Oxygen Supplementation and Hyperoxia in Critically Ill Cardiac Patients

Thomas, Alexander; Diepen, Sean van; Beekman, Rachel; Sinha, Shashank S.; Brusca, Samuel B.; Alviar, Carlos L.; Jentzer, Jacob C.; Bohula, Erin A.; Katz, Jason N.; Shahu, Andi; Barnett, Christopher F.; Morrow, David A.; Gilmore, Emily J.; Solomon, Michael A.; Miller, Paul E.

doi:10.1016/j.jacadv.2022.100065

Cited by 14 publications

(16 citation statements)

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“…13,14 Studies examining hyperoxia in patients receiving ECPR may not apply to the overall CS population, as the potential for anoxic brain injury in cardiac arrest patients could modify the association between hyperoxia and outcomes (particularly if the postanoxic brain is more susceptible to hyperoxia, as has been proposed). 6,9,10,15,[17][18][19][20] Nonetheless, our results closely mirror those of Tonna et al 10 that showed a strong and incremental association between rising PaO2 and higher in-hospital mortality for patients with cardiac arrest receiving ECPR. Notably, we observed similar associations between hyperoxia and adverse outcomes in our CS patients with and without a prior cardiac arrest.…”

Section: Comparison With Other Studiessupporting

confidence: 90%

“…However, hyperoxia is known to have numerous potentially deleterious physiological consequences, including adverse effects on the cardiovascular system and organ perfusion that could explain worse outcomes. 6–8,21,22 This suggests that using a higher PaO2 to increase DO2 may be a poor therapeutic option, particularly as dissolved free oxygen typically contributes only minimally to the oxygen content of arterial blood which is determined primarily by oxygen bound to hemoglobin. 6,8 More importantly, exposure to high levels of free oxygen during hyperoxia may increase oxygen free radical production and compromise beneficial hypoxia-dependent molecular mechanisms, resulting in a multitude of damaging cellular effects on the end organs.…”

Section: Discussionmentioning

confidence: 99%

“…6–8,21,22 This suggests that using a higher PaO2 to increase DO2 may be a poor therapeutic option, particularly as dissolved free oxygen typically contributes only minimally to the oxygen content of arterial blood which is determined primarily by oxygen bound to hemoglobin. 6,8 More importantly, exposure to high levels of free oxygen during hyperoxia may increase oxygen free radical production and compromise beneficial hypoxia-dependent molecular mechanisms, resulting in a multitude of damaging cellular effects on the end organs. 8,22 Our observation that hyperoxia is associated with worse outcomes regardless of the FiO2 suggests that there is likely to be a harmful systemic effect of hyperoxia, as opposed to an effect mediated through oxygen-induced lung injury.…”

Section: Discussionmentioning

confidence: 99%

“…Evidence has accumulated supporting the use of conservative oxygenation targets for many populations of critically ill patients and patients with acute cardiovascular disease. 6,20,[24][25][26] Our analysis potentially expands the concept of conservative oxygen therapy to patients receiving venoarterial ECMO support for CS. While our findings will need to be confirmed by an adequately powered randomized trial, we think that titrating the FiO2 on both the ventilator and ECMO circuit to maintain the PaO2 below 150 mmHg is reasonable for patients with CS who are adequately supported on ECMO.…”

Section: Implications For Clinical Practicementioning

confidence: 96%

“…However, hyperoxia is known to have numerous potentially deleterious physiological consequences, including adverse effects on the cardiovascular system and organ perfusion that could explain worse outcomes. [6][7][8]21,22 This suggests that using a higher PaO2 to increase DO2 may be a poor therapeutic option, particularly as dissolved free oxygen typically contributes only minimally to the oxygen All between-group differences were significant (P<0.05) in each subgroup. content of arterial blood which is determined primarily by oxygen bound to hemoglobin.…”

Section: … …mentioning

confidence: 99%

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Exposure to Arterial Hyperoxia During Extracorporeal Membrane Oxygenator Support and Mortality in Patients With Cardiogenic Shock

