What is acid reflux?

Mechanisms of Reflux
Transient Lower Esophageal Sphincter Relaxations
This is the most common mechanism underlying GER and also accounts for the reflux of gases during belching. Transient LESRs are not associated with antecedent pharyngeal contractions, are unaccompanied by esophageal peristalsis, persist for longer periods (>10 seconds) than swallow-induced LESRs, and are always accompanied by inhibition of the crural diaphragm. Transient LESRs account for nearly all reflux episodes in healthy persons and for 50% to 80% in patients with GERD, depending on the severity of associated esophagitis. However, one study suggested that low basal LES pressure, rather than transient LESRs, may be the primary mechanism of GER in patients with nonreducible hernias. Transient LESRs are not always associated with GER. In healthy persons, about 40% to 60% of transient LESRs are accompanied by reflux episodes, compared with 60% to 70% in patients with GERD. The rate of transient LESR is increased by gastric distention, whether by gas or a meal, by stress, and, to a lesser extent, by subthreshold (for swallowing) stimulation of the pharynx. Under normal circumstances, meals are the major stimuli for transient LESRs, but the importance of specific foods is unknown. Transient LESRs are inhibited by the supine position, sleep, general anesthesia, and vagal cooling. Various drugs also impair transient LESRs including cholecystokinin A antagonists, anticholinergic drugs, morphine, somatostatin, nitric oxide inhibitors, 5-hydroxytryptamine 3 (5-HT 3) antagonists, and d-aminobutyric acid B (GABA B) agonists. Current evidence indicates that transient LESRs are mediated through vagal pathways. Gastric distention activates mechanoreceptors in the proximal stomach adjacent to the gastric cardia that send signals to the brainstem center through vagal afferent pathways. The structured sequence of motor events including LESR, inhibition of the crural diaphragm, and contractions of the esophageal body suggest that this process occurs in a programmed manner, probably controlled by a pattern generator within the vagal nuclei. The motor arm is in the vagus nerve and shares common elements with swallow-induced LESR.
Swallow-Induced Lower Esophageal Sphincter Relaxations
About 5% to 10% of reflux episodes occur during swallow-induced LESRs. Most of these episodes are associated with defective or incomplete peristalsis. During a normal swallow-induced LESR associated with normal peristalsis, reflux is uncommon because of the absence of concomitant crural diaphragm relaxation, the relatively short duration of LES relaxation (5 to 10 seconds), and the prevention of reflux by the oncoming peristaltic wave (see Reflux during swallow-induced LESR is more common in the presence of a hiatus hernia because of pooling of gastric liquids in the hernia sac and the absence of any residual diaphragmatic support during the LESR.
Hypotensive Lower Esophageal Sphincter Pressure
Stress reflux and free reflux are two mechanisms by which GER can be associated with diminished LES. Stress reflux results when a relatively hypotensive LES is overcome and is “blown open” by an abrupt increase in intra-abdominal pressure from coughing, straining, or bending. Stress reflux is unlikely when the LES pressure is greater than 10 mm Hg. Free reflux is characterized by a fall in intraesophageal pH without an identifiable change in intragastric pressure, and it usually occurs when the LES pressure is 0 to 4 mm Hg. Reflux as the result of low or absent LES pressure is uncommon. It is found mostly in patients with severe esophagitis, in whom it may account for up to 23% of reflux episodes, and rarely in patients without endoscopic evidence of esophagitis. The mechanisms of a low LES pressure are poorly understood. The presence of a hiatus hernia reduces LES pressure because the intrinsic support of the crural diaphragm is lost. Some LES weakness may be secondary to impairment of the excitatory cholinergic pathways to the LES as a result of esophagitis. Induction of experimental esophagitis in cats affects the release of acetylcholine and lowers LES pressures; changes that are reversible on healing of the esophagitis. However, healing of esophagitis in humans is rarely accompanied by an increase in LES pressure.