In one breath
The right ventricle pushes the same cardiac output through the lung as the left ventricle pushes round the body, but at a tenth of the resistance: mean pulmonary arterial pressure is only about 15 mmHg. Thin, wide, compliant vessels with almost no resting vasoconstrictor tone make that possible, and when flow rises the resistance falls further by capillary recruitment and distension. Because the pressures are so low, gravity dominates: in an upright person blood flow rises steadily from apex to base, which is why the lung is divided into three zones. A separate high-pressure bronchial circulation, only about 1% of cardiac output, feeds the airway walls themselves.
Builds on: Alveolar ventilation · Gas exchange in the lungs · Leads to: Ventilation–perfusion ratio · Pulmonary edema and drowning
The pulmonary and systemic circuits carry equal volumes per minute, yet the pulmonary bed holds far less blood and generates far less pressure. The difference is resistance: systemic vessels offer a great deal, pulmonary vessels very little, so total pulmonary resistance is about one-tenth of the systemic value.
Functional organization
- Pulmonary arteries branch alongside the airways, so each airway branch has an arterial branch running parallel to it.
- Pulmonary capillaries are wide and freely anastomosing. A branch of the pulmonary artery gives arterioles, and these form a capillary lattice around a single alveolus, so every alveolus sits inside a capillary basket. The lattice drains into a pulmonary vein branch.
- The pulmonary vessels, with the blood in them, make up about 40% of the weight of the lungs.
Functions of pulmonary circulation
- Gas exchange. Venous blood arriving from every part of the body is laid out against the alveoli: CO₂ passes out into the alveolus, O₂ passes in. This is the primary job of the circuit.
- Filter. Thrombi and emboli arriving from the veins and the right heart are trapped here, and the endothelium releases fibrinolytic agents that lyse them. This keeps them out of the coronary, cerebral and other arteries.
- Metabolic — vasoactive hormones are handled in transit:
- ACE, sited mainly on the pulmonary capillary endothelium, converts angiotensin I → angiotensin II;
- bradykinin, serotonin, prostaglandins E₁, E₂ and F₂α, and norepinephrine are inactivated.
- Blood reservoir — about 500 mL of the circulating blood sits in this circuit.
Special features of pulmonary circulation
- Low pressure, low resistance. Mean pulmonary arterial pressure is about 15 mmHg.
- Arteries are thin-walled, short and wide, with little smooth muscle, so they are highly compliant. When a person lies down from standing, a large volume shifts out of the legs into the lungs, and this compliance absorbs it.
- Arterioles are thin-walled with little muscle too, so they constrict far less than the muscular systemic arterioles.
- Veins, too, are thin-walled and very compliant.
- Capillaries form a sheet, not a network. They lie as a lattice in the alveolar wall and blood flows through as a thin sheet, unlike the tubular network of systemic capillaries. Their walls are so thin that they collapse whenever alveolar pressure exceeds capillary pressure.
- Pulmonary venous and left atrial pressures strongly affect gas exchange, and are estimated indirectly by the pulmonary wedge pressure.
- Pulmonary vascular resistance (PVR) is about one-tenth of systemic, for two reasons: the resistance vessels are thin, short, wide and compliant; and there is virtually no resting vasoconstrictor tone, so the arterioles sit mostly dilated. Systemic arterioles and precapillary sphincters, by contrast, are partly constricted by resting sympathetic tone.
- PVR falls when pulmonary arterial pressure rises — a feature unique to this circuit. Two mechanisms:
- Capillary recruitment: many apical capillaries are partly closed at rest because perfusion pressure there is low. Higher flow opens them, and overall resistance drops. This is the main mechanism.
- Capillary distension: the exceedingly thin, compliant capillaries widen as pressure rises.
Applied: pulmonary wedge pressure
A Swan-Ganz catheter is introduced through a vein and advanced across the right heart until its tip wedges in a small pulmonary artery. Beyond the tip there is an uninterrupted column of blood continuous with the left atrium, so the pressure recorded reflects left atrial pressure. It is the bedside way of asking whether a rising left atrial pressure is behind a patient’s pulmonary edema.
Why a low PVR matters
The fall in resistance when cardiac output rises brings three benefits.
- Time for exchange: lower resistance means lower velocity even at high flow rates, so capillary blood still has enough contact time to take up O₂ and give off CO₂.
- More surface area: the capillary distension that lowers resistance also widens the exchange surface, easing diffusion across the alveolar-capillary membrane.
- Protection from edema: a high capillary pressure would drive fluid into the lung. In hard exercise cardiac output rises enormously, but the falling PVR unloads the right ventricle and keeps capillary pressure down, preventing pulmonary edema.
Pulmonary blood flow
About 500 mL of blood is in the pulmonary circuit at any moment, roughly 10% of total blood volume.
| Compartment | Volume |
|---|---|
| Pulmonary arteries | 150 mL |
| Pulmonary veins | 270 mL |
| Pulmonary capillaries | 80 mL |
Distribution: stand a person up and flow rises steadily from the apex down to the base — least at the top, most at the bottom. Gravity is the reason.
