2003 OPEN FORUM Abstracts
Ventilator Self-triggering Masquerades as Brainstem Activity ? A CASE REPORT
Charles G. Durbin, Jr,., MD, Brian Walsh, RRT, Michelle Dumont, RRT, University of Virginia Health Systems, Charlottesville, VA
INTRODUCTION: Absence of all brainstem activity, including absence of breathing, is an essential part of determining brain death. Some modes of ventilation may inhibit this determination. We report a case of a brain dead individual in whom pressure support ventilation was able to support normal gas exchange of over period of more than 4 hours.
CASE: A 30 year old man was transferred to the University Hospital in coma following a two week course of declining mental status. He had a normal lumbar puncture and CT scan. An MRI showed hypothalamic edema. His admission exam showed intact corneal reflexes, doll's eyes, normal oculocephalic reflexes and a normal respiratory drive. He was non-responsive to verbal or painful stimuli and was areflexic throughout. He was empirically treated. He was intubated and maintained on PSV delivered with flow-triggering by a Puritan Bennet 840 ventilator. His condition declined with loss of brainstem reflexes and development of hemodynamic instability.
On IMV (with PSV) he occasionally self-triggered breaths indicating some minimal brain stem function. 24 hours later, he was without any evidence of spontaneous ventilations. During assessment for brain death, he was placed on an IMV rate of 4 and his PaCO2 was allowed to rise. He began spontaneous ventilations when he reached a pH of 7.32 and PaCO2 of 53. With absence of other brain activity and brain death eminent, we continued PSV (8cm H20) alone and monitored spontaneous respiratory rate. About 2 hours later, apnea occurred. IMV was instituted and the patient was ventilated over night. At 4 am the clinicians noted that the patient appeared to be occasionally triggering the ventilator. He was placed on PSV (flow-triggering, sensitivity of 0.5L/min) alone and had an apparent spontaneous rate of 12-14 breaths per minute. On this setting the following gas was obtained: PaO2 = 117, PaCO2 = 38, pH = 7.44. Next morning, he was receiving PSV and had a spontaneous rate of 12 to 16 breaths/min. On examination, there was no movement of the chest wall nor negative defection of the pressure-flow curve preceding each "spontaneous" breath. When the sensitivity of flow-triggering was decreased (2 L/min) the patient became apneic. After several minutes of observed apnea, the PaO2 = 100, PaCO2 = 76, pH 7.21. A complete neurologic examination confirmed brain death.
DISCUSSION: The advent of flow-triggering has increased the ability of the mechanical ventilator to match patient demand for gas flow. This has lowered the work of breathing considerably allowing patients who would otherwise be unable to breathe spontaneously to do so. The increased sensitivity may also be a problem in that slight movement of air in the patient's tracheobronchial tree or ventilator circuit may result in delivery of an unneeded ventilator breath. While we are not sure of the exact mechanism responsible for triggering a PS supported breath in our patient, we believe that cardiac activity may have been responsible. The patient was slender and receiving pressors and the ventilator rate was approximately 1/3 of the cardiac rate. Transmitted cardiac pulsations may have created enough air flow in the trachea to trigger a PSV breath. We believe that setting the sensitivity of the flow-triggering at such a low minute flow (0.5L/min) was a contributing factor and that sensitivity need not be less than 2 L/min when using the PB 840 ventilator in adult patients with reasonable muscle strength and especially during apnea testing.