Heart-lungs interactions are related to the interplay between the cardiovascular and the respiratory system. They result from the respiratory-induced changes in intrathoracic pressure, which are transmitted to the cardiac cavities and to the changes in alveolar pressure, which may impact the lung microvessels. In spontaneously breathing patients, consequences of heart-lungs interactions are during inspiration an increase in right ventricular preload and afterload, a decrease in left ventricular preload and an increase in left ventricular afterload. In mechanically ventilated patients, consequences of heart-lungs interactions are during mechanical insufflation a decrease in right ventricular preload, an increase in right ventricular afterload, an increase in left ventricular preload and a decrease in left ventricular afterload. Physiologically and during normal breathing, heart-lungs interactions do not lead to significant hemodynamic consequences. Nevertheless, in some clinical settings such as acute exacerbation of chronic obstructive pulmonary disease, acute left heart failure or acute respiratory distress syndrome, heart-lungs interactions may lead to significant hemodynamic consequences. These are linked to complex pathophysiological mechanisms, including a marked inspiratory negativity of intrathoracic pressure, a marked inspiratory increase in transpulmonary pressure and an increase in intra-abdominal pressure. The most recent application of heart-lungs interactions is the prediction of fluid responsiveness in mechanically ventilated patients. The first test to be developed using heart-lungs interactions was the respiratory variation of pulse pressure. Subsequently, many other dynamic fluid responsiveness tests using heart-lungs interactions have been developed, such as the respiratory variations of pulse contour-based stroke volume or the respiratory variations of the inferior or superior vena cava diameters. All these tests share the same limitations, the most frequent being low tidal volume ventilation, persistent spontaneous breathing activity and cardiac arrhythmia. Nevertheless, when their main limitations are properly addressed, all these tests can help intensivists in the decision-making process regarding fluid administration and fluid removal in critically ill patients.

Background and Objectives: Intra-abdominal hypertension (IAH) and acute respiratory distress syndrome (ARDS) are common concerns in intensive care unit patients with acute respiratory failure (ARF). Although both conditions lead to impairment of global respiratory parameters, their underlying mechanisms differ substantially. Therefore, a separate assessment of the different respiratory compartments should reveal differences in respiratory mechanics. Materials and Methods: We prospectively investigated alterations in lung and chest wall mechanics in 18 mechanically ventilated pigs exposed to varying levels of intra-abdominal pressures (IAP) and ARDS. The animals were divided into three groups: group A (IAP 10 mmHg, no ARDS), B (IAP 20 mmHg, no ARDS), and C (IAP 10 mmHg, with ARDS). Following induction of IAP (by inflating an intra-abdominal balloon) and ARDS (by saline lung lavage and injurious ventilation), respiratory mechanics were monitored for six hours. Statistical analysis was performed using one-way ANOVA to compare the alterations within each group. Results: After six hours of ventilation, end-expiratory lung volume (EELV) decreased across all groups, while airway and thoracic pressures increased. Significant differences were noted between group (B) and (C) regarding alterations in transpulmonary pressure (TPP) (2.7 ± 0.6 vs. 11.3 ± 2.1 cmH2O, p < 0.001), elastance of the lung (EL) (8.9 ± 1.9 vs. 29.9 ± 5.9 cmH2O/mL, p = 0.003), and elastance of the chest wall (ECW) (32.8 ± 3.2 vs. 4.4 ± 1.8 cmH2O/mL, p < 0.001). However, global respiratory parameters such as EELV/kg bodyweight (-6.1 ± 1.3 vs. -11.0 ± 2.5 mL/kg), driving pressure (12.5 ± 0.9 vs. 13.2 ± 2.3 cmH2O), and compliance of the respiratory system (-21.7 ± 2.8 vs. -19.5 ± 3.4 mL/cmH2O) did not show significant differences among the groups. Conclusions: Separate measurements of lung and chest wall mechanics in pigs with IAH or ARDS reveals significant differences in TPP, EL, and ECW, whereas global respiratory parameters do not differ significantly. Therefore, assessing the compartments of the respiratory system separately could aid in identifying the underlying cause of ARF.