Factors affecting pulmonary blood flow
- Pulmonary vascular resistance — itself set by lung volume, hormones and oxygen tension
- Gravity — the dominant one in an upright person
- Alveolar pressure
- The pressure gradient from the arterial to the venous side
Pulmonary vascular resistance
PVR itself is set by lung volume, hormones and oxygen tension.
Lung volumes
Pulmonary capillaries have little structural support, so surrounding pressure distends or collapses them. Functionally there are two sets of vessels:
- Alveolar vessels — arterioles, capillaries, venules — exposed to alveolar pressure.
- Extra-alveolar vessels — pulmonary arteries and veins — exposed to pleural pressure.
| Lung volume | Extra-alveolar vessels | Alveolar vessels | PVR |
|---|---|---|---|
| High | Pleural pressure more negative → distended | Alveoli wider → compressed | ↑ |
| Low | Pleural pressure positive → compressed | Not compressed | ↑ |
PVR is lowest at functional residual capacity and rises on either side of it, giving the classic U-shaped curve.
Hormones
| Raise PVR (vasoconstrictors) | Lower PVR (vasodilators) |
|---|---|
| Serotonin, norepinephrine, histamine | Adenosine, acetylcholine |
| Thromboxane A₂, leukotrienes | Prostacyclin (PG-I₂), isoproterenol |
The constrictors bite hardest when lung volume is already low and the vessels are squeezed to begin with.
Oxygen tension
A low oxygen tension raises PVR by causing vasoconstriction.
Effect of gravity: the three zones
In the upright lung the apex lies above and the base below the level of the heart, and hydrostatic pressure changes by 0.74 mmHg per cm of height. The apex is about 10 cm above the heart, so its arterial pressure is 7.4 mmHg lower.
| Site | Pulmonary arterial pressure |
|---|---|
| Level of the heart | 14 mmHg |
| Apex (10 cm above) | 6.6 mmHg |
| Base (5 cm below) | 17.7 mmHg |
- Worth knowing, though not in your pages: at 0.74 mmHg per cm, 5 cm below the heart works out to 3.7 mmHg more, which is what gives 17.7 mmHg. The book prints the increment as 3.4 mmHg, which does not fit its own rule or its own total.
Gravity shifts both arterial and venous pressures, so it changes flow and also the Ventilation–perfusion ratio. On this basis the lung is divided into three zones.
Upper zone (Zone 1)
- Capillary pressure at the apex is close to alveolar (atmospheric) pressure.
- Arterial pressure is only just enough to perfuse it. If arterial pressure falls or alveolar pressure rises, the capillaries collapse and gas exchange stops.
- The zone is therefore well ventilated but poorly perfused, so it adds to alveolar dead space.
- In health Zone 1 is very small or does not exist. It enlarges when alveolar pressure rises or pulmonary arterial pressure falls — for example in hemorrhagic shock.
Middle zone (Zone 2)
- Arterial and capillary pressures exceed alveolar pressure, but venous pressure is lower than alveolar pressure, so the veins are squeezed shut from outside.
- Blood therefore dams up in the capillaries. Because pulmonary veins are compliant, they collect whatever blood escapes past the constriction — the waterfall effect.
- Flow here is set by arterial minus alveolar pressure, not by the arterio-venous difference.
Lower zone (Zone 3)
- Every vessel here — artery, capillary and venule — carries a higher pressure than the alveolus, the veins most clearly of all.
- Flow is therefore driven by the ordinary arterio-venous pressure difference, and the extra flow in this zone comes mainly from capillary distension.
Draw it: the three zones of the lung
Draw an upright lung outline and mark the level of the heart across its middle. Divide it into Zone 1 (apex), Zone 2 (middle) and Zone 3 (base) with two horizontal lines. Beside each zone write the pressure ranking: Zone 1 — PA greater than Pa greater than Pv; Zone 2 — Pa greater than PA greater than Pv; Zone 3 — Pa greater than Pv greater than PA (PA = alveolar, Pa = arterial, Pv = venous). Draw the capillary collapsed in Zone 1, partly pinched at its venous end in Zone 2 (label “waterfall effect”), and wide open in Zone 3. Add a blood-flow arrow down the side that thickens towards the base, and write the three arterial pressures 6.6 / 14 / 17.7 mmHg.
PVR is lowest in the middle, not at the top
Both high and low lung volumes raise pulmonary vascular resistance; the minimum is at FRC. Students often assume resistance keeps falling as the lung inflates, but at high volumes the stretched alveoli squash the alveolar vessels.
Alveolar pressure and the arterio-venous gradient
- Alveolar pressure follows lung volume, so anything that changes lung volume changes alveolar pressure and with it pulmonary blood flow.
- Arterio-venous pressure gradient: how fast blood moves through this circuit depends on the gap between its arterial and venous pressures, and alveolar pressure itself alters that gap.
