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Human Physiology · Respiratory system

Mechanics of Breathing

Breathing is a pump: muscles change the size of the chest, pressures change, and air flows. This page explains the pressures, the muscles, the elastic and resistive loads they work against, and how physiotherapists measure and train the respiratory muscles.

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Part 4 · Respiratory System · Chapter 16 of 47

Learning objectives

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

  • Describe the pressures that drive airflow during a breath.
  • Name the muscles of quiet and forced breathing.
  • Explain lung compliance, elastic recoil and the role of surfactant.
  • Explain airway resistance and dynamic airway compression.
  • Describe how respiratory muscle strength is measured.
  • Summarise the evidence for inspiratory muscle training.

Why it matters

Respiratory physiotherapy is built on mechanics. Positioning changes how well the diaphragm works, breathing exercises change lung volume, and airway clearance relies on airflow and pressure.

When a patient with COPD is breathless, a patient with a high spinal cord injury cannot cough, or a ventilated patient fails to wean, the explanation is usually mechanical.

Pressures that move air

Air flows from high pressure to low. At rest, with the airway open and no flow, alveolar pressure equals atmospheric pressure, which we call zero.

The lungs sit inside the chest wall, separated by a thin film of pleural fluid. The lungs tend to recoil inward and the chest wall outward. This pulls pleural pressure below atmospheric, to about −5 cmH2O at rest.

PressureMeaningAt restDuring quiet inspiration
AtmosphericPressure at the mouth00
AlveolarPressure inside the alveoli0About −1 cmH2O
PleuralPressure between lung and chest wallAbout −5About −7.5
TranspulmonaryAlveolar minus pleural; holds the lung openAbout +5About +6.5 at peak

Figure 1 · One quiet breath

Lung volume, alveolar pressure and pleural pressure during a quiet breath Three stacked traces over four seconds. Lung volume rises by about half a litre during inspiration and falls during expiration. Alveolar pressure dips to about minus one centimetre of water during inspiration and rises to plus one during expiration. Pleural pressure falls from about minus five to minus seven and a half, then returns. 00.5Lung volume change (L)−1+1Alveolar pressure (cmH2O)−8−5Pleural pressure (cmH2O)Inspiration (about 2 s)Expiration (about 2 s)
Air follows pressure. Inspiratory muscles make pleural pressure more negative, the lungs expand, alveolar pressure falls below atmospheric and air flows in. Values are typical for quiet breathing.

When the inspiratory muscles contract, the chest enlarges and pleural pressure becomes more negative. The lungs expand, alveolar pressure falls below atmospheric and air flows in. At the end of inspiration flow stops; then elastic recoil pushes alveolar pressure above atmospheric and air flows out.

Specialist laboratories measure pleural pressure with a balloon in the oesophagus [1].

Pneumothorax

If air enters the pleural space through a wound or a ruptured lung surface, pleural pressure rises to atmospheric. The lung recoils and collapses. Never apply positive pressure techniques to a patient with an undrained pneumothorax.

The respiratory muscles

Figure 2 · The breathing muscles

Diaphragm movement and the muscles of quiet and forced breathing A front view of the thorax with ribs and the diaphragm. The diaphragm dome is shown at rest and lower during inspiration, and arrows show the ribs lifting outward. A list names the muscles of quiet and forced inspiration and expiration. Diaphragm: rest (solid), inspiration (dashed)Ribs lift up and out (arrows); diaphragm descendsQuiet inspirationDiaphragm (main), external intercostalsForced inspirationPlus scalenes, sternocleidomastoid,upper trapezius, pectoralsQuiet expirationPassive elastic recoilForced expiration, coughAbdominals, internal intercostals
Quiet breathing is mostly the diaphragm. Expiration is passive at rest; muscles are recruited for forced breathing and coughing. Anatomy of these muscles is covered in the Human Anatomy series.

The diaphragm is a dome of muscle supplied by the phrenic nerves, from spinal segments C3 to C5. When it contracts the dome descends, pushing the abdominal contents down and lifting the lower ribs. It does most of the work of quiet breathing.

The external intercostals lift the ribs upward and outward. During heavy breathing the accessory muscles join in. Quiet expiration is passive, but coughing and forced expiration use the abdominal and internal intercostal muscles.

