Respiratory drive: a journey from health to disease.

Respiratory drive is defined as the intensity of respiratory centers output during the breath and is primarily affected by cortical and chemical feedback mechanisms. During the involuntary act of breathing, chemical feedback, primarily mediated through CO2, is the main determinant of respiratory drive. Respiratory drive travels through neural pathways to respiratory muscles, which execute the breathing process and generate inspiratory flow (inspiratory flow-generation pathway). In a healthy state, inspiratory flow-generation pathway is intact, and thus respiratory drive is satisfied by the rate of volume increase, expressed by mean inspiratory flow, which in turn determines tidal volume. In this review, we will explain the pathophysiology of altered respiratory drive by analyzing the respiratory centers response to arterial partial pressure of CO2 (PaCO2) changes. Both high and low respiratory drive have been associated with several adverse effects in critically ill patients. Hence, it is crucial to understand what alters the respiratory drive. Changes in respiratory drive can be explained by simultaneously considering the (1) ventilatory demands, as dictated by respiratory centers activity to CO2 (brain curve); (2) actual ventilatory response to CO2 (ventilation curve); and (3) metabolic hyperbola. During critical illness, multiple mechanisms affect the brain and ventilation curves, as well as metabolic hyperbola, leading to considerable alterations in respiratory drive. In critically ill patients the inspiratory flow-generation pathway is invariably compromised at various levels. Consequently, mean inspiratory flow and tidal volume do not correspond to respiratory drive, and at a given PaCO2, the actual ventilation is less than ventilatory demands, creating a dissociation between brain and ventilation curves. Since the metabolic hyperbola is one of the two variables that determine PaCO2 (the other being the ventilation curve), its upward or downward movements increase or decrease respiratory drive, respectively. Mechanical ventilation indirectly influences respiratory drive by modifying PaCO2 levels through alterations in various parameters of the ventilation curve and metabolic hyperbola. Understanding the diverse factors that modulate respiratory drive at the bedside could enhance clinical assessment and the management of both the patient and the ventilator.

Driving pressure of respiratory system and lung stress in mechanically ventilated patients with active breathing.

BACKGROUND: During control mechanical ventilation (CMV), the driving pressure of the respiratory system (ΔPrs) serves as a surrogate of transpulmonary driving pressure (ΔPlung). Expiratory muscle activity that decreases end-expiratory lung volume may impair the validity of ΔPrs to reflect ΔPlung. This prospective observational study in patients with acute respiratory distress syndrome (ARDS) ventilated with proportional assist ventilation (PAV+), aimed to investigate: (1) the prevalence of elevated ΔPlung, (2) the ΔPrs-ΔPlung relationship, and (3) whether dynamic transpulmonary pressure (Plungsw) and effort indices (transdiaphragmatic and respiratory muscle pressure swings) remain within safe limits. METHODS: Thirty-one patients instrumented with esophageal and gastric catheters (n = 22) were switched from CMV to PAV+ and respiratory variables were recorded, over a maximum of 24 h. To decrease the contribution of random breaths with irregular characteristics, a 7-breath moving average technique was applied. In each patient, measurements were also analyzed per deciles of increasing lung elastance (Elung). Patients were divided into Group A, if end-inspiratory transpulmonary pressure (PLEI) increased as Elung increased, and Group B, which showed a decrease or no change in PLEI with Elung increase. RESULTS: In 44,836 occluded breaths, ΔPlung ≥ 12 cmH2O was infrequently observed [0.0% (0.0-16.9%) of measurements]. End-expiratory lung volume decrease, due to active expiration, was associated with underestimation of ΔPlung by ΔPrs, as suggested by a negative linear relationship between transpulmonary pressure at end-expiration (PLEE) and ΔPlung/ΔPrs. Group A included 17 and Group B 14 patients. As Elung increased, ΔPlung increased mainly due to PLEI increase in Group A, and PLEE decrease in Group B. Although ΔPrs had an area receiver operating characteristic curve (AUC) of 0.87 (95% confidence intervals 0.82-0.92, P < 0.001) for ΔPlung ≥ 12 cmH2O, this was due exclusively to Group A [0.91 (0.86-0.95), P < 0.001]. In Group B, ΔPrs showed no predictive capacity for detecting ΔPlung ≥ 12 cmH2O [0.65 (0.52-0.78), P > 0.05]. Most of the time Plungsw and effort indices remained within safe range. CONCLUSION: In patients with ARDS ventilated with PAV+, injurious tidal lung stress and effort were infrequent. In the presence of expiratory muscle activity, ΔPrs underestimated ΔPlung. This phenomenon limits the usefulness of ΔPrs as a surrogate of tidal lung stress, regardless of the mode of support.

