The use of ultrasonography has become increasingly popular in the everyday management of critically ill patients. It has been demonstrated to be a safe and handy bedside tool that allows rapid hemodynamic assessment and visualization of the thoracic, abdominal and major vessels structures. More recently, M-mode ultrasonography has been used in the assessment of diaphragm kinetics. Ultrasounds provide a simple, non-invasive method of quantifying diaphragmatic movement in a variety of normal and pathological conditions. Ultrasonography can assess the characteristics of diaphragmatic movement such as amplitude, force and velocity of contraction, special patterns of motion and changes in diaphragmatic thickness during inspiration. These sonographic diaphragmatic parameters can provide valuable information in the assessment and follow up of patients with diaphragmatic weakness or paralysis, in terms of patient-ventilator interactions during controlled or assisted modalities of mechanical ventilation, and can potentially help to understand post-operative pulmonary dysfunction or weaning failure from mechanical ventilation. This article reviews the technique and the clinical applications of ultrasonography in the evaluation of diaphragmatic function in ICU patients.

This report summarizes current physiological and technical knowledge on esophageal pressure (Pes) measurements in patients receiving mechanical ventilation. The respiratory changes in Pes are representative of changes in pleural pressure. The difference between airway pressure (Paw) and Pes is a valid estimate of transpulmonary pressure. Pes helps determine what fraction of Paw is applied to overcome lung and chest wall elastance. Pes is usually measured via a catheter with an air-filled thin-walled latex balloon inserted nasally or orally. To validate Pes measurement, a dynamic occlusion test measures the ratio of change in Pes to change in Paw during inspiratory efforts against a closed airway. A ratio close to unity indicates that the system provides a valid measurement. Provided transpulmonary pressure is the lung-distending pressure, and that chest wall elastance may vary among individuals, a physiologically based ventilator strategy should take the transpulmonary pressure into account. For monitoring purposes, clinicians rely mostly on Paw and flow waveforms. However, these measurements may mask profound patient-ventilator asynchrony and do not allow respiratory muscle effort assessment. Pes also permits the measurement of transmural vascular pressures during both passive and active breathing. Pes measurements have enhanced our understanding of the pathophysiology of acute lung injury, patient-ventilator interaction, and weaning failure. The use of Pes for positive end-expiratory pressure titration may help improve oxygenation and compliance. Pes measurements make it feasible to individualize the level of muscle effort during mechanical ventilation and weaning. The time is now right to apply the knowledge obtained with Pes to improve the management of critically ill and ventilator-dependent patients.

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Despite identical ventilator settings, the different PPV modes lead to substantial differences in VT, PTP, and breathing variability in the presence spontaneous efforts. Clinicians should be aware of the possible harmful effects of i-synchronization especially when high VT is undesirable.

Respiratory rate is one of the key variables we set and monitor during mechanical ventilation. As part of our increasing efforts to optimise mechanical ventilation, it is prudent that we expand our understanding of the potential harmful effects not only of volume and pressures, but also of respiratory rate. The mechanisms by which respiratory rate may become injurious during mechanical ventilation can be distinguished in two broad categories. In the first well-recognised category, concerning both controlled and assisted ventilation, the respiratory rate per se may promote ventilator-induced lung injury, dynamic hyperinflation, ineffective efforts and respiratory alkalosis. It may also be misinterpreted as distress delaying the weaning process. In the second category, which concerns only assisted ventilation, the respiratory rate may induce injury in a less apparent way, by remaining relatively quiescent while being challenged by chemical feedback. By responding minimally to chemical feedback, respiratory rate leaves the control of minute ventilation almost exclusively to inspiratory effort. In such cases, when assist is high, weak inspiratory efforts promote ineffective triggering, periodic breathing and diaphragmatic atrophy. Conversely, when assist is low, diaphragmatic efforts are intense and increase the risk for respiratory distress, asynchronies, ventilator-induced lung injury, diaphragmatic injury, and cardiovascular complications. This review thoroughly presents the multiple mechanisms by which respiratory rate may induce injury during mechanical ventilation, drawing the attention of critical care physicians to the potential injurious effects of respiratory rate insensitivity to chemical feedback during assisted ventilation.

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Noninvasive ventilation (NIV) has an established efficacy to improve gas exchange and reduce the work of breathing in patients with hypoxemic acute respiratory failure. The clinical efficacy in terms of meaningful outcome is less clear and depends very much on patient selection and assessment of the risks of the technique. The potential risks include an insufficient reduction of the oxygen consumption of the respiratory muscles in case of shock, an excessive increase in tidal volume in case of lung injury, and a risk of delayed or emergent intubation. With a careful selection of patients and a rapid decision regarding the need for intubation in case of failure, great benefits can be offered to patients. Emerging indications include its use in patients with treatment limitations, in the postoperative period, and in patients with immunosuppression. This last indication will necessitate reappraisal because the prognosis of the conditions associated with immunosuppression has improved over the years. In all cases, there is both a time window and a severity window for NIV to work, after which delaying endotracheal intubation may worsen outcome. The preventive use of NIV seems promising in this setting but needs more research. An emerging interesting new option is the use of high flow humidified oxygen, which seems to be intermediate between oxygen alone and NIV.