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Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center, Dallas, Texas
Address correspondence and reprint requests to William E. Johnston, MD, Department of Anesthesiology and Pain Management, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75230-9068. Address e-mail to william.johnston{at}utsouthwestern.edu.
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The objective of care is restoration of normal physiology and normal function of organs, with a normal blood volume, functional body water, and electrolytes. This can never be accomplished by inundation.— F. D. Moore and G. T. Shires. Moderation. Annals of Surgery 1967;166:300–1.
The current practice of perioperative fluid administration remains controversial with regard to how much to infuse. Practice guidelines span a wide range, and this issue becomes more critical in the patient with cardiopulmonary disease. Because fluid is a drug, its administration to each patient must be individualized according to the benefits and risks of intravascular fluid administration.
Benefits of Intravascular Fluid Administration
IV fluids are administered perioperatively to replete and expand the extracellular fluid volume (ECFV) space, which is composed of plasma volume (PV) and interstitial fluid volume (ISFV) spaces. Increasing PV could produce several beneficial effects to improve arterial blood pressure, tissue oxygen delivery, and urine output; increasing ISFV could replace the intrinsic fluid loss associated with surgery, trauma, and hemorrhage. These benefits appear intuitively obvious but require further analysis.
Intravascular Fluid Administration to Restore Perfusion Pressure and Oxygen Delivery
PV expansion should increase left ventricular end-diastolic volume and, consequently, stroke volume, by the Frank-Starling relationship. However, there are multiple interrelated factors to improve systemic perfusion pressure and tissue oxygen delivery. Fluid infusions reduce serum hemoglobin, which adversely affects systemic vascular resistance and arterial oxygen content. In a recent human study of large volume saline infusion, stroke volume increased significantly, not from an increment in end-diastolic volume but from a reduced end-systolic volume secondary to reductions in hematocrit and systemic vascular resistance (1). Because the increase in stroke volume was counterbalanced by a proportionate reduction in vascular resistance and hemoglobin, arterial blood pressure and oxygen delivery were not improved. The delicate interplay of various factors controlling perfusion pressure and oxygen delivery limits the efficacy of volume expansion using nonblood solutions.
Intravascular Fluid Administration to Maintain Urine Output
In conscious animals, volume kinetic studies after crystalloid administration demonstrate modest fluid accumulation in the ISFV space with rapid urine elimination (2). After 25 mL/kg saline infusion, the ratio of change in ISFV to urine output is 1:2. In contrast, in anesthetized animals, volatile anesthetics significantly alter fluid handling, so that substantial accumulation occurs in the ISFV space with the ratio of change in ISFV to urine output being 6:1. The increase in ISFV attributable to isoflurane is 3 times more than that seen in conscious animals and may be related to enhanced antidiuretic hormone production. If crystalloid fluids are routinely administered to maintain urine output during anesthesia and surgery, massive fluid accumulation can occur in the ISFV space.
Intravascular Fluid Administration to Replete ECFV Loss
In 1961, Shires et al. (3), using an isotope dilution technique, reported that major operations decreased ECFV by 30%, which correlated linearly with surgical trauma. Radioactive isotopes were injected IV with periodic arterial sampling; the ECFV space was calculated as the amount of injected tracer divided by the serum isotope concentration at equilibrium. This ECFV loss was attributed to a regional redistribution of water expanding the intracellular fluid volume compartment secondary to reduced efficiency of the electrogenic sodium ion pump on the cell membrane, with a secondary increase in intracellular sodium (4).
The clinical practice of preemptive intravascular fluid administration using balanced salt solutions to replace calculated or anticipated fluid deficits has persisted despite other studies that fail to substantiate reductions in ISFV and ECFV spaces with hemorrhagic shock, trauma, and abdominal and cardiac surgery (5,6). Discrepancies in ECFV assessment are attributed to several methodological errors including 1) different isotope sampling sites (aortic arch versus femoral artery), 2) different times for fluid and isotope equilibration before and after surgery, and 3) failure to account for isotope elimination by repetitive arterial sampling and renal excretion (5,6). If sources of experimental error are avoided, resuscitated shock causes no, or minimal, ECFV deficit. The clinical dilemma is that the ECFV space cannot be routinely and accurately measured in patients, so that the potential to overexpand the ISFV space becomes real. In 1967, Moore and Shires (7) acknowledged this fact in an editorial urging moderation of fluid administration.
