IN an unprotected airway, distribution of ventilation volume between the lungs and stomach depends mainly on patient variables such as lower esophageal sphincter pressure (LESP), airway resistance, and respiratory system compliance.1The combination of these variables and ventilatory techniques determines upper airway pressure and therefore gas distribution between the lungs, esophagus, and stomach.2In an animal model, investigators showed that LESP decreases during cardiac arrest from approximately 20 H2O to approximately 5 cm H2O.3,4When such a pressure is used in a bench model of simulated ventilation of an unprotected airway,5stomach ventilation is almost inevitable. Stomach inflation increases intragastric pressure,6elevates the diaphragm, restricts lung movement, and in turn reduces respiratory system compliance and lung ventilation,7,8which may cause severe complications such as aspiration, pneumonia, and possibly death.9,10
Unfortunately, knowledge about LESP physiology during cardiopulmonary resuscitation is limited to one animal model.3The objective of the current study was to verify the rate of decline of LESP before, during, and after cardiovascular collapse and cardiac arrest in humans. After institutional review board approval, we measured LESP in three patients undergoing withdrawal of life support in an intensive care unit. This study may be as close as it is possible to get to realistically assessing human LESP physiology immediately before, during, and after sudden cardiac arrest.
We studied three adult individuals, ranging in age from 53 to 77 yr, all affected by devastating hemorrhagic strokes and in deep coma. Arterial blood gases or arterial oxygen saturation was compatible with good arterial oxygenation during mechanical ventilation.
After confirmation of irreversible devastating neurologic injury in all patients and family decision to withdraw care, informed consent was obtained. While the patient was still supported by mechanical ventilation, esophageal manometry was performed via the nares with a low-compliance perfusion esophageal manometry system (Arndorfer Infusion, Greendale, WI; Medtronic Polygraph, Minneapolis, MN). After recording a baseline measurement, continuous pressure measurements of the LESP were then taken upon extubation until the patient expired (asystole) and for few minutes after the cardiac arrest up to reaching a steady state nadir. Normal LESP in our laboratory is 15–40 mmHg. Withdrawal of care was performed through discontinuation of all medications except morphine and extubation of the trachea to room air. In all cases, the patients' peripheral oximetry desaturated rapidly, and they became bradycardic and then asystolic while esophageal pressure was recorded (fig. 1).
Lower esophageal sphincter pressure decreased rapidly from normal baseline during cardiocirculatory collapse in all three patients undergoing withdrawal of life support, which is similar to previous observations of LESP in an animal model of cardiac arrest.3
Lower esophageal sphincter pressure is one the mechanisms that prevents stomach inflation during positive-pressure ventilation. If our observations of LESP physiology before, during, and after cardiovascular collapse in three intensive care unit patients can be extrapolated to critically ill victims or during cardiac arrest, emergency ventilation management should be always performed in a manner that assumes that the LESP may be unable to prevent air from entering the stomach. Therefore, emergency ventilation should be performed in a manner that minimizes peak inspiratory pressure, because respiratory physiology favors substantial stomach inflation when LESP is critically decreased.2For example, any ventilation strategy generating peak airway pressures above 5 cm H2O in a cardiac arrest patient with an unprotected airway may cause massive stomach inflation before the airway can be protected with an advanced airway device.5Stomach inflation can also be prevented in many patients by applying pressure over the cricoid to seal off the esophagus, when feasible.11,12A recent study of out-of-hospital cardiac arrest showed that professional rescuers use ventilation techniques that would make stomach inflation very likely in the presence of an unprotected airway.13Furthermore, even after a period of intensive retraining, rescuers continued to apply ventilation that resulted in excessive airway pressure. Therefore, basic and advanced life support training courses may require special emphasis on teaching the psychomotor skills necessary for good airway management practices to prevent harm.
Previously, we have developed several strategies to prevent stomach inflation during ventilation of a cardiac arrest victim with an unprotected airway by decreasing peak airway pressure with small instead of large tidal volumes,14decreasing peak inspiratory flow,15,16or using pure oxygen instead of room air.17For example, proper oxygenation and carbon dioxide elimination could be achieved with tidal volumes of 350 ml pure oxygen in anesthetized supine patients.18Because ventilation requirements during cardiopulmonary resuscitation may be less than during intact circulation19and excessive ventilation may decrease the time for life-saving chest compressions and decrease venous return,13it may be important to limit tidal volume to 300–500 ml, a goal usually achieved by observing an adequate chest rise after resuscitation using bag ventilation.20
Although the role of ventilation strategies to prevent stomach inflation in an unprotected airway has been discussed in general during cardiac arrest,1–3,5,8it may be important to extrapolate ventilation strategies for unintubated cardiac arrest patients to other unintubated patients with severe shock states, who often need basic life support ventilation before undergoing intubation. Intuitively, cricoid pressure should be always attempted when an extra set of hands is available.
There are several limitations to the current case report series. First, our patients had severe underlying neurologic injury and may not be exactly comparable to patients with other prehospital conditions of sudden cardiac arrest, dysrhythmia, or hypoxia. Second, two of three patients received vasoactive medications before life support was withdrawn, which may have affected measurements. Third, the mechanism of death in our patients reflects initial hypoxia, hypercapnia, and a rapid decreasing perfusion always resulting in asystolic cardiac arrest, which may be different when compared with out-of-hospital patients with sudden ventricular fibrillation.
In conclusion, after withdrawal of life support in intensive care unit patients, LESP decreased rapidly before cardiac arrest, from a baseline of approximately 20 cm H2O. Invariably, at the time of cardiac arrest, LESP averaged 5 cm H2O.