High-Flow Nasal Oxygen for Severe COVID-19 Pneumonia in Greek Patients: A Prospective Observational Study.

INTRODUCTION: High-flow nasal oxygen (HFNO) and prone positioning may improve outcomes of coronavirus disease 2019 (COVID-19) patients treated in the intensive care unit (ICU). The aim of this study was to describe outcomes following the timely application of HFNO and prone positioning in COVID-19 patients treated in a ward setting. METHODS: The study included 89 prospectively recruited subjects at the COVID-19 ward unit of the University Hospital of Heraklion, Greece, between March and December 2020. RESULTS: Seventy-four (83%) of the 89 subjects in the study had severe COVID-19. Of those, 33 (45%) required HFNO treatment and prone positioning and 15 (45%) were transferred to the ICU, with 4 of them being intubated. Severe COVID-19 and HFNO needs were associated with an increased pneumonia severity index (PSI) score on admission and a worse PaO2/FiO2 ratio. In multivariate analysis, PSI was the only independent predictor of subsequent HFNO needs (OR=1.022). Overall intubation and mortality rates were 5.6% and 3.4%, respectively. CONCLUSION: This study shows that for patients with severe COVID-19 hospitalized in medical wards, standard COVID-19 treatment, along with the timely utilization of HFNO and prone positioning, resulted in excellent outcomes with fewer ICU admission rates.

Hiccup-like Contractions in Mechanically Ventilated Patients: Individualized Treatment Guided by Transpulmonary Pressure.

Hiccups-like contractions, including hiccups, respiratory myoclonus, and diaphragmatic tremor, refer to involuntary, spasmodic, and inspiratory muscle contractions. They have been repeatedly described in mechanically ventilated patients, especially those with central nervous damage. Nevertheless, their effects on patient-ventilator interaction are largely unknown, and even more overlooked is their contribution to lung and diaphragm injury. We describe, for the first time, how the management of hiccup-like contractions was individualized based on esophageal and transpulmonary pressure measurements in three mechanically ventilated patients. The necessity or not of intervention was determined by the effects of these contractions on arterial blood gases, patient-ventilator synchrony, and lung stress. In addition, esophageal pressure permitted the titration of ventilator settings in a patient with hypoxemia and atelectasis secondary to hiccups and in whom sedatives failed to eliminate the contractions and muscle relaxants were contraindicated. This report highlights the importance of esophageal pressure monitoring in the clinical decision making of hiccup-like contractions in mechanically ventilated patients.

The oesophageal balloon for respiratory monitoring in ventilated patients: updated clinical review and practical aspects.

There is a well-recognised importance for personalising mechanical ventilation settings to protect the lungs and the diaphragm for each individual patient. Measurement of oesophageal pressure (P oes) as an estimate of pleural pressure allows assessment of partitioned respiratory mechanics and quantification of lung stress, which helps our understanding of the patient's respiratory physiology and could guide individualisation of ventilator settings. Oesophageal manometry also allows breathing effort quantification, which could contribute to improving settings during assisted ventilation and mechanical ventilation weaning. In parallel with technological improvements, P oes monitoring is now available for daily clinical practice. This review provides a fundamental understanding of the relevant physiological concepts that can be assessed using P oes measurements, both during spontaneous breathing and mechanical ventilation. We also present a practical approach for implementing oesophageal manometry at the bedside. While more clinical data are awaited to confirm the benefits of P oes-guided mechanical ventilation and to determine optimal targets under different conditions, we discuss potential practical approaches, including positive end-expiratory pressure setting in controlled ventilation and assessment of inspiratory effort during assisted modes.

Neural Network-Enabled Identification of Weak Inspiratory Efforts during Pressure Support Ventilation Using Ventilator Waveforms.

During pressure support ventilation (PSV), excessive assist results in weak inspiratory efforts and promotes diaphragm atrophy and delayed weaning. The aim of this study was to develop a classifier using a neural network to identify weak inspiratory efforts during PSV, based on the ventilator waveforms. Recordings of flow, airway, esophageal and gastric pressures from critically ill patients were used to create an annotated dataset, using data from 37 patients at 2-5 different levels of support, computing the inspiratory time and effort for every breath. The complete dataset was randomly split, and data from 22 patients (45,650 breaths) were used to develop the model. Using a One-Dimensional Convolutional Neural Network, a predictive model was developed to characterize the inspiratory effort of each breath as weak or not, using a threshold of 50 cmH2O*s/min. The following results were produced by implementing the model on data from 15 different patients (31,343 breaths). The model predicted weak inspiratory efforts with a sensitivity of 88%, specificity of 72%, positive predictive value of 40%, and negative predictive value of 96%. These results provide a 'proof-of-concept' for the ability of such a neural-network based predictive model to facilitate the implementation of personalized assisted ventilation.