SituationWhat changesClinical example
Flattened diaphragmShorter fibres, less pressure for the same effortHyperinflation in COPD
Loss of phrenic supplyDiaphragm weak or paralysedSpinal cord injury at or above C3–C5
Weak abdominal musclesPoor coughThoracic spinal cord injury, neuromuscular disease
Use of accessory muscles at restDiaphragm overloadedAcute exacerbation, respiratory distress

Elastic properties of the lungs

Compliance describes how easily the lungs stretch: the change in volume for each unit change in distending pressure. A compliant lung fills easily. A stiff lung needs larger pressure swings and so more muscle work.

Figure 3 · Lung compliance

Pressure-volume curves of normal, emphysematous and fibrotic lungs Three curves of lung volume against distending pressure. The emphysema curve is steepest and highest, the normal curve is in between, and the fibrosis curve is flattest and lowest. NormalEmphysema: floppy, high complianceFibrosis: stiff, low complianceDistending (transpulmonary) pressureLung volume
Compliance is the slope. Stiff fibrotic lungs need more pressure, so more muscle work, for each breath. Floppy emphysematous lungs fill easily but recoil poorly, so air is trapped. Schematic.

Elastic recoil comes from two sources: elastic fibres in the lung tissue and surface tension at the air–liquid interface in the alveoli. Surface tension is the larger part.

The functional residual capacity, the volume at the end of a quiet breath, is the point where inward lung recoil exactly balances outward chest wall recoil.

Surfactant

Figure 4 · Why the lungs need surfactant

Effect of surfactant on two connected alveoli of different size Left: without surfactant, a small alveolus connected to a large one has higher pressure and empties into it. Right: with surfactant molecules lining both, surface tension falls most in the small alveolus and both remain open. Without surfactantsmalllargeHigher pressure in the small alveolusempties it into the large oneWith surfactantstablestableSurfactant lowers surface tension mostin small alveoli, so both stay openLaplace: pressure = 2 × surface tension ÷ radius
Surfactant stabilises alveoli and reduces the work of breathing. Premature babies who lack it develop stiff, collapsing lungs.

Type II alveolar cells secrete surfactant, a mixture of lipids and proteins. It lowers surface tension, which increases compliance and reduces the work of breathing. Because it lowers tension more in small alveoli, it stops them emptying into larger ones and helps keep the lungs dry.

Airway resistance

Airflow also meets resistance in the airways. As with blood vessels, resistance rises steeply as the airway narrows. Most resistance lies in the medium-sized bronchi; the very small airways are so numerous that together they offer little resistance.

Bronchoconstriction, mucus and airway wall swelling raise resistance, as in asthma and COPD. Lung volume matters too: airways are wider at high lung volumes, because surrounding tissue pulls them open.

Dynamic airway compression

During forced expiration, pleural pressure becomes positive and squeezes the airways. In healthy lungs they stay open. In emphysema, loss of elastic tissue lets small airways collapse early, trapping air.

Pursed-lip breathing adds back-pressure at the mouth, which helps hold the airways open and slows breathing. Huffing, used in airway clearance, deliberately uses controlled compression to move secretions.

The work of breathing

The respiratory muscles must overcome elastic recoil and airway resistance. At rest this uses only a few per cent of total oxygen uptake. In lung disease the work can rise many times, and breathlessness and fatigue follow.

Stiff lungs favour rapid shallow breathing, which reduces elastic work. Narrow airways favour slow deep breathing, which reduces resistive work. Patients choose their pattern for a reason.

Measuring the respiratory muscles

The European Respiratory Society task force reviewed respiratory muscle tests [1]. The simplest are maximal mouth pressures. Maximal inspiratory pressure (MIP) is measured during a maximal effort from low lung volume; maximal expiratory pressure (MEP) from high lung volume.

Sniff nasal pressure is an easier alternative for some patients. Ultrasound of the diaphragm and specialised electrical and magnetic tests are also available [1].

TestWhat it showsNotes
Maximal inspiratory pressureGlobal inspiratory strengthEffort-dependent; repeat until consistent [1]
Maximal expiratory pressureExpiratory and cough strengthLow values mean a weak cough
Sniff nasal inspiratory pressureInspiratory strengthNatural manoeuvre; useful in neuromuscular disease [1]
Diaphragm ultrasoundThickness and movementBedside; growing role in intensive care [1]
Peak cough flowCough effectivenessGuides airway clearance needs

Training the respiratory muscles

Figure 5 · Training the breathing muscles

Pooled effects of inspiratory muscle training in COPD and in critically ill adults Left: in COPD, inspiratory muscle training increased inspiratory strength by 13 centimetres of water, walking distance by 32 metres and reduced breathlessness by 0.9 Borg points. Right: in intensive care, it increased strength by 6 centimetres of water and shortened ventilation by 4.1 days and weaning by 2.3 days. COPD: 32 trials [2]Inspiratory strength+13 cmH2O6-minute walk+32 mBreathlessness (Borg)−0.9 pointsIntensive care: 20 RCTs [3]Inspiratory strength+6 cmH2OTime on ventilator4.1 days shorterWeaning time2.3 days shorterPooled mean differences versus control
Respiratory muscles are trainable. Strength-type loading works better than endurance-type loading in COPD [2]. ICU effects on ventilation time are promising but low certainty [3].

