Pulmonary Circulation Physiology
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Direct answer
The pulmonary circuit is a low-pressure, low-resistance, high-compliance system: pulmonary artery pressure runs about 25/10 with a mean near 15 mmHg — one-sixth of systemic — and pulmonary vascular resistance is roughly one-tenth of systemic (about 100 dyn.s.cm-5). Pulmonary capillary hydrostatic pressure of only 7-10 mmHg keeps alveoli dry, since oedema appears only when it exceeds 25-28 mmHg against a plasma colloid osmotic pressure of 28. Resistance falls further on exercise because vessels recruit and distend rather than pressure-rise, and capillary transit time of about 0.75 seconds carries a threefold diffusion reserve over the 0.25 seconds gas equilibration needs. Its one great eccentricity is hypoxic pulmonary vasoconstriction — the Euler-Liljestrand response — the opposite of the vasodilation hypoxia produces everywhere else.
What you must remember
- Pressures: PA systolic 25, diastolic 8-10, mean 15 mmHg; left atrial (wedge) pressure 5-8 mmHg; pulmonary capillary pressure 7-10 mmHg.
- Resistance: about one-tenth of the systemic circuit; walls are thin with little smooth muscle — built for capacity, not control.
- Recruitment and distension: when cardiac output rises fivefold in exercise, PVR actually falls because closed capillaries open and open ones stretch; pressure rises only modestly.
- West zones: zone 1 (alveolar pressure above arterial — no flow, dead space), zone 2 (arterial above alveolar above venous — flow depends on the arterial-alveolar difference, the waterfall or Starling resistor), zone 3 (all pressures above alveolar — continuous flow); zones shift with posture, haemorrhage and mechanical ventilation.
- Hypoxic vasoconstriction: alveolar hypoxia constricts local arterioles to divert blood to better-ventilated alveoli; generalised at altitude or in COPD it produces pulmonary hypertension and cor pulmonale; in the fetus it diverts flow away from the unventilated lung.
- Transit time: 0.75 seconds at rest against a 0.25-second equilibration need; the reserve shrinks in exercise and collapses in diffuse fibrosis, producing exertional desaturation.
- Fluid balance: low capillary pressure plus protein-poor interstitium keeps alveoli dry; the safety margin is breached in left heart failure (mitral stenosis, LV failure) above about 25 mmHg wedge pressure.
Working through a mitral stenosis patient
A young woman with rheumatic mitral stenosis climbs a flight of stairs and coughs pink-tinged sputum. Trace the pressure chain backwards. Her stenotic mitral valve raises left atrial pressure; the atrium has no valve guarding the pulmonary veins, so the pressure transmits directly to the pulmonary capillary bed. At rest her wedge pressure of 18 mmHg still sits below the plasma oncotic pressure of 28, so the Starling balance holds. Exertion raises transmitral flow, left atrial pressure climbs past 25-28 mmHg, and fluid floods the interstitium then the alveoli — dyspnoea, orthopnoea, haemoptysis from ruptured bronchial-anastomotic capillaries. The pulmonary arterioles respond over years with medial hypertrophy (a secondary, organic pulmonary hypertension), eventually producing right ventricular failure: the classic history of rheumatic heart disease written entirely in pulmonary haemodynamics.
Now the contrast case: a high-altitude resident with chronic hypoxic vasoconstriction develops the same right-sided failure (cor pulmonale) without any left heart disease — vasoconstriction, not venous obstruction, raised the afterload.
Where students slip
First, the direction of the hypoxia response: systemic arterioles dilate to hypoxia (feed the tissue), pulmonary ones constrict (avoid the poorly ventilated alveolus) — inverting this is the commonest single-mark loss. Second, zone physiology is not fixed anatomy: zone 1 appears when arterial pressure falls (haemorrhage, positive-pressure ventilation raising alveolar pressure), converting perfused lung to dead space; lying supine makes nearly the whole lung zone 3. Third, pulmonary vascular resistance is calculated, not measured directly — PVR = 80 × (mean PA pressure minus wedge pressure) divided by cardiac output — and the 80 converts Wood units to dyn.s.cm-5.
Frequently asked questions
What are the normal pulmonary artery pressures?
Approximately 25/10 mmHg with a mean of 15 mmHg — about one-sixth of systemic arterial pressures.
Why does pulmonary vascular resistance fall during exercise?
Rising pressure and flow recruit previously closed capillaries and distend open ones, enlarging the total cross-sectional area so resistance drops despite a several-fold rise in cardiac output.
What is hypoxic pulmonary vasoconstriction and its purpose?
Alveolar hypoxia constricts local arterioles (the Euler-Liljestrand mechanism), diverting blood from poorly ventilated to well-ventilated regions to preserve V/Q matching.
What are West's zones of the lung?
Zone 1: alveolar pressure exceeds arterial — no flow; zone 2: arterial exceeds alveolar, which exceeds venous — flow set by the arterial-alveolar gradient (waterfall zone); zone 3: venous pressure exceeds alveolar — continuous flow throughout the cycle.
At what capillary pressure does pulmonary oedema develop?
Typically above 25-28 mmHg, when hydrostatic pressure overwhelms the plasma colloid osmotic pressure of about 28 mmHg and the lymphatic reserve.