PPV May Be a Starting Point to Achieve Circulatory Protective Mechanical Ventilation

Pulse pressure variation (PPV) is a mandatory index for hemodynamic monitoring during mechanical ventilation. The changes in pleural pressure (Ppl) and transpulmonary pressure (PL) caused by mechanical ventilation are the basis for PPV and lead to the effect of blood flow. If the state of hypovolemia exists, the effect of the increased Ppl during mechanical ventilation on the right ventricular preload will mainly affect the cardiac output, resulting in a positive PPV. However, PL is more influenced by the change in alveolar pressure, which produces an increase in right heart overload, resulting in high PPV. In particular, if spontaneous breathing is strong, the transvascular pressure will be extremely high, which may lead to the promotion of alveolar flooding and increased RV flow. Asynchronous breathing and mediastinal swing may damage the pulmonary circulation and right heart function. Therefore, according to the principle of PPV, a high PPV can be incorporated into the whole respiratory treatment process to monitor the mechanical ventilation cycle damage/protection regardless of the controlled ventilation or spontaneous breathing. Through the monitoring of PPV, the circulation-protective ventilation can be guided at bedside in real time by PPV.

Awake prone position reduces work of breathing in patients with COVID-19 ARDS supported by CPAP

Background The use of awake prone position concomitant to non-invasive mechanical ventilation in acute respiratory distress syndrome (ARDS) secondary to COVID-19 has shown to improve gas exchange, whereas its effect on the work of breathing remain unclear. The objective of this study was to evaluate the effects of awake prone position during helmet continuous positive airway pressure (CPAP) ventilation on inspiratory effort, gas exchange and comfort of breathing. Methods Forty consecutive patients presenting with ARDS due to COVID-19 were prospectively enrolled. Gas exchange, esophageal pressure swing (ΔPes), dynamic transpulmonary pressure (dTPP), modified pressure time product (mPTP), work of breathing (WOB) and comfort of breathing, were recorded on supine position and after 3 h on prone position. Results The median applied PEEP with helmet CPAP was 10 [8–10] cmH2O. The PaO2/FiO2 was higher in prone compared to supine position (Supine: 166 [136–224] mmHg, Prone: 314 [232–398] mmHg, p < 0.001). Respiratory rate and minute ventilation decreased from supine to prone position from 20 [17–24] to 17 [15–19] b/min (p < 0.001) and from 8.6 [7.3–10.6] to 7.7 [6.6–8.6] L/min (p < 0.001), respectively. Prone position did not reduce ΔPes (Supine: − 7 [− 9 to − 5] cmH2O, Prone: − 6 [− 9 to − 5] cmH2O, p = 0.31) and dTPP (Supine: 17 [14–19] cmH2O, Prone: 16 [14–18] cmH2O, p = 0.34). Conversely, mPTP and WOB decreased from 152 [104–197] to 118 [90–150] cmH2O/min (p < 0.001) and from 146 [120–185] to 114 [95–151] cmH2O L/min (p < 0.001), respectively. Twenty-six (65%) patients experienced a reduction in WOB of more than 10%. The overall sensation of dyspnea was lower in prone position (p = 0.005). Conclusions Awake prone position with helmet CPAP enables a reduction in the work of breathing and an improvement in oxygenation in COVID-19-associated ARDS.

Negative Transpulmonary Pressure Disrupts Airway Morphogenesis by Suppressing Fgf10

Mechanical forces are increasingly recognized as important determinants of cell and tissue phenotype and also appear to play a critical role in organ development. During the fetal stages of lung morphogenesis, the pressure of the fluid within the lumen of the airways is higher than that within the chest cavity, resulting in a positive transpulmonary pressure. Several congenital defects decrease or reverse transpulmonary pressure across the developing airways and are associated with a reduced number of branches and a correspondingly underdeveloped lung that is insufficient for gas exchange after birth. The small size of the early pseudoglandular stage lung and its relative inaccessibility in utero have precluded experimental investigation of the effects of transpulmonary pressure on early branching morphogenesis. Here, we present a simple culture model to explore the effects of negative transpulmonary pressure on development of the embryonic airways. We found that negative transpulmonary pressure decreases branching, and that it does so in part by altering the expression of fibroblast growth factor 10 (Fgf10). The morphogenesis of lungs maintained under negative transpulmonary pressure can be rescued by supplementing the culture medium with exogenous FGF10. These data suggest that Fgf10 expression is regulated by mechanical stress in the developing airways. Understanding the mechanical signaling pathways that connect transpulmonary pressure to FGF10 can lead to the establishment of novel non-surgical approaches for ameliorating congenital lung defects.

