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Human Physiology · Respiratory system

Ventilation, Perfusion and Gas Exchange

Getting air into the lungs is only half the job. Oxygen must meet blood in the right place, in the right amount, and cross a barrier thinner than a cell. This page explains ventilation, blood flow, their matching, diffusion, and why positioning patients can change their oxygen levels and even their survival.

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Part 4 · Respiratory System · Chapter 17 of 47

Learning objectives

By the end of this page you should be able to:

  • Define minute ventilation, alveolar ventilation and dead space.
  • Describe the partial pressures of oxygen and carbon dioxide from air to tissues.
  • Explain the regional distribution of ventilation and blood flow.
  • Explain ventilation–perfusion matching, dead space and shunt.
  • Describe the factors that govern diffusion across the alveolar wall.
  • List the causes of low arterial oxygen and apply positioning principles.

Why it matters

Physiotherapists change ventilation and blood flow every day by positioning, mobilising and breathing exercises. A patient’s oxygen saturation can rise or fall within minutes of being turned.

Understanding why lets you choose positions deliberately, recognise when a fall in saturation is expected, and explain treatments such as prone lying in intensive care.

Ventilation

Minute ventilation is tidal volume multiplied by breathing rate: about 500 mL × 12 = 6 L/min at rest. Not all of this reaches the alveoli. About 150 mL of each breath stays in the conducting airways, the anatomical dead space.

Alveolar ventilation is therefore about (500 − 150) × 12 = 4.2 L/min. This is the ventilation that takes part in gas exchange.

Shallow breathing wastes air

Breathing 250 mL at 24 breaths per minute gives the same minute ventilation as 500 mL at 12, but alveolar ventilation falls from 4.2 to 2.4 L/min. Rapid shallow breathing after surgery or in fatigue is inefficient.

Arterial carbon dioxide is set by alveolar ventilation: halve alveolar ventilation and arterial PCO2 roughly doubles. This is why hypoventilation causes carbon dioxide retention.

Partial pressures

Figure 1 · The oxygen cascade

Partial pressures of oxygen and carbon dioxide from inspired air to working muscle Paired bars. Oxygen partial pressure falls from about 150 millimetres of mercury in humidified inspired air to 100 in alveolar gas, 95 in arterial blood, 40 in mixed venous blood and about 20 or less in working muscle. Carbon dioxide rises from near zero to 40 in alveolar gas and arterial blood and 46 or more in venous blood. 1500Inspired air10040Alveolar gas9540Arterial blood4046Mixed venous blood2050Working muscle050100150Partial pressure (mmHg)PO2PCO2
Gases move down partial pressure gradients. Oxygen steps down from air to mitochondria; carbon dioxide steps up in the other direction. Typical sea-level values.

Each gas moves according to its own partial pressure. Dry air at sea level is about 21% oxygen, giving a partial pressure near 160 mmHg; humidification in the airways lowers it to about 150. Mixing with carbon dioxide in the alveoli lowers alveolar PO2 to about 100 mmHg.

The small drop from alveolar to arterial oxygen, the alveolar–arterial gradient, is normally only a few mmHg. A widened gradient points to a problem with gas exchange rather than with breathing effort.

Distribution of blood flow and ventilation

The pulmonary circulation is a low-pressure system, so gravity has a large effect. West and colleagues showed that regional blood flow depends on the relation between pulmonary arterial, venous and alveolar pressures [1]. In the upright lung, flow is least at the apex and greatest at the base.

ZonePressure relation [1]Blood flowWhere
Zone 1Alveolar > arterial > venousNone; capillaries squashedNot normally present; may appear with low blood pressure or high ventilator pressure
Zone 2Arterial > alveolar > venousIntermittent, set by arterial minus alveolar pressureUpper lung
Zone 3Arterial > venous > alveolarContinuous, set by arterial minus venous pressureLower lung

Ventilation also increases towards the base, because dependent alveoli start smaller and sit on a steeper part of their compliance curve. But blood flow increases more steeply, so the ratio of ventilation to perfusion falls from top to bottom.

