Decreasing intraosseous pressure and increasing respiratory variability track fluid volume reduction in a porcine hypovolemia model [poster]
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Study Objectives: Central venous pressure (CVP) provides an invasive and imprecise but accepted method for estimating fluid volume status. Intraosseous (IO) pressure monitoring may provide an alternative to CVP for estimating changes in fluid volume status. To investigate this possibility, we measured intraosseous pressure changes in a porcine model during a hemorrhagic shock protocol. Methods: Our preparation included placement of femoral artery and central venous pressure lines. IO access was obtained by standard technique (EZ-IO, Vidacare Corporation, San Antonio, TX) to monitor pressures in the femur, humerus and tibia. All pressure signals were transmitted to a data acquisition system (Dataq Instruments,Inc., Akron, OH). To create vascular fluid volume changes, 17% of each pig's estimated total blood volume was bled every 10 minutes until physiologic signs of hemorrhagic shock were recorded (mean arterial pressure <50 mmHg and tachycardia >150/min). To estimate fluid volume status, we tracked changes in absolute arterial, venous and IO pressures. As increasing respiratory variability is an accepted indicator of developing hypovolemia, we evaluated pressure variability due to respiration in all pressures after each 10 minute bleed period using the following formula: systolic pressure/pulse pressure. Results: A hypotensive state was achieved in all six animals after bleeding each animal to 66.1±11.7% (1706.57±210 ml) of their estimated baseline fluid volume. Arterial, CVP and all IO mean pressures decreased at a constant rate during the bleeding sessions. The proportional decrease pre/post bleed (mmHg) was not statistically different among all pressures: arterial 78.5 34.0 (-57%), humerus 17.9 6.5 (-64%), femur 17.1 9.8 (-43%), tibia 14.8 8.4 (-43%), CVP 6.6 -0.9. The respiratory variability ratio increased in arterial, CVP and IO pressures to a similar extent and rate from 0.2 to 0.8 as the hypovolemic state developed. Conclusions: IO pressure decreased consistently at each IO site during a controlled hemorrhagic shock protocol, indicating IO pressures can be tracked as indicators of change in fluid volume status. Increasing variability in IO pressure during the respiratory cycle was also associated with decreasing vascular fluid volume. IO pressure appears to be accessible and equivalent to CVP as an indicator of fluid volume status.