Gosselink and colleagues pooled 32 randomised trials of inspiratory muscle training in COPD. Training increased maximal inspiratory pressure by about 13 cmH2O and walking distance by 32 metres, and reduced breathlessness [2]. Strength-type training worked better than endurance-type training [2].

In intensive care, Vorona and colleagues found inspiratory training feasible and safe. It increased inspiratory pressure and was linked with shorter ventilation and weaning, though the certainty was low [3].

Practical skill · prescribing threshold training

Measure baseline MIP. Start at a load the patient can manage for short sets, commonly a moderate percentage of MIP, and progress as strength improves. Focus on patients with weakness, such as MIP below about 60 cmH2O in COPD [2].

Clinical relevance for the physiotherapist

  • Positioning. Upright sitting lets the diaphragm descend; slumped sitting and abdominal distension restrict it.
  • Breathing exercises. Deep breaths increase transpulmonary pressure and re-expand collapsed areas after surgery.
  • COPD. Hyperinflation flattens the diaphragm; pursed-lip breathing and inspiratory training can help [2].
  • Spinal cord injury. The level of injury predicts which muscles remain; test cough strength.
  • Weaning. Measure inspiratory strength and consider inspiratory training in difficult weaning [1, 3].

Assessment and application

ObservationMechanical meaningResponse
Rapid shallow breathing in a patient with fibrosisLow compliance; elastic work highPacing, positioning, oxygen as prescribed
Prolonged expiration and wheezeHigh airway resistancePursed-lip breathing; check medication use
Abdomen moves in while chest moves out on inspirationPossible diaphragm weaknessMeasure MIP or sniff pressure [1]
Weak cough after abdominal surgeryPain and expiratory muscle inhibitionSupported coughing, pain control, huffing

Common mistakes

  • Thinking the lungs expand on their own; they follow the chest wall through pleural pressure.
  • Calling expiration active at rest; quiet expiration is passive recoil.
  • Confusing compliance with elastic recoil; they are opposites.
  • Using endurance-type breathing devices when strength-type training works better in COPD [2].
  • Assuming respiratory muscle weakness cannot be measured at the bedside [1].

Exam preparation

Long answer

Describe the mechanics of breathing. Add a note on surfactant.

  • Pressures: atmospheric, alveolar, pleural, transpulmonary (Figure 1).
  • Muscles of quiet and forced breathing (Figure 2).
  • Compliance and elastic recoil (Figure 3).
  • Surfactant and the law of Laplace (Figure 4).
  • Airway resistance and work of breathing.
  • Clinical tests of muscle strength [1].

Short notes

  • Intrapleural pressure.
  • Lung compliance.
  • Surfactant.
  • Inspiratory muscle training [2, 3].

Viva and practical

  • “Why is pleural pressure negative?” — opposing recoil of lung and chest wall.
  • “What happens in pneumothorax?” — pleural pressure rises to atmospheric and the lung collapses.
  • “Which IMT type works best in COPD?” — strength-type training [2].
  • OSCE: measure maximal inspiratory pressure [1].

Current evidence

Exam and traditional teaching

Respiratory muscles are described anatomically, and weakness is often inferred from the breathing pattern rather than measured.

What the evidence adds

Respiratory muscle strength can be measured with standard tests, and newer imaging methods add detail [1].

Inspiratory muscle training improves strength, walking distance and breathlessness in COPD [2], and appears safe in intensive care [3].

What the student should understand

Treat the respiratory muscles like any other muscles: measure them, load them progressively, and position the patient so they can work well.

Check yourself

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

Q1. During quiet inspiration, pleural pressure typically:
  1. (A) Becomes positive
  2. (B) Falls from about −5 to −7.5 cmH2O
  3. (C) Stays at zero
  4. (D) Equals atmospheric pressure

Answer: (B) Pleural pressure becomes more negative as the inspiratory muscles act; such pressures are measured with oesophageal balloons [1].