Patients with acute exacerbation of lung fibrosis with usual interstitial pneumonia (EUIP) pattern are at increased risk for ventilator-induced lung injury (VILI) and mortality when exposed to mechanical ventilation (MV). Yet, lack of a mechanical model describing UIP-lung deformation during MV represents a research gap. Aim of this study was to develop a constitutive mathematical model for UIP-lung deformation during lung protective MV based on the stress-strain behavior and the specific elastance of patients with EUIP as compared to that of acute respiratory distress syndrome (ARDS) and healthy lung. Partitioned lung and chest wall mechanics were assessed for patients with EUIP and primary ARDS (1:1 matched based on body mass index and PaO2/FiO2 ratio) during a PEEP trial performed within 24 h from intubation. Patient\'s stress-strain curve and the lung specific elastance were computed and compared with those of healthy lungs, derived from literature. Respiratory mechanics were used to fit a novel mathematical model of the lung describing mechanical-inflation-induced lung parenchyma deformation, differentiating the contributions of elastin and collagen, the main components of lung extracellular matrix. Five patients with EUIP and 5 matched with primary ARDS were included and analyzed. Global strain was not different at low PEEP between the groups. Overall specific elastance was significantly higher in EUIP as compared to ARDS (28.9 [22.8-33.2] cmH2O versus 11.4 [10.3-14.6] cmH2O, respectively). Compared to ARDS and healthy lung, the stress/strain curve of EUIP showed a steeper increase, crossing the VILI threshold stress risk for strain values greater than 0.55. The contribution of elastin was prevalent at lower strains, while the contribution of collagen was prevalent at large strains. The stress/strain curve for collagen showed an upward shift passing from ARDS and healthy lungs to EUIP lungs. During MV, patients with EUIP showed different respiratory mechanics, stress-strain curve and specific elastance as compared to ARDS patients and healthy subjects and may experience VILI even when protective MV is applied. According to our mathematical model of lung deformation during mechanical inflation, the elastic response of UIP-lung is peculiar and different from ARDS. Our data suggest that patients with EUIP experience VILI with ventilatory setting that are lung-protective for patients with ARDS.

The use of transpulmonary pressure monitoring based on measurement of esophageal pressure has contributed importantly to the personalization of mechanical ventilation based on respiratory pathophysiology in critically ill patients. However, esophageal pressure monitoring is still underused in the clinical practice. This technique allows partitioning of the respiratory mechanics between the lungs and the chest wall, provides information on lung recruitment and risk of barotrauma, and helps titrating mechanical ventilation settings in patients with respiratory failure. In assisted ventilation modes and during non-invasive respiratory support, esophageal pressure monitoring provides important information on the inspiratory effort and work of breathing. Nonetheless, several controversies persist on technical aspects, interpretation and clinical decision-making based on values derived from this monitoring technique. The aim of this review is to summarize the physiological bases of esophageal pressure monitoring, discussing the pros and cons of its clinical applications and different interpretations in critically ill patients undergoing invasive and non-invasive respiratory support.

Advanced respiratory monitoring encompasses a diverse range of mini- or noninvasive tools used to evaluate various aspects of respiratory function in patients experiencing acute respiratory failure, including those requiring extracorporeal membrane oxygenation (ECMO) support. Among these techniques, key modalities include esophageal pressure measurement (including derived pressures), lung and respiratory muscle ultrasounds, electrical impedance tomography, the monitoring of diaphragm electrical activity, and assessment of flow index. These tools play a critical role in assessing essential parameters such as lung recruitment and overdistention, lung aeration and morphology, ventilation/perfusion distribution, inspiratory effort, respiratory drive, respiratory muscle contraction, and patient-ventilator synchrony. In contrast to conventional methods, advanced respiratory monitoring offers a deeper understanding of pathological changes in lung aeration caused by underlying diseases. Moreover, it allows for meticulous tracking of responses to therapeutic interventions, aiding in the development of personalized respiratory support strategies aimed at preserving lung function and respiratory muscle integrity. The integration of advanced respiratory monitoring represents a significant advancement in the clinical management of acute respiratory failure. It serves as a cornerstone in scenarios where treatment strategies rely on tailored approaches, empowering clinicians to make informed decisions about intervention selection and adjustment. By enabling real-time assessment and modification of respiratory support, advanced monitoring not only optimizes care for patients with acute respiratory distress syndrome but also contributes to improved outcomes and enhanced patient safety.

