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187 result(s) for "Assisted mechanical ventilation"
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Surface EMG-based quantification of inspiratory effort: a quantitative comparison with P es
Inspiratory patient effort under assisted mechanical ventilation is an important quantity for assessing patient-ventilator interaction and recognizing over and under assistance. An established clinical standard is respiratory muscle pressure [Formula: see text], derived from esophageal pressure ([Formula: see text]), which requires the correct placement and calibration of an esophageal balloon catheter. Surface electromyography (sEMG) of the respiratory muscles represents a promising and straightforward alternative technique, enabling non-invasive monitoring of patient activity. A prospective observational study was conducted with patients under assisted mechanical ventilation, who were scheduled for elective bronchoscopy. Airway flow and pressure, esophageal/gastric pressures and sEMG of the diaphragm and intercostal muscles were recorded at four levels of pressure support ventilation. Patient efforts were quantified via the [Formula: see text]-time product ([Formula: see text]), the transdiaphragmatic pressure-time product ([Formula: see text]) and the EMG-time products (ETP) of the two sEMG channels. To improve the signal-to-noise ratio, a method for automatically selecting the more informative of the sEMG channels was investigated. Correlation between ETP and [Formula: see text] was assessed by determining a neuromechanical conversion factor [Formula: see text] between the two quantities. Moreover, it was investigated whether this scalar can be reliably determined from airway pressure during occlusion maneuvers, thus allowing to quantify inspiratory effort based solely on sEMG measurements. In total, 62 patients with heterogeneous pulmonary diseases were enrolled in the study, 43 of which were included in the data analysis. The ETP of the two sEMG channels was well correlated with [Formula: see text] ([Formula: see text] and [Formula: see text] for diaphragm and intercostal recordings, respectively). The proposed automatic channel selection method improved correlation with [Formula: see text] ([Formula: see text]). The neuromechanical conversion factor obtained by fitting ETP to [Formula: see text] varied widely between patients ([Formula: see text]) and was highly correlated with the scalar determined during occlusions ([Formula: see text], [Formula: see text]). The occlusion-based method for deriving [Formula: see text] from ETP showed a breath-wise deviation to [Formula: see text] of [Formula: see text] across all datasets. These results support the use of surface electromyography as a non-invasive alternative for monitoring breath-by-breath inspiratory effort of patients under assisted mechanical ventilation.
The Diaphragm Acts as a Brake during Expiration to Prevent Lung Collapse
Abstract Rationale The diaphragm is the major inspiratory muscle and is assumed to relax during expiration. However, electrical postinspiratory activity has been observed. Whether there is an expiratory diaphragmatic contraction that preserves lung patency has yet to be explored. Objectives We hypothesized the occurrence of an expiratory diaphragmatic contraction directed at stabilizing peripheral airways and preventing or reducing cyclic expiratory lung collapse. Methods Mild acute respiratory distress syndrome was induced in 10 anesthetized, spontaneously breathing pigs. Lung volume was decreased by lowering end-expiratory airway pressure in a stepwise manner. We recorded the diaphragmatic electric activity during expiration, dynamic computed tomographic scans, and respiratory mechanics. In five pigs, the same protocol was repeated during mechanical ventilation after muscle paralysis. Measurements and Main Results Diaphragmatic electric activity during expiration increased by decreasing end-expiratory lung volume during spontaneous breathing. This enhanced the diaphragm muscle force, to a greater extent with lower lung volume, indicating a diaphragmatic electromechanical coupling during spontaneous expiration. In turn, the resulting diaphragmatic contraction delayed and reduced the expiratory collapse and increased lung aeration compared with mechanical ventilation with muscle paralysis and absence of diaphragmatic activity. Conclusions The diaphragm is an important regulator of expiration. Its expiratory activity seems to preserve lung volume and to protect against lung collapse. The loss of diaphragmatic expiratory contraction during mechanical ventilation and muscle paralysis may be a contributing factor to unsuccessful respiratory support.
