Response to fluid boluses in the fluid and catheter treatment trial

Abstract

Background: Recent emphasis has been placed on methods to predict fluid responsiveness, but the usefulness of using fluid boluses to increase cardiac index in critically ill patients with ineffective circulation or oliguria remains unclear.

Methods: This retrospective analysis investigated hemodynamic responses of critically ill patients in the ARDS Network Fluid and Catheter Treatment Trial (FACTT) who were given protocol-based fluid boluses. Fluid responsiveness was defined as ≥ 15% increase in cardiac index after a 15 mL/kg fluid bolus.

Results: A convenience sample of 127 critically ill patients enrolled in FACTT was analyzed for physiologic responses to 569 protocolized crystalloid or albumin boluses given for shock, low urine output (UOP), or low pulmonary artery occlusion pressure (PAOP). There were significant increases in mean central venous pressure (9.9 ± 4.5 to 11.1 ± 4.8 mm Hg, P < .0001) and mean PAOP (11.6 ± 3.6 to 13.3 ± 4.3 mm Hg, P < .0001) following fluid boluses. However, there were no significant changes in UOP, and there were clinically small changes in heart rate, mean arterial pressure, and cardiac index. Only 23% of fluid boluses led to a ≥ 15% change in cardiac index. There was no significant difference in the frequency of fluid responsiveness between boluses given for shock or oliguria vs boluses given only for low PAOP (24.0% vs 21.8%, P = .59). There were no significant differences in 90-day survival, need for hemodialysis, or return to unassisted breathing between patients defined as fluid responders and fluid nonresponders.

Conclusions: In this cohort of critically ill patients with ARDS who were previously resuscitated, the rate of fluid responsiveness was low, and fluid boluses only led to small hemodynamic changes.

Figures

Figure 1 –

Sample bedside flow sheet. To be included in this “no fluids” analysis, variables were collected at a time point at least 6 h after a fluid bolus or diuretic dose; these same variables were then collected 1 to 4 h later. At the top, “pre” (time 1000) represents hemodynamic variables prior to a fluid bolus, and “post” (1100) refers to hemodynamic variables 1 h after the fluid bolus was started. No fluid bolus or diuretic was given for > 6 h from 1100 to 1900; therefore, variables measured at 1900 are “pre” and at 2300 are “post” for the “no fluids” analysis, as described in the Materials and Methods section. CI = cardiac index; CVP = central venous pressure; HR = heart rate; MAP = mean arterial pressure; PAOP = pulmonary artery occlusion pressure; UOP = urine output.

Figure 2 –

Change in hemodynamic variables before a fluid bolus (“pre”) and after a fluid bolus (“post”). Changes are stratified by indication, with solid lines and black symbols representing patients with shock or low UOP and dotted lines and gray symbols representing patients with acceptable MAP and UOP but low PAOP. A, MAP (mm Hg) and HR (beats/min). B, Cardiac index (L/min/m2) and UOP (mL/kg/h). C, CVP (mm Hg) and PAOP (mm Hg). See Figure 1 legend for expansion of abbreviations.

Figure 3 –

A, B, Correlations between change in cardiac index and change in MAP (A) and change in U/O (B). U/O = urine output. See Figure 1 legend for expansion of other abbreviation.

Figure 4 –

Frequency of fluid responsiveness stratified by indication for fluid bolus. “Fluid response” is a ≥ 15% increase in cardiac index after a fluid bolus, and “No fluid response” is a