In one breath
Fluid movement across pulmonary capillaries follows the same Starling forces as anywhere else, but with two extras: alveolar surface tension pulls fluid out, and alveolar pressure pushes it back in. Capillary hydrostatic pressure is only 8 to 10 mmHg against an oncotic pressure of 25 mmHg, so the lung is kept almost dry, and the little fluid that does escape is carried off by a well developed lymphatic system. Pulmonary edema appears when that balance tips — a high capillary pressure, a high surface tension, a low plasma oncotic pressure or a leaky capillary. Drowning is the same physics run backwards: fresh water is pulled into the blood and kills by hemolysis and ventricular fibrillation, while salt water pulls plasma into the alveoli and kills by asphyxia.
Builds on: Pulmonary circulation · Leads to: Ventilation–perfusion ratio · Hypoxia
Filtration across pulmonary capillaries
The Starling forces — hydrostatic and osmotic gradients — govern filtration here as they do in the systemic capillaries. Two forces are added that exist only in the lung:
| Extra force | Interstitial pressure | Effect |
|---|---|---|
| Alveolar surface tension (pulls the wall inward) | Falls | Favours filtration |
| Alveolar pressure (compresses the space) | Rises | Opposes filtration |
Hydrostatic and oncotic pressures
- Pulmonary capillary hydrostatic pressure is low: about 8 to 10 mmHg.
- Plasma oncotic pressure is 25 mmHg, far higher.
- The balance therefore favours net absorption of fluid from interstitium into capillary blood. This is the opposite of the systemic capillary, and it is what keeps the alveoli dry.
Surface tension, and the fluid that does escape
- Alveolar surface tension favours filtration, cancelling part of the protection that the low hydrostatic pressure gives.
- So a small volume of fluid does escape the capillaries into the interstitium.
- From the interstitium it is taken up by the perivascular and peribronchial spaces, and passes on into lymphatic channels.
Role of lymphatics
- The pulmonary lymphatic system is extensive and well developed.
- The lymphatics lie mainly near the terminal bronchioles, ideally placed to drain the peribronchial space.
Draw it: forces at the pulmonary capillary
Draw an alveolus with a capillary in its wall and a narrow interstitial space between them. Put four labelled arrows on the interstitium: capillary hydrostatic pressure 8–10 mmHg pushing out, plasma oncotic pressure 25 mmHg pulling in, alveolar surface tension pulling the alveolar wall inward (mark it “favours filtration”), and alveolar pressure pressing on the interstitium (mark it “opposes filtration”). Draw a small arrow of fluid leaving into the interstitium, then to the peribronchial space, then into a lymphatic beside a terminal bronchiole. Write “net effect: absorption, lung stays dry”.
Pulmonary edema
Pulmonary edema is the accumulation of excess free fluid in the interstitial spaces and alveoli.
Causes
- Raised capillary hydrostatic pressure — the commonest cause. Usually an abnormally high pulmonary venous pressure, as in left heart failure or mitral stenosis.
- Raised alveolar surface tension — high surface tension lowers interstitial hydrostatic pressure and so favours filtration. Reduced surfactant synthesis does this, as in ARDS.
- Reduced oncotic pressure — plasma colloid osmotic pressure falls in hypoproteinemia, for example in starvation.
- Increased capillary permeability — also a major cause, following pulmonary vascular injury:
- oxidant damage — ozone toxicity, oxygen therapy;
- inflammatory reactions — the action of endotoxins;
- neurogenic shock; head injury is a major cause.
Effects on the lung
- Gas exchange falls → hypoxemia and hypercapnia.
- Small airways are obstructed → airway resistance rises.
- Compliance falls, both from interstitial swelling and from the raised alveolar surface tension.
- Work of breathing rises, because of the low compliance and the airway obstruction.
Applied: why oxygen therapy can cut both ways
Oxidant damage from oxygen therapy is itself listed as a cause of the increased capillary permeability that produces pulmonary edema. So the treatment for the hypoxemia of edema can, given long enough at a high enough concentration, feed the cause — the reason oxygen therapy is titrated rather than given at full strength indefinitely.
Basis of treatment
The aim is to lower pulmonary capillary hydrostatic pressure.
| Measure | How it lowers capillary pressure |
|---|---|
| Diuretics | Reduce blood volume |
| Digitalis | Improve left ventricular function |
| Vasodilators | Relax systemic vessels |
Digitalis makes sense because the usual trigger is a left ventricle that cannot pump effectively, so blood dams back into the pulmonary veins.
Drowning
Fresh-water drowning
Water is aspirated, but death is not from pulmonary edema.
- Death is usually from ventricular fibrillation.
- Aspirated water passes from the alveoli into the capillary blood, drawn in by the low capillary hydrostatic pressure and the high oncotic pressure.
- The water dilutes the plasma, making it hypotonic for the red cells.
- The red cells therefore hemolyse, which produces hyperkalemia and hyponatremia.
- Hyperkalemia plus hypoxemia sets off the ventricular fibrillation.
Salt-water drowning
What is aspirated here is hypertonic, since sea water is rich in Na⁺ and Cl⁻.
- Hypertonic fluid in the alveoli draws plasma out, producing pulmonary edema.
- Death is from asphyxia.
Don't swap the two drownings
Fresh water moves into the blood (hemolysis → hyperkalemia → ventricular fibrillation). Salt water pulls fluid into the alveoli (pulmonary edema → asphyxia). The edema belongs to salt water, the arrhythmia to fresh water. Remember it by direction of water movement: water always follows the higher solute.
Exam-answer skeleton: "Pulmonary edema: causes, effects and physiological basis of treatment" (short note)
- Definition: excess free fluid in interstitium and alveoli.
- Normal balance: capillary hydrostatic 8–10 mmHg against oncotic 25 mmHg, so absorption predominates.
- The two lung-specific forces: surface tension favours filtration, alveolar pressure opposes it.
- Lymphatic drainage near terminal bronchioles as the safety valve.
- Four mechanisms of edema: raised capillary pressure (mitral stenosis, left heart failure), raised surface tension (ARDS), low oncotic pressure (hypoproteinemia), increased permeability (oxidants, endotoxin, head injury).
- Effects: hypoxemia and hypercapnia, raised airway resistance, reduced compliance, increased work of breathing.
- Treatment aimed at lowering capillary hydrostatic pressure: diuretics, digitalis, vasodilators.