Transpulmonary pressure (PL) calculation requires esophageal pressure (PES) as a surrogate of pleural pressure (Ppl), but its calibration is a cumbersome technique. Central venous pressure (CVP) swings may reflect tidal variations in Ppl and could be used instead of PES, but the interpretation of CVP waveforms could be difficult due to superposition of heartbeat-induced pressure changes. Thus, we developed a digital filter able to remove the cardiac noise to obtain a filtered CVP (f-CVP). The aim of the study was to evaluate the accuracy of CVP and filtered CVP swings (ΔCVP and Δf-CVP, respectively) in estimating esophageal respiratory swings (ΔPES) and compare PL calculated with CVP, f-CVP and PES; then we tested the diagnostic accuracy of the f-CVP method to identify unsafe high PL levels, defined as PL>10 cmH2O. Twenty patients with acute respiratory failure (defined as PaO2/FiO2 ratio below 200 mmHg) treated with invasive mechanical ventilation and monitored with an esophageal balloon and central venous catheter were enrolled prospectively. For each patient a recording session at baseline was performed, repeated if a modification in ventilatory settings occurred. PES, CVP and airway pressure during an end-inspiratory and -expiratory pause were simultaneously recorded; CVP, f-CVP and PES waveforms were analyzed off-line and used to calculate transpulmonary pressure (PLCVP, PLf-CVP, PLPES, respectively). Δf-CVP correlated better than ΔCVP with ΔPES (r = 0.8, p = 0.001 vs. r = 0.08, p = 0.73), with a lower bias in Bland Altman analysis in favor of PLf-CVP (mean bias - 0.16, Limits of Agreement (LoA) -1.31, 0.98 cmH2O vs. mean bias - 0.79, LoA - 3.14, 1.55 cmH2O). Both PLf-CVP and PLCVP correlated well with PLPES (r = 0.98, p < 0.001 vs. r = 0.94, p < 0.001), again with a lower bias in Bland Altman analysis in favor of PLf-CVP (0.15, LoA - 0.95, 1.26 cmH2O vs. 0.80, LoA - 1.51, 3.12, cmH2O). PLf-CVP discriminated high PL value with an area under the receiver operating characteristic curve 0.99 (standard deviation, SD, 0.02) (AUC difference = 0.01 [-0.024; 0.05], p = 0.48). In mechanically ventilated patients with acute respiratory failure, the digital filtered CVP estimated ΔPES and PL obtained from digital filtered CVP represented a reliable value of standard PL measured with the esophageal method and could identify patients with non-protective ventilation settings.

UNASSIGNED: Esophageal pressure (Pes) has been used as a surrogate of pleural pressure (Ppl) to titrate positive end-expiratory pressure (PEEP) in acute respiratory distress syndrome (ARDS) patients. The relationship between Pes and PEEP remains undetermined.
UNASSIGNED: A gastric tube with a balloon catheter was inserted to monitor Pes in moderate to severe ARDS patients who underwent invasive mechanical ventilation. To assess the end-expiratory Pes response (ΔPes) to PEEP changes (ΔPEEP), the PEEP level was decreased and increased subsequently (with an average change of 3 cmH2O). The patients underwent the following two series of PEEP adjustment: (I) from PEEP-3 cmH2O to PEEPbaseline; and (II) from PEEPbaseline to PEEP+3 cmH2O. The patients were classified as \"PEEP-dependent type\" if they had ΔPes ≥30% ΔPEEP and were otherwise classified as \"PEEP-independent type\" (ΔPes <30% ΔPEEP in any series).
UNASSIGNED: In total, 54 series of PEEP adjustments were performed in 18 ARDS patients. Of these patients, 12 were classified as PEEP-dependent type, and six were classified as PEEP-independent type. During the PEEP adjustment, end-expiratory Pes changed significantly in the PEEP-dependent patients, who had a Pes of 10.8 (7.9, 12.3), 12.5 (10.5, 14.9), and 14.5 (13.1, 18.3) cmH2O at PEEP-3 cmH2O, PEEPbaseline, and PEEP+3 cmH2O, respectively (median and quartiles; P<0.0001), while end-expiratory transpulmonary pressure (PL) was maintained at an optimal range [-0.1 (-0.7, 0.4), 0.1 (-0.6, 0.5), and 0.3 (-0.3, 0.7) cmH2O, respectively]. In the PEEP-independent patients, the Pes remained unchanged, with a Pes of 15.4 (11.4, 17.8), 15.5 (11.6, 17.8), and 15.4 (11.7, 18.30) cmH2O at each of the three PEEP levels, respectively. Meanwhile, end-expiratory PL significantly improved [from -5.5 (-8.5, -3.4) at PEEP-3 cmH2O to -2.5 (-5.0, -1.6) at PEEPbaseline to -0.5 (-1.8, 0.3) at PEEP+3 cmH2O; P<0.01].
UNASSIGNED: Two types of Pes phenotypes were identified according to the ΔPes to ΔPEEP. The underlying mechanisms and implications for clinical practice require further exploration.