Regulation of pulmonary blood flow
Regulation is by active factors (neural, hormonal, chemical) and passive factors.
Active factors
Neural. The pulmonary vessels are richly supplied with sympathetic nerves, yet their diameter is virtually unaffected by autonomic activity in normal conditions, because the resting sympathetic tone is almost absent. Sympathetic stimulation gives only mild vasoconstriction, parasympathetic stimulation only mild vasodilation.
Hormonal. Constrictors reduce flow, dilators increase it.
- Vasoconstrictors: serotonin, norepinephrine, endothelin, angiotensin, thromboxane A₂, leukotrienes.
- Vasodilators: adenosine, acetylcholine, prostacyclin (PG-I₂), bradykinin, nitric oxide.
Several agents do both, depending on which receptor they reach:
| Agent | Constricts via | Dilates via |
|---|---|---|
| Catecholamines | α₁ | α₂, β₂* |
| Purinergics | P2x | P2y* |
| Tachykinins | NK₂ | NK₁* |
| Adenosine | A₁ | A₂ |
| Angiotensin II | AT₁ | AT₂ |
| Endothelin | ETA | ETB* |
| Serotonin | 5-HT₁ | 5-HT₁C* |
| Thromboxane | TP | — |
Dilator-only agents: VIP, CGRP, ANP (at ANPA and ANPB), bradykinin (B₁, B₂*), histamine (H₁*, H₂), vasopressin (V₁*).
An asterisk marks dilators that need an intact endothelium to work.
- Worth knowing, though not in your pages: the book’s table labels the dilator angiotensin II receptor “A2”; the standard name is AT₂, which is what is written above so it is not confused with adenosine A₂.
Chemical. Alveolar hypoxia or hypoxemia constricts the small pulmonary arteries, the opposite of what hypoxia does in the systemic circulation, where it dilates.
- The exact mechanism is unknown; hypoxia is thought to make pulmonary vascular smooth muscle contract directly.
- Probably hypoxia inhibits K⁺ channels, so the muscle cell depolarizes.
- Depolarization opens voltage-gated Ca²⁺ channels, and Ca²⁺ influx causes constriction.
- The response is accentuated by a high CO₂ and a low pH.
Hypoxia: lungs constrict, everywhere else dilates
This is the single most asked trap from the chapter. In the lung, hypoxia constricts; in systemic vessels it dilates. The pulmonary response is useful — it diverts blood away from poorly ventilated alveoli and protects the Ventilation–perfusion ratio — but when the whole alveolar gas is hypoxic, as at high altitude, every vessel constricts at once and pulmonary arterial pressure rises.
Passive factors
Cardiac output, gravity and lung volumes. A rise in cardiac output increases pulmonary blood flow.
Bronchial circulation
The bronchial circulation supplies the walls of the conducting airways and the tissue around them.
- It perfuses the upper respiratory tract, and does not supply respiratory bronchioles or alveoli — those are fed by the pulmonary circulation.
- Its venous blood returns by the bronchial veins, or by bronchopulmonary veins into the pulmonary veins.
- It takes only 1% of cardiac output, but in inflammatory airway disease such as chronic bronchitis this can rise to 10%.
- Bronchial arterial pressure is nearly as high as aortic, and its vascular resistance far exceeds that of the pulmonary bed. It is a high-pressure, high-resistance circuit sitting beside a low-pressure one.
Physiological importance
The bronchial circulation, not the pulmonary circulation, can undergo angiogenesis — it grows new vessels.
- That gives the lung parenchyma collaterals when the pulmonary supply is compromised.
- When a clot or embolus blocks pulmonary flow, the parenchyma beyond it can survive on these new vessels.
Because bronchial venous blood is deoxygenated and drains into oxygenated pulmonary venous blood, this circuit is also the normal physiological shunt — see Ventilation–perfusion ratio.
Exam-answer skeleton: "Write short notes on the pulmonary circulation" (short note)
- Functional organization: arteries parallel to airways, capillary basket round each alveolus, vessels about 40% of lung weight.
- Four functions: gas exchange, filter, metabolic (ACE), reservoir of 500 mL.
- Special features: mean pressure 15 mmHg, thin compliant wide vessels, sheet flow, PVR one-tenth of systemic, no resting tone.
- Why PVR falls when flow rises: capillary recruitment and distension; the three benefits of a low PVR.
- Blood volume 500 mL, split 150 / 270 / 80 mL between arteries, veins and capillaries.
- Factors affecting flow: PVR (lung volume, hormones, O₂ tension), gravity, alveolar pressure, arterio-venous gradient.
- Effect of gravity: the three zones with their pressure rankings and the waterfall effect — draw the diagram.
- Regulation: active (neural, hormonal, hypoxic vasoconstriction) and passive (cardiac output, gravity, lung volume).
Asked in exams
- Pulmonary circulation: May 2022, MCQ