The Role of Noninvasive Respiratory Management in Patients with Severe COVID-19 Pneumonia.

Acute hypoxemic respiratory failure is the principal cause of hospitalization, invasive mechanical ventilation and death in severe COVID-19 infection. Nearly half of intubated patients with COVID-19 eventually die. High-Flow Nasal Oxygen (HFNO) and Noninvasive Ventilation (NIV) constitute valuable tools to avert endotracheal intubation in patients with severe COVID-19 pneumonia who do not respond to conventional oxygen treatment. Sparing Intensive Care Unit beds and reducing intubation-related complications may save lives in the pandemic era. The main drawback of HFNO and/or NIV is intubation delay. Cautious selection of patients with severe hypoxemia due to COVID-19 disease, close monitoring and appropriate employment and titration of HFNO and/or NIV can increase the rate of success and eliminate the risk of intubation delay. At the same time, all precautions to protect the healthcare personnel from viral transmission should be taken. In this review, we summarize the evidence supporting the application of HFNO and NIV in severe COVID-19 hypoxemic respiratory failure, analyse the risks associated with their use and provide a path for their proper implementation.

A rational approach on the use of extracorporeal membrane oxygenation in severe hypoxemia: advanced technology is not a panacea.

Veno-venous extracorporeal membrane oxygenation (ECMO) is a helpful intervention in patients with severe refractory hypoxemia either because mechanical ventilation cannot ensure adequate oxygenation or because lung protective ventilation is not feasible. Since ECMO is a highly invasive procedure with several, potentially devastating complications and its implementation is complex and expensive, simpler and less invasive therapeutic options should be first exploited. Low tidal volume and driving pressure ventilation, prone position, neuromuscular blocking agents and individualized ventilation based on transpulmonary pressure measurements have been demonstrated to successfully treat the vast majority of mechanically ventilated patients with severe hypoxemia. Veno-venous ECMO has a place in the small portion of severely hypoxemic patients in whom these strategies fail. A combined analysis of recent ARDS trials revealed that ECMO was used in only 2.15% of patients (n = 145/6736). Nevertheless, ECMO use has sharply increased in the last decade, raising questions regarding its thoughtful use. Such a policy could be harmful both for patients as well as for the ECMO technique itself. This narrative review attempts to describe together the practical approaches that can be offered to the sickest patients before going to ECMO, as well as the rationale and the limitations of ECMO. The benefit and the drawbacks associated with ECMO use along with a direct comparison with less invasive therapeutic strategies will be analyzed.

Esophageal and transdiaphragmatic pressure swings as indices of inspiratory effort.

AIM: To describe the correlation between the inspiratory esophageal and transdiaphragmatic pressure swings (ΔPes and ΔPdi), easily measured indices of inspiratory effort, with the gold-standard, the transdiaphragmatic pressure time product (PTPPdi/min), and assess the accuracy of swing pressures in predicting very high or low effort. METHOD: Retrospective analysis of data from patients enrolled in four previous studies. ROC curves of ΔPes and ΔPdi values for specific PTPPdi/min thresholds (50, 150, 200 cmH2O × sec/min) were constructed, and the diagnostic accuracy of different thresholds of swing values were computed. RESULTS: A threshold of inspiratory ΔP<7cmH2O can be used to identify most patients with low effort, as lower ΔP thresholds have low sensitivity. Thresholds of inspiratory ΔP>14-18cmH2O can be used to identify patients with very high inspiratory effort (PTPPdi/min> 200 cmH2O × sec/min). CONCLUSIONS: The results of this study can help clinicians better select and interpret thresholds of ΔP to evaluate inspiratory effort.

Hemophagocytic lymphohistiocytosis syndrome associated with Epstein-Barr infection in an immunocompetent patient. A case study.

