Learn — Respiratory system

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Openings in the diaphragm

The diaphragm is pierced at three main levels so that structures can pass between the thorax and the abdomen, and each opening lies at a fixed vertebral level in a different part of the muscle. Knowing them explains why a hiatus hernia occurs at T10 and nowhere else, why the inferior vena cava is held open during inspiration, and where congenital defects let abdominal viscera climb into the chest.

The caval opening lies at the level of T8 in the central tendon, to the right of the midline, and transmits the inferior vena cava and the right phrenic nerve.
Because the caval opening lies in the fibrous central tendon it is pulled open as the diaphragm descends, so inspiration widens it and helps venous return — the opposite of what happens at the oesophagus.
The oesophageal opening lies at T10 in the muscular sling of the right crus and transmits the oesophagus, the anterior and posterior vagal trunks and the oesophageal branches of the left gastric vessels.
The right crus around the oesophagus acts as a physiological sphincter and pinches it shut during inspiration; when that sling is weak the stomach slides upward as a hiatus hernia and the patient has reflux.
The aortic opening lies at T12 behind the median arcuate ligament between the two crura; it is osseoaponeurotic, so the aorta is never compressed by the contracting muscle, and it transmits the aorta, the thoracic duct and the azygos vein.
Smaller passages: the left phrenic nerve pierces the muscle of the left dome, the superior epigastric vessels pass through the sternocostal gap of Larrey, the splanchnic nerves pierce the crura, and the sympathetic trunk passes behind the medial arcuate ligament.
The diaphragm arches over the abdominal viscera as high as the fifth rib on the right and the fifth intercostal space on the left, the right dome about one space higher because of the liver — which is why a stab wound below the nipple line is a chest injury and an abdominal injury at once.
Congenital defects: the foramen of Bochdalek is a posterolateral defect and accounts for most congenital diaphragmatic hernias, about 85 to 90 per cent of them on the left, while the foramen of Morgagni is a small anterior retrosternal defect and is far less common.
The diaphragm develops from four parts — the septum transversum, the pleuroperitoneal membranes, the dorsal mesentery of the oesophagus and the body wall — and failure of the pleuroperitoneal membrane to close produces the Bochdalek hernia.

Diaphragm physiology

The diaphragm is the principal muscle of inspiration, a musculotendinous dome running from the lower ribs, xiphoid process and lumbar vertebrae to a central tendon, and it is supplied entirely by the phrenic nerve from C3, C4 and C5. When it contracts the dome flattens, the vertical dimension of the thorax increases, the intrapleural pressure falls further below atmospheric and air is drawn in — which is why anything that splints or denervates it causes respiratory failure.

The motor supply is the phrenic nerve alone, from C3, C4 and C5; sensation from the central part is also phrenic, while the peripheral rim is supplied by the lower intercostal nerves.
In quiet breathing the diaphragm does about 70 to 75 per cent of the work and descends 1 to 1.5 cm; in deep breathing it can descend up to about 10 cm.
Contraction lowers the intrapleural pressure from about -5 cm of water at the end of expiration to about -8 cm at the end of inspiration, and alveolar pressure falls roughly 1 cm of water below atmospheric so that air flows in.
Quiet expiration is entirely passive, driven by the elastic recoil of lung and chest wall; forced expiration recruits the abdominal muscles and the internal intercostals.
The accessory muscles of inspiration are the sternocleidomastoid, the scalenes and the pectorals, and their visible use with nasal flaring and intercostal recession is a nursing sign of increased work of breathing before any monitored number changes.
The right dome sits about one intercostal space higher than the left because of the liver, reaching the fifth rib on the right and the fifth intercostal space on the left in quiet expiration.
Because the phrenic supply is C3 to C5, a complete cord injury above C3 stops spontaneous breathing and needs immediate ventilation, an injury at C4 leaves breathing precarious, and one below C5 spares the diaphragm but paralyses the intercostal and abdominal muscles so the cough is weak.
Position changes the work of the diaphragm: sitting upright lets the abdominal contents fall away and raises the functional residual capacity, while lying flat, obesity, late pregnancy, ascites and abdominal distension splint the diaphragm and lower it.
Hiccup is a sudden involuntary contraction of the diaphragm with abrupt closure of the glottis, mediated by the phrenic and vagus nerves; persistent hiccup suggests diaphragmatic irritation from a subphrenic abscess, uraemia or a lesion along the phrenic nerve.

Visceral pleura

The pleura is a double serous membrane: the visceral layer is fused to the lung surface and dips into every fissure, while the parietal layer lines the chest wall, diaphragm and mediastinum, and the two become continuous at the hilum and the pulmonary ligament. Between them lies a potential space holding only a few millilitres of fluid at a negative pressure, and the different nerve supply of the two layers decides where — and whether — a patient feels pleural disease.