Assisted mechanical ventilation promotes recovery of diaphragmatic thickness in critically ill patients: a prospective observational study
Background Diaphragm atrophy and dysfunction are consequences of mechanical ventilation and are determinants of clinical outcomes. We hypothesize that partial preservation of diaphragm function, such as during assisted modes of ventilation, will restore diaphragm thickness. We also aim to correlate the changes in diaphragm thickness and function to outcomes and clinical factors. Methods This is a prospective, multicentre, observational study. Patients mechanically ventilated for more than 48 h in controlled mode and eventually switched to assisted ventilation were enrolled. Diaphragm ultrasound and clinical data collection were performed every 48 h until discharge or death. A threshold of 10% was used to define thinning during controlled and recovery of thickness during assisted ventilation. Patients were also classified based on the level of diaphragm activity during assisted ventilation. We evaluated the association between changes in diaphragm thickness and activity and clinical outcomes and data, such as ventilation parameters. Results Sixty-two patients ventilated in controlled mode and then switched to the assisted mode of ventilation were enrolled. Diaphragm thickness significantly decreased during controlled ventilation (1.84 ± 0.44 to 1.49 ± 0.37 mm, p  < 0.001) and was partially restored during assisted ventilation (1.49 ± 0.37 to 1.75 ± 0.43 mm, p  < 0.001). A diaphragm thinning of more than 10% was associated with longer duration of controlled ventilation (10 [5, 15] versus 5 [4, 8.5] days, p  = 0.004) and higher PEEP levels (12.6 ± 4 versus 10.4 ± 4 cmH 2 O, p  = 0.034). An increase in diaphragm thickness of more than 10% during assisted ventilation was not associated with any clinical outcome but with lower respiratory rate (16.7 ± 3.2 versus 19.2 ± 4 bpm, p  = 0.019) and Rapid Shallow Breathing Index (37 ± 11 versus 44 ± 13, p  = 0.029) and with higher Pressure Muscle Index (2 [0.5, 3] versus 0.4 [0, 1.9], p  = 0.024). Change in diaphragm thickness was not related to diaphragm function expressed as diaphragm thickening fraction. Conclusion Mode of ventilation affects diaphragm thickness, and preservation of diaphragmatic contraction, as during assisted modes, can partially reverse the muscle atrophy process. Avoiding a strenuous inspiratory work, as measured by Rapid Shallow Breathing Index and Pressure Muscle Index, may help diaphragm thickness restoration.
Reduction of patient-ventilator asynchrony by reducing tidal volume during pressure-support ventilation
Objective To identify ventilatory setting adjustments that improve patient-ventilator synchrony during pressure-support ventilation in ventilator-dependent patients by reducing ineffective triggering events without decreasing tolerance. Design and setting Prospective physiological study in a 13-bed medical intensive care unit in a university hospital. Patients and participants Twelve intubated patients with more than 10% of ineffective breaths while receiving pressure-support ventilation. Interventions Flow, airway-pressure, esophageal-pressure, and gastric-pressure signals were used to measure patient inspiratory effort. To decrease ineffective triggering the following ventilator setting adjustments were randomly adjusted: pressure support reduction, insufflation time reduction, and change in end-expiratory pressure. Measurements and results Reducing pressure support from 20.0 cm H 2 O (IQR 19.5–20) to 13.0 (12.0–14.0) reduced tidal volume [10.2 ml/kg predicted body weight (7.2–11.5) to 5.9 (4.9–6.7)] and minimized ineffective triggering events [45% of respiratory efforts (36–52) to 0% (0–7)], completely abolishing ineffective triggering in two-thirds of patients. The ventilator respiratory rate increased due to unmasked wasted efforts, with no changes in patient respiratory rate [26.5 breaths/min (23.1–31.9) vs. 29.4 (24.6–34.5)], patient effort, or arterial PCO 2 . Shortening the insufflation time reduced ineffective triggering events and patient effort, while applying positive end-expiratory pressure had no influence on asynchrony. Conclusions Markedly reducing pressure support or inspiratory duration to reach a tidal volume of about 6 ml/kg predicted body weight eliminated ineffective triggering in two-thirds of patients with weaning difficulties and a high percentage of ineffective efforts without inducing excessive work of breathing or modifying patient respiratory rate.
Monitoring of invasive assisted mechanical ventilation: a good clinical practice document by the Italian Society of Anesthesia, Analgesia, Resuscitation, and Intensive Care (SIAARTI)
The Italian Society of Anesthesia, Analgesia, Resuscitation, and Intensive Care (SIAARTI) developed a good clinical practice document providing consensus-based statements on the monitoring of respiratory variables during weaning from invasive mechanical ventilation in adult patients. The aim was to summarize key parameters and available monitoring techniques to support healthcare professionals in daily clinical practice. The statements and supporting rationales were drafted by a panel of 10 experts to assist clinicians in selecting appropriate monitoring tools for the various respiratory functions involved during assisted ventilation. A total of 13 statements were issued, grouped into 8 items (rationale for monitoring, choice of the level of assistance, monitoring of respiratory patterns, respiratory effort, diaphragm functionality, respiratory drive, patient-ventilator synchrony, discontinuation of invasive assisted ventilation). The panel’s work offers a practical bedside tool designed to optimize monitoring while acknowledging the heterogeneity of practices and equipment across Italian intensive care units.