Figure 2 · Ventilation and blood flow down the lung

Ventilation, blood flow and their ratio from apex to base of the upright lung Both ventilation and blood flow increase from the top of the upright lung to the bottom, but blood flow increases much more steeply. The ventilation-perfusion ratio is therefore high at the apex, about 3, and low at the base, about 0.6. upright lungapexbaseFlow per unit lung volumeVentilationBlood flowV/Q ratioabout 3Top: wasted ventilationabout 1Middleabout 0.6Base: relatively over-perfused
Gravity shapes the lung. Blood flow depends on the balance of arterial, venous and alveolar pressures at each height [1]. Ventilation varies less, so the ratio falls from top to bottom. Schematic.

Ventilation–perfusion matching

For efficient exchange, each alveolus should receive air and blood in proportion. The overall ratio of alveolar ventilation (about 4 L/min) to blood flow (about 5 L/min) is close to 0.8.

Figure 3 · Matching air and blood

Normal unit, dead space unit and shunt unit Three alveolar units. In the normal unit both air and blood arrive. In the dead space unit air arrives but the capillary is blocked, so ventilation is wasted. In the shunt unit the airway is blocked, so blood passes without picking up oxygen. NormalV/Q about 1good exchangeno blood flow (clot)Dead spaceV/Q high (∞)ventilation wastedblockedShuntV/Q zeroblood leaves unoxygenated
Most real lungs lie between these extremes. Mismatch is the commonest cause of low arterial oxygen in lung disease. Extra oxygen corrects mismatch well but corrects a true shunt poorly.
SituationV/QExampleResponse to extra oxygen
Dead spaceHighPulmonary embolus; apex in low blood pressureLittle change in oxygen; CO2 may rise
MismatchLow in some areasCOPD, pneumonia, sputum retentionGood
ShuntZeroCollapsed lobe, consolidation, some heart defectsPoor

The lung partly corrects mismatch by itself. Low alveolar oxygen constricts the local pulmonary arterioles, diverting blood to better-ventilated areas. This hypoxic vasoconstriction is the opposite of what systemic vessels do.

Diffusion across the alveolar wall

Oxygen and carbon dioxide cross the alveolar–capillary barrier by simple diffusion. The rate rises with surface area and partial pressure difference and falls with barrier thickness. Carbon dioxide diffuses about twenty times more readily than oxygen, so oxygen transfer fails first.

FactorNormalReduced in
Surface areaAbout 50–100 m2Emphysema, lung resection
Barrier thicknessLess than 1 μmFibrosis, pulmonary oedema
Pressure differenceAbout 60 mmHg for oxygen at the capillary startHigh altitude, hypoventilation
Time in capillaryAbout 0.75 s at restShortened in exercise

Figure 4 · How quickly oxygen loads

Rise of oxygen partial pressure along the pulmonary capillary Capillary oxygen partial pressure rises from 40 towards the alveolar value of 100. In a normal lung it reaches equilibrium within about a quarter of a second, well within the three-quarters of a second available. With a thickened barrier it rises more slowly and may not reach equilibrium when transit time shortens in exercise. alveolar PO2 100exercise transit0.000.250.500.754070100Time in pulmonary capillary (s); about 0.75 s at restCapillary PO2 (mmHg)Normal: equilibrium in about 0.25 sThickened barrier: may not finish, especially in exercise
A large safety margin. Diffusion limitation usually shows only on exertion, which is why patients with fibrosis desaturate when they walk. Schematic.

Why arterial oxygen falls

CauseAlveolar–arterial gradientClue
Low inspired oxygenNormalAltitude
HypoventilationNormalHigh PaCO2; sedation, weakness, obesity
V/Q mismatchWidenedLung disease; improves with oxygen
ShuntWidenedLittle improvement with oxygen
Diffusion limitationWidened, mainly in exerciseFibrosis; desaturation on walking

Positioning and gas exchange

Because gravity sends blood to dependent regions, the lung that is lowermost receives most of the blood flow. In disease confined to one lung, oxygenation is better when the healthy lung is dependent: ‘good lung down’ [2].

Prone positioning applies the same idea to severe lung injury. In ARDS, the back of the lung is heavy and collapsed in supine lying, yet it receives much of the blood flow. Turning prone reopens these regions and evens out ventilation.

