Targeting Arterial Partial Pressure of Carbon Dioxide in Acute Respiratory Distress Syndrome Patients using Extracorporeal Carbon Dioxide Removal

2021 ◽  
Author(s):  
John K. Leypoldt ◽  
Jörg Kurz ◽  
Jorge Echeverri ◽  
Markus Storr ◽  
Kai Harenski
2015 ◽  
Vol 122 (3) ◽  
pp. 631-646 ◽  
Author(s):  
Andreas Güldner ◽  
Thomas Kiss ◽  
Thomas Bluth ◽  
Christopher Uhlig ◽  
Anja Braune ◽  
...  

Abstract Background: To investigate the role of ultraprotective mechanical ventilation (UP-MV) and extracorporeal carbon dioxide removal with and without spontaneous breathing (SB) to improve respiratory function and lung protection in experimental severe acute respiratory distress syndrome. Methods: Severe acute respiratory distress syndrome was induced by saline lung lavage and mechanical ventilation (MV) with higher tidal volume (VT) in 28 anesthetized pigs (32.8 to 52.5 kg). Animals (n = 7 per group) were randomly assigned to 6 h of MV (airway pressure release ventilation) with: (1) conventional P-MV with VT ≈6 ml/kg (P-MVcontr); (2) UP-MV with VT ≈3 ml/kg (UP-MVcontr); (3) UP-MV with VT ≈3 ml/kg and SB (UP-MVspont); and (4) UP-MV with VT ≈3 ml/kg and pressure supported SB (UP-MVPS). In UP-MV groups, extracorporeal carbon dioxide removal was used. Results: The authors found that: (1) UP-MVcontr reduced diffuse alveolar damage score in dorsal lung zones (median[interquartile]) (12.0 [7.0 to 16.8] vs. 22.5 [13.8 to 40.8]), but worsened oxygenation and intrapulmonary shunt, compared to P-MVcontr; (2) UP-MVspont and UP-MVPS improved oxygenation and intrapulmonary shunt, and redistributed ventilation towards dorsal areas, as compared to UP-MVcontr; (3) compared to P-MVcontr, UP-MVcontr and UP-MVspont, UP-MVPS yielded higher levels of tumor necrosis factor-α (6.9 [6.5 to 10.1] vs. 2.8 [2.2 to 3.0], 3.6 [3.0 to 4.7] and 4.0 [2.8 to 4.4] pg/mg, respectively) and interleukin-8 (216.8 [113.5 to 343.5] vs. 59.8 [45.3 to 66.7], 37.6 [18.8 to 52.0], and 59.5 [36.1 to 79.7] pg/mg, respectively) in dorsal lung zones. Conclusions: In this model of severe acute respiratory distress syndrome, MV with VT ≈3 ml/kg and extracorporeal carbon dioxide removal without SB slightly reduced lung histologic damage, but not inflammation, as compared to MV with VT = 4 to 6 ml/kg. During UP-MV, pressure supported SB increased lung inflammation.


2016 ◽  
Vol 125 (1) ◽  
pp. 159-167 ◽  
Author(s):  
Tommaso Mauri ◽  
Giacomo Grasselli ◽  
Grazia Suriano ◽  
Nilde Eronia ◽  
Savino Spadaro ◽  
...  