The P0.1 maneuver as an alternative method for assessing the validity of esophageal pressure measurements during assisted ventilation: an exploratory analysis
Background Transpulmonary pressure, calculated as the difference between airway pressure (Paw) and esophageal pressure (Pes), is an important monitoring parameter during assisted mechanical ventilation, provided Pes is measured via a correctly placed and filled esophageal pressure probe. The reference method to verify Pes accuracy in spontaneously breathing patients requires calculating the ratio of changes in Pes and Paw (ΔPes/ΔPaw) during an inspiratory effort against an occluded airway. We hypothesized that the P0.1 maneuver, a brief and repeatable test, could provide an alternative means to assess ΔPes/ΔPaw during assisted mechanical ventilation. Methods We performed an exploratory secondary analysis of data from a multicenter prospective observational study (ICEBERG study; NCT05203536). In 35 patients receiving assisted mechanical ventilation, ΔPes/ΔPaw obtained during P0.1 maneuvers (Ratio P0.1 , experimental method) was compared with ΔPes/ΔPaw from prolonged expiratory occlusion maneuvers (Ratio occ , reference method) using linear regression and Bland–Altman analysis. Results Among 25 patients with 65 evaluable measurements, Ratio P0.1 showed a moderate correlation ( R 2 :0.647, p  < 0.0001) with Ratio occ . Bland–Altman analysis demonstrated minimal bias and acceptable agreement between methods. Using the occlusion maneuver as reference, Ratio P0.1 identified incorrect Pes measurement with a sensitivity of 93% and a specificity for identifying correct Pes measurement of 71%. Results were consistent across patient subgroups. Conclusions Our exploratory analysis suggests that the P0.1 maneuver may support semi-continuous screening of esophageal pressure signal validity during assisted ventilation. While abnormal P0.1 values should prompt confirmatory occlusion testing, values within the expected range may help rule out major measurement errors. These findings provide a rationale for prospective validation studies including different ventilator types. Trial registration : clinicaltrials.gov, NCT05203536. Registered 24. January 2022—Retrospectively registered, https://classic.clinicaltrials.gov/ct2/show/NCT05203536
Bedside waveforms interpretation as a tool to identify patient-ventilator asynchronies
During assisted modes of ventilatory support the ventilatory output is the final expression of the interaction between the ventilator and the patient's controller of breathing. This interaction may lead to patient-ventilator asynchrony, preventing the ventilator from achieving its goals, and may cause patient harm. Flow, volume, and airway pressure signals are significantly affected by patient-ventilator interaction and may serve as a tool to guide the physician to take the appropriate action to improve the synchrony between patient and ventilator. This review discusses the basic waveforms during assisted mechanical ventilation and how their interpretation may influence the management of ventilated patients. The discussion is limited on waveform eye interpretation of the signals without using any intervention which may interrupt the process of mechanical ventilation. Flow, volume, and airway pressure may be used to (a) identify the mode of ventilator assistance, triggering delay, ineffective efforts, and autotriggering, (b) estimate qualitatively patient's respiratory efforts, and (c) recognize delayed and premature opening of exhalation valve. These signals may also serve as a tool for gross estimation of respiratory system mechanics and monitor the effects of disease progression and various therapeutic interventions. Flow, volume, and airway pressure waveforms are valuable real-time tools in identifying various aspects of patient-ventilator interaction.
Determination of respiratory system compliance during pressure support ventilation by small variations of pressure support
In mechanically ventilated patients, measurement of respiratory system compliance (Crs) is of high clinical interest. Spontaneous breathing activity during pressure support ventilation (PSV) can impede the correct assessment of Crs and also alter the true Crs by inducing lung recruitment. We describe a method for determination of Crs during PSV and assess its accuracy in a study on 20 mechanically ventilated patients. To assess Crs during pressure support ventilation (Crs,PSV), we performed repeated changes in pressure support level by ± 2 cmH2O. Crs,PSV was calculated from the volume change induced by these changes in pressure support level, taking into account the inspiration time and the expiratory time constant. As reference methods, we used Crs, measured during volume controlled ventilation (Crs,VCV). In a post-hoc analysis, we assessed Crs during the last 20% of the volume-controlled inflation (Crs,VCV20). Values were compared by linear regression and Bland–Altman methods comparison. Comparing Crs,PSV to the reference value Crs,VCV, we found a coefficient of determination (r2) of 0.90, but a relatively high bias of − 7 ml/cm H2O (95% limits of agreement − 16.7 to + 2.7 ml/cmH2O). Comparison with Crs,VCV20 resulted in a negligible bias (− 1.3 ml/cmH2O, 95% limits of agreement − 13.9 to + 11.3) and r2 of 0.81. We conclude that the novel method provides an estimate of end-inspiratory Crs during PSV. Despite its limited accuracy, it might be useful for non-invasive monitoring of Crs in patients undergoing pressure support ventilation.
