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Introduction: Pressure support ventilation (PSV) should allow spontaneous breathing with a "normal" neuro-ventilatory drive. Low neuro-ventilatory drive puts the patient at risk of diaphragmatic atrophy while high neuro-ventilatory drive may causes dyspnea and patient self-inflicted lung injury. We continuously assessed for 12 h the electrical activity of the diaphragm (EAdi), a close surrogate of neuro-ventilatory drive, during PSV. Our aim was to document the EAdi trend and the occurrence of periods of "Low" and/or "High" neuro-ventilatory drive during clinical application of PSV., Method: In 16 critically ill patients ventilated in the PSV mode for clinical reasons, inspiratory peak EAdi peak (EAdi PEAK ), pressure time product of the trans-diaphragmatic pressure per breath and per minute (PTP DI/b and PTP DI/min , respectively), breathing pattern and major asynchronies were continuously monitored for 12 h (from 8 a.m. to 8 p.m.). We identified breaths with "Normal" (EAdi PEAK 5-15 μV), "Low" (EAdi PEAK  < 5 μV) and "High" (EAdi PEAK  > 15 μV) neuro-ventilatory drive., Results: Within all the analyzed breaths (177.117), the neuro-ventilatory drive, as expressed by the EAdi PEAK , was "Low" in 50.116 breath (28%), "Normal" in 88.419 breaths (50%) and "High" in 38.582 breaths (22%). The average times spent in "Low", "Normal" and "High" class were 1.37, 3.67 and 0.55 h, respectively (p < 0.0001), with wide variations among patients. Eleven patients remained in the "Low" neuro-ventilatory drive class for more than 1 h, median 6.1 [3.9-8.5] h and 6 in the "High" neuro-ventilatory drive class, median 3.4 [2.2-7.8] h. The asynchrony index was significantly higher in the "Low" neuro-ventilatory class, mainly because of a higher number of missed efforts., Conclusions: We observed wide variations in EAdi amplitude and unevenly distributed "Low" and "High" neuro ventilatory drive periods during 12 h of PSV in critically ill patients. Further studies are needed to assess the possible clinical implications of our physiological findings.

Purpose: High-flow oxygen therapy delivered through nasal cannulae improves oxygenation and decreases work of breathing in critically ill patients. Little is known of the physiological effects of high-flow oxygen therapy applied to the tracheostomy cannula (T-HF). In this study, we compared the effects of T-HF or conventional low-flow oxygen therapy (conventional O 2 ) on neuro-ventilatory drive, work of breathing, respiratory rate (RR) and gas exchange, in a mixed population of tracheostomized patients at high risk of weaning failure., Methods: This was a single-center, unblinded, cross-over study on fourteen patients. After disconnection from the ventilator, each patient received two 1-h periods of T-HF (T-HF1 and T-HF2) alternated with 1 h of conventional O 2 . The inspiratory oxygen fraction was titrated to achieve an arterial O 2 saturation target of 94-98% (88-92% in COPD patients). We recorded neuro-ventilatory drive (electrical diaphragmatic activity, EAdi), work of breathing (inspiratory muscular pressure-time product per breath and per minute, PTP musc/b and PTP musc/min , respectively) respiratory rate and arterial blood gases., Results: The EAdi peak remained unchanged (mean ± SD) in the T-HF1, conventional O 2 and T-HF2 study periods (8.8 ± 4.3 μV vs 8.9 ± 4.8 μV vs 9.0 ± 4.1 μV, respectively, p = 0.99). Similarly, PTP musc/b and PTP musc/min , RR and gas exchange remained unchanged., Conclusions: In tracheostomized patients at high risk of weaning failure from mechanical ventilation, T-HF did not improve neuro-ventilatory drive, work of breathing, respiratory rate and gas exchange compared with conventional O 2 after disconnection from the ventilator. The present findings might suggest that physiological effects of high-flow therapy through tracheostomy substantially differ from nasal high flow.