Abstract Background The amount of extracorporeal carbon dioxide removal may influence respiratory drive in acute respiratory distress syndrome (ARDS) patients undergoing extracorporeal membrane oxygenation (ECMO). The authors evaluated the effects of different levels of extracorporeal carbon dioxide removal in patients recovering from severe ARDS undergoing pressure support ventilation (PSV) and neurally adjusted ventilatory assist (NAVA). Methods The authors conducted a prospective, randomized, crossover study on eight spontaneously breathing ARDS patients undergoing venovenous ECMO since 28 ± 20 days. To modulate carbon dioxide extraction, ECMO gas flow (GF) was decreased from baseline resting protective conditions (i.e., GF100%, set to obtain pressure generated in the first 100 ms of inspiration against an occluded airway less than 2 cm H2O, respiratory rate less than or equal to 25 bpm, tidal volume less than 6 ml/kg, and peak airway pressure less than 25 cm H2O) to GF50%-GF25%-GF0% during both PSV and NAVA (random order for ventilation mode). Continuous recordings of airway pressure and flow and esophageal pressure were obtained and analyzed during all study phases. Results At higher levels of extracorporeal carbon dioxide extraction, pressure generated in the first 100 ms of inspiration against an occluded airway decreased from 2.8 ± 2.7 cm H2O (PSV, GF0%) and 3.0 ± 2.1 cm H2O (NAVA, GF0%) to 0.9 ± 0.5 cm H2O (PSV, GF100%) and 1.0 ± 0.8 cm H2O (NAVA, GF100%; P < 0.001) and patients’ inspiratory muscle pressure passed from 8.5 ± 6.3 and 6.5 ± 5.5 cm H2O to 4.5 ± 3.1 and 4.2 ± 3.7 cm H2O (P < 0.001). In time, decreased inspiratory drive and effort determined by higher carbon dioxide extraction led to reduction of tidal volume from 6.6 ± 0.9 and 7.5 ± 1.2 ml/kg to 4.9 ± 0.8 and 5.3 ± 1.3 ml/kg (P < 0.001) and of peak airway pressure from 21 ± 3 and 25 ± 4 cm H2O to 21 ± 3 and 21 ± 5 cm H2O (P < 0.001). Finally, transpulmonary pressure linearly decreased when the amount of carbon dioxide extracted by ECMO increased (R2 = 0.823, P < 0.001). Conclusions In patients recovering from ARDS undergoing ECMO, the amount of carbon dioxide removed by the artificial lung may influence spontaneous breathing. The effects of carbon dioxide removal on spontaneous breathing during the earlier acute phases of ARDS remain to be elucidated.


2018 ◽  
Vol 20 (1) ◽  
pp. 40-45 ◽  
Author(s):  
Hariharan Regunath ◽  
Nathanial Moulton ◽  
Daniel Woolery ◽  
Mohammed Alnijoumi ◽  
Troy Whitacre ◽  
...  

Background Tidal hyperinflation can still occur with mechanical ventilation using low tidal volume (LVT) (6 mL/kg predicted body weight (PBW)) in acute respiratory distress syndrome (ARDS), despite a well-demonstrated reduction in mortality. Methods Retrospective chart review from August 2012 to October 2014. Inclusion: Age >18years, PaO2/FiO2<200 with bilateral pulmonary infiltrates, absent heart failure, and ultra-protective mechanical ventilation (UPMV) defined as tidal volume (VT) <6 mL/kg PBW. Exclusion: UPMV use for <24 h. Demographics, admission Acute Physiology and Chronic Health Evaluation II (APACHE II) scores, arterial blood gas, serum bicarbonate, ventilator parameters for pre-, during, and post-UPMV periods including modes, VT, peak inspiratory pressure (PIP), plateau pressure (Pplat), driving pressure, etc. were gathered. We compared lab and ventilator data for pre-, during, and post-UPMV periods. Results Fifteen patients (male:female = 7:8, age 42.13 ± 11.29 years) satisfied criteria, APACHEII 20.6 ± 7.1, mean days in intensive care unit and hospitalization were 18.5 ± 8.85 and 20.81 ± 9.78 days, 9 (60%) received paralysis and 7 (46.67%) required inotropes. Eleven patients had echocardiogram, 7 (63.64%) demonstrated right ventricular volume or pressure overload. Eleven patients (73.33%) survived. During-UPMV, VT ranged 2–5 mL/kg PBW(3.99 ± 0.73), the arterial partial pressure of carbon dioxide (PaCO2) was higher than pre-UPMV values (84.81 ± 18.95 cmH2O vs. 69.16 ± 33.09 cmH2O), but pH was comparable and none received extracorporeal carbon dioxide removal (ECCO2-R). The positive end-expiratory pressure (14.18 ± 7.56 vs. 12.31 ± 6.84 cmH2O), PIP (38.21 ± 12.89 vs. 32.59 ± 9.88), and mean airway pressures (19.98 ± 7.61 vs. 17.48 ± 6.7 cm H2O) were higher during UPMV, but Pplat and PaO2/FiO2 were comparable during- and pre-UPMV. Driving pressure was observed to be higher in those who died than who survived (24.18 ± 12.36 vs. 13.42 ± 3.25). Conclusion UPMV alone may be a safe alternative option for ARDS patients in centers without ECCO2-R.


