Thoracic Wall and Diaphragm

Part 4 · The trunk

The cage, the intercostals and the mechanics of breathing

Why this is a physiotherapy chapter

Cardiorespiratory physiotherapy is one of the three great domains of the profession, and it rests entirely on this chapter. Every technique — positioning, breathing exercises, manual hyperinflation, cough assist, inspiratory muscle training, chest wall mobilisation — is an intervention on the mechanics described here.

Two ideas run through everything:

• The lungs do not breathe. The chest wall breathes, and the lungs follow — coupled by the pleural seal. If the seal is broken (pneumothorax) or the wall is stiff, immobile or paralysed, ventilation fails no matter how healthy the lung tissue.
• The diaphragm is the muscle of quiet breathing, contributing 70–80% of tidal volume. Everything else is a reserve, recruited only when demand rises — and a patient using accessory muscles at rest is telling you their reserve is already committed.

Learning outcomes

• Describe the thoracic cage, its apertures and the classification of ribs.
• Describe the costovertebral and costotransverse joints and explain pump-handle and bucket-handle motion.
• Describe the intercostal spaces, their muscles and the neurovascular bundle.
• Describe the diaphragm: attachments, openings, nerve supply, and its dome mechanics.
• Name the accessory muscles of inspiration and expiration and state when each is recruited.
• Explain the pleura, intrapleural pressure and the mechanics of a breath.
• Explain lung volumes and capacities and the muscles responsible for each.
• Describe the surface anatomy of the lungs and pleura and the levels for auscultation and chest drainage.
• Explain the effect of body position on ventilation and perfusion, and apply it to positioning.
• Explain the respiratory consequences of spinal cord injury, COPD, rib fracture and flail chest, and the basis of the cough.

The thoracic cage

Figure 1 · The thoracic cage and a typical rib

The sternum

The sternal angle marks, all at once:

• The second costal cartilage — so rib counting always starts here
• The level of the intervertebral disc between T4 and T5
• The bifurcation of the trachea (carina)
• The beginning and end of the aortic arch
• The bifurcation of the pulmonary trunk
• The upper limit of the pericardium
• The division between superior and inferior mediastinum

Learn this one landmark thoroughly and half of thoracic surface anatomy follows.

Classification of ribs

The costal groove on the inferior internal border of each rib carries the intercostal vein, artery and nerve — VAN, from superior to inferior — which dictates where a needle or chest drain is placed (§18.4).

Rib joints and the mechanics of the cage

Figure 2 · Why the upper and lower ribs move differently

Pump-handle and bucket-handle motion

The axis of rib movement runs through the costovertebral and costotransverse joints, and its orientation changes down the cage:

Both mechanisms operate at every level; the terms describe which predominates. Together they can increase thoracic volume substantially, and their loss — from ankylosing spondylitis, kyphosis, prolonged mechanical ventilation, burns, or simply age — reduces vital capacity independently of lung disease.

Chest expansion measurement (at the axilla, the nipple line and the xiphisternum) quantifies this and is a standard, underused assessment. Normal is roughly 3–7 cm at the xiphoid level; less than 2.5 cm at the fourth intercostal space is a diagnostic criterion for ankylosing spondylitis.

The intercostal spaces

Figure 3 · Inside an intercostal space

Eleven spaces, each containing three muscle layers and a neurovascular bundle.

The neurovascular bundle — vein, artery, nerve from above downwards (VAN) — runs in the costal groove at the inferior border of the rib above, between the internal and innermost layers. A smaller collateral bundle runs along the superior border of the rib below, which is why no part of the space is entirely safe.

Where to put a needle or a chest drain — and why

Insert immediately ABOVE the upper border of the rib below, in the middle of the intercostal space, to avoid the main neurovascular bundle in the costal groove above.

The “safe triangle” for intercostal drain insertion is bounded by the anterior border of latissimus dorsi, the lateral border of pectoralis major, a line superior to the horizontal level of the nipple (roughly the 5th intercostal space), and the apex below the axilla. It avoids the internal thoracic artery medially, the long thoracic nerve posteriorly, the diaphragm and liver/spleen inferiorly, and the thick musculature above.