Figure 5 · Lying prone in severe lung injury

Mortality with prone versus supine positioning in severe ARDS Paired bars. Twenty-eight-day mortality was 32.8 per cent supine and 16.0 per cent prone. Ninety-day mortality was 41.0 per cent supine and 23.6 per cent prone. 32.8%Supine16.0%Prone 16 h or more28-day mortality41.0%Supine23.6%Prone 16 h or more90-day mortality
Position changes survival. In 466 ventilated patients with severe ARDS, long prone sessions halved 28-day mortality [3]. Prone lying improves the matching of ventilation and perfusion.

Guérin and colleagues randomised 466 patients with severe ARDS to prone sessions of at least 16 hours or to supine lying. Mortality at 28 days fell from 32.8% to 16.0% [3]. Complications were similar, except that cardiac arrests were more frequent in the supine group [3].

Practical skill · positioning for oxygenation

In one-sided lung disease, try side-lying with the good lung down and watch the saturation [2]. For airway clearance you may deliberately place the affected lung uppermost; expect saturation to fall and limit the time. Prone positioning in intensive care needs a trained team and protocol [3].

Clinical relevance for the physiotherapist

  • Post-operative patients. Shallow breathing and lying flat cause basal collapse and shunt; upright positions and deep breaths reverse it.
  • Unilateral disease. Good lung down improves oxygenation [2]; affected lung up aids drainage.
  • Intensive care. Prone positioning improves survival in severe ARDS [3].
  • Interstitial lung disease. Expect exertional desaturation from diffusion limitation; monitor and titrate oxygen during exercise.
  • Pulmonary embolus. Dead space raises breathing effort; sudden breathlessness needs urgent medical review.

Assessment and application

FindingProbable mechanismPhysiotherapy response
Saturation drops when patient lies on the affected sideMore blood to diseased lung [2]Reposition with good lung down
Saturation normal at rest, falls on walkingDiffusion limitationExercise with oxygen titrated to target
Low saturation barely improves with high oxygenShunt, such as collapseRecruit lung: positioning, deep breathing, airway clearance
Rapid shallow breathing with rising CO2Low alveolar ventilationSeek medical review; consider ventilatory support

Common mistakes

  • Equating minute ventilation with alveolar ventilation.
  • Expecting ventilation and blood flow to be the same in every region [1].
  • Assuming any side-lying position is equally good in one-sided disease [2].
  • Thinking prone positioning is only a comfort measure [3].
  • Treating every low saturation with more oxygen without asking why.

Exam preparation

Long answer

Explain ventilation–perfusion relationships in the lung and their clinical importance.

  • Alveolar ventilation and dead space.
  • Regional blood flow and West’s zones [1] (Figure 2).
  • V/Q ratio, dead space and shunt (Figure 3).
  • Hypoxic pulmonary vasoconstriction.
  • Clinical: positioning in unilateral disease [2] and prone positioning [3].

Short notes

  • Dead space.
  • Zones of the lung [1].
  • Diffusion across the respiratory membrane.
  • Prone positioning in ARDS [3].

Viva and practical

  • “Where is V/Q highest?” — at the apex [1].
  • “Which side should a patient with left pneumonia lie on to oxygenate best?” — the right [2].
  • “What did PROSEVA show?” — prone sessions halved 28-day mortality [3].
  • OSCE: interpret saturation changes with position.

Current evidence

Exam and traditional teaching

West’s zones and V/Q matching are taught as theory, with little link to treatment.

What the evidence adds

Positioning changes arterial oxygen in predictable ways in one-sided disease [2].

In severe ARDS, prolonged prone lying reduced 28-day mortality from 32.8% to 16.0% [3].

What the student should understand

Gravity distributes blood; you control gravity by positioning. Use it deliberately to match air and blood.

Check yourself

10 questions on this page. Tap one to see the answer and the reasoning.

Q1. In the upright lung, blood flow per unit volume is greatest at the:
  1. (A) Apex
  2. (B) Base
  3. (C) Middle
  4. (D) It is the same everywhere

Answer: (B) Gravity raises vascular pressure in dependent regions, so flow is greatest at the base [1].

Q2. The ventilation–perfusion ratio is highest at the:
  1. (A) Apex
  2. (B) Base
  3. (C) Hilum
  4. (D) Diaphragm

Answer: (A) Blood flow falls more steeply than ventilation towards the apex, which depends on vascular and alveolar pressures [1].

