Pulmonary circulation

What it normally does

• The whole cardiac output, about 5 L/min, passes through the lungs at roughly a sixth of systemic pressure — mean pulmonary artery pressure around 14 mmHg against a systemic mean near 90. The vessels are thin and stretchy, and when flow rises they open unused capillaries (recruitment) and widen open ones (distension), so resistance falls and pressure barely moves. The right ventricle is a thin bellows built to shift volume, not to generate pressure.

  Explains why the right ventricle fails when resistance rises suddenly (pulmonary embolism) and why a sustained pressure load remodels then kills it (pulmonary hypertension, cor pulmonale).

• Pulmonary capillary hydrostatic pressure is only about 8-10 mmHg, well below the roughly 25 mmHg of plasma oncotic pressure pulling fluid back in. Net filtration is tiny and the lymphatics clear it, so the alveoli stay dry and gas crosses a barrier well under a micrometre thick.

  Explains why anything that raises left atrial pressure floods the alveoli — water on the lungs (pulmonary oedema).

• When an alveolus is poorly ventilated its own arteriole constricts (hypoxic pulmonary vasoconstriction) — the opposite of most systemic beds, where hypoxia dilates. Low alveolar oxygen shuts voltage-gated potassium channels in the smooth muscle, the cell depolarises, calcium enters through L-type channels, the vessel narrows, and blood is redirected to alveoli that actually have air in them.

  Explains how blood and air stay matched in patchy lung disease, why the reflex becomes destructive when the whole lung is hypoxic, and why correcting alveolar hypoxia dilates the pulmonary bed.

• Essentially all systemic venous blood passes through the lung before it returns to the systemic arteries, through vessels that taper down to capillaries about the width of a single red cell. The exception is small: bronchial and Thebesian venous blood drains straight into the left heart, a normal anatomical shunt of a few per cent of cardiac output, which is why arterial PO2 always sits a little below alveolar. The lung is the filter of the circulation: clots, fat, air and debris from the systemic veins lodge here first.

  Explains why a clot in a calf vein becomes an emergency in the chest (pulmonary embolism).

What goes wrong

• Pulmonary embolism← from “Essentially all systemic venous blood passes t…”

  A clot forms in a deep leg or pelvic vein — stasis, vessel injury, a hypercoagulable state (Virchow triad) — breaks off, floats through the right heart and wedges where the pulmonary arteries narrow. That segment is now ventilated but not perfused: wasted ventilation (dead space). Vasoactive mediators released by platelets in the clot, chiefly thromboxane and serotonin, constrict neighbouring vessels, so pulmonary vascular resistance jumps further. A previously normal, thin right ventricle cannot acutely generate a mean pulmonary artery pressure much above about 40 mmHg. It dilates, bulges the septum into the left ventricle, left-sided filling falls, and the patient is shocked with a clear chest.

  Breathless far out of proportion to the chest examination; venous thromboembolism remains one of the commonest preventable causes of death in Australian hospitals, and unresolved clot is a route to chronic thromboembolic pulmonary hypertension.

  You would find: Sudden breathlessness and pleuritic chest pain, tachycardia, often hypoxaemia with a low PaCO2, clear lung fields, near-normal chest x-ray. Raised JVP with hypotension means the right ventricle is failing now. D-dimer helps rule out only in patients already assessed as low risk; the diagnosis is usually made on CT pulmonary angiogram, with a ventilation-perfusion scan used instead when contrast or radiation is the problem (renal impairment, pregnancy). The ECG is usually just sinus tachycardia.

• Pulmonary hypertension and cor pulmonale← from “The whole cardiac output, about 5 L/min, passe…”

  Mean pulmonary artery pressure sits above 20 mmHg at rest. Four common routes get you there: a failing or obstructed left heart backing pressure up the pulmonary veins (much the commonest), chronic hypoxic lung disease driving vasoconstriction and then remodelling, unresolved thromboembolism, and primary disease of the small pulmonary arteries. Whatever the cause, the thin-walled right ventricle is now a pressure pump. It hypertrophies, then dilates; the tricuspid ring stretches so the valve leaks backwards (tricuspid regurgitation); pressure rises in the systemic veins behind it.

  Cor pulmonale means right heart failure caused by disease of the lung or its vessels — in Australia think COPD and obstructive sleep apnoea, and in Aboriginal and Torres Strait Islander communities also bronchiectasis, which is far more common there. Rheumatic mitral stenosis, also disproportionately common in remote northern and central Australia, raises pulmonary pressure too, but as left heart disease it is not cor pulmonale — the distinction matters because the treatment is the valve.

  You would find: Exertional breathlessness and fatigue first. Then a loud pulmonary second heart sound, a heave felt at the left sternal edge, raised JVP with a large V wave, a pulsatile liver, ankle oedema. Echocardiography estimates right ventricular systolic pressure from the tricuspid regurgitant jet; right heart catheterisation confirms the diagnosis and separates pre- from post-capillary disease.

• Ventilation-perfusion mismatch when hypoxic vasoconstriction is overwhelmed← from “When an alveolus is poorly ventilated its own …”

  Pneumonia, collapse (atelectasis), oedema or a mucus plug fills or shuts alveoli. Hypoxic vasoconstriction shunts blood away, but it is only a partial reflex — it cannot divert flow from a whole lobe. Blood keeps sliding past unventilated alveoli and returns to the left heart still desaturated. Well-ventilated regions cannot compensate because the oxyhaemoglobin curve is flat at the top, so they cannot add extra oxygen to make up the deficit, and PaO2 falls. Run it the other way — hypoxia across the entire lung, at altitude or in COPD or during sleep apnoea — and the reflex constricts everything at once, driving up pulmonary vascular resistance and loading the right ventricle.

  This is the vascular bed where hypoxia constricts rather than dilates; that single reversal is what matches blood to air, and it is also what turns chronic lung disease into right heart failure.

  You would find: Hypoxaemia that lifts nicely with a bit of oxygen is V/Q mismatch. Hypoxaemia that barely moves on high inspired oxygen is a true shunt — a consolidated lobe, a collapsed lung, a right-to-left cardiac shunt. Uneven vasoconstriction at altitude over-perfuses the segments still open and is thought to produce high-altitude pulmonary oedema.

• Cardiogenic pulmonary oedema← from “Pulmonary capillary hydrostatic pressure is on…”

  Left ventricular failure or a tight mitral valve raises left atrial pressure. The pressure backs into the pulmonary veins and then the capillaries. Once capillary hydrostatic pressure rises enough that filtration outruns the lymphatics, fluid fills the interstitium first — breathless, wheezy, Kerley B lines — then floods into the alveoli. The barrier that made gas exchange effortless is now a diffusion problem, and the flooded alveoli shunt on top.

  Non-cardiogenic oedema (ARDS) looks similar on the film, but there the capillary is leaky rather than overloaded — left atrial pressure is normal and diuretics are not the answer.

  You would find: Breathless lying flat (orthopnoea), waking gasping at night (paroxysmal nocturnal dyspnoea), fine crackles at both bases, a third heart sound, raised JVP, sometimes frothy pink sputum. Chest x-ray: upper lobe blood diversion, Kerley B lines, bat wing shadowing, small pleural effusions.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.