Visceral pleura is supplied by autonomic fibres from the pulmonary plexus and is insensitive to pain, touch and temperature, while parietal pleura has somatic innervation and is exquisitely sensitive — so pleuritic pain always means the parietal layer is involved.
The costal and peripheral diaphragmatic parietal pleura are supplied by the intercostal nerves and refer pain to the overlying chest wall, while the mediastinal and central diaphragmatic pleura are supplied by the phrenic nerve (C3 to C5) and refer pain to the tip of the shoulder.
The pleural cavity normally holds only about 5 to 15 mL of serous fluid, roughly 0.1 to 0.2 mL per kilogram — enough to lubricate but never to separate the layers.
Intrapleural pressure stays negative throughout quiet breathing, about -5 cm of water at the end of expiration and -8 cm at the end of inspiration; this negativity holds the lung expanded against its elastic recoil, and losing it collapses the lung.
The parietal pleura has four parts — costal, diaphragmatic, mediastinal and cervical; the cervical pleura or cupola rises about 2.5 cm above the medial third of the clavicle, which is why a supraclavicular block or a subclavian line can cause a pneumothorax.
Surface markings: the lower border of the lung crosses the 6th rib in the midclavicular line, the 8th in the midaxillary line and the 10th beside the vertebral column, while the pleural reflection runs two ribs lower at the 8th, 10th and 12th.
An intercostal drain is inserted in the safe triangle bounded by the lateral border of pectoralis major, the anterior border of latissimus dorsi and a line at the level of the nipple, usually in the 4th or 5th intercostal space.
The needle or drain is always passed along the upper border of the lower rib, because the intercostal vein, artery and nerve run in the subcostal groove at the lower border of the rib above, in that order from above downwards.
Fluid in the space is a pleural effusion, air a pneumothorax, blood a haemothorax and pus an empyema; in pleurisy the inflamed layers rub together and produce the creaking rub heard with breathing.

Lung volumes and capacities

Lung volumes are the four non-overlapping compartments of the air the lungs move and hold, while capacities are the sums of two or more of them; the standard figures quoted are for a young adult male, and a woman's are about 20 to 25 per cent lower. They matter at the bedside because incentive spirometry, weaning from a ventilator and the decision to intubate a weakening neuromuscular patient all rest on measured volumes rather than on how breathless the patient looks.

Tidal volume is about 500 mL, the air moved with each quiet breath, roughly 6 to 8 mL per kilogram of ideal body weight.
Inspiratory reserve volume is about 3,000 mL and expiratory reserve volume about 1,100 mL — the extra air that can be forcibly taken in above, and pushed out below, a normal tidal breath.
Residual volume is about 1,200 mL, the air that remains after the most forceful expiration and can never be exhaled; it keeps the alveoli open and lets gas exchange continue between breaths.
Inspiratory capacity is tidal volume plus inspiratory reserve volume, about 3,500 mL, and functional residual capacity is expiratory reserve volume plus residual volume, about 2,300 mL — the air left in the lung at the end of a quiet expiration, and the oxygen store a patient lives on during intubation.
Vital capacity is tidal plus inspiratory reserve plus expiratory reserve volume, about 4,600 mL, and total lung capacity is vital capacity plus residual volume, about 5,800 mL.
Any value that contains the residual volume — residual volume itself, functional residual capacity and total lung capacity — cannot be measured by simple spirometry and needs helium dilution, nitrogen washout or body plethysmography.
Anatomical dead space is about 150 mL, roughly 2 mL per kilogram, so alveolar ventilation is the tidal volume minus the dead space multiplied by the respiratory rate — about 350 mL times 12, or roughly 4.2 litres a minute; slow deep breaths ventilate the alveoli far better than rapid shallow ones at the same minute volume.
The forced expiratory ratio separates the two great patterns: an FEV1 to FVC ratio below 0.7 with a low FEV1 means obstruction as in asthma and chronic obstructive pulmonary disease, while a normal or high ratio with a reduced FVC and total lung capacity means restriction as in fibrosis, kyphoscoliosis, obesity or neuromuscular weakness.
Functional residual capacity falls with supine posture, obesity, pregnancy, abdominal distension, anaesthesia and pain after upper abdominal surgery — the physiological reason for sitting patients up, mobilising early and using incentive spirometry.

Larynx anatomy

The larynx is the organ of phonation and the sphincter that guards the airway, lying in front of the pharynx from the third to the sixth cervical vertebra in the adult and built from nine cartilages joined by membranes and moved by intrinsic muscles. Its nerve supply is the reason a thyroid operation can leave a patient hoarse, or in the worst case unable to breathe at all.

