD infusion induced an extravascular volume contraction of 6.8 ± 1.4 mL/kg shortly after the end of infusion (or 170% of IV). This contraction of the extravascular volume was roughly equivalent to the intravascular expansion at the end of infusion. At T120, net extravascular contraction was about 13.1 ± 2.8 mL/kg, the vascular expansion was 3.6 ± 0.8 mL/kg, and 13.5 ± 2.5 mL/kg had been lost in the urine.
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Electrolytes
Serum Na+ concentration increased from 141 ± 1 mmol/L and peaked at 150 ± 1 mmol/L (P < 0.05) at the end of the HSD infusion. Thereafter, serum Na+ decreased to 145 ± 1 mmol/L at study end (Table 1). The serum osmolality increased with its maximal value at the end of the HSD infusion, 307 ± 1.8 mOsm/kg. The LR infusion produced no changes in serum Na+ concentration or in serum osmolality. Serum K+ concentration was only significantly changed in relation to HSD infusion and was reduced by 0.5 mmol/L 30 min after the infusion ended (P < 0.05).
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Hemodynamics
The two infusion regimens induced similar and relatively mild hemodynamic changes, with small increases in all blood pressures during the infusions and declines back to the preinfusion levels at the end of the observation period (Table 2).
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Discussion |
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In conscious normovolemic sheep, IV infusion of 25 mL/kg LR or 4 mL/kg HSD over 30 minutes produced nearly identical hemodilution and diuresis during the infusion and the subsequent 120-minute observation period, despite a sixfold larger IV of LR. Most of the infused LR was rapidly redistributed, first to the extravascular compartment, and later to urinary output, resulting in low intravascular VEE. Infusion of HSD induced blood volume expansion by shifting fluid from the extravascular to the vascular compartment during the entire infusion. Net fluid movement from the extravascular compartment into the vascular space continued after the end of the HSD infusion because intravascular volume declined less than urine output increased. At the end of the observation period, the cumulative diuresis was more than three times the IV in the HSD group.
An intravascular volume expansion of <10% of the infused LR volume is less than the value suggested by current anesthesia and surgical textbooks quoting a "3:1 rule," implying that 1/3 of infused crystalloid remains intravascular (18). However, clinical studies and volunteer studies measuring vascular volume expansion after crystalloid infusion show a VEE typically <0.2 soon after infusion (Table 3). In the present study, VEE was 0.27 at the end of infusion (T30), diminished to 0.15 by 10 minutes (T40) and equaled 0.07 at 30 minutes after the infusion ended (T60). Theoretically, assuming an interstitial space 4 times the size of the plasma space, an even distribution of LR throughout the extracellular compartment, and zero urine output, only 20% of IV would remain intravascularly. Because of increased diuresis after LR, in fact <20% of infused blood volume expansion would remain. Based on these deliberations, the ratio between infused and intravascularly retained volume should be more than 5:1.
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Volume expansion can be somewhat larger and more sustained in animals and humans under conditions of hypovolemia (1,8,19) in which VEE as high as 0.18 to 0.30 are reported immediately after infusion. The reduced VEE of LR under normovolemia versus hypovolemia seems to depend on the preinfusion set point of the mechanisms that regulate fluid exchange between the circulatory volume, the kidneys, and the extravascular space. Many early volume expansion studies were done under conditions of hypovolemia and/or anesthesia. Hypovolemia increases antidiuretic hormone and aldosterone and reduces renal blood flow, all of which decrease urine output. Anesthesia can have similar effects. During hypovolemia, capillary pressure and lymphatic return are lower than normovolemia, tending to favor intravascular volume expansion and increasing the effective volume of infused fluid.
During LR infusion, there is an accelerated loss of intravascular volume, initially to the extravascular space and subsequently to urine, commencing at infusion start and continuing for 15 minutes after the infusion ends. These findings are generally consistent with the volume kinetic analysis model of Ståhle et al. (12), which stipulates extravasation rates proportional to the increased intravascular volume.
The decrease in VEE during a constant infusion of LR suggests a time lag before the physiologic responses to IV hydration occur. Peak urine rates occurred 40 minutes after the start of infusion. A previous study of volume infusion reported that the atrial natruretic peptides ir-ANF (1–98) and ir-ANF (98–126) began to act 45 minutes after the start of infusion (20).
