Nausea and Vomiting

Nausea is an unpleasant sensation of the need to vomit

• Much of the research into vomiting is based on animal models, which has limitations for understanding the physiological basis of nausea
• Although nausea and vomiting often coincide, evidence for separate neural systems for nausea comes from:
• 5-HT₃ antagonists treat chemotherapy-induced vomiting but 50% still get nausea; vomiting is easier to treat
• Raised ICP, pregnancy and radiotherapy cause vomiting with nausea
• Although abdominal vagal afferents contribute to both nausea and vomiting, patients will still experience nausea post-bilateral vagotomy
• The sensation of nausea requires neural areas above the brainstem, where conscious sensations are formed

Vomiting is a reflexive, forceful expulsion of stomach contents from the mouth

• It is different from:
• Reflux - the retrograde passage of gastric acid up the oesophagus through the lower oesophageal sphincter
• Regurgitation - the passive passage of gastric acid past the upper oesophageal sphincter into the pharynx

• There is no anatomical 'vomiting centre'; it is considered the area of the medulla that integrates emetic signals

• The GI tract
• Toxic materials in the gut lumen triggers enterochromaffin cells to secrete paracrine intermediates (serotonin, CCK, substance P)
• Stimulation of 5-HT₃ receptors opens Na⁺ channels
• This propagates an afferent signal via the vagus nerve to nucleus tractus solitarius and then the brainstem


• The bloodstream
• Toxic materials in the bloodstream are sensed by the chemoreceptor trigger zone (CTZ) a.k.a. the area postrema, which lies on the floor of the 4^th ventricle
• The area postrema is one of the 7 circumventricular organs and functionally lies outside the BBB
• It expresses 5-HT₃, D_{2 - 4}, NK₁ and opioid receptors


• CNS stimuli
• Stimulation of the limbic system e.g. due to raised ICP, pain, fear, anxiety, CNS trauma
• Tends to cause vomiting without nausea/retching
• Exact mechanisms are unclear, although we know some e.g. use of opioid drugs, which act on mu opioid receptors in the CTZ


• Disturbances of the vestibulocochlear system
• Postulated that vestibulocochlear disturbance modulates the sensitivity of the brainstem to emetogenic stimuli
• Involves H₁ histamine and M₃ & M₅ mAChR receptors


• Visceral pathology e.g. MI, renal failure, GI tract via vagal afferents

1. Autonomic outflow from the vagus nerve, which causes:
• Gastric relaxation
• Retrograde gastric and oesophageal peristalsis


2. Corticospinal efferents, which lead to:
• Abdominal wall and intercostal muscle contraction

• Gastric relaxation and retrograde gastric peristalsis
• Deep breath elevating hyoid bone and larynx, which opens upper oesophageal sphincter

• Glottic closure and soft palate elevation to protect the nasopharynx

• Abdominal wall muscle and diaphragmatic contraction, with simultaneous relaxation of the diaphragmatic crura
• Retrograde oesophageal peristalsis
• Further dilation of upper oesophageal sphincter

→ The combination of these lead to expulsion of gastric contents

• Gastric acid ionic omposition:

• Thus in excessive fluid loss through vomiting there will be:
• Metabolic alkalosis, due to loss of H⁺
• Hypochloraemia, which further contributes to the alkalosis
• Hypokalaemia
• Dehydration/hypovolaemia from loss of water
• An associated large rise in serum bicarbonate levels


• Replacement fluid should therefore aim to correct these abnormalities e.g. with 0.9% NaCl + K⁺