Hypercapnia

Masterson, Claire; Otulakowski, Gail; Kavanagh, Brian P.

doi:10.1097/mcc.0000000000000164

Cited by 18 publications

(8 citation statements)

References 46 publications

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“…Interestingly, systemic blood pressures were very similar across the PaCO 2 subgroups in this cohort. PaCO 2 could yet be an important mediator in vascular effects, cardiopulmonary resuscitation and cerebral perfusion [ 13 , 33 ]. In view of that, the association between hypocapnia and mortality may be explained by cerebral vasoconstriction, whereas hypercapnia may be less harmful due to increased peripheral tissue oxygenation [ 34 – 38 ].…”

Section: Discussionmentioning

confidence: 99%

Associations of arterial carbon dioxide and arterial oxygen concentrations with hospital mortality after resuscitation from cardiac arrest

et al. 2015

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IntroductionArterial concentrations of carbon dioxide (PaCO2) and oxygen (PaO2) during admission to the intensive care unit (ICU) may substantially affect organ perfusion and outcome after cardiac arrest. Our aim was to investigate the independent and synergistic effects of both parameters on hospital mortality.MethodsThis was a cohort study using data from mechanically ventilated cardiac arrest patients in the Dutch National Intensive Care Evaluation (NICE) registry between 2007 and 2012. PaCO2 and PaO2 levels from arterial blood gas analyses corresponding to the worst oxygenation in the first 24 h of ICU stay were retrieved for analyses. Logistic regression analyses were performed to assess the relationship between hospital mortality and both categorized groups and a spline-based transformation of the continuous values of PaCO2 and PaO2.ResultsIn total, 5,258 cardiac arrest patients admitted to 82 ICUs in the Netherlands were included. In the first 24 h of ICU admission, hypocapnia was encountered in 22 %, and hypercapnia in 35 % of included cases. Hypoxia and hyperoxia were observed in 8 % and 3 % of the patients, respectively. Both PaCO2 and PaO2 had an independent U-shaped relationship with hospital mortality and after adjustment for confounders, hypocapnia and hypoxia were significant predictors of hospital mortality: OR 1.37 (95 % CI 1.17–1.61) and OR 1.34 (95 % CI 1.08–1.66). A synergistic effect of concurrent derangements of PaCO2 and PaO2 was not observed (P = 0.75).ConclusionsThe effects of aberrant arterial carbon dioxide and arterial oxygen concentrations were independently but not synergistically associated with hospital mortality after cardiac arrest.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-015-1067-6) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Associations of arterial carbon dioxide and arterial oxygen concentrations with hospital mortality after resuscitation from cardiac arrest

et al. 2015

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“…Several years ago, it has been hypothesized that inducing hypercapnia could have been beneficial in patients with acute respiratory failure by attenuating lung inflammation and injury 4 . However, hypercapnia has been associated with impaired alveolar epithelial function, induced immunosuppression, pulmonary hypertension and diaphragmatic dysfunction [5][6][7][8][9][10] . Along these lines, devices allowing extracorporeal CO 2 removal (ECCO2R) to facilitate ultraprotective ventilation have been recently developed [11][12][13] .…”

Section: Introductionmentioning

confidence: 99%

Impact of Arterial CO₂Retention in Patients With Moderate or Severe ARDS

et al. 2023

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HAL is a multi-disciplinary open access archive for the deposit and dissemination of scientific research documents, whether they are published or not. The documents may come from teaching and research institutions in France or abroad, or from public or private research centers. L'archive ouverte pluridisciplinaire HAL, est destinée au dépôt et à la diffusion de documents scientifiques de niveau recherche, publiés ou non, émanant des établissements d'enseignement et de recherche français ou étrangers, des laboratoires publics ou privés.

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“…HCA also attenuates the inflammatory activation of p42/44 MAP-kinase, an enzyme that has numerous effects on cytoskeletal and focal adhesion proteins that are directly involved in endothelial permeability. 5 , 6 We have shown that airway pressure is synergistic with vascular pressure in altering K f ; 7 thus, the ability of HCA to mitigate alveolar injury during VILI prompted us to hypothesize that HCA may also influence endothelial barrier function during mechanical stress.…”

Section: Introductionmentioning

confidence: 99%

Hypercapnic acidosis attenuates pressure‐dependent increase in whole‐lung filtration coefficient (K_f)

et al. 2017

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Hypercapnic acidosis (HCA) has beneficial effects in experimental models of lung injury by attenuating inflammation and decreasing pulmonary edema. However, HCA increases pulmonary vascular pressure that will increase fluid filtration and worsen edema development. To reconcile these disparate effects, we tested the hypothesis that HCA inhibits endothelial mechanotransduction and protects against pressure-dependent increases in the whole lung filtration coefficient (Kf). Isolated perfused rat lung preparation was used to measure whole lung filtration coefficient (Kf) at two levels of left atrial pressure (PLA = 7.5 versus 15 cm H2O) and at low tidal volume (LVt) versus standard tidal volume (STVt) ventilation. The ratio of Kf2/Kf1 was used as the index of whole lung permeability. Double occlusion pressure, pulmonary artery pressure, pulmonary capillary pressures, and zonal characteristics (ZC) were measured to assess effects of HCA on hemodynamics and their relationship to Kf2/Kf1. An increase in PLA2 from 7.5 to 15 cm H2O resulted in a 4.9-fold increase in Kf2/Kf1 during LVt and a 4.8-fold increase during STVt. During LVt, HCA reduced Kf2/Kf1 by 2.7-fold and reduced STVt Kf2/Kf1 by 5.2-fold. Analysis of pulmonary hemodynamics revealed no significant differences in filtration forces in response to HCA. HCA interferes with lung vascular mechanotransduction and prevents pressure-dependent increases in whole lung filtration coefficient. These results contribute to a further understanding of the lung protective effects of HCA.

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Hypercapnia

Cited by 18 publications

References 46 publications

Associations of arterial carbon dioxide and arterial oxygen concentrations with hospital mortality after resuscitation from cardiac arrest

Associations of arterial carbon dioxide and arterial oxygen concentrations with hospital mortality after resuscitation from cardiac arrest

Impact of Arterial CO₂Retention in Patients With Moderate or Severe ARDS

Hypercapnic acidosis attenuates pressure‐dependent increase in whole‐lung filtration coefficient (K_f)

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Hypercapnia

Cited by 18 publications

References 46 publications

Associations of arterial carbon dioxide and arterial oxygen concentrations with hospital mortality after resuscitation from cardiac arrest

Associations of arterial carbon dioxide and arterial oxygen concentrations with hospital mortality after resuscitation from cardiac arrest

Impact of Arterial CO2Retention in Patients With Moderate or Severe ARDS

Hypercapnic acidosis attenuates pressure‐dependent increase in whole‐lung filtration coefficient (Kf)

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Impact of Arterial CO₂Retention in Patients With Moderate or Severe ARDS

Hypercapnic acidosis attenuates pressure‐dependent increase in whole‐lung filtration coefficient (K_f)