Jentzer

Miller

Alviar

et al. 2023

Circ: Heart Failure

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Background: Exposure to hyperoxia, a high arterial partial pressure of oxygen (PaO2), may be associated with worse outcomes in patients receiving extracorporeal membrane oxygenator (ECMO) support. We examined hyperoxia in the Extracorporeal Life Support Organization (ELSO) Registry among patients receiving venoarterial (VA) ECMO for cardiogenic shock (CS). Methods: We included ELSO Registry patients from 2010 to 2020 who received VA ECMO for CS, excluding extracorporeal CPR. Patients were grouped based on PaO2 after 24 hours of ECMO: normoxia (PaO2 60-150 mmHg), mild hyperoxia (PaO2 151-300 mmHg), and severe hyperoxia (PaO2 >300 mmHg). In-hospital mortality was evaluated using multivariable logistic regression. Results: Among 9959 patients, 3005 (30.2%) patients had mild hyperoxia and 1972 (19.8%) had severe hyperoxia. In-hospital mortality increased across groups: normoxia, 47.8%; mild hyperoxia, 55.6% (adjusted OR 1.37, 95% CI 1.23-1.53, p <0.001); severe hyperoxia, 65.4% (adjusted OR 2.20, 95% CI 1.92-2.52, p <0.001). A higher PaO2 was incrementally associated with increased in-hospital mortality (adjusted OR 1.14 per 50 mmHg higher, 95% CI 1.12-1.16, p <0.001). Patients with a higher PaO2 had increased in-hospital mortality in each subgroup and when stratified by ventilator settings, airway pressures, acid-base status, and other clinical variables. Higher PaO2 was the second strongest predictor of in-hospital mortality, after older age. Conclusions: Exposure to hyperoxia during VA ECMO support for CS is strongly associated with increased in-hospital mortality, independent from hemodynamic and ventilatory status. Until clinical trial data are available, we suggest targeting a normal PaO2 and avoiding hyperoxia in CS patients receiving VA ECMO.

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Section: Comparison With Other Studiessupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Implications For Clinical Practicementioning

confidence: 96%

“…However, hyperoxia is known to have numerous potentially deleterious physiological consequences, including adverse effects on the cardiovascular system and organ perfusion that could explain worse outcomes. [6][7][8]21,22 This suggests that using a higher PaO2 to increase DO2 may be a poor therapeutic option, particularly as dissolved free oxygen typically contributes only minimally to the oxygen All between-group differences were significant (P<0.05) in each subgroup. content of arterial blood which is determined primarily by oxygen bound to hemoglobin.…”

Section: … …mentioning

confidence: 99%

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Exposure to Arterial Hyperoxia During Extracorporeal Membrane Oxygenator Support and Mortality in Patients With Cardiogenic Shock

Jentzer

Miller

Alviar

et al. 2023

Circ: Heart Failure

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Hypocapnia is associated with increased in‐hospital mortality and 1 year mortality in acute heart failure patients

Zhang,

Sun,

Sui

et al. 2024

ESC Heart Failure

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AimsBoth hypercapnia and hypocapnia are common in patients with acute heart failure (AHF), but the association between partial pressure of arterial carbon dioxide (PaCO2) and AHF prognosis remains unclear. The objective of this study was to investigate the connection between PaCO2 within 24 h after admission to the intensive care unit (ICU) and mortality during hospitalization and at 1 year in AHF patients.Methods and resultsAHF patients were enrolled from the Medical Information Mart for Intensive Care IV database. The patients were divided into three groups by PaCO2 values of <35, 35–45, and >45 mmHg. The primary outcome was to investigate the connection between PaCO2 and in‐hospital mortality and 1 year mortality in AHF patients. The secondary outcome was to assess the prediction value of PaCO2 in predicting in‐hospital mortality and 1 year mortality in AHF patients. A total of 2374 patients were included in this study, including 457 patients in the PaCO2 < 35 mmHg group, 1072 patients in the PaCO2 = 35–45 mmHg group, and 845 patients in the PaCO2 > 45 mmHg group. The in‐hospital mortality was 19.5%, and the 1 year mortality was 23.9% in the PaCO2 < 35 mmHg group. Multivariate logistic regression analysis showed that the PaCO2 < 35 mmHg group was associated with an increased risk of in‐hospital mortality [hazard ratio (HR) 1.398, 95% confidence interval (CI) 1.039–1.882, P = 0.027] and 1 year mortality (HR 1.327, 95% CI 1.020–1.728, P = 0.035) than the PaCO2 = 35–45 mmHg group. The PaCO2 > 45 mmHg group was associated with an increased risk of in‐hospital mortality (HR 1.387, 95% CI 1.050–1.832, P = 0.021); the 1 year mortality showed no significant difference (HR 1.286, 95% CI 0.995–1.662, P = 0.055) compared with the PaCO2 = 35–45 mmHg group. The Kaplan–Meier survival curves showed that the PaCO2 < 35 mmHg group had a significantly lower 1 year survival rate. The area under the receiver operating characteristic curve for predicting in‐hospital mortality was 0.591 (95% CI 0.526–0.656), and the 1 year mortality was 0.566 (95% CI 0.505–0.627) in the PaCO2 < 35 mmHg group.ConclusionsIn AHF patients, hypocapnia within 24 h after admission to the ICU was associated with increased in‐hospital mortality and 1 year mortality. However, the increase in 1 year mortality may be influenced by hospitalization mortality. Hypercapnia was associated with increased in‐hospital mortality.

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