INTRODUCTION: Hemophagocytic lymphohistiocytosis (HLH) is a life-threatening rare disease resulting from the uncontrolled activation of the immune system, leading to unrestrained cytokine release and macrophage activation. It can be either hereditary or acquired due to infections, hematological disease or malignancy. CASE REPORT: We present the case of a 19-year old woman that presented with high fever and acute cholestatic hepatitis. She was initially admitted to the Gastroenterology department and the following days she developed respiratory distress and multiorgan insufficiency that necessitated intubation and support in the Intensive Care Unit. Fever, splenomegaly, hypertriglyceridemia, increased ferritin levels and hemophagocytosis in the bone marrow were found, thus, fulfilling the criteria of hemophagocytic lymphohistiocytosis. Laboratory examination was notable for positive serology (IgM and IgG) and PCR for EBV in the serum. An extensive workup including virology and immunologic workup, blood cultures, a CT of the thorax and the abdomen and a bone marrow biopsy did not reveal any cause of secondary HLH other than the EBV infection. The patient was treated with high dose corticosteroids and intravenous immunoglobulins with slow resolution of her symptoms. CONCLUSIONS: In patients with EBV infection who exhibit persistent high fever and unresponsiveness to antibiotics, the possibility of HLH should be considered. Early diagnosis and rapid initiation of appropriate treatment may avert an unfavorable outcome.

Airway pressure morphology and respiratory muscle activity during end-inspiratory occlusions in pressure support ventilation.

BACKGROUND: The driving pressure of the respiratory system is a valuable indicator of global lung stress during passive mechanical ventilation. Monitoring lung stress in assisted ventilation is indispensable, but achieving passive conditions in spontaneously breathing patients to measure driving pressure is challenging. The accuracy of the morphology of airway pressure (Paw) during end-inspiratory occlusion to assure passive conditions during pressure support ventilation has not been examined. METHODS: Retrospective analysis of end-inspiratory occlusions obtained from critically ill patients during pressure support ventilation. Flow, airway, esophageal, gastric, and transdiaphragmatic pressures were analyzed. The rise of gastric pressure during occlusion with a constant/decreasing transdiaphragmatic pressure was used to identify and quantify the expiratory muscle activity. The Paw during occlusion was classified in three patterns, based on the differences at three pre-defined points after occlusion (0.3, 1, and 2 s): a "passive-like" decrease followed by plateau, a pattern with "clear plateau," and an "irregular rise" pattern, which included all cases of late or continuous increase, with or without plateau. RESULTS: Data from 40 patients and 227 occlusions were analyzed. Expiratory muscle activity during occlusion was identified in 79% of occlusions, and at all levels of assist. After classifying occlusions according to Paw pattern, expiratory muscle activity was identified in 52%, 67%, and 100% of cases of Paw of passive-like, clear plateau, or irregular rise pattern, respectively. The driving pressure was evaluated in the 133 occlusions having a passive-like or clear plateau pattern in Paw. An increase in gastric pressure was present in 46%, 62%, and 64% of cases at 0.3, 1, and 2 s, respectively, and it was greater than 2 cmH2O, in 10%, 20%, and 15% of cases at 0.3, 1, and 2 s, respectively. CONCLUSIONS: The pattern of Paw during an end-inspiratory occlusion in pressure support cannot assure the absence of expiratory muscle activity and accurate measurement of driving pressure. Yet, because driving pressure can only be overestimated due to expiratory muscle contraction, in everyday practice, a low driving pressure indicates an absence of global lung over-stretch. A measurement of high driving pressure should prompt further diagnostic workup, such as a measurement of esophageal pressure.

Validation of a Proposed Algorithm for Assistance Titration During Proportional Assist Ventilation With Load-Adjustable Gain Factors.

BACKGROUND: The present study aimed to validate a recently proposed algorithm for assistance titration during proportional assist ventilation with load-adjustable gain factors, based on a noninvasive estimation of maximum inspiratory pressure (peak Pmus) and inspiratory effort (pressure-time product [PTP] peak Pmus). METHODS: Retrospective analysis of the recordings obtained from 26 subjects ventilated on proportional assist ventilation with load-adjustable gain factors under different conditions, each considered as an experimental case. The estimated inspiratory output (peak Pmus) and effort (PTP-peak Pmus) were compared with the actual-determined by the measurement of transdiaphragmatic pressure- and the derived PTP. Validation of the algorithm was performed by assessing the accuracy of peak Pmus in predicting the actual inspiratory muscle effort and indicating the appropriate level of assist. RESULTS: In the 63 experimental cases analyzed, a limited agreement was observed between the estimated and the actual inspiratory muscle pressure (-11 to 10 cm H2O) and effort (-82 to 125 cm H2O × s/min). The sensitivity and specificity of peak Pmus to predict the range of the actual inspiratory effort was 81.2% and 58.1%, respectively. In 49% of experimental cases, the level of assist indicated by the algorithm differed from that indicated by the transdiaphragmatic pressure and PTP. CONCLUSIONS: The proposed algorithm had limited accuracy in estimating inspiratory muscle effort and with indicating the appropriate level of assist.

