Neurally adjusted ventilatory assist (NAVA) is a mode of mechanical ventilation that delivers assistance to spontaneous breathing based on the detection of electrical activity of the diaphragm. Neural control of respiration originates in the respiratory center, and signals are transmitted through the phrenic nerve to excite and contract the diaphragm. The neural method monitors electrical signals to the diaphragm. These signals are a proxy for phrenic nerve activity. Bipolar electrodes attached to a nasogastric tube are positioned in the esophagus at the level of the diaphragm. The online monitoring system differentially amplifies signals from each electrode pair and digitizes them. The resulting signal can help monitor the patient’s respiration or control the timing and/or levels of the ventilatory assist. We wanted to use this technology to assess diaphragmatic function with exertion.
Our patient is a 64-year old male who developed fatigue and dyspnea on exertion and six months later presented with left facial paralysis. After clinical evaluation and serologies, he was diagnosed with Lyme disease and was started on oral antibiotics with significant improvement of symptoms. After stopping antibiotics the dyspnea on exertion returned. He was a well developed male, in no acute distress, body mass index of 34. Physical exam and routine labs were within normal limits except for an elevation in Lyme titers, particularly during the periods of time when he was off antibiotics. A ventilation/perfusion scan showed no perfusion defects. Computed tomography of chest was normal. A nuclear stress test did not show any signs of ischemia and left ventricular ejection fraction of 55%. Was the dyspnea the result of neurologic effects of Lyme disease causing diaphragmatic weakness? The patient had normal spirometry. A fluoroscopic exam of the diaphragm (“sniff test”) showed no paradoxical diaphragmatic movement. Then we asked permission to perform an unconventional test. With the patient sitting a NAVA catheter (16 french) was placed through the left nostril without difficulty perpendicular to the level of the diaphragm. Minor adjustments were needed due to patient position and changes in posture. Edi (Electrical activity of diaphragm) Peak ranged from 7.8 to 22 (all measured in microvolts) and EdiMin from 0.4 to 2.8 during breathing at rest, while with deep inspiration EdiPeak 170 and EdiMin 0.4, all within normal limits. Then we proceeded to have the patient exert himself by walking up three flights of stairs while having the ventilator monitor attached to the NAVA catheter. Walking in the hallway to the stairwell EdiPeak was 54 while EdiMin was 16. After the first flight of stairs the Edi Peak was 113 while EdiMin was 8.2 which coincided with slight dyspnea. When he reached the 3rd floor landing, he was experiencing increased level of dyspnea while EdiPeak was recorded at 170 and EdiMin was 3.5.
Despite a normal fluoroscopic exam there was still a question as whether there was diaphragmatic dysfunction limited only to exercise since the symptoms presented exclusively after exertion. Since we were unable to perform a fluoroscopic examination of the diaphragm during exercise, we decided to proceed with a different approach. At the end we were able to demonstrate that the patient had effective neuro-ventilatory coupling which appeared to respond appropriately to the increased demand and that the diaphragm did not seem to be affected by Lyme disease.
We concluded in this first reported study of trans-esophageal measurement of diaphragmatic function during ambulation that the NAVA system is an alternative way to assess diaphragmatic activity in the ambulatory setting and could be the only practical way to do it while the patient is exercising .
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