BACKGROUND: We have previously reported a simple correction method for estimating pleural pressure (Ppl) using central venous pressure (CVP). However, it remains unclear whether this method is applicable to patients with varying levels of intravascular volumes and/or chest wall compliance. This study aimed to investigate the accuracy of our method under different conditions of intravascular volume and chest wall compliance.
RESULTS: Ten anesthetized and paralyzed pigs (43.2 ± 1.8 kg) were mechanically ventilated and subjected to lung injury by saline lung lavage. Each pig was subjected to three different intravascular volumes and two different intraabdominal pressures. For each condition, the changes in the esophageal pressure (ΔPes) and the estimated ΔPpl using ΔCVP (cΔCVP-derived ΔPpl) were compared to the directly measured change in pleural pressure (Δd-Ppl), which was the gold standard estimate in this study. The cΔCVP-derived ΔPpl was calculated as κ × ΔCVP, where \"κ\" was the ratio of the change in airway pressure to the change in CVP during the occlusion test. The means and standard deviations of the Δd-Ppl, ΔPes, and cΔCVP-derived ΔPpl for all pigs under all conditions were 7.6 ± 4.5, 7.2 ± 3.6, and 8.0 ± 4.8 cmH2O, respectively. The repeated measures correlations showed that both the ΔPes and cΔCVP-derived ΔPpl showed a strong correlation with the Δd-Ppl (ΔPes: r = 0.95, p < 0.0001; cΔCVP-derived ΔPpl: r = 0.97, p < 0.0001, respectively). In the Bland-Altman analysis to test the performance of the cΔCVP-derived ΔPpl to predict the Δd-Ppl, the ΔPes and cΔCVP-derived ΔPpl showed almost the same bias and precision (ΔPes: 0.5 and 1.7 cmH2O; cΔCVP-derived ΔPpl: - 0.3 and 1.9 cmH2O, respectively). No significant difference was found in the bias and precision depending on the intravascular volume and intraabdominal pressure in both comparisons between the ΔPes and Δd-Ppl, and cΔCVP-derived ΔPpl and Δd-Ppl.
CONCLUSIONS: The CVP method can estimate the ΔPpl with reasonable accuracy, similar to Pes measurement. The accuracy was not affected by the intravascular volume or chest wall compliance.

BACKGROUND: Data concerning the depth of neuromuscular blockade (NMB) required for effective relaxation of the respiratory muscles in ARDS are scarce. We hypothesised that complete versus partial NMB can modify respiratory mechanics.
METHODS: Prospective study to compare the respiratory mechanics of ARDS patients according to the NMB depth. Each patient was analysed at two times: deep NMB (facial train of four count (TOFC) = 0) and intermediate NMB (TOFC >0). The primary endpoint was the comparison of chest wall elastance (ELCW) according to the NMB level.
RESULTS: 33 ARDS patients were analysed. There was no statistical difference between the ELCW at TOFC = 0 compared to TOFC >0: 7 cmH2O/l [5.7-9.5] versus 7 cmH2O/l [5.3-10.8] (p = 0.36). The depth of NMB did not modify the expiratory nor inspiratory oesophageal pressure (Pesexp = 8 cmH2O [5-9.5] at TOFC = 0 versus 7 cmH2O [5-10] at TOFC >0; (p = 0.16) and Pesinsp = 10 cmH2O [8.2-13] at TOFC = 0 versus 10 cmH2O [8-13] at TOFC >0; (p = 0.12)).
CONCLUSIONS: In ARDS, the relaxation of the respiratory muscles seems to be independent of the NMB level.

Objective. Understanding a patient\'s respiratory effort and mechanics is essential for the provision of individualized care during mechanical ventilation. However, measurement of transpulmonary pressure (the difference between airway and pleural pressures) is not easily performed in practice. While airway pressures are available on most mechanical ventilators, pleural pressures are measured indirectly by an esophageal balloon catheter. In many cases, esophageal pressure readings take other phenomena into account and are not a reliable measure of pleural pressure.Approach.A system identification approach was applied to provide accurate pleural measures from esophageal pressure readings. First, we used a closed pressurized chamber to stimulate an esophageal balloon and model its dynamics. Second, we created a simplified version of an artificial lung and tried the model with different ventilation configurations. For validation, data from 11 patients (five male and six female) were used to estimate respiratory effort profile and patient mechanics.Main results.After correcting the dynamic response of the balloon catheter, the estimates of resistance and compliance and the corresponding respiratory effort waveform were improved when compared with the adjusted quantities in the test bench. The performance of the estimated model was evaluated using the respiratory pause/occlusion maneuver, demonstrating improved agreement between the airway and esophageal pressure waveforms when using the normalized mean squared error metric. Using the corrected muscle pressure waveform, we detected start and peak times 130 ± 50 ms earlier and a peak amplitude 2.04 ± 1.46 cmH2O higher than the corresponding estimates from esophageal catheter readings.Significance.Compensating the acquired measurements with system identification techniques makes the readings more accurate, possibly better portraying the patient\'s situation for individualization of ventilation therapy.