2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Nicolò Sella ◽  
Tommaso Pettenuzzo ◽  
Michele Della Paolera ◽  
Giulio Andreatta ◽  
Annalisa Boscolo ◽  
...  

Veno-venous extracorporeal membrane oxygenation (V-V ECMO) may be required to treat critically ill patients with COVID-19-associated severe acute respiratory distress syndrome (ARDS). We report the case of a 43-year-old peripartum patient, who underwent two sequential V-V ECMO runs. The first extracorporeal support was established for COVID-19 ARDS, as characterized by severe hypoxemia and hypercapnia (arterial partial pressure of oxygen to inspired oxygen fraction ratio 85 mmHg and arterial partial pressure of carbon dioxide 95 mmHg) and reduction of respiratory system static compliance to 25 mL/cmH2O, unresponsive to mechanical ventilation and prone positioning. After 22 days of lung rest, V-V ECMO was successfully removed and ventilator weaning initiated. A second V-V ECMO was required 7 days later, because of newly onset ARDS due to Pseudomonas aeruginosa ventilator-associated pneumonia. The second V-V ECMO run lasted 12 days. During both V-V ECMO runs, anticoagulation and ventilator settings were titrated through bedside thromboelastometry and electrical impedance tomography, respectively, without major complications. The patient was successfully decannulated, weaned from mechanical ventilation, and finally discharged home without oxygen therapy. At one-month follow-up, she showed good general conditions and no sign of respiratory failure.


2007 ◽  
Vol 113 (6) ◽  
pp. 279-285 ◽  
Author(s):  
Shang Jyh Kao ◽  
Diana Yu-Wung Yeh ◽  
Hsing I. Chen

FES (fat embolism syndrome) is a clinical problem, and, although ARDS (acute respiratory distress syndrome) has been considered as a serious complication of FES, the pathogenesis of ARDS associated with FES remains unclear. In the present study, we investigated the clinical manifestations, and biochemical and pathophysiological changes, in subjects associated with FES and ARDS, to elucidate the possible mechanisms involved in this disorder. A total of eight patients with FES were studied, and arterial blood pH, PaO2 (arterial partial pressure of O2), PaCO2 (arterial partial pressure of CO2), biochemical and pathophysiological data were obtained. These subjects suffered from crash injuries and developed FES associated with ARDS, and each died within 2 h after admission. In the subjects, chest radiography revealed that the lungs were clear on admission, and pulmonary infiltration was observed within 2 h of admission. Arterial blood pH and PaO2 declined, whereas PaCO2 increased. Plasma PLA2 (phospholipase A2), nitrate/nitrite, methylguanidine, TNF-α (tumour necrosis factor-α), IL-1β (interleukin-1β) and IL-10 (interleukin-10) were significantly elevated. Pathological examinations revealed alveolar oedema and haemorrhage with multiple fat droplet depositions and fibrin thrombi. Fat droplets were also found in the arterioles and/or capillaries in the lung, kidney and brain. Immunohistochemical staining identified iNOS (inducible nitric oxide synthase) in alveolar macrophages. In conclusion, our clinical analysis suggests that PLA2, NO, free radicals and pro-inflammatory cytokines are involved in the pathogenesis of ARDS associated with FES. The major source of NO is the alveolar macrophages.


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