Esophagus

In adults, the esophagus is approximately 25 cm long and the esophagogastric junction is approximately 40 cm from the incisor teeth. In humans, the proximal one-third of the esophagus is composed of striated muscle, but the distal end contains only smooth muscle. Muscular sphincters at both ends are normally closed. The cricopharyngeal or upper esophageal sphincter prevents the entry of air into the esophagus during respiration, and the gastroesophageal or lower esophageal sphincter prevents the reflux of gastric contents. The lower esophageal sphincter is characterized anatomically and manometrically as a 3-cm zone of specialized muscle that maintains tonic activity. The end-expiratory pressure in the sphincter is 8 to 20 mm Hg above the end-expiratory gastric pressure. The lower esophageal sphincter is kept in place by the phrenoesophageal ligament, which inserts into the esophagus approximately 3 cm above the diaphragmatic opening ( Fig. 28.2 ). The lower esophageal sphincter is not always closed; transient relaxations occur that account for the gastroesophageal reflux that healthy subjects experience.

The stomach and its relationship to the diaphragm in nonpregnancy (left) and pregnancy (right) . The stomach consists of a fundus, body, antrum, and pylorus. The function of the lower esophageal sphincter depends on the chronic contraction of circular muscle fibers, the wrapping of the esophagus by the crus of the diaphragm at the esophageal hiatus, and the length of the esophagus exposed to intra-abdominal pressure. The gravid uterus may encroach on the stomach and alter the effectiveness of the lower esophageal sphincter.

(Illustration by Naveen Nathan, MD, Northwestern University Feinberg School of Medicine, Chicago, IL.)

Gastrointestinal Motility

Differences in fasting and fed patterns of gut motility are firmly established. During fasting, the main component of peristalsis is the migrating motor complex (MMC). Each MMC cycle lasts 90 to 120 minutes and comprises four phases: Phase I has little or no electrical spike activity and thus no measurable contractions; phase II has intermittent spike activity; phase III has spikes of large amplitude and is associated with strong contractile activity; and phase IV is a brief period of intermittent activity leading back to phase I. The MMC first appears in the lower esophageal sphincter and stomach, followed by the duodenum, and finally the terminal ileum, at which time a new cycle begins in the lower esophageal sphincter and stomach. The phase of the MMC at the time of administration of certain drugs can affect absorption and thereby the onset of therapeutic effect. Eating abolishes the MMC and induces a pattern of intermittent spike activity that appears similar to that in phase II. The duration of the fed pattern is determined both by the calorie content and the type of nutrients in the meal.

The stomach, through the processes of receptive relaxation and gastric accommodation, can accept 1.0 to 1.5 L of food before intragastric pressure begins to increase. The contraction waves that propel food into the small intestine begin in the antrum. The pylorus closes midway through the contraction wave, allowing some fluid to exit into the duodenum but causing the remaining fluid to move retrograde toward the body of the stomach. The jet of fluid that exits the pylorus contains primarily liquid and fine particles. Large particles that lag behind are caught in the retrograde flow of fluid, which assists in their disintegration. Therefore, the manner by which individual components of a meal pass through the stomach depends on the particle size and the viscosity of the suspension. Small particles and fluids exit the stomach faster than larger particles. The outlet of the stomach—the pylorus—limits outflow by means of both its chronic tone and its anatomic position. The pylorus is higher than the most dependent portion of the stomach in both the supine and standing positions.

Gastric Secretion

In one day, the stomach produces as much as 1500 mL of highly acidic fluid containing the proteolytic enzyme pepsin. Normal individuals can produce a peak acid output of 38 mmol/h. Acid is secreted at a low basal rate of approximately 10% of maximal output, even when the stomach is empty. There is diurnal variation in this basal rate of gastric acid secretion, with the lowest and highest outputs occurring in the morning and evening, respectively.

The stomach lining has two types of glands: pyloric and oxyntic. The pyloric glands contain chief cells, which secrete pepsinogen, the precursor for pepsin. The oxyntic glands contain the oxyntic cells, which secrete hydrochloric acid. Water molecules and carbon dioxide in the oxyntic cells combine to form carbonic acid, which dissociates into hydrogen ions and bicarbonate. The bicarbonate leaves the cell for the bloodstream, and the hydrogen ions are actively exchanged for potassium ions in the canaliculi connecting with the lumen of the oxyntic gland. The secretions of the oxyntic cell can contain a hydrochloric acid concentration as great as 160 mmol/L (pH 0.8). Proton-pump inhibitors (PPIs) block the hydrogen ion pump on the canaliculi to decrease acid production.