Respiratory Drive in Critically Ill Patients. Pathophysiology and Clinical Implications.

Respiratory drive, the intensity of the respiratory center's output, determines the effort exerted in each breath. The increasing awareness of the adverse effects of both strong and weak respiratory efforts during mechanical ventilation on patient outcome brings attention to the respiratory drive of the critically ill patient. Critical illness can affect patients' respiratory drive through multiple pathways, mainly operating through three feedback systems: cortical, metabolic, and chemical. The chemical feedback system, defined as the response of the respiratory center's output to changes in arterial blood gases and pH, is one of the most important determinants of respiratory drive. The purpose of this state-of-the-art review is to describe the determinants of respiratory drive in critically ill patients, review the tools available to assess respiratory drive at the bedside, and discuss the implications of altered respiratory drive during mechanical ventilation. An analysis that relates arterial carbon dioxide levels with brain's response to this stimulus will be presented, contrasting the brain's responses to the patient's ability to generate effective alveolar ventilation, both during unassisted breathing and with different modes of ventilatory assist. This analysis may facilitate comprehension of the pathophysiology of respiratory drive in critically ill patients. As we aim to avoid both over- and under-assistance with mechanical ventilation, considering the patients' respiratory drive at the bedside may improve clinical assessment and management of the patient and the ventilator.

Driving pressure during proportional assist ventilation: an observational study.

BACKGROUND: During passive mechanical ventilation, the driving pressure of the respiratory system is an important mediator of ventilator-induced lung injury. Monitoring of driving pressure during assisted ventilation, similar to controlled ventilation, could be a tool to identify patients at risk of ventilator-induced lung injury. The aim of this study was to describe driving pressure over time and to identify whether and when high driving pressure occurs in critically ill patients during assisted ventilation. METHODS: Sixty-two patients fulfilling criteria for assisted ventilation were prospectively studied. Patients were included when the treating physician selected proportional assist ventilation (PAV+), a mode that estimates respiratory system compliance. In these patients, continuous recordings of all ventilator parameters were obtained for up to 72 h. Driving pressure was calculated as tidal volume-to-respiratory system compliance ratio. The distribution of driving pressure and tidal volume values over time was examined, and periods of sustained high driving pressure (≥ 15 cmH2O) and of stable compliance were identified and analyzed. RESULTS: The analysis included 3200 h of ventilation, consisting of 8.8 million samples. For most (95%) of the time, driving pressure was < 15 cmH2O and tidal volume < 11 mL/kg (of ideal body weight). In most patients, high driving pressure was observed for short periods of time (median 2.5 min). Prolonged periods of high driving pressure were observed in five patients (8%). During the 661 periods of stable compliance, high driving pressure combined with a tidal volume ≥ 8 mL/kg was observed only in 11 cases (1.6%) pertaining to four patients. High driving pressure occurred almost exclusively when respiratory system compliance was low, and compliance above 30 mL/cmH2O excluded the presence of high driving pressure with 90% sensitivity and specificity. CONCLUSIONS: In critically ill patients fulfilling criteria for assisted ventilation, and ventilated in PAV+ mode, sustained high driving pressure occurred in a small, yet not negligible number of patients. The presence of sustained high driving pressure was not associated with high tidal volume, but occurred almost exclusively when compliance was below 30 mL/cmH2O.

The Injurious Effects of Elevated or Nonelevated Respiratory Rate during Mechanical Ventilation.

Respiratory rate is one of the key variables that is set and monitored during mechanical ventilation. As part of increasing efforts to optimize mechanical ventilation, it is prudent to expand understanding of the potential harmful effects of not only volume and pressures but also 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-recognized 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 V. e 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.

Can proportional ventilation modes facilitate exercise in critically ill patients? A physiological cross-over study : Pressure support versus proportional ventilation during lower limb exercise in ventilated critically ill patients.