Circulating Skeletal Troponin During Weaning From Mechanical Ventilation and Their Association to Diaphragmatic Function: A Pilot Study
Background: Patients with acute respiratory failure (ARF) may need mechanical ventilation (MV), which can lead to diaphragmatic dysfunction and muscle wasting, thus making difficult the weaning from the ventilator. Currently, there are no biomarkers specific for respiratory muscle and their function can only be assessed trough ultrasound or other invasive methods. Previously, the fast and slow isoform of the skeletal troponin I (fsTnI and ssTnI, respectively) have shown to be specific markers of muscle damage in healthy volunteers. We aimed therefore at describing the trend of skeletal troponin in mixed population of ICU patients undergoing weaning from mechanical ventilation and compared the value of fsTnI and ssTnI with diaphragmatic ultrasound derived parameters. Methods: In this prospective observational study we enrolled consecutive patients recovering from acute hypoxemic respiratory failure (AHRF) within 24 h from the start of weaning. Every day an arterial blood sample was collected to measure fsTnI, ssTnI, and global markers of muscle damage, such as ALT, AST, and CPK. Moreover, thickening fraction (TF) and diaphragmatic displacement (DE) were assessed by diaphragmatic ultrasound. The trend of fsTnI and ssTnI was evaluated during the first 3 days of weaning. Results: We enrolled 62 consecutive patients in the study, with a mean age of 67 ± 13 years and 43 of them (69%) were male. We did not find significant variations in the ssTnI trend ( p = 0.623), but fsTnI significantly decreased over time by 30% from Day 1 to Day 2 and by 20% from Day 2 to Day 3 ( p < 0.05). There was a significant interaction effect between baseline ssTnI and DE [ F (2) = 4.396, p = 0.015], with high basal levels of ssTnI being associated to a higher decrease in DE. On the contrary, the high basal levels of fsTnI at day 1 were characterized by significant higher DE at each time point. Conclusions: Skeletal muscle proteins have a distinctive pattern of variation during weaning from mechanical ventilation. At day 1, a high basal value of ssTnI were associated to a higher decrease over time of diaphragmatic function while high values of fsTnI were associated to a higher displacement at each time point.
A surgical Decision-making scoring model for spontaneous ventilation- and mechanical ventilation-video-assisted thoracoscopic surgery in non-small-cell lung cancer patients
Backgrounds Spontaneous ventilation-video-assisted thoracoscopic surgery (SV-VATS) has been applied to non-small cell lung cancer (NSCLC) patients in many centers. Since it remains a new and challenging surgical technique, only selected patients can be performed SV-VATS. We aim to conduct a retrospective single-center study to develop a clinical decision-making model to make surgery decision between SV-VATS and MV (mechanical ventilation) -VATS in NSCLC patients more objectively and individually. Methods Four thousand three hundred sixty-eight NSCLC patients undergoing SV-VATS or MV-VATS in the department of thoracic surgery between 2011 and 2018 were included. Univariate and multivariate regression analysis were used to identify potential factors influencing the surgical decisions. Factors with statistical significance were selected for constructing the Surgical Decision-making Scoring (SDS) model. The performance of the model was validated by area under the receiver operating characteristic curve (AUC), calibration curves and decision curve analysis (DCA). Results The Surgical Decision-making Scoring (SDS) model was built guided by the clinical judgment and statistically significant results of univariate and multivariate regression analyses of potential predictors, including smoking status ( p  = 0.03), BMI ( p  < 0.001), ACCI ( p  = 0.04), T stage ( p  < 0.001), N stage ( p  < 0.001), ASA grade ( p  < 0.001) and surgical technique ( p  < 0.001). The AUC of the training group and the testing group were 0.72 and 0.70, respectively. The calibration curves and the DCA curve revealed that the SDS model has a desired performance in predicting the surgical decision. Conclusions This SDS model is the first clinical decision-making model developed for an individual NSCLC patient to make decision between SV-VATS and MV-VATS.