Does persistent red blood cell overproduction raise hematocrit and impede microvascular flow?

Persistent absolute erythrocytosis—whether primary or secondary—raises circulating red-cell mass and is expected to increase hematocrit. The resulting rheological changes provide a well-established mechanism by which excess red cells can impair microvascular flow.

Hematocrit, viscosity, and flow resistance

• Higher hematocrit is the principal driver of increased whole-blood viscosity and yield stress in erythrocytosis. The relationship is nonlinear, with disproportionately larger viscosity increases at higher hematocrit; under otherwise similar blood properties, a 1-percentage-point hematocrit increase has been estimated to increase high-shear viscosity by about 4%.
• Increased viscosity raises resistance within individual microvessels. At capillary-scale Reynolds numbers (~0.001), viscous forces dominate over inertial forces. In vivo microviscometry found that isovolemic hemodilution reduced local apparent viscosity and microvessel flow resistance by 25.1 ± 6.1%, supporting the reciprocal effect of higher viscosity increasing resistance.
• Greater microvascular resistance can reduce microvascular perfusion. This is particularly relevant where tissue oxygen delivery is already vulnerable.

Mechanistic and clinical context

• The size of the viscosity effect is individualized: shear rate, plasma viscosity, red-cell aggregation, and erythrocyte deformability all modify it. Aggregation matters especially at low shear, whereas hematocrit and deformability have greater influence at higher shear.
• Capillary adaptations—including the Fåhraeus effect, plasma skimming, and the cell-depleted near-wall layer underlying the Fåhraeus–Lindqvist effect—can lower capillary apparent viscosity relative to systemic blood, but do not eliminate the resistance-increasing effect.
• Iron deficiency with microcytosis, including after repeated phlebotomy, may worsen rheology at a given hematocrit. Persistent erythrocytosis should also be distinguished from relative hemoconcentration and assessed for primary and secondary causes.

Bottom line

• The claim is strongly supported: sustained red-cell overproduction raises hematocrit, increases blood viscosity, and thereby increases resistance to microvascular flow; the clinical magnitude depends on the hematocrit level and individual blood and vascular properties.