Practical gastric physiology
Diana M Jolliffe BSc FRCP FRCA
The functions of the stomach are:
† temporary storage of food input;
† mechanical breakdown of food into
smaller particles;
† chemical digestion, with breakdown of
proteins;
† regulation of output of chyme into the
duodenum;
† secretion of intrinsic factor, vital for
vitamin B12 absorption.
Most anaesthetists are wary of this part of
the gastrointestinal tract because of the poten-
tial for tracheobronchial aspiration of stomach
contents. Nevertheless, we are required to
administer anaesthesia to patients with full
stomachs and an understanding of the relevant
gastric physiology can help avoid and reduce
the consequences of gastric aspiration.
For aspiration of stomach contents to occur
there must first be gastro-oesophageal reflux,
when gastric contents breach the lower oeso-
phageal sphincter (LOS). The acid material
must then flow back along the 30 cm oesopha-
gus and be regurgitated ( pass the upper oeso-
phageal sphincter) to contaminate the pharynx.
If the patient’s level of consciousness is
reduced, the normally protective gag and cough
reflexes will be obtunded and gastric contents
may then reach the tracheobronchial tree
(aspiration). Solid matter may obstruct the
airways and the acidic liquid can cause broncho-
spasm, resulting in severe hypoxia and respir-
atory failure.
Measures to reduce the
incidence and effects of
aspiration of gastric contents
(i) Minimize the amount of gastro-
oesophageal reflux, by:
(a) maintaining the tone of the LOS;
(b) reducing the gastro-oesophageal
pressure gradient;
(c) using gravity.
(ii) Reduce gastric volume.
(iii) Increase gastric emptying.
(iv) Reduce acidity of gastric contents.
doi:10.1093/bjaceaccp/mkp033
Continuing Education in Anaesthesia, Critical Care & Pain | Volume 9 Number 6 2009
& The Author [2009]. Published by Oxford University Press on behalf of the British Journal of Anaesthesia.
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Gastro-oesophageal reflux and Key points
the lower oesophageal
Gastro-oesophageal reflux
sphincter
is a normal physiological
The distal oesophagus passes through the crura of event.
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the diaphragm and joins the stomach at an acute The lower oesophageal
angle, the gastro-oesophageal junction, which sphincter (LOS) may relax
normally lies just below the diaphragmatic hiatus. spontaneously.
The LOS is formed by the intrinsic circular The barrier pressure of the
smooth muscle of the lowest 2–4 cm of the oeso- LOS is one of the defences
phagus, tonic contraction of which separates the against acid reflux.
gastric and oesophageal lumens. The LOS is a The head-up position
physiological sphincter which is normally closed discourages reflux and
with a resting pressure of 15–25 mm Hg above regurgitation.
gastric pressure (termed the barrier pressure). It
Antacids raise the pH of
relaxes on swallowing, a reflex mediated by the
stomach contents but
inhibitory neurotransmitters nitric oxide and increase gastric volume.
vasoactive intestinal polypeptide. This allows
saliva, ingested liquids, and food boluses, which
are transported from the pharynx on the oesopha-
geal peristaltic wave, to pass through into the
stomach. The LOS then regains its tone.
LOS tone was thought to be the main defence
mechanism against reflux of acidic gastric con-
tents into the lower oesophagus. It was found that
many patients with severe erosive oesophagitis
had LOS pressures below 10 mm Hg. In these
cases small increases in intra-gastric or
intra-abdominal pressure resulted in free reflux of
gastric acid into the oesophagus. Various factors
are known to alter LOS tone and may affect the
incidence of gastro-oesophageal reflux (Table 1).
However, studies in normal individuals have
since demonstrated that gastro-oesophageal reflux
is a physiological event and healthy asympto-
matic people have acid reflux sufficient to lower
the pH in the distal oesophagus to below 4 for up
to 4% of the time. It is now recognized that there
are transient, unprovoked relaxations of the LOS
which are of longer duration (10–45 s) than those
associated with swallowing (6–8 s).1 The fre-
quency of these spontaneous relaxations corre- Diana M Jolliffe BSc FRCP FRCA
lates with the severity of oesophagitis, and Consultant Anaesthetist
Department of Anaesthesia
explains how patients can have severe heartburn
Northampton General Hospital
with a normal resting LOS tone. However, the Cliftonville
severity of symptoms correlates poorly with the Northampton NN1 5BD
UK
degree of acid reflux and the presence or extent of
Tel: þ44 1604 545671/2
mucosal damage. Excessive gastro-oesophageal Fax: þ44 1604 545663
reflux also occurs in patients with disordered E-mail: diana.jolliffe@ngh.nhs.uk
oesophageal motility and those with gastric (for correspondence)
173
Practical gastric physiology

