Re-examining Permissive Hypercapnia in ARDS

Barnes, Thomas A; Zochios, Vasileios; Parhar, Kuljit

doi:10.1016/j.chest.2017.11.010

Cited by 62 publications

(43 citation statements)

References 85 publications

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“…Lung-protective ventilation with lower tidal volumes (6 mL/kg) is desirable but may lead to hypercapnia and acidaemia [73]. However, permissive hypercapnia may have a negative effect on the kidney through reduced renal plasma flow and increased renal vascular resistance [119]. In theory, RRT helps compensate respiratory acidosis and may remove CO 2 through additional filters included in the CRRT circuit [extracorporeal CO 2 removal (ECCO 2 R)] [96,120,121].…”

Section: Rationalementioning

confidence: 99%

Lung–kidney interactions in critically ill patients: consensus report of the Acute Disease Quality Initiative (ADQI) 21 Workgroup

et al. 2019

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Background: Multi-organ dysfunction in critical illness is common and frequently involves the lungs and kidneys, often requiring organ support such as invasive mechanical ventilation (IMV), renal replacement therapy (RRT) and/or extracorporeal membrane oxygenation (ECMO). Methods:A consensus conference on the spectrum of lung-kidney interactions in critical illness was held under the auspices of the Acute Disease Quality Initiative (ADQI) in Innsbruck, Austria, in June 2018. Through review and critical appraisal of the available evidence, the current state of research, and both clinical and research recommendations were described on the following topics: epidemiology, pathophysiology and strategies to mitigate pulmonary dysfunction among patients with acute kidney injury and/or kidney dysfunction among patients with acute respiratory failure/acute respiratory distress syndrome. Furthermore, emphasis was put on patients receiving organ support (RRT, IMV and/or ECMO) and its impact on lung and kidney function. Conclusion:The ADQI 21 conference found significant knowledge gaps about organ crosstalk between lung and kidney and its relevance for critically ill patients. Lung protective ventilation, conservative fluid management and early recognition and treatment of pulmonary infections were the only clinical recommendations with higher quality of evidence. Recommendations for research were formulated, targeting lung-kidney interactions to improve care processes and outcomes in critical illness.

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Section: Rationalementioning

confidence: 99%

Lung–kidney interactions in critically ill patients: consensus report of the Acute Disease Quality Initiative (ADQI) 21 Workgroup

et al. 2019

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“…37,38 Acute respiratory distress patients often attempt to increase minute ventilation, thus potentially worsening ventilator dyssynchrony, secondary to a multitude of reasons including anxiety and compensation for permissive hypercapnia. 39 While deep sedation can blunt this high respiratory drive and minute ventilation, and ventilator setting adjustments can reduce ventilator dyssynchrony, 40 complete control of the ventilator-patient interface may only be accomplished via paralysis.…”

Section: Potential Physiologic Benefitsmentioning

confidence: 99%

“…The primary endpoint was oxygenation during the 120 hours after randomization, as measured by serial P/F ratios. The authors found the cisatracurium group had a significant improvement in oxygenation over the 120-hour study time Table 2 Potential physiologic benefits and harms of neuromuscular blockade in acute respiratory distress syndrome 24,[36][37][38][39][40][41][42][43][44][45][46][47][48][49][50][51][52][53][54][55]…”

Section: Randomized Clinical Trialsmentioning

confidence: 99%

Role of Pharmacologic Paralysis in Acute Respiratory Distress Syndrome

Syed

Kobzik

Huang

2019

Semin Respir Crit Care Med

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The pharmacology and history of neuromuscular blockade in clinical care are complex, with multiple theoretical and observed potential benefits and potential harms. Past studies raised concern for long-term paresis, but more recent studies have not found evidence for harm, possibly due to changes in background care, neuromuscular blocking agent, and duration of blockade. Current use is highly variable, likely due to limited evidence for efficacy beyond short-term physiologic improvement and lingering concerns for harm. A recently completed large multicenter trial will provide further information on the role of pharmacologic paralysis in acute respiratory distress syndrome.

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“…Ventilations are always needed to correct hypoxemia [3,4] To avoid or reduce pulmonary morbidity, the low tidal volume ventilation is often applied [5,6]. The ventilation strategy will certainly result in hypercapnia, which is called "permissive hypercapnia" [7,8]. Our previous study found that hypercapnia could induce IL-1β overproduction in hypoxia-activated microglia [9].…”

Section: Introductionmentioning

confidence: 99%

Hypercapnia promotes microglial pyroptosis via inhibiting mitophagy: implication in neuroinflammation in hypoxemic adult rats

Ding

Liu

et al. 2019

Preprint

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Background: Hypoxemia is a typical symptom of acute respiratory distress syndrome (ARDS). Ventilations are always needed for correcting hypoxemia. To avoid pulmonary morbidity, low tidal volume ventilation is often applied. The ventilation strategy will certainly result in hypercapnia. Our previous study found that hypercapnia could induce IL-1β overproduction in hypoxia-activated microglia. However, the underlying mechanism has remained unclear. This study aimed to explore whether hypercapnia would promote microglial pyroptosis via inhibiting mitophagy in adult rats with hypoxemia. Methods: Cerebral oxygen extraction ratio (CERO2), partial pressure of brain tissue oxygen (PbtO2), and reactive oxygen species (ROS) production in brain tissue in a rat model of hypercapnia/hypoxemia were evaluated. Along with this, the oxygen consumption rate (OCR) and ROS production of BV-2 microglial cells were evaluated after 15% CO2/0.2% O2 treatment. Mitophagy was observed using transmission electron microscopy (TEM). The protein expression level of LC3-II/I, p62, caspase-1, gasdermin D-N domains (GSDMD-N), IL-1β and IL-18 in microglial cells were detected before and after application of a ROS scavenger in vivo and in vitro. Results: PbtO2 level was elevated by hypercapnia in the hypoxemic rats in the first 1.5 h, but it was significantly decreased 2 h after ventilation. This was further evident by the increased levels of CERO2 at 3 h after ventilation. Besides, a high concentration of CO2 treatment could increase the levels of OCR in hypoxic BV-2 microglial cells in vitro. Expression levels of LC3-II were reduced, while those of p62 were increased by hypercapnia in the hypoxic hippocampus and BV-2 microglia. Autophagosomes could be seen in hypoxia treated microglial cells under TEM, while those were rarely observed in hypercapnia + hypoxia treated microglia. Hypercapnia markedly increased the production of ROS and the expression of caspase-1, GSDMD-N, IL-1β, and IL-18 in hypoxia-activated microglia both in vivo and in vitro. Pharmacological scavenging ROS inhibited microglial pyroptosis and expression of IL-1β and IL-18.Conclusion: Hypercapnia-induced mitophagy inhibition may promote pyroptosis and enhance IL-1β and IL-18 release in hypoxia-activated microglia.

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Re-examining Permissive Hypercapnia in ARDS

Cited by 62 publications

References 85 publications

Lung–kidney interactions in critically ill patients: consensus report of the Acute Disease Quality Initiative (ADQI) 21 Workgroup

Lung–kidney interactions in critically ill patients: consensus report of the Acute Disease Quality Initiative (ADQI) 21 Workgroup

Role of Pharmacologic Paralysis in Acute Respiratory Distress Syndrome

Hypercapnia promotes microglial pyroptosis via inhibiting mitophagy: implication in neuroinflammation in hypoxemic adult rats

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