Q3. A region with ventilation but no blood flow is called:
  1. (A) Shunt
  2. (B) Dead space
  3. (C) Atelectasis
  4. (D) Diffusion block

Answer: (B) Without perfusion the ventilation is wasted; pulmonary flow depends on vascular versus alveolar pressure [1].

Q4. A patient with right lower lobe pneumonia usually oxygenates best when lying:
  1. (A) On the right side
  2. (B) On the left side
  3. (C) Flat supine
  4. (D) Position makes no difference

Answer: (B) In unilateral lung disease, oxygenation is better with the good lung dependent [2].

Q5. The physiological reason for ‘good lung down’ is that:
  1. (A) The bad lung receives more air
  2. (B) Gravity sends more blood to the dependent, healthy lung
  3. (C) It reduces heart rate
  4. (D) It stops coughing

Answer: (B) Positional changes in arterial oxygen in one-sided disease reflect redistribution of blood flow [2].

Q6. In the PROSEVA trial, 28-day mortality in severe ARDS was:
  1. (A) The same prone and supine
  2. (B) 16.0% prone vs 32.8% supine
  3. (C) 32.8% prone vs 16.0% supine
  4. (D) Not measured

Answer: (B) Prolonged prone sessions roughly halved 28-day mortality [3].

Q7. How long were the prone sessions in that trial?
  1. (A) 10 minutes
  2. (B) At least 16 hours
  3. (C) 1 hour
  4. (D) Only at night for 4 hours

Answer: (B) Sessions lasted at least 16 hours [3].

Q8. Which statement about complications in the prone trial is correct?
  1. (A) Prone had many more complications
  2. (B) Complications were similar; cardiac arrests were more frequent supine
  3. (C) The trial was stopped for harm
  4. (D) No data were collected

Answer: (B) Complication rates did not differ, except for more cardiac arrests in the supine group [3].

Q9. Severe ARDS in that trial was defined partly by a PaO2/FiO2 ratio below:
  1. (A) 400 mmHg
  2. (B) 300 mmHg
  3. (C) 150 mmHg
  4. (D) 50 mmHg

Answer: (C) Inclusion required a ratio under 150 mmHg with FiO2 of at least 0.6 [3].

Q10. Pulmonary blood flow in each lung region depends on:
  1. (A) Arterial, venous and alveolar pressures
  2. (B) Only heart rate
  3. (C) Only the bronchial arteries
  4. (D) Surfactant alone

Answer: (A) The relation of vascular to alveolar pressures determines regional flow [1].

Quick review

Key takeaways

  • Alveolar ventilation = (tidal volume − dead space) × rate; it sets PaCO2.
  • PO2: about 150 inspired, 100 alveolar, 95 arterial, 40 mixed venous.
  • Blood flow rises steeply from apex to base; V/Q falls [1].
  • Dead space = air without blood; shunt = blood without air.
  • Diffusion fails first for oxygen and shows in exercise.
  • Good lung down [2]; prone lying in severe ARDS saves lives [3].

Further reading

SourceWhy it earns its place
West JB — Respiratory Physiology: The EssentialsThe standard account of V/Q
West JB et al. — J Appl Physiol, 1964The original zones paper [1]
Remolina C et al. — NEJM, 1981Positioning in one-sided lung disease [2]
Guérin C et al. — NEJM, 2013The prone positioning trial [3]

References

  1. West JB, Dollery CT, Naimark A. Distribution of blood flow in isolated lung; relation to vascular and alveolar pressures. Journal of Applied Physiology. 1964 Jul;19:713–724. doi:10.1152/jappl.1964.19.4.713 PMID 14195584 Experimental study
  2. Remolina C, Khan AU, Santiago TV, Edelman NH. Positional hypoxemia in unilateral lung disease. New England Journal of Medicine. 1981;304(9):523–525. doi:10.1056/NEJM198102263040906 PMID 6779161 Clinical study
  3. Guérin C, Reignier J, Richard JC, et al. Prone positioning in severe acute respiratory distress syndrome. New England Journal of Medicine. 2013;368(23):2159–2168. doi:10.1056/NEJMoa1214103 PMID 23688302 Randomised controlled trial

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Reviewed by the Physiotherapist India Team. · Human Physiology contents