A physiotherapist does not insert drains, but must know this to understand drain position, to mobilise a patient safely with a drain in situ, and to recognise a malpositioned one.

Arterial supply: posterior intercostal arteries — the upper two from the superior intercostal artery (from the costocervical trunk of the subclavian), the rest directly from the thoracic aorta; and anterior intercostal arteries from the internal thoracic artery and its musculophrenic branch.

Nerve supply:

• the anterior rami of T1–T11 are the intercostal nerves
• the anterior ramus of T12 is the subcostal nerve. T1 largely joins the brachial plexus
• T7–T11 continue into the abdominal wall as thoracoabdominal nerves. Each gives a lateral cutaneous branch (mid-axillary) and an anterior cutaneous branch

Clinically: the intercostobrachial nerve (lateral cutaneous branch of T2) supplies the medial arm and axilla — routinely sacrificed in axillary dissection, producing predictable medial arm numbness. Herpes zoster classically follows a single intercostal dermatome. And the segmental innervation is why T4 = nipple and T10 = umbilicus are such reliable landmarks.

The diaphragm

Figure 4 · The diaphragm seen from below

The principal muscle of respiration, a dome-shaped musculotendinous sheet separating thorax from abdomen.

Attachments

The right dome is higher than the left (because of the liver), reaching approximately the 5th rib in expiration; the left reaches the 5th intercostal space.

The three major openings — learn by level

Mnemonic: “I ate ten eggs at twelve” — IVC 8, Esophagus 10, Aorta 12. Or count the letters: VenaCava (T8, 3 letters ×… ) — most students find the sentence easier.

Minor structures pass elsewhere: the superior epigastric vessels behind the sternal slips; the splanchnic nerves pierce the crura; the sympathetic trunk passes behind the medial arcuate ligament; the hemiazygos vein pierces the left crus.

Nerve supply and the C3–C5 rule

Motor supply is exclusively from the phrenic nerve (C3, C4, C5) — “C3, 4, 5 keeps the diaphragm alive.” Sensory supply to the central part is also phrenic; the peripheral part is supplied by the lower intercostal nerves (T7–T11).

Two consequences of enormous clinical importance:

• Referred pain. Irritation of the central diaphragm — by blood, pus, air, or an inflamed viscus — refers to the tip of the shoulder (C3–C5 dermatomes), because the diaphragm develops in the cervical region and migrates caudally, dragging its nerve supply (Chapter 8). Hence shoulder-tip pain after laparoscopy, splenic rupture, subphrenic abscess or hepatic irritation. Peripheral diaphragmatic irritation refers to the lower chest wall and abdomen instead.
• Spinal cord injury level determines survival. A lesion above C3 abolishes diaphragmatic function and requires permanent ventilation. A lesion at C4–C5 usually preserves diaphragmatic function, though vital capacity is markedly reduced by loss of the intercostals and abdominals. This single fact structures the entire respiratory management of tetraplegia.

How the diaphragm works

On contraction, the dome descends — flattening and increasing the vertical dimension of the thorax — and, once the central tendon meets the resistance of the abdominal viscera, the zone of apposition (the cylindrical portion of the diaphragm applied to the inner chest wall) contracts to lift and evert the lower ribs, increasing the transverse diameter. It therefore does two jobs, and the second depends on abdominal wall tone providing a fulcrum.

Quiet inspiration: diaphragmatic descent of ~1.5 cm, contributing 70–80% of tidal volume. Deep inspiration: descent of ~6–10 cm.

Why hyperinflation is so disabling in COPD

A hyperinflated chest flattens the diaphragm. A flattened diaphragm has:

• A shorter zone of apposition, so it cannot lift the ribs — it may even pull them inwards (Hoover’s sign: paradoxical inward movement of the lower costal margin on inspiration, a specific clinical sign of hyperinflation)
• Shortened fibres, placing it on an unfavourable part of the length–tension curve (Chapter 5)
• A reduced radius of curvature, so by Laplace’s law it generates less pressure for the same tension

The COPD patient’s diaphragm is mechanically disadvantaged, not merely weak. That is why they recruit accessory muscles at rest, why they adopt forward-lean positions (which push the abdominal contents up, restoring the dome and the zone of apposition), and why pursed-lip breathing helps by reducing dynamic airway collapse and air trapping. Every one of those observations is anatomy applied.