The pylorus contains G cells, which secrete gastrin into the bloodstream when stimulated by the vagus nerve, stomach distention, tactile stimuli, or chemical stimuli (e.g., amino acids, certain peptides). Gastrin binds to gastrin receptors on the oxyntic cell to stimulate the secretion of hydrochloric acid. Acetylcholine binds to muscarinic (M ₁ ) receptors on the oxyntic cell to cause an increase in intracellular calcium ion concentration, which results in hydrochloric acid secretion. Histamine potentiates the effects of both acetylcholine and gastrin by combining with H ₂ receptors on the oxyntic cell to increase the intracellular cyclic adenosine monophosphate concentration, leading to a dramatic increase in the production of acid. H ₂ -receptor antagonists (e.g., ranitidine, famotidine) prevent histamine’s potentiation of acid production ( Fig. 28.3 ).

The oxyntic cell produces hydrogen ions that are secreted into the gastric lumen and bicarbonate ions that are secreted into the bloodstream. H ₂ -receptor antagonists (e.g., ranitidine, famotidine) and proton-pump inhibitors (e.g., omeprazole) act on the oxyntic cell to reduce gastric acid secretion. H ₂ -receptor antagonists block the histamine receptor on the basal membrane to decrease hydrogen ion production in the oxyntic cell. Omeprazole blocks the active transport of the hydrogen ions into the gastric lumen. ACh, acetylcholine; ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate; CO ₂ , carbon dioxide; H ⁺ , hydrogen ion; HCO ₃ ⁻ , bicarbonate; H ₂ O, water; K ⁺ , potassium.

Ingestion of Food

When a meal is eaten, the mechanisms that control the secretion of gastric juice and the motility and emptying of the stomach interact in a complex manner to coordinate the functions of the stomach. The response to eating is divided into three phases: cephalic, gastric, and intestinal. Chewing, tasting, and smelling cause an increase in the vagal stimulation of the stomach, which in turn increases gastric acid production. This represents the cephalic phase of digestion. In this phase, gastric acid output increases to approximately 55% of peak output. The gastric phase begins with the release of gastrin. Gastric acid secretion depends on antral distention, vagal activity, gastrin concentration, and the composition of the meal. Gastric acid secretion during a mixed-composition meal increases to approximately 80% of peak acid output. The intestinal phase begins with the movement of food into the small intestine and is largely inhibitory. Hormones (e.g., gastrin, cholecystokinin, secretin) and an enterogastric reflex further modulate gastric acid secretion and motility depending on the composition and volume of the food in the duodenum. This inhibition of gastric emptying by food in the duodenum enables the duodenal contents to be processed before more material is delivered from the stomach.

After the ingestion of a meal, gastric emptying depends on (1) the premeal volume, (2) the volume ingested, (3) the composition of the meal, (4) the size of the solids, (5) the amount of gastric secretion, (6) the physical characteristics of the stomach contents entering the duodenum, and (7) patient position. A mixture of liquids and solids passes through the stomach much more slowly than liquids alone. Gastric emptying is slowed by high lipid content, high caloric load, and large particle size. Thus, predicting an exact time for the passage of liquids and solids through the stomach is very difficult. For non-nutrient liquids (e.g., normal saline), the gastric volume decreases exponentially with respect to time. In one study, 90% of a 150-mL saline meal given to fasting adults in the sitting position passed through the stomach in a median time of 14 minutes; however, in adults in the left lateral position, the median time for gastric emptying was 28 minutes. In a subject eating a 400-mL meal of steak, bread, and vanilla ice cream, 800 mL of gastric juice was secreted ( Fig. 28.4 ). Consequently, the volume in the stomach remained high for almost 2 hours despite early, rapid emptying. These studies indicate that the volume and composition of the test meal, the resulting gastric secretions, and even patient positioning can impact gastric emptying and residual gastric content.

Volume of gastric contents and rate of gastric emptying in a subject eating a 400-mL meal of steak, bread, and vanilla ice cream.

(From Malagelada JR, Longstreth GF, Summerskill WHJ, et al. Measurements of gastric functions during digestion of ordinary solid meals in man. Gastroenterology. 1976;70:203–210.)

Effects of Pregnancy on Gastric Function

Gastroesophageal reflux, resulting in heartburn, is a common complication of late pregnancy. Pregnancy compromises the integrity of the lower esophageal sphincter; it alters the anatomic relationship of the esophagus to the diaphragm and stomach, raises intragastric pressure, and in some women limits the ability of the lower esophageal sphincter to increase its tone. Progesterone, which relaxes smooth muscle, probably accounts for the inability of the lower esophageal sphincter to increase its tone. Lower esophageal pH monitoring has shown a higher incidence of reflux in pregnant women at term, even in those who are asymptomatic, than in nonpregnant controls. Therefore, at term gestation the pregnant woman who requires anesthesia should be regarded as having an incompetent lower esophageal sphincter. These physiologic changes return to their prepregnancy levels by 48 hours after delivery.

Serial studies assessing gastric acidity during pregnancy have proved difficult to perform because they require repeated placement of nasogastric tubes. However, in the most comprehensive study of gastric acid secretion during pregnancy, basal and histamine-augmented gastric acid secretion was measured in 10 controls and 30 pregnant women equally distributed throughout the three trimesters of pregnancy. No significant differences in basal gastric acid secretion were seen between the pregnant and nonpregnant women.