Novel method of transpulmonary pressure measurement with an air-filled esophageal catheter

Background There is a strong rationale for proposing transpulmonary pressure-guided protective ventilation in acute respiratory distress syndrome. The reference esophageal balloon catheter method requires complex in vivo calibration, expertise and specific material order. A simple, inexpensive, accurate and reproducible method of measuring esophageal pressure would greatly facilitate the measure of transpulmonary pressure to individualize protective ventilation in the intensive care unit. Results We propose an air-filled esophageal catheter method without balloon, using a disposable catheter that allows reproducible esophageal pressure measurements. We use a 49-cm-long 10 Fr thin suction catheter, positioned in the lower-third of the esophagus and connected to an air-filled disposable blood pressure transducer bound to the monitor and pressurized by an air-filled infusion bag. Only simple calibration by zeroing the transducer to atmospheric pressure and unit conversion from mmHg to cmH2O are required. We compared our method with the reference balloon catheter both ex vivo, using pressure chambers, and in vivo, in 15 consecutive mechanically ventilated patients. Esophageal-to-airway pressure change ratios during the dynamic occlusion test were close to one (1.03 ± 0.19 and 1.00 ± 0.16 in the controlled and assisted modes, respectively), validating the proper esophageal positioning. The Bland–Altman analysis revealed no bias of our method compared with the reference and good precision for inspiratory, expiratory and delta esophageal pressure measurements in both the controlled (largest bias −0.5 cmH2O [95% confidence interval: −0.9; −0.1] cmH2O; largest limits of agreement −3.5 to 2.5 cmH2O) and assisted modes (largest bias −0.3 [−2.6; 2.0] cmH2O). We observed a good repeatability (intra-observer, intraclass correlation coefficient, ICC: 0.89 [0.79; 0.96]) and reproducibility (inter-observer ICC: 0.89 [0.76; 0.96]) of esophageal measurements. The direct comparison with pleural pressure in two patients and spectral analysis by Fourier transform confirmed the reliability of the air-filled catheter-derived esophageal pressure as an accurate surrogate of pleural pressure. A calculator for transpulmonary pressures is available online. Conclusions We propose a simple, minimally invasive, inexpensive and reproducible method for esophageal pressure monitoring with an air-filled esophageal catheter without balloon. It holds the promise of widespread bedside use of transpulmonary pressure-guided protective ventilation in ICU patients.

A new mode of mechanical ventilation: positive + negative synchronized ventilation

Often, in supporting patients suffering from severe respiratory diseases with mechanical ventilation, obstacles are encountered due to pulmonary and/or thoracic alterations, reductions in the ventilable lung parenchyma, increases in airway resistance, alterations in thoraco-pulmonary compliance, advanced age of the subjects. All this involves difficulties in finding the right ventilation parameters and an adequate driving pressure to guarantee sufficient ventilation. Therefrom, new mechanical ventilation techniques were sought that could help overcome the aforementioned obstacles. A new mode of mechanical ventilation is being presented, i.e., a Positive + Negative Synchronized Ventilation (PNSV), characterized by the association and integration of two pulmonary ventilators; one acting inside the chest with positive pressures and one externally with negative pressure. The peculiarity of this combination is the complete synchronization, which takes place with specific electronic modifications. The PNSV can be applied both in a completely non-invasive and invasive way and, therefore, be used both in acute care wards and in ICU. The most relevant effect found, due to the compensation of opposing pressures acting on the chest, is that, during the entire inspiratory act created by the ventilators, the pressure at the alveolar level is equal to zero even if adding together the two ventilators’ pressures; thus, the transpulmonary pressure is doubled. The application of this pressure for 1 hour on elderly patients suffering from severe acute respiratory failure, resulted in a significant improvement in blood gas analytical and clinical parameters without any side effects. An increased pulmonary recruitment, including posterior lung areas, and a reduction in spontaneous ventilatory rate have also been demonstrated with PNSV. This also paves the way to the search for the best ventilatory treatment in critically ill or ARDS patients. The compensation of intrathoracic pressures should also lead, although not yet proven, to an improvement in venous return, systolic and cardiac output. In the analysis of the study in which this method was applied, the total transpulmonary pressure delivered was the sum of the individual pressures applied by the two ventilators. However, this does not exclude the possibility of reducing the pressures of the two machines to modulate a lower but balanced total transpulmonary pressure within the chest.

