Detection of Ventilator Autotriggering by an Esophageal Catheter Used to Monitor the Neural Input and Diaphragm Excitation.

Patient-ventilator synchrony has been the focus of attention in the field of mechanical ventilation for quite some time now. Toward that end, the modern ventilators are equipped with very sensitive pneumatic triggering mechanisms, which allow for minimal wasting of patient effort. The increasingly sensitive pneumatic triggers have the potential to cause autotriggering, where stimuli other than neural signals (eg, cardiac oscillations) can trigger the mechanical breath. Although autotriggering has been well documented in brain-dead patients, its existence is difficult to prove in patients who have the ability to trigger breath through neural diaphragmatic activity. The only way to be sure that the triggered breath is indeed from the neural diaphragmatic activity rather than a spurious change in pressure or flow is to monitor neural signals during triggered mechanical breaths. Autotriggering can have deleterious effects including diaphragmatic atrophy, increased duration on the mechanical ventilator, and increased stay in the intensive care unit. Esophageal catheters, with the ability to measure phrenic nerve and diaphragmatic activity, allow for the detection of the extent of autotriggering. This article demonstrates the hitherto unknown but potentially common occurrence of autotriggering through nonneural stimuli and their amelioration by making the pneumatic autotriggering less sensitive. The full extent of the phenomenon and its deleterious effects remain to be explored in larger patient populations.

Ultra-protective mechanical ventilation without extra-corporeal carbon dioxide removal for acute respiratory distress syndrome.

BACKGROUND: Tidal hyperinflation can still occur with mechanical ventilation using low tidal volume (LVT) (6 mL/kg predicted body weight (PBW)) in acute respiratory distress syndrome (ARDS), despite a well-demonstrated reduction in mortality. METHODS: Retrospective chart review from August 2012 to October 2014. Inclusion: Age >18years, PaO2/FiO2<200 with bilateral pulmonary infiltrates, absent heart failure, and ultra-protective mechanical ventilation (UPMV) defined as tidal volume (VT) <6 mL/kg PBW. Exclusion: UPMV use for <24 h. Demographics, admission Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, arterial blood gas, serum bicarbonate, ventilator parameters for pre-, during, and post-UPMV periods including modes, VT, peak inspiratory pressure (PIP), plateau pressure (Pplat), driving pressure, etc. were gathered. We compared lab and ventilator data for pre-, during, and post-UPMV periods. RESULTS: Fifteen patients (male:female = 7:8, age 42.13 ± 11.29 years) satisfied criteria, APACHEII 20.6 ± 7.1, mean days in intensive care unit and hospitalization were 18.5 ± 8.85 and 20.81 ± 9.78 days, 9 (60%) received paralysis and 7 (46.67%) required inotropes. Eleven patients had echocardiogram, 7 (63.64%) demonstrated right ventricular volume or pressure overload. Eleven patients (73.33%) survived. During-UPMV, VT ranged 2-5 mL/kg PBW(3.99 ± 0.73), the arterial partial pressure of carbon dioxide (PaCO2) was higher than pre-UPMV values (84.81 ± 18.95 cmH2O vs. 69.16 ± 33.09 cmH2O), but pH was comparable and none received extracorporeal carbon dioxide removal (ECCO2-R). The positive end-expiratory pressure (14.18 ± 7.56 vs. 12.31 ± 6.84 cmH2O), PIP (38.21 ± 12.89 vs. 32.59 ± 9.88), and mean airway pressures (19.98 ± 7.61 vs. 17.48 ± 6.7 cm H2O) were higher during UPMV, but Pplat and PaO2/FiO2 were comparable during- and pre-UPMV. Driving pressure was observed to be higher in those who died than who survived (24.18 ± 12.36 vs. 13.42 ± 3.25). CONCLUSION: UPMV alone may be a safe alternative option for ARDS patients in centers without ECCO2-R.