A variety of techniques have been used to study gastric emptying during pregnancy and labor ( Table 28.1 ). Overall, the data suggest that pregnancy does not significantly alter the rate of gastric emptying. In addition, gastric emptying has not been found to be delayed in either obese or nonobese term pregnant women who ingested 300 mL of water after an overnight fast. However, management of obese parturients should take into account the possible presence of other associated problems in this group of patients (e.g., hiatal hernia or difficult airway). Gastric emptying appears to be normal in early labor but becomes delayed as labor advances ; the cause is uncertain. Pain is known to delay gastric emptying, but even when labor pain is abolished with epidural analgesia using a local anesthetic alone, the delay still occurs. Parenteral opioids cause a significant delay in gastric emptying, as do bolus doses of epidural and intrathecal opioids. Continuous epidural infusion of low-dose local anesthetic with fentanyl does not appear to delay gastric emptying until the total dose of fentanyl exceeds 100 µg.

TABLE 28.1

Studies of Gastric Emptying during Pregnancy and Labor

Method of Assessment	Study	Study Period and Subjects	Gastric Emptying
Radiographic	Hirsheimer et al. (1938)	Labor (10 subjects)	Delay in 2 subjects
	La Salvia and Steffen (1950)	Third trimester and labor	Third trimester: no delay Third trimester + opioids: marked delay Labor: slight delay Labor + opioids: marked delay
	Crawford (1956)	Labor (12 subjects)	Delay in 1 subject
Large-volume test meal	Hunt and Murray (1958)	Serial study Small numbers Second and third trimesters, postpartum	No change
Double-sampling test meal	Davison et al. (1970)	Third trimester and labor	Labor: delay, with altered pattern of emptying
Epigastric impedance	O’Sullivan et al. (1987)	Nonpregnant controls, third trimester, 60 minutes postpartum	No delay
Applied potential tomography	Sandhar et al. (1992)	Sequential study 10 mothers: 37–40 weeks’ gestation, 2–3 days postpartum, 6 weeks postpartum	No delay
Acetaminophen absorption	Nimmo et al. (1975)	Labor with intramuscular opioids Postpartum 2–5 days	Labor: No delay Labor + opioids: marked delay Postpartum: no delay
	Nimmo et al. (1977)	Labor	Labor: slight delay Labor + epidural analgesia (no opioid): slight delay
	Simpson et al. (1988)	Nonpregnant controls, 8–11 weeks’ gestation, 12–14 weeks’ gestation	8–11 weeks: no delay 12–14 weeks: delay
	Macfie et al. (1991)	Nonpregnant controls, first, second, and third trimesters	No delay in any trimester
	Geddes et al. (1991)	Postcesarean delivery Epidural fentanyl 100 µg	Delay
	Gin et al. (1991)	Postpartum: day 1 and day 3, 6 weeks	No delay
	Wright et al. (1992)	Labor with epidural bolus: (1) bupivacaine 0.375%; (2) bupivacaine 0.375% + fentanyl 100 µg	Epidural opioids: delay
	Whitehead et al. (1993)	Nonpregnant controls, first, second, and third trimesters Postpartum: 2, 18–24, and 24–48 hours	Pregnancy: No change Postpartum: 2 hours: delay 18–24 hours: no delay 24–48 hours: no delay
	Ewah et al. (1993)	Labor with epidural infusion: (1) bupivacaine 0.25%; (2) bupivacaine 0.25% + fentanyl 50 or 100 µg, or diamorphine 2.5 or 5 mg	Epidural opioids: delay
	Levy et al. (1994)	Nonpregnant controls, 8–12 weeks’ gestation	Delay
	Stanley et al. (1995)	Second and third trimesters and 8 weeks postpartum	No delay
	Zimmermann et al. (1996)	Labor with epidural infusion: (1) bupivacaine 0.125%; (2) bupivacaine 0.125% + fentanyl 2 µg/mL	No delay
	Porter et al. (1997)	Labor with epidural infusion: (1) bupivacaine 0.125%; (2) bupivacaine 0.125% + fentanyl 2.5 µg/mL	Epidural fentanyl total: < 100 µg: no delay > 100 µg: delay
	Kelly et al. (1997)	Labor with neuraxial bolus: (1) epidural bupivacaine 0.375%; (2) epidural bupivacaine 0.25% + fentanyl 50 µg; (3) intrathecal bupivacaine 2.5 mg + fentanyl 25 µg	Epidural fentanyl: no delay Intrathecal fentanyl: delay
Real-time ultrasonography	Carp et al. (1992)	Nonpregnant controls, third trimester	No delay
	Chiloiro et al. (2001)	Serial study in 11 women: first and third trimesters, 4–6 months postpartum	No delay
Real-time ultrasonography and acetaminophen absorption	Wong et al. (2002)	Third trimester Cross-over study	50-mL or 300-mL water: no delay Faster gastric emptying with 300 mL
	Wong et al. (2007)	10 obese parturients Third trimester Cross-over study	50-mL or 300-mL water: no delay

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