Pulmonary vascular resistance

Vivian Imbriotis | Sept. 23, 2025

Pulmonary vascular resistance is the hydraulic resistance of the pulmonary vessels (veins, capillaries, arteries).


$$\Delta P = \text{PVR} \cdot Q$$


This flow is laminar, so the resistance is given by the Hagen-Poiseuille equation:


$$R = \frac{8 \mu l}{\pi r^4}$$


Where l is the tube length, r is the pipe (total cross-sectional) radius, and \(\mu\) is the fluid viscosity.


It is influenced by six factors

Confusingly, PVR is not independent of pressure. Resistance falls roughly with \(\frac{1}{\Delta P}\), due to

  1. Recruitment: Collapsed cappillaries are reexpaned by higher pulmonary arterial pressures \(\to\) added in parallel
  2. Distension: Elastic capillaries are stretched by higher pulmonary arterial pressures \(\to\) increased vessel radius

Therefore, the relationship between PAP and pulmonary blood flow is roughly parabolic:


$$Q \propto {\Delta P}^2 \text{ (roughly)}$$



PVR is minimal at FRC.

At volumes greater than FRC, the expanded alveoli compress the small pulmonary capillaries, increasing PVR.

At volumes less than FRC, the larger pulmonary arterial vessels, which are thin-walled and stented open by radial tension from the elastic lung parenchyma, collapse due to loss of this radial tension.

Mechanism:

  1. Low O2 sensed by pulmonary endothelial cells. Exact mechanism unknown (possibly direct effect on O2-sensitive K channels)
  2. Suppression of normal eNOS activity
  3. Decreased NO release \(\to\) diffuses into smooth muscle cells
  4. Decreased cGMP
  5. Decreased protein kinase G \(\to\) smooth muscle relaxation
  6. (note that sildenafil blocks this pathway by preventing cGMP breakdown by PDE5)

And:

  1. Endothelin-1 released from pulmonary endothelial cells
  2. Binds to endothelin-A receptors on smooth muscle
  3. Calcium influx
  4. Potent vascoconstriction
  5. (note that bosentan blocks this pathway by antagonizing endothelin receptor)


In normal physiology, HPV improves v/q matching by directing blood away from areas of low ventilation. In global pulmonary hypoxia, however, increases PVR substantially.

Biphasic process: rapid, then slow, with very gradual return to normal after withdrawal of hypoxic stimulus.


Just a laundry list of things that ALL increase PVR...

  1. Histamine
  2. Catecholamines
  3. thromboxane A2
  4. PaCO2 (mildly)
  5. Acidaemia

Pulmonary vasodilators

  1. Milrinone (PDE3i)†
  2. Levosimendin (calcium sensitizer that also opens endothelial \(K_{ATP}\) receptors)
  3. (note NOT dobutamine!)
  4. **Vasopressin**
  5. CCBs, ACEIs, PDE5is e.g. sildenafil, endothelin antagonists e.g. bosentan
  6. Nitric oxide / nitroglycerin†
  7. Prostacyclin†

†inhaled agent


Pulmonary vasoconstrictors (basically all non-vasopressin systemic vasocostrictors...)

  1. Catecholamines
  2. Methylene blue

Because of Poiseuille:

  1. Paraproteinaemia (MM, WM)
  2. Polycythaemia
  3. Raging leukaemia
  4. Thrombocytosis