Analysis of non-invasive ventilation effects on gastric inflation using a non-linear mathematical model

Summary

A non-linear mathematical model of the oesophagus was developed to study the effects of non-invasive ventilation variables on the severity of gastric inflation. The model was based on the non-linear physical characteristics of biological tissue. The model simulated oesophageal mechanical function during non-invasive ventilation in cardiac arrest (2:30 ventilations/chest compressions cycles) and respiratory arrest (1:5 ventilations/s) as recommended by the European Resuscitation Council (ERC) in its 2005 guidelines for adult basic and advanced life support. Model predictions establish a strong correlation between the expiratory time and the occurrence of gastric inflation. For cardiac arrest, when using ventilation pressure lower than 12 cmH₂O, expiratory time between consequent ventilations and time until the occurrence of gastric inflation were linearly dependant (r = 0.98). This linear correlation changed abruptly when airway pressure exceeded the threshold pressure of 12 cmH₂O, indicating that air had entered the stomach during the first ventilation. The interval at which the pressure at the distal section of the oesophagus was above the lower oesophageal sphincter (LES) opening pressure was significantly prolonged in the model of cardiac arrest (approximately 5.5 s compared to 3 s in respiratory arrest), thus allowing a greater amount of air to enter the stomach at relatively low airway pressures. During cardiac arrest, the mean pressure at the distal section of the oesophagus and the amplitude of air backflow were higher compared to the mean pressure and amplitude during respiratory arrest. This is also due to the shorter expiratory intervals in the 2:30 ventilations/chest compressions technique. The model indicates that the time required for the air trapped in the oesophagus to completely deflate is approximately 2 s. This may be longer than the expiratory time recommended by the 2005 guidelines. Model predictions support the 2005 guidelines regarding the decrease in the tidal volume and in the inspiratory pressure in an effort to minimise gastric inflation.

Introduction

Non-invasive ventilation (NIV) during cardiopulmonary resuscitation (CPR) involves a potential risk of gastric inflation (GI), especially when the airway is unprotected. GI compresses the lungs, thereby decreasing their compliance and demanding higher airway ventilation pressure.² The latter is also associated with increased risk of GI, thus generating a vicious cycle. Serious complications of GI are regurgitation of gastric contents and pulmonary aspiration, leading to higher mortality rates within 24–96 h after successful resuscitation.

The distribution of ventilation volume between lungs and stomach in the unprotected airway depends on patient variables such as airway resistance, lower oesophageal sphincter (LES) pressure, respiratory system compliance and the applied technique in both basic and advanced airway support. Variables that may affect GI are head position, inflation flow rate,³ inspiratory time (TI), and tidal volume.⁴ Airway pressure depends on inspiratory time, airway resistance and tidal volume. Large tidal volumes, high airway resistance and short TI's lead to higher airway pressure and an increased probability of air entering the stomach. This was confirmed in studies undertaken in both bench⁵ and clinical6, 7 settings during respiratory arrest with an unprotected airway and during CPR. These studies also demonstrated the beneficial effects of small (∼500 ml) rather than large (800–1200 ml) tidal volumes as long as oxygen supplementation is used.

Lower oesophageal sphincter pressure is the pressure at the oesophageal–gastric junction that prevents regurgitation of stomach contents into the pharynx, and insufflation of air into the gastro-intestinal tract during ventilation. The lower oesophageal sphincter pressure in a healthy adult is approximately 20–25 cmH₂O. During cardiac arrest, LES tone decreases rapidly⁸ and requires a smaller pressure gradient to open, thus making GI more likely to occur also at relatively low airway pressures.

In an effort to minimise gastric inflation, the European Resuscitation Council (ERC), in its 2005¹ and 2000⁹ guidelines for Adult Basic Life Support, recommended a decrease in the tidal volume during non-invasive ventilation. According to the 2005 guidelines, it is recommended that for adult resuscitation each rescue breath (mouth-to-mouth and bag-valve-mask; with and without supplemental oxygen) should deliver the volume of air needed to produce a visible chest rise. Tidal volumes of 500–600 ml (6–7 ml kg⁻¹) are recommended. The 2005 guidelines state that low minute ventilation (i.e., low tidal volume and ventilation rate) can maintain oxygenation without significant stomach inflation.

The 2005 guidelines for adult basic and advanced life support refer to two main ventilation strategies: (a) combined ventilations and chest compressions, in 2:30 ratio, at approximately 22-s cycles. Each cycle consists of two ventilations followed by 30 chest compressions. This technique is used during adult cardiopulmonary resuscitation when signs of spontaneous circulation are not detected; (b) ventilations alone at a rate of 10–12 breaths min⁻¹ (1:5). This is the common strategy of ventilation during respiratory arrest, when there is no breathing but there is a pulse.

To study the effects of different NIV variables on gastric inflation, we developed a mathematical model of the primary components that are involved in the procedure. The multi-element non-linear model includes 25 serially connected oesophageal subsections.