The impact of blood pressure targets on venous return physiology during post cardiac arrest care.

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Venous return (VR) physiology may be elucidated using a calculated mean systemic filling pressure analogue (Pmsa) that reflects the stressed intravascular volume. The aim of this study was to explore differences in VR physiological variables with the hypothesis that vasopressor therapy targeting a higher mean arterial pressure (MAP) would associate with an increased volume state. This would be important to appreciate the intravascular volume effect of an intervention that traditionally is judged by the pressure response alone. This exploratory study used data from the BOX trial that investigated a higher (MAP of 77 mmHg, MAP77) versus a lower (63 mmHg, MAP63) blood pressure target during intensive care of survivors from out-of-hospital cardiac arrest. Data from 730 patients (MAP63, n = 362 and MAP77, n = 368) were used to calculate Pmsa, the driving pressure for VR (VRdP, the difference between Pmsa and central venous pressure [CVP]), the resistance to venous return (RVR, the VRdP divided by the cardiac output [CO]) and heart efficiency (Eh, the VRdP divided by Pmsa). Linear mixed models were used to evaluate longitudinal haemodynamic data captured from admission to the intensive care unit and over 36 h. The Pmsa was consistently higher in the MAP77 group (p < .03) while the CVP was not statistically different. The greater Pmsa translated into a progressively increasing VRdP (p < .0001) and thus an increased CO (p < .001). Similar stroke volumes in both groups meant that CO was maintained by an increased heart rate in MAP77 (p < .001). The RVR was higher in MAP77 (p < .04) but gradually decreased in both groups, while the Eh was similar overall. In conclusion, a higher MAP target effectively increased the stressed intravascular volume to sustain a higher CO. This post-hoc analysis of the BOX trial explores VR physiology and how it is influenced by the use of various doses of noradrenaline and dopamine. A higher blood pressure target appears to increase VR by increasing the stressed intravascular volume. This results in an increase in the CO. These findings are important given the worry about the effect of a higher afterload on cardiac function.