The Physiological Process of Vomiting
Vomiting is a coordinated multistep reflex controlled by the brainstem that results from afferent impulses to the vomiting center in the medulla from the chemoreceptor trigger zone, gastrointestinal tract via vagal fibers, pharynx, and cerebral cortex, followed by efferent signals to the salivation center, abdominal muscles, respiratory center, and cranial nerves to forcefully expel gastric contents. 1
Neural Control Architecture
The vomiting center is located in the medulla between the obex and retrofacial nucleus, extending from the nucleus of the solitary tract through the lateral tegmental field of the reticular formation to the ventrolateral medulla 2. The central pattern generator that hierarchically organizes all three digestive tract correlates of vomiting may be located in the Bötzinger nucleus of the brainstem 3.
Afferent Pathways (Triggers)
The vomiting center receives input from four primary sources 1:
- Chemoreceptor trigger zone (CTZ) in the area postrema, which detects circulating toxins, drugs, and metabolites in the blood 1
- Gastrointestinal tract via vagal afferent fibers, responding to mucosal irritation, distension, or inflammation 1
- Pharynx through direct neural connections 1
- Cerebral cortex mediating psychological triggers, anticipatory responses, and the subjective sensation of nausea 1, 2
Neurotransmitter Systems
Multiple neurotransmitter receptors are distributed throughout the chemoreceptor trigger zone, vomiting center, and gastrointestinal tract 1:
- Primary receptors: Serotonin (5-HT3) and dopamine receptors are the principal neuroreceptors involved in the emetic response 1
- Secondary receptors: Acetylcholine, corticosteroid, histamine, cannabinoid, opiate, and neurokinin-1 (NK-1) receptors located in the vomiting and vestibular centers 1
Activation of these receptors by chemotherapeutic agents, toxins, or their metabolites triggers the emetic cascade 1. Antiemetic agents work by blocking different neuronal pathways at various points during the emetic response, though no single agent provides complete protection since no final common pathway has been identified 1.
Efferent Pathways (Motor Response)
When the vomiting center is activated, efferent impulses are transmitted to 1:
- Salivation center: Produces increased saliva (ptyalism) as a prodromal sign 4
- Abdominal muscles: Contract forcefully to generate expulsive pressure 1
- Respiratory center: Coordinates closure of the glottis and respiratory muscle activity 1
- Cranial nerves: Orchestrate pharyngeal, esophageal, and gastric motor responses 1
Three-Phase Digestive Tract Response
The actual vomiting process involves three independently organized but hierarchically coordinated digestive tract correlates 3:
Phase 1: Preparatory Relaxation and Contraction
- Upper stomach relaxation allows gastroesophageal reflux 3
- Lower pharyngeal contraction prevents supra-esophageal reflux and aspiration 3
- Both responses persist throughout the entire vomiting episode 3
Phase 2: Retrograde Giant Contraction
- Empties the proximal digestive tract of noxious contents 3
- Supplies the stomach with intestinal fluids to neutralize gastric acid, protecting the esophagus from damage during expulsion 3
Phase 3: Retching and Expulsion
- Retching mixes gastric contents with acid neutralizer and provides momentum to the expelled bolus 3
- Expulsion involves maximal longitudinal esophageal stretching that stiffens the esophageal wall for rapid transport as suprahyoid muscles and diaphragmatic dome contract while hiatal fibers relax 3
Prodromal Signs
Clinical manifestations preceding vomiting include 4:
- Ptyalism (excessive salivation)
- Tachycardia
- Depression or behavioral changes
- Hiding behavior
- Yawning
Nausea vs. Vomiting
Nausea and vomiting are related but may occur via different mechanisms 1. Nausea is a subjective sensation thought to involve the cerebral cortex and is more difficult to control than vomiting itself 1, 2. Patients receiving effective antiemetic regimens often experience more nausea than vomiting, with younger patients and women being particularly susceptible 1.
Clinical Relevance in Gastrointestinal Disorders
In patients with gastrointestinal disorders, the area postrema may be activated to inhibit orthograde digestive tract motility and reflux-blocking reflexes that would interfere with the anterograde movement that is the basic purpose of vomiting 3. Common initiating causes include gastritis, gastrointestinal ulceration, pancreatitis, uremia, and drug administration 4.