Vasopressor Responsiveness Beyond Arterial Pressure: A Conceptual Systematic Review Using Venous Return Physiology

Abstract

We performed a systematic review to investigate the effects of vasopressor-induced hemodynamic changes in adults with shock. We applied a physiological approach using the interacting domains of intravascular volume, heart pump performance, and vascular resistance to structure the interpretation of responses to vasopressors. We hypothesized that incorporating changes in determinants of cardiac output and vascular resistance better reflect the vasopressor responsiveness beyond mean arterial pressure alone. We identified 28 studies including 678 subjects in Pubmed, EMBASE, and CENTRAL databases. All studies demonstrated significant increases in mean arterial pressure (MAP) and systemic vascular resistance during vasopressor infusion. The calculated mean systemic filling pressure analogue increased (16 AE 3.3 mmHg to 18 AE 3.4 mmHg; P ¼ 0.02) by vasopressors with variable effects on central venous pressure and the pump efficiency of the heart leading to heterogenous changes in cardiac output. Changes in the pressure gradient for venous return and cardiac output, scaled by the change in MAP, were positively correlated (r 2 ¼ 0.88, P < 0.001). Changes in the mean systemic filling pressure analogue and heart pump efficiency were negatively correlated (r 2 ¼ 0.57, P < 0.001) while no correlation was found between changes in MAP and heart pump efficiency. We conclude that hemodynamic changes induced by vasopressor therapy are inadequately represented by the change in MAP alone despite its common use as a clinical endpoint. The more comprehensive analysis applied in this review illustrates how vasopressor administration may be optimized.

Changes in the venous return system and mortality in patients with constrictive pericarditis after pericardial stripping: a retrospective cohort study

“…Another study reported that Pmsf was 12 mmHg 1 minute after cardiac arrest and 5 mmHg 8 min after death; use of norepinephrine at the time of death was associated with higher Pmsf [24]. Pmsf can increase from 16 to 18 mmHg during infusion of vasoactive drugs [25]. Systemic venous stasis is the main clinical manifestation of constrictive pericarditis and is caused by right heart insu ciency [34].…”

“…Changes in Pmsf re ect changes in circulating blood volume and indicate changes in volume status [12,15,16,21,22]. Pmsf varies according to clinical condition, volume status, and vasodilatory tone [23] and increases after uid infusion and vasopressor administration [24,25]. In patients receiving positive pressure ventilation, elevated RAP causes an increase in Pmsf to maintain an adequate venous return pressure gradient [26,27].…”

Analogue Mean Systemic Filling Pressure: a New Volume Management Approach During Percutaneous Left Ventricular Assist Device Therapy

“…Preserved right ventricular function ensures that right atrial pressure is lower than Pmsa, thus providing driving pressure for venous return which is equal to cardiac output [ 18 ]. These physiological concepts of Pmsa and venous return were recently further clinically validated [ 19 , 20 ].…”

Reply to: vasopressor effects on venous return in septic patients: a review

“…We fully agree with this statement and further add that the data are complicated by variable disease stages and severity, different methodologies and high variability of volume status and/or catecholamine therapy. To illustrate the complexity of these mechanisms, a recent meta-analysis calculated the MSFP analogue of 28 studies and found that it increased in response to vasopressor infusion but with variable effects on central venous pressure and the pump efficiency of the heart leading to heterogenous changes in cardiac output 5 . Hyperdynamic states, the extent of capillary leakage, the vasoplegia, a reduced plasma volume as well as cardiac dysfunction are highly variable factors influencing the MCFP.…”