Table 1 Factors affecting LOS tone
Factors that increase LOS tone
and so make reflux less likely
Physiological
Cholinergic stimulation
Pharmacological
Anti-cholinesterases, e.g. neostigmine
Factors that decrease LOS tone
and so make reflux more likely
Swallowing
Oestrogen, progesterone
Anti-muscarinics, e.g. atropine,
laparoscopic surgery) and is associated with a higher incidence of
gastro-oesophageal reflux. The patient with gastrointestinal obstruc-
tion develops distension of the gut proximal to the obstruction due
to sequestration of fluid and gas. It may be possible to lessen this by
inserting and intermittently aspirating a large-bore nasogastric tube
which will help to decompress the gut and relieve the raised
intra-abdominal pressure. The patient will be more comfortable if
they are allowed to sit propped up with their hips and knees flexed
as this reduces the tension in their abdominal wall muscles.

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glycopyrrolate
D2 antagonists, e.g. metoclopramide, Dopamine
prochlorperazine, domperidone
Cyclizine Opioids
Succinylcholine Thiopental
Pathological
Alcohol
dysmotility. Therefore, LOS tone is probably only part of the defence
against acid reflux and two other mechanisms may contribute:
(i) the acute angle at which the oesophagus enters the stomach
may help seal the gastro-oesophageal junction.
(ii) the muscle fibres around the diaphragmatic hiatus may reinforce
LOS function, helping to prevent reflux into the oesophagus,
particularly when intra-abdominal pressure is raised.
Gastro-oesophageal reflux increases in those with a sliding
hiatus hernia (when the upper part of the stomach passes through
the diaphragmatic hiatus into the thorax). In this situation the angle
of the gastro-oesophageal junction is straightened out, there is no
diaphragmatic contribution to sphincter function and increases in
intra-abdominal pressure are transmitted to the stomach. The dis-
torted gastro-oesophageal junction now lies above the diaphragm
within the thorax at low pressure, and stomach contents tend to be
forced through the LOS (unreinforced by the diaphragmatic fibres)
into the lower oesophagus.
Gastro-oesophageal pressure gradient
If intra-gastric or intra-abdominal pressure (which is transmitted to
the stomach) is elevated there will be an increased pressure gradi-
ent across the LOS increasing the chance of gastro-oesophageal
reflux occurring.
The stomach converts the episodic input of food from the
oesophagus into a more continuous output of chyme into the duo-
denum. The fundus and body (the proximal stomach) act as a
reservoir and their relatively thin, highly distensible smooth
muscle layers relax as the stomach expands. It might be anticipated
that as the stomach filled the intra-gastric pressure would increase,
but there is little increase in intra-gastric pressure until gastric
volume exceeds a litre. This accommodation results from a vagal
reflex initiated by stretch receptors in the oesophagus (‘receptive
relaxation’) and as a consequence of the presence of food in the
proximal stomach (‘adaptive relaxation’).2
Intra-abdominal pressure is increased in various situations
(including obesity, pregnancy, intestinal obstruction, and during
Gastro-oesophageal reflux and gravity
Both reflux and regurgitation are passive processes which are influ-
enced by gravity and so are less likely to occur if the patient is
semi-recumbent rather than supine. For mechanically ventilated
patients the time spent supine is a critical factor associated with
aspiration.3 Elevation of the head of the patient’s bed is included in
the Institute for Healthcare Improvement’s ventilator care bundle for
reducing the high mortality of ventilator-acquired pneumonia.4
Cricoid pressure is used during induction of anaesthesia in the
patient with a potentially full stomach. This manoeuvre uses external
pressure to compress the oesophagus against the cervical body of C6
and so discourages regurgitation of stomach contents through the
upper oesophageal sphincter. This anatomical sphincter comprises
the inferior pharyngeal constrictor muscle (the cricopharyngeus)
which lies at the level of C5 and C6. Cricoid pressure is effective in
reducing regurgitation even if a nasogastric tube is present.5
Gastric volume
The volume of the stomach is determined by:
† the amount of food and drink ingested;
† the volume of gastric juice produced;
† the rate at which the stomach empties.
Gastric volume is reduced by keeping a patient ‘nil by mouth’
not only because input is omitted but also because less gastric
juice is secreted. Gastric juice is produced in response to eating.
Normally the stomach produces about 2 litres a day but during
fasting there is little or no secretion. It consists of hydrochloric
acid, intrinsic factor, pepsinogens, and mucus (the secretions of the
gastric gland cells, Table 2) and also contains water and electro-
lytes, particularly Kþ and Cl2. It has a pH of 1–1.5.
Physical methods may be used to empty the stomach: a large-
bore nasogastric tube may be inserted and aspirated occasionally but
otherwise allowed to drain freely. Emetic agents are no longer used.
Gastric emptying
For the stomach to empty, the pressure generated by the antral pump
must exceed the resistance of the pyloric sphincter. In general, emp-
tying occurs at an exponential rate proportional to the volume of the
stomach, that is, the fuller the stomach, the more rapidly it empties
(Table 3). This is mediated by vagal excitatory reflexes (provoked
by gastric distension). Gastrin is also released in response to antral

