Article Hemodynamics · Rheology · ⏱ 8 min read

Blood Rheology: Why Blood Refuses to Be a Simple Newtonian Fluid

The classic Poiseuille law (the standard equation for how fluid flows through a pipe under pressure) assumes a constant viscosity — true for water, false for blood. Blood is a concentrated suspension of deformable, aggregating red blood cells, and that microstructure makes its viscosity depend on how fast it's sheared and how narrow the vessel is.

TL;DR: Blood's viscosity isn't constant: red blood cells clump into stacks at low shear rates and align and flatten at high shear rates, so blood thins as it flows faster. The Casson model captures its yield stress, the Carreau-Yasuda model smooths that for simulations, and the Fåhræus-Lindqvist effect explains why apparent viscosity drops in narrow vessels.

1. What "Newtonian" actually means

A Newtonian fluid obeys Newton's law of viscosity: shear stress is directly proportional to shear rate, with a single constant of proportionality — the viscosity μ, independent of how hard you shear it.

Newton's law of viscosity τ = μ · (du/dy)

where τ = shear stress, du/dy = shear rate (velocity gradient), μ = constant viscosity

Water, air, and glycerin are essentially Newtonian across the shear rates you'll ever encounter in a syringe or a pipe. Blood is not — plot τ against shear rate for blood and you get a curved, not a straight, line.

2. Why blood isn't Newtonian

Blood is roughly 55% plasma (which is Newtonian, close to water) and ~45% red blood cells (RBCs) by volume (the hematocrit), plus much smaller amounts of white cells and platelets. At low shear rates the RBCs are not being pulled apart by flow, so they clump into stacks called rouleaux — held together by plasma proteins like fibrinogen — which raises the effective viscosity a lot. As shear rate increases, three things happen in sequence:

  • Rouleaux breakup — the stacks are torn apart by the flow, reducing effective particle size.
  • RBC alignment — individual cells rotate to align with the flow, reducing drag.
  • RBC deformation — the biconcave discs elongate into ellipsoid "bullet" shapes that slip past each other more easily.

All three reduce resistance to flow as shear rate rises — this is shear-thinning (pseudoplastic) behaviour: apparent viscosity decreases as shear rate increases. It's the opposite of shear-thickening fluids like cornflour-and-water suspensions.

Where it matters clinically

In large arteries, shear rates are high (100–1000 s⁻¹) and blood behaves nearly Newtonian, so Poiseuille's law is a decent approximation. In small vessels, post-stenotic regions, veins, or during stasis, shear rates fall below ~10 s⁻¹ and non-Newtonian effects — including a yield stress — become significant, which matters for modelling thrombosis risk and microcirculation.

3. The Casson model and yield stress

The most widely used clinical model for blood is the Casson equation. It captures a striking feature: blood appears to need a minimum stress before it flows at all — a yield stress τy, caused by the rouleaux network needing to be broken before flow can start.

Casson model √τ = √τy + √(μc · γ̇)    for τ > τy
γ̇ = 0    for τ ≤ τy

where γ̇ = shear rate, μc = Casson viscosity coefficient, τy ≈ 0.005 Pa (normal hematocrit)

τy depends strongly on hematocrit and fibrinogen concentration — it rises in conditions like polycythemia or hyperfibrinogenemia, and can contribute to the "sluggish flow" seen clinically in those states.

4. The Carreau-Yasuda model

For CFD simulations, the Casson model's √ singularity at low shear is numerically awkward, so the smoother Carreau-Yasuda model is often preferred. It interpolates continuously between a high, near-constant viscosity at very low shear rate and a low, near-constant viscosity at very high shear rate:

Carreau-Yasuda model μ(γ̇) = μ + (μ₀ − μ) · [1 + (λγ̇)a](n−1)/a

μ₀ ≈ 0.056 Pa·s (zero-shear plateau), μ ≈ 0.0035 Pa·s (infinite-shear plateau, ≈ plasma), λ ≈ 3.31 s (transition time constant), n ≈ 0.3568 (power-law index), a ≈ 2 (transition sharpness)

At γ̇ → 0, μ → μ₀ (thick, near-yield behaviour). At γ̇ → ∞, μ → μ (blood behaves almost like plasma alone, since RBCs are fully aligned and deformed).

5. The Fåhræus-Lindqvist effect

There's a second, geometric non-Newtonian effect specific to microcirculation. In vessels below roughly 300 μm in diameter, the apparent viscosity of blood decreases as the tube gets narrower — the opposite of what a simple viscosity model would predict.

The mechanism: RBCs migrate away from the vessel wall toward the centreline (axial migration), leaving a thin, RBC-poor, low-viscosity plasma skimming layer next to the wall. In very narrow capillaries this cell-free layer becomes a significant fraction of the tube radius, effectively lubricating the flow and lowering the pressure drop needed to push blood through — this is the Fåhræus-Lindqvist effect (Fåhræus & Lindqvist, 1931), and it reverses again below ~10 μm as individual RBCs (≈7–8 μm) must squeeze through single-file.

Why it matters physiologically

Without the Fåhræus-Lindqvist effect, the pressure required to perfuse capillary beds through vessels only slightly wider than a red cell would be far higher than the heart can generate. The cell-free layer is a passive, purely mechanical adaptation that keeps microcirculatory resistance manageable.

6. Pseudocode

Computing local viscosity with the Carreau-Yasuda model inside a flow solver:

function carreauYasudaViscosity(shearRate):
  const mu0    = 0.056   // Pa·s, zero-shear plateau
  const muInf  = 0.0035  // Pa·s, infinite-shear plateau
  const lambda = 3.31    // s, transition time constant
  const n      = 0.3568 // power-law index
  const a      = 2.0     // transition sharpness

  term = Math.pow(1 + Math.pow(lambda * shearRate, a), (n - 1) / a)
  return muInf + (mu0 - muInf) * term

function stepBloodFlow(velocityField, dt):
  for each grid cell:
    shearRate = localVelocityGradient(velocityField, cell)
    mu = carreauYasudaViscosity(shearRate)
    // use mu(x) in place of constant viscosity in the Navier-Stokes solve
    applyViscousStress(cell, mu, dt)

The key difference from a plain Navier-Stokes / SPH solver is that μ is recomputed per cell, per step from the local shear rate, rather than being a single global constant — this is what lets the same solver reproduce both thick, near-stationary flow in small vessels and thin, fast-sliding flow in large arteries.

🩸 Related: Blood Flow & Poiseuille's Law

See the (Newtonian) baseline model this article extends — pressure, resistance, and the fourth-power law for vessel radius.

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