A Protective Tidal Volume Adapted To Lung Compliance and The PEEP Level With Lowest Transpulmonary Driving Pressure May Be Determined By a Rapid PEEP-Step Procedure

Background: A protective ventilation strategy should be based on lung mechanics and transpulmonary pressure, as this is the pressure that directly “hits” the lung. Esophageal pressure has been used for this purpose but has not gained widespread clinical acceptance. Instead, respiratory system mechanics and airway driving pressure have been used as surrogate measures. We have shown that the lung pressure/volume (P/V) curve coincides with the line connecting the end-expiratory airway P/V points of a PEEP trial. Consequently, transpulmonary pressure increases as much as PEEP and lung compliance (CL) can be determined as ΔEELV/ΔPEEP and transpulmonary driving pressure (ΔPTP) as tidal volume divided by ΔEELV/ΔPEEP.Methods: In ten patients with acute respiratory failure, ΔEELV was measured during each 4 cmH2O PEEP-step from 0 to 16 cmH2O and CL for each PEEP interval calculated as ΔEELV/ΔPEEP giving a lung P/V curve for the whole PEEP trial. Similarily, a lung P/V curve was obtained also for the PEEP levels 8, 12, and 16 cmH2O only.Results: A two-step PEEP procedure starting from a clinical PEEP level of 8 cmH2O gave almost identical lung P/V curves as the four PEEP-step procedure. The lung P/V curves showed a marked individual variation with an over-all CL (CLoa ) 50-137 ml/cmH2O. ΔPTP of a tidal volume of 6-7 ml/kg ideal body weight divided by CLoa ranged from 8.6-2.8 cmH2O, while ΔPTP of tidal volume adapted to CLoa ranged from 3.3 in the patient with lowest to 4.3 cmH 2 O in the patient with highest CLoa . The ratio of airway driving pressure to transpulmonary driving pressure (ΔPTP/ΔPAW) varied between patients and changed with PEEP, reducing the value of ΔPAW as surrogate for ΔPTP in individual patients.Conclusion: Only a two PEEP-step procedure is required for obtaining a lung P/V curve from baseline clinical PEEP to end-inspiration at the highest PEEP level, i.e. without esophageal pressure measurements. The best-fit equation for the curve can be used to determine a tidal volume related to lung compliance instead of ideal body weight and the PEEP level where transpulmonary driving pressure is lowest and possibly least injurious for any given tidal volume.

An assessment of esophageal balloon use for the titration of airway pressure release ventilation and controlled mechanical ventilation in a patient with extrapulmonary acute respiratory distress syndrome: a case report

Background Esophageal pressure measurement is a minimally invasive monitoring process that assesses respiratory mechanics in patients with acute respiratory distress syndrome. Airway pressure release ventilation is a relatively new positive pressure ventilation modality, characterized by a series of advantages in patients with acute respiratory distress syndrome. Case presentation We report a case of a 55-year-old chilean female, with preexisting hypertension and recurrent renal colic who entered the cardiosurgical intensive care unit with signs and symptoms of urinary sepsis secondary to a right-sided obstructive urolithiasis. At the time of admission, the patient showed signs of urinary sepsis, a poor overall condition, hemodynamic instability, tachycardia, hypotension, and needed vasoactive drugs. Initially the patient was treated with volume control ventilation. Then, ventilation was with conventional ventilation parameters described by the Acute Respiratory Distress Syndrome Network. However, hemodynamic complications led to reduced airway pressure. Later she presented intraabdominal hypertension that compromised the oxygen supply and her ventilation management. Considering these records, an esophageal manometry was used to measure distending lung pressure, that is, transpulmonary pressure, to protect lungs. Initial use of the esophageal balloon was in a volume-controlled modality (deep sedation), which allowed the medical team to perform inspiratory and expiratory pause maneuvers to monitor transpulmonary plateau pressure as a substitute for pulmonary distension and expiratory pause and determine transpulmonary positive end-expiratory pressure. On the third day of mechanical respiration, the modality was switched to airway pressure release ventilation. The use of airway pressure release ventilation was associated with reduced hemodynamic complications and kept transpulmonary pressure between 0 and 20 cmH2O despite a sustained high positive end-expiratory pressure of 20 cmH2O. Conclusion The application of this technique is shown in airway pressure release ventilation with spontaneous ventilation, which is then compared with a controlled modality that requires a lesser number of sedative doses and vasoactive drugs, without altering the criteria for lung protection as guided by esophageal manometry.