Q2. The main muscle of quiet inspiration is the:
  1. (A) Sternocleidomastoid
  2. (B) Diaphragm
  3. (C) Rectus abdominis
  4. (D) Internal intercostals

Answer: (B) The diaphragm is the principal inspiratory muscle; its function can be assessed by pressure and imaging methods [1].

Q3. Maximal inspiratory pressure (MIP or PI,max) is a measure of:
  1. (A) Lung compliance
  2. (B) Global inspiratory muscle strength
  3. (C) Airway resistance
  4. (D) Gas exchange

Answer: (B) Mouth pressures during maximal efforts are standard tests of respiratory muscle strength [1].

Q4. In the COPD meta-analysis, inspiratory muscle training increased maximal inspiratory pressure by about:
  1. (A) 1 cmH2O
  2. (B) 13 cmH2O
  3. (C) 60 cmH2O
  4. (D) No change

Answer: (B) Pooled PI,max rose by about 13 cmH2O [2].

Q5. In COPD, which type of inspiratory muscle training was less effective?
  1. (A) Strength training
  2. (B) Endurance training
  3. (C) Both equally effective
  4. (D) Neither had any effect

Answer: (B) Endurance-type training was less effective than strength-type training [2].

Q6. The COPD meta-analysis defined inspiratory muscle weakness as PI,max below about:
  1. (A) 20 cmH2O
  2. (B) 60 cmH2O
  3. (C) 150 cmH2O
  4. (D) 300 cmH2O

Answer: (B) Patients with PI,max under 60 cmH2O benefited when training was added to exercise [2].

Q7. In critically ill adults, inspiratory muscle training was:
  1. (A) Unsafe
  2. (B) Feasible, with few adverse events
  3. (C) Impossible during ventilation
  4. (D) Shown to raise mortality

Answer: (B) IMT was feasible and well tolerated, with a median adverse event rate of 0% [3].

Q8. In ICU trials, inspiratory muscle training was associated with weaning that was shorter by about:
  1. (A) 2.3 days
  2. (B) 20 days
  3. (C) 2 hours
  4. (D) No difference

Answer: (A) Weaning was about 2.3 days shorter, though certainty was low [3].

Q9. A lung with fibrosis has:
  1. (A) High compliance
  2. (B) Low compliance
  3. (C) Normal compliance
  4. (D) No elastic recoil

Answer: (B) Stiff lungs require larger pressure swings, which raises the load on the inspiratory muscles that tests of muscle function assess [1].

Q10. Which method is the most common technique of inspiratory muscle training in intensive care?
  1. (A) Threshold loading
  2. (B) Electrical stimulation only
  3. (C) Bed rest
  4. (D) Prone lying

Answer: (A) Inspiratory threshold loading was the most commonly used technique [3].

Quick review

Key takeaways

  • Air flows down pressure gradients; pleural pressure is about −5 cmH2O at rest.
  • Diaphragm does most quiet inspiration; quiet expiration is passive.
  • Compliance = change in volume ÷ change in pressure; surfactant raises it.
  • Most airway resistance is in medium bronchi; forced expiration compresses airways.
  • MIP and MEP measure respiratory muscle strength [1].
  • IMT improves strength and walking in COPD [2] and is safe in ICU [3].

Further reading

SourceWhy it earns its place
West JB — Respiratory Physiology: The EssentialsClear account of mechanics
Laveneziana P et al. — Eur Respir J, 2019How respiratory muscles are tested [1]
Gosselink R et al. — Eur Respir J, 2011IMT in COPD [2]
Vorona S et al. — Ann Am Thorac Soc, 2018IMT in intensive care [3]

References

  1. Laveneziana P, Albuquerque A, Aliverti A, et al. ERS statement on respiratory muscle testing at rest and during exercise. European Respiratory Journal. 2019;53(6):1801214. doi:10.1183/13993003.01214-2018 PMID 30956204 Task force statement
  2. Gosselink R, De Vos J, van den Heuvel SP, Segers J, Decramer M, Kwakkel G. Impact of inspiratory muscle training in patients with COPD: what is the evidence? European Respiratory Journal. 2011;37(2):416–425. doi:10.1183/09031936.00031810 PMID 21282809 Meta-analysis
  3. Vorona S, Sabatini U, Al-Maqbali S, et al. Inspiratory muscle rehabilitation in critically ill adults. A systematic review and meta-analysis. Annals of the American Thoracic Society. 2018;15(6):735–744. doi:10.1513/AnnalsATS.201712-961OC PMID 29584447 Systematic review and meta-analysis

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Reviewed by the Physiotherapist India Team. · Human Physiology contents