Perioperative Anaphylaxis: Comment

We read with great interest the erudite review of anaphylaxis by Tacquaer et al. and summary by Avram which appeared in the January 2023 issue of Anesthesiology. The review is comprehensive and timely. The mechanisms for hypotension associated with anaphylaxis are identified as vasoplegia, distributive shock, vasodilation, and hypovolemia. While the first three describe a state of pathologically reduced vascular tone, the term hypovolemia can be misleading since there are no true volume deficits associated with anaphylaxis. An alternative and more accurate terminology may be decreased stressed volume as described by Guyton et al. in 1955. Stressed volume is the vascular space that contributes to systemic pressure and filling of the heart. This pressure is thought to be the sum of hydrostatic pressure and that mediated through vascular tone (vasoconstriction). Unstressed volume is the intravascular volume not subject to vascular tone; its pressure is determined only by hydrostatic forces—those that result from the effect of gravity on a column of fluid. Unstressed volume is thought to reside largely within the venous reservoir. Vasodilatation produced by the release of proinflammatory mediators results in decreases in stressed volume, systemic pressure, and filling of the heart (fig. 1). This state is difficult to reverse pharmacologically as administration of vasoconstrictors does not reliably increase systemic pressure and filling of the heart.  Instead, volume administration is utilized to fill the unstressed reservoir and, with continued administration of IV fluids, contribute to stressed volume, systemic pressure, and venous return. As with true hypovolemia, administration of intravascular fluids is a treatment, but in this case due to a different etiology, and could result in volume overloading with resolution of vasodilatation. Although driving forces for venous return are still a subject of debate, the work by Guyton et al. contributes substantially our understanding of cardiac physiology, and we believe that the article by Tacquaer et al. is an opportunity to remind our readers about the relevant and complex interplay between systemic pressure and heart filling described more than a half century ago.