The VEE of HSD in the present study was about 2.0, somewhat less than the 3.0–4.0 reported in other studies in which HSD was infused to treat hypovolemia (9,10). This likely reflects the finding that volume expansion of any fluid is more efficient during a hypovolemic state. In normovolemic volunteers, the intravascular volume effect of HSD was significantly lower than in hypovolemic volunteers, and a similar difference has also been reported for LR (8,21). Also, VEE may initially be increased after a bolus infusion. In the present study, a 30-minute infusion was used to deliver HSD, compared with numerous previous studies in which an equal volume of HSD was injected as a rapid 2-minute bolus.
HSD displayed the highest VEE during the first 10 minutes of infusion when the osmotic gradient between the HSD solution and the body water was greatest. It may also be that the HSD-induced osmotic gradient between blood and tissues was maintained to some extent beyond the end of the infusion. Blood volume expansion continued for five minutes after the infusion ended and was followed by a decline toward baseline in blood volume for the remainder of the observation period. Studies in euvolemic sheep comparing expansion with a 2-minute bolus infusion of HS alone and dextran alone showed that HS caused peak expansion immediately postinfusion whereas dextran took 15 to 30 minutes postinfusion to exert its maximal effect (13).
The small volume of HSD produced a similar initial and extended intravascular volume increase, as did the much larger volume of LR. In addition, HSD produced a urinary output that was threefold larger than the infused volume. This prolonged diuresis seemed to correlate over time with the decrease in intravascular volume. After peak expansion, the reduction in blood volume was not explained by fluid returning to the extravascular space, as suggested by Mazzoni et al.(7), but rather by an increased diuresis, as described in a previous study of HSD infusion in volunteers (8). At the end of the observation period, the sheep displayed a relative extravascular dehydration, consistent with other studies (8,22). The extravascular dehydration seems to be limited to the cellular space, because interstitial expansion has been reported in previous HSD studies despite decreases in total body water after HSD and HS infusions (8,22,23) in humans and animals.
Changes in hemodynamic variables were relatively small, with increases in central venous pressure and PAOP in both study groups. The volume expansion of both solutions and the changes in cardiac filling pressures paralleled each other, as peak central venous pressure and PAOP occurred at the end of the infusion.
Knowledge about the effects of IV infusions on intravascular expansion over time may have implications for their timing and administration rates in the clinical setting. The rapid redistribution of isotonic fluids and the loss of blood volume expansion even before the end of infusion suggest that a slower, longer-lasting infusion may be more suitable to maintain some degree of intravascular expansion for a prolonged time interval without infusing additional volume. Volume dynamic measurements made with an initial tracer for determination of plasma volume and subsequently followed by Hb dilution measurements need to be performed in patients and animal models of clinical scenarios of fluid therapy. Such studies may help optimize perioperative volume support and define the best role for different volume expanders.
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Conclusions |
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TopAbstractIntroductionMethodsResultsDiscussionConclusionsReferences |
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Measurements of blood Hb and urine output allowed calculation of blood volume change and fluid shifts to the extravascular compartment during and after infusion of LR and HSD in normovolemic sheep. A 30-minute infusion of 25 mL/kg of LR produced a peak intravascular fluid expansion of 7.2 ± 0.5 mL/kg, which declined to only 1.7 ± 0.06 mL/kg by 30 minutes after the infusion ended. Two-thirds of the infused fluid remained in the extravascular space and the remainder was lost as urine. A 30-minute infusion of 4 mL/kg of HSD produced a slightly higher initial intravascular volume expansion of 7.8 ± 0.9 mL/kg but a more sustained expansion of 5.1 ± 0.9 mL/kg after 30 minutes. HSD mobilized fluid from the extravascular compartment during the whole observation period and produced a diuresis several times its infused volume. The relative volume expansion per volume infused for HSD versus LR was 7:1 and about equal to the solute ratio of the two solutions immediately after infusion. However, the relative VEE rapidly increased to 10:1 and to as high as 20:1 during the subsequent hour.
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Acknowledgments |
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Supported by Shriners Hospital Grant 8720.
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References |
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