Expiratory Muscle Relaxation-Induced Ventilator Triggering: A Novel Patient-Ventilator Dyssynchrony

In critically ill patients receiving mechanical ventilation, expiratory muscles are recruited with high respiratory loading and/or low inspiratory muscle capacity. In this case report, we describe a previously unrecognized patient-ventilator dyssynchrony characterized by ventilator triggering by expiratory muscle relaxation, an observation that we termed expiratory muscle relaxation-induced ventilator triggering (ERIT). ERIT can be recognized with in-depth respiratory muscle monitoring as (1) an increase in gastric pressure (Pga) during expiration, resulting from expiratory muscle recruitment; (2) a drop in Pga (and hence, esophageal pressure) at the time of ventilator triggering; and (3) diaphragm electrical activity onset occurring after ventilator triggering. Future studies should focus on the incidence of ERIT and the impact in the patient receiving mechanical ventilation

Mitochondrial complex I dysfunction and altered NAD(P)H kinetics in rat myocardium in cardiac right ventricular hypertrophy and failure

AIMS: In cardiac hypertrophy (CH) and heart failure (HF), alterations occur in mitochondrial enzyme content and activities but the origin and implications of these changes for mitochondrial function need to be resolved. METHODS AND RESULTS: Right ventricular CH or HF was induced by monocrotaline injection, which causes pulmonary artery hypertension, in rats. Results were compared with saline injection (CON). NAD(P)H and FAD autofluorescence were recorded in thin intact cardiac trabeculae during transitions in stimulation frequency, to assess mitochondrial complex I and complex II function, respectively. Oxygen consumption, mitochondrial morphology, protein content, and enzymatic activity were assessed. NAD(P)H autofluorescence upon an increase in stimulation frequency showed a rapid decline followed by a slow recovery. FAD autofluorescence followed a similar time course, but in opposite direction. The amplitude of the early rapid change in NAD(P)H autofluorescence was severely depressed in CH and HF compared with CON. The rapid changes in FAD autofluorescence in CH and HF were reduced to a lesser extent. Complex I-coupled respiration showed an ∼3.5-fold reduction in CH and HF; complex II-coupled respiration was depressed two-fold in HF. Western blot analyses revealed modest reductions in complex I protein content in CH and HF and in complex I activity in supercomplexes in HF. Mitochondrial volume density was similar, but mitochondrial remodelling was evident from changes in ultrastructure and fusion/fission indices in CH and HF. CONCLUSION: These results suggest that the alterations in mitochondrial function observed in right ventricular CH and HF can be mainly attributed to complex I dysfunction

Ventilating two patients with one ventilator: technical setup and laboratory testing

With a modified circuit, it is feasible to ventilate two patients with one ventilator over a relevant range of compliances. Adding inspiratory resistance allows individual titration of tidal volume, and incorporating one-way valves prevents pendelluft. https://bit.ly/3ex8SYP

Performance of Noninvasive Airway Occlusion Maneuvers to Assess Lung Stress and Diaphragm Effort in Mechanically Ventilated Critically Ill Patients

Background: Monitoring and controlling lung stress and diaphragm effort has been hypothesized to limit lung injury and diaphragm injury. The occluded inspiratory airway pressure (Pocc) and the airway occlusion pressure at 100 ms (P0.1) have been used as noninvasive methods to assess lung stress and respiratory muscle effort, but comparative performance of these measures and their correlation to diaphragm effort is unknown. The authors hypothesized that Pocc and P0.1 correlate with diaphragm effort and lung stress and would have strong discriminative performance in identifying extremes of lung stress and diaphragm effort. Methods: Change in transdiaphragmatic pressure and transpulmonary pressure was obtained with double-balloon nasogastric catheters in critically ill patients (n = 38). Pocc and P0.1 were measured every 1 to 3 h. Correlations between Pocc and P0.1 with change in transdiaphragmatic pressure and transpulmonary pressure were computed from patients from the first cohort. Accuracy of Pocc and P0.1 to identify patients with extremes of lung stress (change in transpulmonary pressure > 20 cm H 2O) and diaphragm effort (change in transdiaphragmatic pressure 12 cm H 2O) in the preceding hour was assessed with area under receiver operating characteristic curves. Cutoffs were validated in patients from the second cohort (n = 13). Results: Pocc and P0.1 correlate with change in transpulmonary pressure (R 2= 0.62 and 0.51, respectively) and change in transdiaphragmatic pressure (R 2= 0.53 and 0.22, respectively). Area under receiver operating characteristic curves to detect high lung stress is 0.90 (0.86 to 0.94) for Pocc and 0.88 (0.84 to 0.92) for P0.1. Area under receiver operating characteristic curves to detect low diaphragm effort is 0.97 (0.87 to 1.00) for Pocc and 0.93 (0.81 to 0.99) for P0.1. Area under receiver operating characteristic curves to detect high diaphragm effort is 0.86 (0.81 to 0.91) for Pocc and 0.73 (0.66 to 0.79) for P0.1. Performance was similar in the external dataset. Conclusions: Pocc and P0.1 correlate with lung stress and diaphragm effort in the preceding hour. Diagnostic performance of Pocc and P0.1 to detect extremes in these parameters is reasonable to excellent. Pocc is more accurate in detecting high diaphragm effort