Trachea and large airways

What it normally does

• The trachea is held open by about 16 to 20 C-shaped cartilage rings — solid at the front and sides, open at the back, where a strip of smooth muscle (trachealis) closes the gap against the oesophagus.

  the airway cannot collapse under the suction of a breath in — and when that cartilage is soft, squashed from outside, or the lining inside it swells, breathing in becomes noisy (stridor).

• The lining is ciliated. Each cilium beats roughly 12 to 15 times a second in a watery periciliary layer, under a blanket of mucus, sweeping trapped dust and bacteria up to the throat to be swallowed — the mucociliary escalator. That watery layer stays deep enough only because CFTR, an ATP-gated chloride channel (not a pump), lets chloride move down its electrochemical gradient onto the surface, with sodium and water following.

  anything that dries the layer out, stills the cilia, or buries them in mucus leaves bacteria sitting in the airway — the shared starting point of cystic fibrosis lung disease, bronchiectasis and smoker's cough.

• In adults the right main bronchus is wider, shorter and more vertical — about 25 degrees off the vertical midline, against roughly 45 on the left. In children under about 3 the two angles are much more similar.

  in adults and older children anything inhaled — a peanut, a tooth, vomit — usually ends up on the right; in toddlers it is only modestly right-sided, so left-sided signs never rule a foreign body out.

• Irritant receptors in the larynx, trachea and especially the carina send signals up the vagus nerve and fire the cough reflex: deep breath in, glottis shut, then an explosive blast out.

  cough is the backup for the escalator — and when it is suppressed by a reduced conscious level, alcohol or a stroke, what should have been coughed out is aspirated instead, most often into the right lung.

What goes wrong

• Inhaled foreign body← from “In adults the right main bronchus is wider, sh…”

  An object drawn past the vocal cords tends to follow the wider, straighter right main bronchus — a right-sided predominance that is strong in adults but only modest in toddlers, whose bronchial angles are nearly symmetric. While it sits at the carina it triggers violent coughing, because that is the most sensitive point in the airway. Once it lodges further down the receptors adapt and the coughing stops — the silent interval that makes everyone relax. Where it sits it acts as a one-way valve: airways widen on inspiration so air gets past, and narrow on expiration so less gets out, and the lobe beyond hyperinflates. Vegetable matter such as a peanut swells and inflames the mucosa around it, so within hours it is stuck fast.

  Peanut, under 3, right side more often than left but either is possible. Unilateral wheeze is a foreign body until rigid bronchoscopy says otherwise.

  You would find: A toddler who suddenly choked, then unilateral wheeze and reduced air entry on one side. An expiratory or lateral decubitus chest film shows the affected side staying hyperinflated with the mediastinum pushed away from it. A normal film does not exclude it — food is radiolucent.

• Cystic fibrosis airway disease← from “The lining is ciliated. Each cilium beats roug…”

  A faulty CFTR channel means chloride, and therefore water, is not secreted onto the airway surface (sodium absorption through ENaC is also unrestrained, drying it further). The periciliary layer the cilia beat in collapses, so the cilia are stuck in glue and stop moving mucus. Stagnant mucus is a culture medium: Staphylococcus aureus early, Pseudomonas aeruginosa later. Neutrophils pour in, die, and spill DNA that makes the sputum thicker still. Repeated infection destroys the airway wall, so the endpoint of cystic fibrosis lung disease is bronchiectasis.

  No chloride, no water, no periciliary layer, no ciliary beat. Almost everything else in the airway picture follows from mucus that cannot move.

  You would find: Roughly 1 in 2500 to 3500 Australian births, nearly all detected on the newborn heel-prick screen (immunoreactive trypsinogen then genotyping). Chronic wet cough, poor weight gain, fatty stools, and a raised sweat chloride, which remains the confirmatory test.

• Bronchiectasis and chronic suppurative lung disease← from “The lining is ciliated. Each cilium beats roug…”

  Anything that stalls the escalator long enough lets infection persist — severe or repeated childhood pneumonia, whooping cough, or a foreign body left in place. Neutrophil elastase and other proteases from the chronic infection digest the elastic tissue and cartilage of the airway wall, so the airway dilates permanently and loses its shape. A wide floppy airway clears even worse than a normal one, holds more infected mucus, and the cycle repeats (the vicious cycle).

  Failed clearance to infection to wall destruction to worse clearance. Wet cough beyond four weeks in a child is the referral trigger.

  You would find: A daily wet productive cough for months, coarse crackles, and dilated thick-walled airways on CT. Aboriginal and Torres Strait Islander children, particularly in central and northern Australia, carry rates among the highest reported anywhere in the world — a wet cough lasting more than four weeks in any child is investigated, not watched.

• Smoker's chronic bronchitis← from “The lining is ciliated. Each cilium beats roug…”

  Smoke slows and then destroys cilia, while driving goblet cells and submucosal glands to multiply. Mucus production rises at exactly the moment the means of moving it fails. Clearance now depends largely on coughing, and mucus that pools between coughs feeds bacteria, so every winter virus turns into a purulent exacerbation.

  More mucus, no escalator. Chronic bronchitis is a clinical definition — cough and sputum, not a spirometry number (airflow obstruction on spirometry is what defines COPD).

  You would find: Cough productive of sputum on most days for at least three months in each of two consecutive years. Worst on waking, after a night lying flat with no working escalator.

• Large airway obstruction with stridor← from “The trachea is held open by about 16 to 20 C-s…”

  Inside the chest, negative pleural pressure helps hold airways open on inspiration. Above the sternal notch the opposite happens: breathing in generates negative pressure inside a trachea surrounded by atmospheric pressure, sucking it narrower, and cartilage and laryngeal muscle are what resist that. Anything eating into the margin — mucosal swelling in croup, a compressing goitre or tumour, or congenitally floppy cartilage (tracheomalacia, when the floppy segment is extrathoracic; a malacic segment inside the chest collapses on expiration instead) — turns smooth flow into noisy turbulent flow. For laminar flow, resistance is inversely proportional to the fourth power of the radius, so halving the radius multiplies resistance about sixteenfold; once flow becomes turbulent the penalty for narrowing is steeper still. Either way, one millimetre of circumferential oedema takes a huge fraction of a toddler's roughly 4 mm subglottis and only a small fraction of an adult's.

  Stridor on inspiration means large or extrathoracic airway; wheeze on expiration means small intrathoracic airways. The r⁴ relationship (resistance ∝ 1/r⁴ for laminar flow, steeper still once flow is turbulent) is why the same millimetre of swelling that an adult tolerates can obstruct a small child.

  You would find: A harsh noise on breathing in, not out. Barking cough and hoarse voice at night in a one to three year old is croup; progressive stridor and a hoarse voice in an adult smoker is a tumour until proven otherwise.

What we give, and how it works

Open a drug to see what it binds, what that does to the cell, and what you then see in the patient.