The muscles of breathing

Figure 5 · Which muscles breathe, and when

Two points of clinical significance:

• Quiet expiration is passive. Any visible expiratory effort at rest is abnormal and indicates increased work of breathing or airflow obstruction.
• The abdominal muscles are the muscles of forced expiration and therefore of the cough. In a patient with abdominal muscle paralysis — a tetraplegic or high paraplegic patient — cough is ineffective, secretions accumulate, and respiratory complications are the leading cause of death. This is why assisted cough (manual abdominal thrust), abdominal binders (which restore the diaphragm’s fulcrum in the upright position), air stacking and mechanical insufflation–exsufflation are core interventions, not optional extras.

Accessory muscle use is a clinical sign. Sternocleidomastoid and scalene hypertrophy or visible activity at rest indicates chronically increased work of breathing.

The pleura and the mechanics of a breath

The pleura

A serous membrane in two continuous layers:

• Parietal pleura — lining the thoracic wall, with costal, mediastinal, diaphragmatic and cervical (cupula) parts. Innervated somatically by the intercostal and phrenic nerves — hence it is pain-sensitive and pain is well localised (or referred to the shoulder tip, if the diaphragmatic part is central).
• Visceral pleura — covering the lung, continuous with the parietal layer at the hilum and the pulmonary ligament. Innervated autonomically — it is insensitive to pain.

Between them, the pleural cavity — a potential space containing a few millilitres of serous fluid.

Recesses: the costodiaphragmatic recess (the deepest, where the lung does not reach in quiet breathing — the site of pleural effusion collection and thoracocentesis) and the costomediastinal recess.

Intrapleural pressure and the mechanics

The lung’s elastic recoil pulls inwards; the chest wall’s recoil pulls outwards. The fluid seal between the pleural layers prevents them separating, so the two opposing recoils generate a negative intrapleural pressure:

The sequence of a breath: 1. Inspiratory muscles contract → thoracic volume increases in all three dimensions (vertical by diaphragmatic descent, anteroposterior by pump-handle, transverse by bucket-handle). 2. Intrapleural pressure becomes more negative. 3. The lung, held to the wall by the fluid seal, expands (transpulmonary pressure rises). 4. Alveolar pressure falls below atmospheric. 5. Air flows in down the pressure gradient (Boyle’s law). 6. Expiration: muscles relax, elastic recoil restores volume, alveolar pressure exceeds atmospheric, air flows out.

Break the seal and the mechanism fails. In a pneumothorax, air enters the pleural cavity, intrapleural pressure rises toward atmospheric, and the lung collapses under its own recoil while the chest wall springs outwards. In a tension pneumothorax, a one-way valve effect raises intrapleural pressure above atmospheric, collapsing the lung completely and displacing the mediastinum — compressing the great veins and causing cardiovascular collapse. This is an immediate emergency: tracheal deviation away from the side, absent breath sounds, hyperresonance, distended neck veins and hypotension.

Compliance (Δvolume/Δpressure) falls in fibrosis, ARDS, pulmonary oedema, obesity and chest wall restriction; it rises in emphysema (destroyed elastic tissue), which is why emphysematous lungs inflate easily but empty poorly.

Surfactant, secreted by type II pneumocytes from ~24 weeks gestation, reduces alveolar surface tension, increases compliance, prevents alveolar collapse and equalises pressures between alveoli of different sizes (Laplace’s law). Its deficiency causes neonatal respiratory distress syndrome.

Lung volumes and capacities

In neuromuscular disease, vital capacity is the number that matters. A VC below ~1 litre (or ~15 mL/kg) indicates impending respiratory failure; a fall of more than ~25% from sitting to supine indicates significant diaphragmatic weakness. Serial bedside VC in Guillain–Barré syndrome or motor neurone disease is a core physiotherapy and nursing measurement.