There are nine cartilages: three unpaired — thyroid, cricoid and epiglottis — and three paired — arytenoid, corniculate of Santorini and cuneiform of Wrisberg.
The thyroid, the cricoid and the greater part of the arytenoid are hyaline cartilage and calcify with age, while the epiglottis, the corniculate and cuneiform cartilages and the apex and vocal process of the arytenoid are elastic cartilage and do not.
The vocal ligament runs from the vocal process of the arytenoid behind to the angle of the thyroid cartilage in front, and the gap between the cords, the rima glottidis, is the narrowest part of the adult airway.
All the intrinsic muscles are supplied by the recurrent laryngeal nerve except the cricothyroid, which is supplied by the external branch of the superior laryngeal nerve — the tensor of the cords, and the nerve whose injury takes away the high notes.
The posterior cricoarytenoid is the only abductor of the vocal cords and therefore the only muscle that opens the airway, so its bilateral paralysis is life-threatening; the lateral cricoarytenoids and the transverse arytenoid adduct them.
Sensation is divided at the cords: above them by the internal branch of the superior laryngeal nerve and below them by the recurrent laryngeal nerve, so blocking the internal laryngeal nerve abolishes the cough reflex from above the cords.
The left recurrent laryngeal nerve hooks under the arch of the aorta at the ligamentum arteriosum and the right under the right subclavian artery, so the left has a far longer course and is more often involved by a lung tumour, an aortic aneurysm or an enlarged left atrium.
The recurrent laryngeal nerve runs in the tracheo-oesophageal groove in close relation to the inferior thyroid artery, which is why it is at risk in thyroidectomy; unilateral injury gives a hoarse breathy voice and bilateral injury gives stridor and airway obstruction.
The blood supply is from the superior laryngeal artery, a branch of the superior thyroid artery from the external carotid, and the inferior laryngeal artery from the inferior thyroid artery of the thyrocervical trunk.

Lung epithelium lining

The lining of the airway changes step by step from the nose to the alveolus, becoming thinner and losing its cilia and glands as it nears the gas-exchanging surface. Above, the pseudostratified ciliated columnar epithelium with goblet cells forms the mucociliary escalator that clears inhaled particles; below, a single layer of flat type I pneumocytes lets oxygen cross in a fraction of a micrometre.

The nasal vestibule is lined by stratified squamous keratinised epithelium with hairs, and from the nasal cavity through the trachea and bronchi the lining is pseudostratified ciliated columnar epithelium with goblet cells — the classic respiratory epithelium.
Bronchioles are lined by simple ciliated columnar epithelium, terminal bronchioles by simple cuboidal cells with club (Clara) cells and almost no goblet cells, and respiratory bronchioles by cuboidal cells interrupted by alveolar openings.
Alveoli have two cell types: type I pneumocytes, flat squamous cells that cover about 95 per cent of the alveolar surface and across which gas diffuses, and type II pneumocytes, which are more numerous but cover only about 5 per cent of the surface.
Type II pneumocytes secrete surfactant, chiefly dipalmitoyl phosphatidylcholine or lecithin, which lowers alveolar surface tension, prevents the collapse of small alveoli and reduces the work of breathing; they are also the stem cells that replace damaged type I cells.
By the law of Laplace the collapsing pressure of an alveolus is twice the surface tension divided by the radius, so without surfactant the small alveoli would empty into the large ones — the mechanism of the diffuse collapse seen in respiratory distress syndrome.
Surfactant appears from about 24 to 28 weeks of gestation and is adequate by about 34 to 36 weeks; a lecithin to sphingomyelin ratio of 2 to 1 or more indicates lung maturity, and antenatal corticosteroids accelerate its production.
Cilia beat about 10 to 20 times a second and move the mucus blanket towards the pharynx at roughly 1 cm a minute; the escalator is slowed by cigarette smoke, dehydration, dry inspired gas, hypoxia, general anaesthesia and high concentrations of oxygen.
Alveolar macrophages, the dust cells, are the phagocytes of the alveolus, and when they take up red cells in pulmonary congestion they become the haemosiderin-laden heart failure cells found in sputum.
The blood-gas barrier is only about 0.2 to 0.5 micrometres thick across a total alveolar surface of roughly 70 square metres in some 300 million alveoli, which is why any thickening of that membrane, as in fibrosis or oedema, affects oxygen before it affects carbon dioxide.

