Competence is a subtraction
and it can be lost with the tone unchanged.

1. Three phases, one voluntary. Oral (voluntary), pharyngeal (involuntary), oesophageal (involuntary). The reflex is coordinated in the swallowing centre of the medulla; afferents arrive by the glossopharyngeal and vagus nerves and efferents leave by the nucleus ambiguus.
2. The airway is closed, not merely covered. The vocal cords adduct, the aryepiglottic folds close, the larynx is pulled up and forward under the tongue base, and only then does the epiglottis tilt over the inlet. Breathing stops for 1 to 2 seconds.
3. Two sphincters, and only one is anatomical. The upper is cricopharyngeus, a named skeletal muscle. The lower has no discrete muscle to dissect and is identified by a high-pressure zone on manometry, which is what “physiological sphincter” means.
4. Two muscular components, two different nerves. Intrinsic oesophageal smooth muscle on the vagus, and the crural diaphragm on the phrenic. An answer naming one has described half the sphincter.
5. Barrier pressure = sphincter pressure − intragastric pressure. About 15 to 25 mmHg. Competence is the difference, so it falls either because the sphincter weakens or because the stomach pushes harder.
6. Transient relaxations are normal. Vagally mediated, unrelated to swallowing, triggered by fundal distension, and the route by which most physiological reflux occurs. They are the dominant mechanism of reflux in obesity, not a low resting tone.

The commonest wrong answer here is “the epiglottis covers the larynx”, as though that were the mechanism rather than the last step of it. Patients whose epiglottis has been removed can still swallow safely. What actually protects the airway is a sequence, and it works from the inside out.

1. The vocal cords adduct, closing the glottis. Lateral cricoarytenoid, and the oblique and transverse arytenoids, all supplied by the recurrent laryngeal nerve.
2. The aryepiglottic folds adduct, closing the laryngeal inlet above the cords. A second seal, above the first.
3. The larynx and hyoid are pulled upwards and forwards, by the digastric and stylohyoid. This tucks the laryngeal inlet under the base of the tongue and out of the bolus’s path, and it simultaneously opens the upper oesophageal sphincter by traction.
4. The epiglottis tilts down over the inlet, deflecting the bolus laterally into the piriform fossae. This is a diversion, not a lid.
5. Respiration is inhibited for 1 to 2 seconds. Deglutition apnoea is brief enough to go unnoticed, and it means that no inspiratory effort can draw the bolus towards the cords at the moment they are most exposed.

Two velocities are worth carrying because they explain why the pharyngeal phase feels instantaneous and the oesophageal phase does not. The bolus crosses the pharynx at about 30 cm/s and the oesophagus at about 3 cm/s. Gravity moves fluids faster than this in the upright position, which is why a drink reaches the stomach before the peristaltic wave does, and why swallowing works upside down but more slowly.

The upper oesophageal sphincter is cricopharyngeus, the lowest and most horizontal part of the inferior constrictor, reinforced by the inferior constrictor proper and the circular muscle of the upper oesophagus. It lies at the level of the cricoid cartilage. It is skeletal muscle, so it is an anatomical sphincter in a way the lower one is not: you can find it, name it and dissect it.

Its job is bidirectional. It stops air entering the oesophagus during inspiration, and it stops oesophageal contents entering the pharynx. It relaxes during the pharyngeal phase — partly by active inhibition, partly by the traction of laryngeal elevation — and then contracts behind the bolus. Because it is skeletal muscle it has tone only while the patient is awake: it relaxes in sleep and under anaesthesia, which is why regurgitated material that reaches the oesophagus of an anaesthetised patient meets no upper barrier at all.

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A coronal section through the gastro-oesophageal junction. The oesophagus descends from the top, passing through the oesophageal hiatus in the diaphragm, where the right crus is shown encircling it as a sling. The phreno-oesophageal ligament is drawn anchoring the oesophagus to the diaphragm. Below the hiatus, the intra-abdominal segment of oesophagus enters the stomach at the angle of His, an acute angle between the oesophagus and the gastric fundus, with the mucosal rosette at the junction itself. A blue arrow within the lumen points downwards, labelled lower oesophageal sphincter pressure; a red arrow rising from the gastric lumen points upwards, labelled intragastric pressure. An inset panel at upper right shows the mucosal rosette in cross-section as radiating folds occluding the lumen.

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The five-component list matters more than any single one of them, because it is what makes a hiatus hernia intelligible. A hiatus hernia removes three of the five at once: the intrinsic sphincter is displaced above the hiatus so it no longer acts at the same level as the crus, the intra-abdominal segment is lost, and the angle of His is straightened. The muscle itself may be entirely normal.

A swallow-related relaxation is a different event. The sphincter relaxes 1 to 2 seconds after the swallow begins, stays relaxed for 8 to 9 seconds, and then contracts 1 to 15 mmHg above its resting tone for 10 to 15 seconds before settling. Both relaxations are mediated by the same transmitters: nitric oxide and vasoactive intestinal peptide, released from the inhibitory non-adrenergic non-cholinergic neurones of the myenteric plexus.

Resting tone is largely myogenic: the muscle maintains a contractile state independent of neural input, and increases it when stretched. Everything below modulates that baseline. The five groups are the structure of the answer, and giving both directions within each group matters more than the length of any one list.

Stated as absolute pressures, the sphincter sits at about 20 to 30 mmHg against an intragastric pressure of about 5 to 10 mmHg, and the two framings agree once the subtraction is done. Lead with the difference: it is the quantity that determines whether anything moves, and one published source gives two different absolute ranges for the sphincter two pages apart, which is on its own a reason not to quote an absolute as though it were settled.

Everybody refluxes. Physiological reflux occurs mainly during transient sphincter relaxations, and it is cleared by three mechanisms: secondary peristalsis, which strips the refluxate back into the stomach; gravity, in the upright position; and swallowed saliva, whose bicarbonate neutralises what is left. All three fail at night, in the supine position, which is why symptoms are nocturnal and why smoking — which reduces both sphincter tone and salivary bicarbonate — makes reflux disease worse by two mechanisms at once.

The pattern is otherwise consistent and unhelpful. Volatile agents, propofol, thiopentone, opioids and anticholinergics all reduce tone, and they do it at exactly the moment the airway reflexes of section 03 are being abolished. Positioning works the same way: the supine position removes the gravitational assistance that keeps gastric contents below the junction, and lithotomy and head-down positioning raise intra-abdominal pressure on top of that. A head-up induction is protective on both counts.