Gastroesophageal reflux disease and pulmonary function: A potential role of the dead space extension

Abstract

SummaryBackgroundTo evaluate the differences in the existence and size of dead space in patients with and without Gastroesophageal Reflux Disease (GERD and non-GERD) expressed through the size of intrapulmonary shunt (QS/QT).Material/MethodsThe study enrolled 86 subjects – 43 patients referred for endoscopy because of symptoms of GERD (heartburn, acid regurgitation, dysfagia) and 43 healthy subjects with similar anthropometric characteristics without GERD symptoms. Based on endoscopy findings, patients were classified into the erosive reflux disease (ERD) group and non-erosive reflux disease (NERD) group. Spirometry values, single-breath diffusing capacity of the lung for carbon monoxide (DLCO) and intrapulmonary shunt (venous shunt – QS/QT) determined by the oxygen method were measured in all participants.ResultsStatistically significant differences between GERD and non-GERD groups in FVC (p=0.034), FEV1 (p=0.002), FEV1/FVC (p=0.001), and PEF (p=0.001) were observed. There were no statistically significant differences in FEF 25% (p=0.859), FEF 50% (p=0.850), and FEF 75% (p=0.058). Values of DLCO (p=0.006) and DLCO/VA (p=0.001) were significantly lower and QS/QT was significantly higher (p=0.001) in the GERD group than in the non-GERD group. However, in both groups the average values of DLCO and DLCO/VA expressed as a percentage of predictive values were within normal range, while the value of QS/QT in the GERD group showed pathological (6.0%) mean value (normal value ≤5.0%). There were no significant differences in respiratory function test results between patients with ERD and NERD.ConclusionsOur results suggest that microaspiration of stomach contents may cause surfactant damage, development of microatelectasis, and dead space expansion with consequent increase of intrapulmonary (venous) shunt.

The prevalence of gastro-esophageal reflux disease and esophageal dysmotility in Chinese patients with idiopathic pulmonary fibrosis

“…Mise et al [ 30 ] reported lower DLCO in patients with recently diagnosed GERD in comparison with healthy controls. Bonacin et al [ 31 ] showed statistically significant increases in FVC in the GERD group as compared with the non-GERD group. Among the GERD group, values of DLCO and DLCO/VA were significantly lower, and intrapulmonary shunt was significantly higher in comparison with the non-GERD group, which confirmed the correlation between GERD and damaged lung function.…”

A pilot randomized clinical trial assessing the effect of cricoid pressure on risk of aspiration

“…Observational studies have suggested an association between risk factors for microaspiration (eg obesity, GERD, and diabetes mellitus) and development of serious hospital‐acquired conditions such as ARDS and HAP. Beyond its association with ARDS and HAP, microaspiration can also result in bronchospasm, and hypoxia during intubation . In this context, interventions that may be employed to reduce the risk of microaspiration are clearly of great interest.…”

“…Macroaspiration (grossly visible aspiration) has been clearly associated with severe pulmonary injury . More recently, microaspiration (aspiration without grossly visible gastric material) has also been associated with significant morbidity including acute respiratory distress syndrome (ARDS), ventilator associated pneumonia (VAP), and acute respiratory failure due to bronchoconstriction and ventilation‐perfusion mismatching …”

Prospect in Pediatric Diseases Medicine

“…A higher frequency of proximal GERs is in line with findings from other studies (Embarak et al 2015;Gao et al 2015;Savarino et al 2013). It has been observed that pulmonary function, as represented, for instance, by carbon monoxide diffusion lung capacity (DL CO ) and carbon monoxide diffusion lung capacity per unit alveolar volume (DL CO /VA) measurements, is appreciably lower in GERD patients (Bonacin et al 2012;Mise et al 2010). It is possible that microaspirations cause surfactant damage, which stimulates the development of an intrapulmonary shunt.…”