174 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 9 Number 6 2009
 Practical gastric physiology

Table 2 Secretions of gastric gland cells

Released from Release stimulated by Release inhibited by Function

HCl 0.15 M Parietal cells, mainly in the Gastrin Acidity Facilitates breakdown of protein
fundus and body of the stomach ACh Anti-muscarinics Activates pepsinogens and provides optimal
Vagal stimulation Vagotomy conditions for pepsin activity
Distension of body of Somatostatin Improves solubility and hence absorption of
stomach (vagal reflex) Prostaglandin E2 calcium and iron
Histamine (H2 receptors) H2 receptor antagonists Kills pathogenic micro-organisms
PPIs

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Pepsin Chief cells, mainly in the body of Vagal stimulation A proteolytic enzyme, stored as inactive
the stomach ACh pepsinogens, which facilitates protein digestion
Acid pH
Secretin (from the duodenum)

Intrinsic Parietal cells, mainly in the Same factors that stimulate This glycoprotein binds ingested B12 (cobalamin)
factor fundus of the stomach release of gastric acid in the stomach, protecting it from enzymatic
destruction. The complex is absorbed in the
terminal ileum

Mucus Mucus cells Vagal stimulation Forms a layer protecting the mucosa from
Prostaglandins E2 and I2 mechanical trauma and digestion by gastric acid
and proteolytic enzymes