Respiratory centre stimulants

Breathing is generated by the respiratory centres in the medulla and pons and adjusted moment to moment by chemoreceptors that sample carbon dioxide, hydrogen ion and oxygen. The central chemoreceptors in the medulla respond to the hydrogen ion produced when carbon dioxide crosses into the cerebrospinal fluid and supply the greater part of the drive, while the peripheral chemoreceptors in the carotid and aortic bodies are the only ones that respond to a fall in arterial oxygen.

The medulla contains the dorsal respiratory group, which drives inspiration and sets the basic rhythm, and the ventral respiratory group, which is largely silent in quiet breathing and is recruited for forced breathing.
The pons modifies that rhythm: the pneumotaxic centre in the upper pons limits inspiration and so raises the rate, while the apneustic centre in the lower pons prolongs it.
Central chemoreceptors lie on the ventral surface of the medulla and respond to hydrogen ion in the cerebrospinal fluid; carbon dioxide crosses the blood-brain barrier freely while hydrogen ion does not, so carbon dioxide acts through the acid it generates.
Peripheral chemoreceptors are the carotid bodies at the bifurcation of the common carotid artery, with afferents in the glossopharyngeal nerve, and the aortic bodies on the arch, with afferents in the vagus; they respond to a fall in arterial oxygen tension and also to a rise in carbon dioxide and hydrogen ion.
The hypoxic drive from the peripheral chemoreceptors becomes significant only when the arterial oxygen tension falls below about 60 mmHg, which corresponds to a saturation of about 90 per cent on the steep part of the oxygen dissociation curve.
In health carbon dioxide is by far the most powerful stimulus to breathing, and a rise of only a few mmHg greatly increases ventilation; in chronic carbon dioxide retention the central receptors adapt and the hypoxic drive takes over, which is why oxygen must be titrated in these patients.
The Hering-Breuer inflation reflex, carried by vagal stretch receptors in the airway, ends inspiration when the lung is greatly distended; it protects against over-inflation but is not active at normal adult tidal volumes.
The arterial values to interpret against are pH 7.35 to 7.45, PaCO2 35 to 45 mmHg, PaO2 80 to 100 mmHg and bicarbonate 22 to 26 mEq/L.
Other influences on the centre are voluntary cortical control, emotion through the limbic system, joint and muscle proprioceptors at the start of exercise, body temperature, and drugs — opioids and sedatives depress the medullary centre directly and slow the rate before they reduce the depth.

Oxygenated vs deoxygenated blood

The circulation is two pumps in series: the right heart drives deoxygenated blood through the pulmonary circuit to be loaded with oxygen, and the left heart drives oxygenated blood through the systemic circuit to deliver it. The naming trap that examiners love is that artery and vein are defined by the direction of flow relative to the heart and not by oxygen content, which is why the pulmonary artery is the one artery carrying deoxygenated blood and the pulmonary veins are the only veins carrying oxygenated blood.

Deoxygenated route: systemic veins and the coronary sinus drain into the right atrium, through the tricuspid valve to the right ventricle, through the pulmonary valve into the pulmonary trunk and its two arteries to the lungs.
Oxygenated route: four pulmonary veins carry blood to the left atrium, through the mitral valve to the left ventricle, through the aortic valve into the aorta and on to the systemic arteries and capillaries.
Arterial blood normally has an oxygen tension of 80 to 100 mmHg with a saturation of 95 to 100 per cent and a carbon dioxide tension of 35 to 45 mmHg; mixed venous blood has an oxygen tension of about 40 mmHg and a saturation of about 75 per cent, so only about a quarter of the delivered oxygen is extracted at rest.
Oxygenated blood is bright scarlet and deoxygenated blood is dark purplish-red; the blue appearance of veins under the skin is an optical effect, not the colour of the blood inside.
Cyanosis becomes visible only when reduced haemoglobin in capillary blood exceeds about 5 g/dL, which means a severely anaemic patient can be dangerously hypoxic without looking blue, while a polycythaemic patient looks blue early.
Central cyanosis is seen in the tongue and buccal mucosa and means arterial blood is desaturated; peripheral cyanosis is confined to the fingers, toes, nose and ears and usually means slow flow from cold or low output with normal arterial saturation.
The fetus reverses the same rule in the umbilical vessels: the single umbilical vein carries oxygenated blood from the placenta to the fetus and the two umbilical arteries carry deoxygenated blood back, and fetal shunting through the ductus venosus, foramen ovale and ductus arteriosus means fetal blood is always partly mixed.
A right-to-left shunt, as in tetralogy of Fallot or transposition of the great arteries, sends deoxygenated blood straight into the systemic circulation, and its hallmark is cyanosis that barely improves when oxygen is given.
The lungs also receive oxygenated blood of their own through the bronchial arteries from the aorta, and that blood drains into the pulmonary veins, adding a small normal physiological shunt.

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