Complications From Intravascular Fluid Administration
There are numerous complications from intravascular fluid administration in patients, including tissue edema formation with impaired oxygen transfer, prolonged time for excretion, coagulation abnormalities, hyperchloremic metabolic acidosis, and increased morbidity and mortality in critically ill patients (8–10). Patients with compromised pulmonary or cardiac function appear more prone to complications than normal counterparts. With left ventricular dysfunction, small amounts of saline (10 mL/kg) cause significant reductions in diffusion capacity, alveolar-capillary membrane conductance, and peak expiratory flow rate (11,12) These changes are not produced in normal subjects and are attributed to up-regulation of sodium transport with water diffusion into the interstitium (12).
In patients with underlying heart failure, the risk of intravascular fluid administration is an acute increase in end-diastolic pressure from reduced myocardial compliance. Consequently, developed pressure, defined as the difference between left ventricular systolic and diastolic pressures, flattens with intravascular fluid administration because end-diastolic pressure increases at a more rapid rate than stroke volume and arterial blood pressure (13). Preload-recruitable cardiac reserves are available at larger end-diastolic volumes from intravascular fluid administration but with marked increases in diastolic filling pressures (13,14).
With experimental right ventricular ischemia, intravascular fluid administration increased pericardial pressure to the point of reducing collateral blood flow within the area at risk (15). With right coronary ligation and an intact pericardium, intravascular volume expansion reduced collateral blood flow by 50% and increased infarct size by two- to threefold; this effect was eliminated by opening the pericardial sac. Whether similar results would occur with ischemia of the left ventricle is not known, as the pericardium exerts a greater pressure effect on the right side (16).
With experimental mitral regurgitation, orifice area and the severity of regurgitation vary directly with left ventricular volume (17). Similar findings are reported in patients in whom the size of the regurgitant orifice parallels ventricular size (18). These studies clearly demonstrate that intravascular fluid administration under conditions of reduced ventricular compliance or functional mitral regurgitation can be deleterious.
Outcome Studies Using Fluid Restriction
Several studies indicate that reduced fluid administration can benefit patient outcome. A randomized, observer-blinded, multicenter trial of 172 patients undergoing major colorectal surgery compared standard and restricted fluid management (19). The overall complication rate was reduced from 40% to 21% (P = 0.003) by fluid restriction along with the incidence of cardiopulmonary (24% versus 7%; P = 0.007) and tissue healing complications (31% versus 16%; P = 0.04). Other studies report similar benefits from intraoperative fluid restriction during aortic revascularization (20) and colon resection (21).
Recommendations for Intraoperative Fluid Management
Rather than treating the ECFV space as a whole (Fig. 1), individual components (PV and ISFV spaces) should be individually addressed and separately managed. The distributional compartments for intraoperative fluids should be regarded as separate but interrelated components (Fig. 2). Accordingly, the goals of perioperative fluid management are optimization of intravascular volume, hemoglobin, and ISFV space.
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Intravascular Volume
Intravascular volume assessment has traditionally used static measurements of filling pressures that are problematic because of acute changes in myocardial compliance (22). More reliable techniques use dynamic indices that reflect the changes in biventricular preload and afterload with positive pressure ventilation, such as systolic pressure or stroke volume variability (23). Dynamic measures are more sensitive to predict a beneficial response from subsequent intravascular fluid administration.
Hemoglobin
The optimal hemoglobin value continues to be debated, but blood transfusions should be performed in a manner that maintains normovolemia. Hemorrhage, per se, will reduce hematocrit from the loss of red blood cells plus the leakage of fluid from the ISFV space. Subsequent intravascular fluid administration using nonblood solutions can worsen any reduction in hematocrit. Overzealous administration resulting in hypervolemia with dilutional anemia should be avoided. Although blood transfusion is treated as a separate component, its direct relationship affecting intravascular volume is apparent (Fig. 2).
Interstitial Fluid Volume
The concept that the ISFV space serves as an endless, passive reservoir for intravascular crystalloid fluids appears incorrect, as the excess fluid must be excreted over time and can cause serious morbidity by itself. Unfortunately, there are no practical tests to measure ISFV. Previous studies showing less ECFV deficit made no recommendations for fluid management in surgical patients (5,6). In patients undergoing abdominal aortic surgery, a positive linear relationship was established between intraoperative fluid balance and ISFV where 
ISFV = 0.77 x fluid balance – 2.05 (r = 0.67; P < 0.01) (24). A net positive fluid balance between 2–4 L maintained ECFV unchanged. It is unknown whether these data can be extrapolated to other abdominal pathology.
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Supported, in part, by the Margaret Milam McDermott Distinguished Chair in Anesthesiology and Pain Management.
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This article has been cited by other articles:
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  W. J. Fawcett and N. F. Quiney Fluid Restriction and Major Surgery Anesth. Analg., December 1, 2006; 103(6): 1608 - 1608. [Full Text] [PDF]
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