Table 3 Factors affecting gastric emptying duodenum, and also reduces gastric emptying. If the chyme has too
high a content of amino acids, gastrin is released. This increases con-
Factors that increase gastric emptying Factors that delay gastric emptying
and so make reflux less likely and so make reflux more likely traction of the pyloric sphincter (as well as increasing gastric motility)
and overall delays gastric emptying. Hypertonic chyme is detected by
Physiological duodenal osmoreceptors and gastric emptying is slowed.
Stomach distension Duodenal distension As the duodenum fills, stretch receptors are activated and
Liquid content Chyme high in Hþ, fat, or protein inhibit the vagus which results in reduced gut tone and motility,
Smaller particles Secretin
Parasympathetic stimulation Pain, anxiety, stress temporarily reducing gastric emptying. As the duodenum empties
Sympathetic stimulation this inhibition diminishes, the tone and motility of the gut
Pharmacological increases, and gastric emptying is restored. The neural and hormo-
Anti-cholinesterases, e.g. Anti-muscarinics, e.g. atropine, nal mechanisms which originate from the duodenum and feedback
neostigmine glycopyrrolate to slow gastric emptying constitute the entero-gastric reflex.6 By
Metoclopramide Opioids
Domperidone regulating the rate of delivery of chyme into the duodenum, the
Erythromycin absorption of nutrients in the small intestine is maximized.
Pathological Alcohol and opioids reduce the rate of gastric empting, as do
Alcohol pain, fear, and anxiety (acting via the sympathetic nervous system
Pyloric stenosis which inhibits motility). It is now recognized that pregnancy per se
Intestinal obstruction does not alter gastric empting. However, during labour there is
Previous vagotomy
delay because of pain, anxiety, and administration of opioids.
Prokinetic drugs may be used to stimulate enteral propulsion if
distension, and both these stimuli produce an increase in antral there is no gastrointestinal obstruction, perforation, or haemor-
pump activity. The speed of emptying for liquids, or contents con- rhage. Metoclopramide is a centrally and peripherally acting dopa-
sisting of smaller particles, is faster than for solids. Thus, in the minergic D2 antagonist which increases the rate of gastric
normal stomach, 95% of an ingested clear liquid reaches the duode- emptying and small intestinal transit, and also increases LOS
num within 1 h and 50% of a meal will pass the pylorus in 2 h. constriction. It can be given i.v., i.m., or orally, in a dose of 10 mg
The chemical composition of the chyme entering the duodenum 8 hourly, but is most effective i.v. Its use may be limited by
also affects the rate of gastric emptying and various hormones are adverse effects which include extra-pyramidal effects, tardive
involved (Table 4). If the chyme is too acidic, secretin is released dyskinesia, and hyperprolactinaemia. Domperidone has similar
which slows gastric emptying, reduces the production of gastric acid, pharmacological actions and is better tolerated but can only be
and increases the secretion of alkaline pancreatic juice into the duode- given orally or rectally.
num. If the fat content of the chyme is too high, cholecystokinin The macrolide antibiotic erythromycin has prokinetic properties
(CCK) is released. CCK stimulates contraction of the gall bladder so and may produce abdominal cramps, nausea, and vomiting. It is an
that bile salts (which emulsify the fats) are secreted into the agonist at motilin receptors, stimulating strong antral contractions.

Continuing Education in Anaesthesia, Critical Care & Pain j Volume 9 Number 6 2009 175
Practical gastric physiology

Table 4 Gastric hormones

Released from Release stimulated by Release inhibited by Function

Gastrin G cells in the stomach antrum and Vagal stimulation Gastric acidity Stimulates gastric acid production
duodenum Distension of gastric antrum Somatostatin Increases secretion of pepsinogens
Distension of duodenum Secretin (stimulated by Increases secretion of mucus
Amino acids and peptides duodenal acidity) Increases gastric motility
Alcohol Glucagon Constricts pyloric sphincter
Caffeine Reduces gastric emptying

Secretin S cells in the duodenum and jejunum Increased acidity in duodenal chyme Reduces gastric acid secretion

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Reduces gastric emptying
Increases pancreatic secretions

CCK I cells in the duodenum and jejunum Increased fat in duodenal chyme Reduces gastric acid secretion
Reduces gastric emptying
Contracts gall bladder

Somatostatin D cells in the stomach Gastric acidity Vagal stimulation Inhibits gastrin secretion (and thereby
gastric acid production)
Reduces gastric motility
Reduces gastric emptying

Motilin Entero-chromaffin-like cells in Increases gastric motility

proximal small intestine Increases gastric emptying
Associated with the inter-digestive
migratory motor complex (MMC)