BACKGROUND: Early exercise of critically ill patients may have beneficial effects on muscle strength, mass and systemic inflammation. During pressure support ventilation (PSV), a mismatch between demand and assist could increase work of breathing and limit exercise. A better exercise tolerance is possible with a proportional mode of ventilation (Proportional Assist Ventilation, PAV+ and Neurally Adjusted Ventilatory Assist, NAVA). We examined whether, in critically ill patients, PSV and proportional ventilation have different effects on respiratory muscles unloading and work efficiency during exercise. METHODS: Prospective pilot randomized cross-over study performed in a medico-surgical ICU. Patients requiring mechanical ventilation >48 h were enrolled. At initiation, the patients underwent an incremental workload test on a cycloergometer to determine the maximum level capacity. The next day, 2 15-min exercise, at 60% of the maximum capacity, were performed while patients were randomly ventilated with PSV and PAV+ or NAVA. The change in oxygen consumption (ΔVO2, indirect calorimetry) and the work efficiency (ratio of ΔVO2 per mean power) were computed. RESULTS: Ten patients were examined, 6 ventilated with PSV/PAV+ and 4 with PSV/NAVA. Despite the same mean inspiratory pressure at baseline between the modes, baseline VO2 (median, IQR) was higher during proportional ventilation (301 ml/min, 270-342) compared to PSV (249 ml/min, 206-353). Exercise with PSV was associated with a significant increase in VO2 (ΔVO2, median, IQR) (77.6 ml/min, 59.9-96.5), while VO2 did not significantly change during exercise with proportional modes (46.3 ml/min, 5.7-63.7, p < 0.05). As a result, exercise with proportional modes was associated with a better work efficiency than with PSV. The ventilator modes did not affect patient's dyspnea, limb fatigue, distance, hemodynamics and breathing pattern. CONCLUSIONS: Proportional ventilation during exercise results in higher work efficiency and less increase in VO2 compared to ventilation with PSV. These preliminary findings suggest that proportional ventilation could enhance the training effect and facilitate rehabilitation.

Patient-Ventilator Dyssynchrony.

In mechanically ventilated patients, assisted mechanical ventilation (MV) is employed early, following the acute phase of critical illness, in order to eliminate the detrimental effects of controlled MV, most notably the development of ventilator-induced diaphragmatic dysfunction. Nevertheless, the benefits of assisted MV are often counteracted by the development of patient-ventilator dyssynchrony. Patient-ventilator dyssynchrony occurs when either the initiation and/or termination of mechanical breath is not in time agreement with the initiation and termination of neural inspiration, respectively, or if the magnitude of mechanical assist does not respond to the patient's respiratory demand. As patient-ventilator dyssynchrony has been associated with several adverse effects and can adversely influence patient outcome, every effort should be made to recognize and correct this occurrence at bedside. To detect patient-ventilator dyssynchronies, the physician should assess patient comfort and carefully inspect the pressure- and flow-time waveforms, available on the ventilator screen of all modern ventilators. Modern ventilators offer several modifiable settings to improve patient-ventilator interaction. New proportional modes of ventilation are also very helpful in improving patient-ventilator interaction.

Accuracy of delivered airway pressure and work of breathing estimation during proportional assist ventilation: a bench study.

BACKGROUND: Proportional assist ventilation+ (PAV+) delivers airway pressure (P aw) in proportion to patient effort (P mus) by using the equation of motion of the respiratory system. PAV+ calculates automatically respiratory mechanics (elastance and resistance); the work of breathing (WOB) is estimated by the ventilator. The accuracy of P mus estimation and hence accuracy of the delivered P aw and WOB calculation have not been assessed. This study aimed at assessing the accuracy of delivered P aw and calculated WOB by PAV+ and examining the factors influencing this accuracy. METHODS: Using an active lung model with different respiratory mechanics, we compared (1) the actual delivered P aw by the ventilator to the theoretical P aw as defined by the equation of motion and (2) the WOB value displayed by the ventilator to the WOB measured from a Campbell diagram. RESULTS: Irrespective of respiratory mechanics and gain, the ventilator provided a P aw approximately 25 % lower than expected. This underassistance was greatest at the beginning of the inspiration. Intrinsic PEEP (PEEPi), associated with an increase in trigger delay, was a major factor affecting PAV+ accuracy. The absolute value of total WOB displayed by the ventilator was underestimated, but the changes in WOB were accurately detected by the ventilator. CONCLUSION: The assistance provided by PAV+ well follows P mus but with a constant underassistance. This is associated with an underestimation by the ventilator of the WOB. PEEPi can be a major factor contributing to PAV+ inaccuracy. Clinical recommendations should include using a high trigger sensitivity and a careful PEEP titration.