Vomiting

Describe the neural integration of vomiting, highlighting the site and mechanism of action of antiemetics

Vomiting is the involuntary, forceful expulsion of gastrointestinal contents through the mouth. It is the product of a complex, coordinated reflex involving central and peripheral neural pathways.

Sensory inputs

Vomiting is initiated by afferent signals from multiple sources converging on central emetic pathways:

  1. Cerebral Cortex

    • Stimuli: pain, smell, sight, emotional stress.
    • Directly activates the vomiting centre.
  2. Chemoreceptor trigger zone (CTZ)

    • Located within the area postrema on the floor of the 4th ventricle.
    • Lies outside the blood–brain barrier and can therefore respond to drugs or toxins present in systemic circulation.
    • Has a high density of D₂ (dopamine), 5-HT₃ (serotonin) and opioid receptors.
    • Relays signals to the vomiting centre
  3. Vestibular System (Inner Ear)

    • Triggered by rhythmic motion (motion sickness).
    • Mediated via acetylcholine (ACh) and histamine H1 receptors
    • Pathway: Vestibular labyrinth → CN VIII → vestibular nuclei → CTZ → vomiting centre
  4. Gastrointestinal Tract

    • Stretch (mechanoreceptors) and chemoreceptors activate 5-HT₃ receptors.
    • Afferent signals transmitted via vagal and sympathetic nerves.
    • Signals converge on the nucleus tractus solitarius (NTS), rich in ACh and H1 receptors.
    • The NTS sends signals to the vomiting centre.
  5. Pharynx

    • Mechanical stimulation of glossopharyngeal touch receptors can trigger vomiting.
    • Afferent pathway via glossopharyngeal nerve (CN IX) to the NTS.

Central integration

  • The vomiting centre is located in the lateral medulla and is rich in acetylcholine (ACh) receptors.
  • It integrates all incoming signals to coordinate the emetic response.
  • Efferent output is mediated via cranial nerves (V, VII, IX, X and XII) and spinal motor nerves.

Effector pathways

  1. Pre-ejection

    • Retrograde peristalsis (antiperistalsis)
      • Intestinal contents propelled proximally into the stomach
    • Characterised by nausea and salivation.
  2. Retching

    • Lower oesophageal sphincter relaxes.
    • Deep inspiration with closure of the glottis and nasopharynx.
      • Prevents aspiration and nasal regurgitation.
  3. Expulsion

    • Forceful contraction of pylorus and thoracic and abdominal muscles with descent of the diaphragm.
    • Results in rapid expulsion of gastric contents.
Vomiting - a sprint to the finish

It's helpful to think about vomiting like the start of a 100m sprint!

On your marks

  • The gut gets everything into position with retrograde peristalsis.
  • Other 'preparatory' activities like nausea and salivation take place.

Get set

  • Opening of the lower oesophageal sphincter and closure of the glottis and nasopharynx set the course for the impending vomit.

Go!

  • Rapid, forceful muscle contraction sends the vomitus on its way.

Site and mechanism of action of antiemetics

Class

Primary Site of Action

Drug Examples

H1 antagonists

Vestibular nucleus, NTS

Cyclizine, Promethazine, Prochlorperazine

Anticholinergics

Vestibular nucleus, NTS, vomiting centre

Promethazine, Prochlorperazine, Hyoscine (scopolamine)

D2 antagonists

Chemoreceptor trigger zone (CTZ)

Metoclopramide, Droperidol, Prochlorperazine

5-HT3 antagonists

CTZ, gastrointestinal tract (vagal afferents)

Ondansetron

Other / adjuncts

Central nervous system (various)

Dexamethasone, Propofol, Benzodiazepines, Pyridoxine