Surface anatomy and positioning

Lung and pleural borders

The pleura extends two ribs below the lung at each line — the difference being the costodiaphragmatic recess. Both apices extend 2.5 cm above the medial third of the clavicle, into the neck — which is why a supraclavicular stab wound or a badly placed subclavian line causes a pneumothorax.

Fissures and lobes:

• Oblique fissure (both lungs): follows the line of the medial border of the scapula with the arm fully abducted overhead, running from the T2 spinous process to the 6th costal cartilage
• Horizontal fissure (right lung only): along the 4th costal cartilage, meeting the oblique fissure in the midaxillary line
• Right lung: three lobes. Left lung: two lobes plus the lingula (the left’s homologue of the middle lobe) and the cardiac notch

Auscultation implication: with the patient standing or sitting facing forward, you are listening mostly to upper lobes anteriorly and lower lobes posteriorly. The middle lobe and lingula are best heard in the axilla. Students who auscultate only the back systematically miss right middle lobe pathology.

Position and its effect on ventilation and perfusion

This is where the anatomy becomes directly therapeutic.

• In the upright position, gravity makes both ventilation and perfusion greater at the bases, but perfusion increases more steeply, so V/Q ratio is high at the apices and low at the bases (West zones 1–3).
• In side lying, in an adult, the dependent (lower) lung is better ventilated and better perfused, because the dependent diaphragm is pushed higher by the abdominal contents into a more favourable position on its length–tension curve and with a better radius of curvature. Hence: “good lung down” to optimise oxygenation in unilateral lung disease — the affected lung uppermost.
• In infants, this is reversed — the uppermost lung is better ventilated, because their compliant chest wall and small airways cause the dependent lung to be compressed. “Good lung up” in infants. Getting this backwards is a real and consequential error.
• Supine lying reduces FRC by roughly 0.5–1 litre through cephalad diaphragm displacement, which is a principal mechanism of post-operative hypoxaemia and atelectasis — and the reason early upright positioning and mobilisation are among the most effective respiratory physiotherapy interventions available.
• Prone positioning improves oxygenation in ARDS by making the distribution of transpulmonary pressure more uniform, recruiting dorsal lung units, and improving V/Q matching. The PROSEVA trial demonstrated a mortality benefit, and prone positioning is now standard in severe ARDS.

The cough, and clinical conditions

The cough — four phases

• Inspiration — a deep breath to ~85–90% of TLC, providing the volume and the elastic recoil.
• Compression — glottic closure with abdominal and intercostal contraction, raising intrathoracic pressure to 100–200 cmH₂O.
• Expulsion — glottis opens; airflow reaches ~6–12 L/s (peak cough flow), and dynamic airway compression narrows the airways, increasing linear velocity and shearing secretions from the walls.
• Relaxation.

Failure of any phase produces an ineffective cough:

Peak cough flow below ~270 L/min indicates an at-risk cough; below 160 L/min, cough is ineffective and airway clearance assistance is required.

Clinical conditions

Where students consistently go wrong

• Forgetting quiet expiration is passive.
• Getting the neurovascular bundle order wrong. VAN from above down, in the costal groove of the rib above — so insert above the rib below.
• Misplacing the diaphragmatic openings. T8 IVC, T10 oesophagus, T12 aorta.
• Forgetting the aorta passes behind the diaphragm and is not compressed.
• Confusing pump-handle and bucket-handle. Upper ribs = AP diameter; lower ribs = transverse.
• Saying visceral pleura is pain-sensitive. It is not; parietal pleura is.
• Reversing “good lung down”. Adults good lung down; infants good lung up.
• Thinking the COPD diaphragm is simply weak. It is mechanically disadvantaged by hyperinflation.
• Forgetting the abdominals are the cough muscles. Hence ineffective cough in SCI.
• Applying positive pressure techniques to an undrained pneumothorax.

Check yourself

15 questions on this chapter. Tap one to see the answer and the reasoning.

Quick review

Further reading

Chapter 18 of 24 · Human Anatomy · Physiotherapist India Next: Chapter 19 — Heart and Mediastinum: chambers, valves, the conducting system and the coronary supply.

Reviewed by the Physiotherapist India Team. · Human Anatomy contents