Gastric contents Illustrative clinical example

The morbidity of acid aspiration syndrome correlates with the
volume, acidity, and the particulate nature of the material intro- Suggested management of the patient with a potentially full
duced into the lungs. Therefore, reducing the size of the particles stomach who requires a general anaesthetic
and the acidity of the contents of the stomach will result in less
severe pulmonary damage if aspiration occurs. Before operation:
Parietal cell production of gastric acid is stimulated by various Position the patient with head-up tilt and knees flexed
factors (Table 2). Inhibition of gastric acid secretion will also Insert large-bore nasogastric tube and aspirate
reduce the volume of the stomach’s contents. Leave nasogastric tube on free drainage
Anti-muscarinic agents block acetylcholine (ACh) release from Keep ‘nil by mouth’
vagal postganglionic fibres and reduce gastric acidity. However, they Give ranitidine 50 mg by slow i.v. injection
are not used in practice because they also reduce LOS tone and delay Give metoclopramide 10 mg i.v. if no gastrointestinal
gastric emptying, thereby increasing the risk of gastro-oesophageal obstruction, perforation, or haemorrhage
reflux. H2 receptor antagonists reduce gastric acid secretion and both
cimetidine and ranitidine may be given i.v. Ranitidine is preferred At induction of anaesthesia:
because it has a longer duration of action and fewer drug interactions. Aspirate nasogastric tube
Proton pump inhibitors (PPIs) irreversibly block the Hþ/Kþ ATPase Give sodium citrate 0.3 M (30 ml) orally
enzyme which catalyses the exchange of intracellular Hþ for extra- Check patient positioned with head-up tilt
cellular Kþ, the final step in the production of gastric acid by the par- Pre-oxygenate
ietal cells. With repeated doses PPIs are highly effective at producing Apply cricoid pressure
achlorhydria. Omeprazole 40 mg may be given i.v. but as a single Induce anaesthesia with a rapid sequence induction
preoperative dose has no advantage over H2 receptor antagonists. Intubate with a cuffed oro-tracheal tube to secure the airway
Oral antacids are given to raise the pH of the stomach’s con- Peroperatively:
tents by neutralizing gastric acid, but they increase gastric volume. Maintain head-up position if possible
Sodium citrate 0.3 M is used as it is non-particulate so causes less
Avoid increases in abdominal pressure
pulmonary damage if aspirated. 30 ml will neutralize the gastric
Ensure adequate depth of anaesthesia
contents within 10 min.
Using their knowledge of the relevant gastric physiology, the After operation:
anaesthetist can reduce the incidence and consequences of gastric Extubate in the left lateral position
aspiration when required to administer general anaesthesia to a Extubate when awake and gag and cough reflexes are present
patient with a full stomach, gastro-oesophageal reflux, and/or
obtunded airway reflexes.

176 Continuing Education in Anaesthesia, Critical Care & Pain j Volume 9 Number 6 2009

References
1. Holloway RH, Penagini R, Ireland AC. Criteria for objective definition of
transient lower esophageal sphincter relaxation. Am J Physiol Gastrointest
Liver Physiol 1995; 268: G128– 33
2. Petersen OH. Lecture Notes: Human Physiology, 5th Edn. Oxford:
Blackwell Publishing Ltd, 2007
3. Torres A, Serra-Batlles J, Ros E, Piera C, Puig de la Bellacasa J, Cobos A.
Pulmonary aspiration of gastric contents in patients receiving mechanical
ventilation: the effect of body position. Ann Intern Med 1992; 116: 540–3
Continuing Education in Anaesthesia, Critical Care & Pain j Volume 9 Number 6 2009
Practical gastric physiology
4. Available from www.ihi.org/IHI/Topics/CriticalCare/IntensiveCare/Changes/
ImplementtheVentilatorBundle. Accessed February 20, 2009
5. Aitkenhead AR, Smith G, Rowbotham DJ. Textbook of Anaesthesia,
5th Edn. Elsevier, 2007: Chapter 28, p. 544
6. Pocock G, Richards CD. The storage, mixing, and propulsion of gastric
contents. Human Physiology: The Basis of Medicine, 2nd Edn. Oxford:
Oxford University Press, 2004; 437– 40
Please see multiple choice questions 1– 3
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