BS

Video 2 - Hemodynamics: Resistance, Cross-Sectional Area & Velocity

Physiological Need for Slow Capillary Flow

  • Fundamental purpose: allow adequate time for diffusion of O$2$, CO$2$, glucose, hormones, wastes, etc.
  • Structural prerequisites
    • Capillary wall = one thin endothelial cell → maintains a minimal diffusion barrier.
    • Red blood cells (RBCs) forced into single-file orientation → maximizes membrane contact.
    • Therefore velocity must decrease as blood enters capillary beds.

Determinants of Tissue Blood Flow

  • Two broad categories
    • Driving force (∆P)
    • Generated by cardiac output & arterial blood pressure (BP).
    • Blood moves high → low pressure analogous to diffusion.
    • Resistance (R)
    • Frictional drag as blood rubs against the vessel wall.
    • Governs how easily flow occurs through a given segment.

Resistance: The Friction Story

  • In any vessel, cells adjacent to the wall experience maximal shear → slowest velocity.
  • RBCs in the axial (centerline) stream encounter less wall contact → faster.
  • The narrower the vessel the higher the proportion of blood near the wall → overall velocity drops.
Variables that Alter Resistance (Poiseuille-like logic)
  1. Length (L) – essentially fixed once growth completed.
  2. Viscosity (η) – regulated within narrow physiologic limits ("not too watery, not too thick").
  3. Radius (r)primary adjustable parameter via vasoconstriction/vasodilation.
    • Small radius → R \uparrow dramatically (remember R \propto \frac{1}{r^4}).
    • Large radius → R \downarrow.
Visual Comparison – Small vs. Large Vessel Cross-Section
  • Small vessel: every RBC touches wall → universal friction.
  • Large vessel: only peripheral ring touches wall; core RBCs interact mostly with other cells → faster axial flow.

Total Cross-Sectional Area (Aₜ) Concept

  • Individual capillary = tiny, high-resistance tube.
  • Capillary bed = thousands of parallel tubes.
    • When bundled ("ponytail" thought experiment) → aggregate lumen area often exceeds that of the supplying arteriole.
  • Consequence: even though each capillary has high R, the enormous collective area slows bulk velocity.

Velocity (v) vs. Total Cross-Sectional Area Relationship

  • At constant flow (Q):
    Q = v \times At → v \propto \frac{1}{At} (inverse proportionality).

Garden-Hose Thumb Analogy

  • Thumb over hose = small outlet (Aₜ ↓) → stream accelerates (v ↑) to reach distant flowers.
  • Thumb removed = outlet widens (Aₜ ↑) → stream slows (v ↓) → water "blooms" out.
  • Applies directly to arteries vs. capillary networks.

Sample Calculations (Q kept at 100 arbitrary units)

ScenariovAₜComment
Baseline1010Balanced
Orifice narrows502Thumb over hose (fast jet)
Orifice widens520Thumb removed (slow, broad)

Branching Pattern & Velocity Profile in the Vascular Tree

  • Diagram logic:
    1. Large artery → moderate Aₜ.
    2. Multiple branches → total Aₜ skyrockets in capillary zone.
    3. Venules/veins converge → Aₜ falls again.
  • Therefore velocity pattern = high → low → modest uptick.
    • Counter-intuitive bump in venules because reduction in Aₜ acts like replacing thumb on hose.
  • Important distinction: Pressure continuously falls along the system; velocity does not mirror pressure.

Flow, Pressure, and Resistance—Clinical Framing

  • Basic hemodynamic identity: Q = \frac{\Delta P}{R}.
  • For blood to move, \Delta P must exceed resistive forces.
  • Types of pressure cited
    • Arterial (systemic) – what we measure as BP.
    • Capillary pressure – drives filtration/reabsorption.
    • Venous pressure – lowest, aided by valves & muscle pump.

Arterial Blood Pressure Numbers

  • Traditional "normal": 120/70\ \text{mmHg} (systolic/diastolic).
  • Clinical nuance
    • Elevation of diastolic (lower number) often considered more worrisome because vessel wall never fully relaxes.
    • Example: 140/70 > transient systolic surge but diastole normal – less concerning than 120/90.

Practical & Conceptual Take-aways

  • Slowed capillary transit time is engineered by two synergistic mechanisms:
    1. Micro-radius → intrinsic high resistance.
    2. Massive total cross-sectional area → velocity suppression.
  • Inverse v–Aₜ principle explains garden-hose behavior, blood velocity dip in capillaries, and modest venous speed increase.
  • Never confuse velocity with pressure; pressure gradient keeps dropping, while velocity can rise or fall depending on area changes.
  • Clinically, blood pressure must be adequate to overcome microvascular resistance; chronic elevation (hypertension) largely reflects maladaptive changes in radius & wall tension.