Accurate assessment of intravascular volume is critical for precise fluid prescription. In people, bedside or point of care ultrasound is used to measure the inferior vena cava, with or without paired aortic measurement, to estimate intravascular volume. To determine if point of care ultrasound measurement of the caudal vena cava (CVC) diameter or the CVC diameter to the abdominal aorta (Ao) diameter (CVC:Ao) at the paralumbar view are associated with changes in intravascular volume, mean arterial pressure (MAP), or cardiac output in normovolemic and hypovolemic dogs. 8 purpose-bred dogs. Pressure-targeted hemorrhagic shock was induced in purpose-bred dogs under general anesthesia. Dogs were exsanguinated to a mean arterial pressure of 40 mmHg, or a maximum 60% blood volume lost, then auto-transfused shed blood. At a left paralumbar view, longitudinal plane measurements of the abdominal CVC diameter and aortic diameter were obtained. Measurements were performed at 4 timepoints: baseline under anesthesia (TP1), after hemorrhagic shock was induced (TP2), after ½ of shed blood had been re-transfused (TP3), and post-resuscitation with completed re-transfusion (TP4). Additional variables collected included cardiac output using thermodilution and arterial blood pressure. CVC:Ao was not significantly different between timepoints and was not associated with changes in CO (p = 0.28) or MAP (p = 0.50). CVC diameter was significantly different between baseline (TP1) and hemorrhagic shock (TP2). CVC diameter was significantly different at TP2 compared to TP1 after controlling for the effect of CO (p = 0.03) and MAP (p = 0.001). Aortic diameter was also significantly different at TP2 (p = 0.002, p = 0.001) and TP3 (p = 0.023, p = 0.017) compared to TP1 after controlling for CO and MAP. Obtaining point of care ultrasound images for CVC:Ao measurement was feasible. With a marked decrease in intravascular volume, both CVC and Ao diameter decreased, resulting in an unchanged CVC:Ao. Despite changes in CVC and Ao diameters, these changes were not associated with measured changes in CO, emphasizing that CO is not a direct estimate of intravascular volume and is affected by many compensatory mechanisms. Additional studies are needed to determine the most accurate method for bedside measurement of intravascular volume status.
Read full abstract