Vomiting and its control !

Regulation
Exam priority: medium

Vomiting is a protective brainstem reflex that expels stomach contents; losing a lot of acid upsets the electrolytes.

Updated 2026-11-01

Also called: Emesis, Chemoreceptor trigger zone

See it in 3D: Medulla oblongata · Fourth ventricle · Vagus nerve · Stomach · Diaphragm · Esophagus

Key points

Chemoreceptor trigger zone: area postrema, in the floor of the fourth ventricle, with no blood–brain barrier; it senses drugs and toxins in blood (D2, 5-HT3, NK1, opioid receptors).
Vagal route: serotonin from enterochromaffin cells (chemotherapy, radiation, infection) activates 5-HT3 receptors on vagal afferents.
Vestibular route (motion sickness): H1 and muscarinic receptors.
Sequence: nausea → deep breath → glottis closes and palate rises → diaphragm and abdominal wall contract while the esophageal sphincters relax.
HCl loss → metabolic alkalosis; hypovolemia activates aldosterone → renal K⁺ and H⁺ loss; urine Cl⁻ is low (< 20 mEq/L), a 'chloride-responsive' alkalosis.
Mechanical complications: Mallory–Weiss tear (mucosa) and Boerhaave syndrome (esophageal perforation).

What it is

Vomiting is a motor programme coordinated by neurons in the medulla (nucleus of the solitary tract and the nearby reticular formation). It takes input from the gut via the vagus, from the chemoreceptor trigger zone in the area postrema (outside the blood–brain barrier), from the vestibular system and from the cortex. Its classic metabolic consequence is hypochloremic, hypokalemic metabolic alkalosis.

How it works, step by step

A signal from the trigger zone, vagus, vestibule or cortex activates the vomiting generator in the medulla.
Nausea appears, with salivation, sweating, pallor and tachycardia (autonomic discharge).
A retrograde contraction carries small-bowel contents back into the stomach.
A deep breath is taken, the glottis closes and the soft palate seals the nasopharynx to protect the airway.
The diaphragm and abdominal muscles squeeze the stomach while the esophageal sphincters relax: contents are expelled.
Repeated loss of gastric juice leaves HCO₃⁻ unmatched (an un-neutralized alkaline tide) and contracts extracellular volume.

Regulation

+Chemoreceptor trigger zone (D2, 5-HT3, NK1): Opioids, digoxin, chemotherapy, uremia and toxins activate the vomiting centre
+Vagal afferents (5-HT3): Gut irritation or distension and mucosal serotonin trigger the reflex
+Vestibular system (H1, M1): Motion and Ménière disease
+Cortex and limbic system: Smells, sights, severe pain, anxiety, anticipatory nausea

Clinical notes

Pyloric stenosis, high bowel obstruction or prolonged vomiting: metabolic alkalosis with hypochloremia and hypokalemia.
Bilious vomiting in a newborn: obstruction below the ampulla (malrotation with volvulus) until proven otherwise.
Vomiting with headache and papilledema: think of raised intracranial pressure, which stimulates the vomiting centre directly.
Antiemetics act on these receptors: D2, 5-HT3, NK1 and H1 antagonists and antimuscarinics.

Test yourself

Think of the answer, then tap the question to see it.

Why can the chemoreceptor trigger zone detect drugs and toxins in the blood?

It lies in the area postrema, in the floor of the fourth ventricle, one of the regions without a blood–brain barrier; its neurons are directly exposed to what circulates in plasma.

Why does prolonged vomiting cause hypokalemia when gastric juice holds little potassium?

Hypovolemia activates aldosterone, and excess filtered HCO₃⁻ carries Na⁺ to the distal tubule; both increase renal K⁺ secretion, which is the main loss.

Which pathway explains the severe nausea caused by chemotherapy?

Chemotherapy damages the mucosa and releases serotonin from enterochromaffin cells, which activates 5-HT3 receptors on vagal afferents and in the trigger zone.

In metabolic alkalosis from vomiting, what urine chloride is expected and why?

Low (< 20 mEq/L). With hypovolemia and little chloride, the kidney avidly retains Na⁺ and Cl⁻, which is why the alkalosis improves when volume is replaced with chloride.

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See it in 3D

The structures of Durgical's 3D anatomy where it happens.

In Pharmacology

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Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.

Sources: 23.4 The Stomach (OpenStax (Rice University), 2022); Alkalosis: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2024); Pyloric Stenosis (StatPearls (NCBI Bookshelf), 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 67). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).

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Representative model, for educational purposes only.