Fluid Therapy and the Microcirculation in Health and Critical Illness

Abstract

Fluid selection and administration during shock is typically guided by consideration of macrovascular abnormalities and resuscitative targets (perfusion parameters, heart rate, blood pressure, cardiac output). However, the microcirculatory unit (comprised of arterioles, true capillaries, and venules) is vital for the effective delivery of oxygen and nutrients to cells and removal of waste products from the tissue beds. Given that the microcirculation is subject to both systemic and local control, there is potential for functional changes and impacts on tissue perfusion that are not reflected by macrocirculatory parameters. This chapter will present an overview of the structure, function and regulation of the microcirculation and endothelial surface layer in health and shock states such as trauma, hemorrhage and sepsis. This will set the stage for consideration of how these microcirculatory characteristics, and the potential disconnect between micro- and macrovascular perfusion, may affect decisions related to acute fluid therapy (fluid type, amount, and rate) and monitoring of resuscitative efforts. Available evidence for the impact of various fluids and resuscitative strategies on the microcirculation will also be reviewed.

Keywords: glycocalyx; hemorrhage; macrocirculation; microcirculation; sepsis; shock.

Figure 1

Schematic of the microcirculation. Boxes on the left represent ranges of vessel diameters at varying levels of the microcirculation. Boxes throughout the diagram represent the average interstitial (tissue) oxygen tension (P_tO₂). Arrows represent direction of blood flow across the microcirculatory unit.

Figure 2

Curve reflecting tissue autoregulation for maintaining consistent blood flow across varying systemic perfusion pressures.

Figure 3

Diagram representing the impact of shear force generated against the endothelium. Through mechanotransduction, intracellular calcium is increased leading to increased nitric oxide (NO) production from stimulation of constitutive nitric oxide synthetase (cNOS). NO diffuses into surrounding smooth muscle cell causing activation of guanylyl cyclase (GC) and conversion of guanosine triphosphate (GTP) into cyclic guanosine monophosphate (cGMP). The resulting decrease in cytosolic calcium causes relaxation of vascular smooth muscle and vasodilation.

Figure 4

Representative images from a sidestream dark-field microscopy device from a healthy dog (A), dog in hemorrhagic shock (B), and dog in septic shock (C). Note the decreased density of capillaries in patients with shock.