Scandinavian journal of gastroenterology · 2003
The gastro-oesophageal pressure inversion point revisited.
СтатьяВалидационное исследованиеНазвание и аннотация: Перевод пока не подготовлен
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Bredenoord A J, Weusten B L A M, Roelofs J M M, Smout A J P M
Аннотация
BACKGROUND: The pressure inversion point (PIP) is defined as the point at which, during stationary pull-through manometry of the oesophago-gastric junction, the polarity of the respiratory-associated pressure variations changes. Traditionally, the PIP is ascribed to transition of the pressure sensor from the abdominal to the thoracic cavity. We used high-resolution manometry to investigate the validity of this concept in six healthy volunteers and six patients with a sliding hiatus hernia.
METHODS: In the analysis, the position of the PIP was identified. When there was a second, more distal, PIP, its position was also noted. The amplitude of the respiratory-associated pressure variations, defined as the difference between end-expiratory and end-inspiratory pressure, was measured.
RESULTS: Double PIPs were found both in healthy controls (23 +/- 8% of time) and in patients (38 +/- 9% of time). Amplitudes of the respiratory-associated pressure variations were significantly higher at the proximal and distal border of the PIP (3.36 +/- 0.2 kPa and 2.29 +/- 0.2 kPa) than in the oesophageal body (0.54 +/- 0.03 kPa, P < 0.001) and in the stomach (0.54 +/- 0.03 kPa, P < 0.001). We also observed a relationship between the localization of the highest end-expiratory pressure and the position of the PIP. During TLOSRs respiratory variation amplitudes at the proximal and distal border of the PIP decreased to 0.61 +/- 0.02 kPa and 0.29 +/- 0.01 kPa, approximating respiratory pressure variation in oesophagus and stomach.
CONCLUSION: Our findings suggest that the PIP is caused by sliding of the high-pressure zone along pressure sensors rather than by the transition from the thoracic to the abdominal compartment.
METHODS: In the analysis, the position of the PIP was identified. When there was a second, more distal, PIP, its position was also noted. The amplitude of the respiratory-associated pressure variations, defined as the difference between end-expiratory and end-inspiratory pressure, was measured.
RESULTS: Double PIPs were found both in healthy controls (23 +/- 8% of time) and in patients (38 +/- 9% of time). Amplitudes of the respiratory-associated pressure variations were significantly higher at the proximal and distal border of the PIP (3.36 +/- 0.2 kPa and 2.29 +/- 0.2 kPa) than in the oesophageal body (0.54 +/- 0.03 kPa, P < 0.001) and in the stomach (0.54 +/- 0.03 kPa, P < 0.001). We also observed a relationship between the localization of the highest end-expiratory pressure and the position of the PIP. During TLOSRs respiratory variation amplitudes at the proximal and distal border of the PIP decreased to 0.61 +/- 0.02 kPa and 0.29 +/- 0.01 kPa, approximating respiratory pressure variation in oesophagus and stomach.
CONCLUSION: Our findings suggest that the PIP is caused by sliding of the high-pressure zone along pressure sensors rather than by the transition from the thoracic to the abdominal compartment.