Hyperoxia and cardiopulmonary resuscitation outcome: where is the data? (original) (raw)
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JAMA, 2010
S UDDEN CARDIAC ARREST IS THE most common lethal consequence of cardiovascular disease. Even if return of spontaneous circulation (ROSC) from cardiac arrest is achieved, approximately 60% of patients will not survive to hospital discharge. 1,2 The high mortality is attributed to the postcardiac arrest syndrome, which involves global ischemiareperfusion injury, myocardial stunning, and anoxic brain injury. The recent success of therapeutic hypothermia for post-ROSC neuroprotection 4,5 has increased momentum for investigating post-ROSC factors that can improve outcomes.
BMC Cardiovascular Disorders, 2021
Background High levels of arterial oxygen pressures (PaO2) have been associated with increased mortality in extracorporeal cardiopulmonary resuscitation (ECPR), but there is limited information regarding possible mechanisms linking hyperoxia and death in this setting, notably with respect to its hemodynamic consequences. We aimed therefore at evaluating a possible association between PaO2, circulatory failure and death during ECPR. Methods We retrospectively analyzed 44 consecutive cardiac arrest (CA) patients treated with ECPR to determine the association between the mean PaO2 over the first 24 h, arterial blood pressure, vasopressor and intravenous fluid therapies, mortality, and cause of deaths. Results Eleven patients (25%) survived to hospital discharge. The main causes of death were refractory circulatory shock (46%) and neurological damage (24%). Compared to survivors, non survivors had significantly higher mean 24 h PaO2 (306 ± 121 mmHg vs 164 ± 53 mmHg, p < 0.001), lower...
2021
BackgroundHyperoxia has been associated with adverse outcomes in post cardiac arrest (CA) patients. However, little data are available from mixed cohorts, where extracorporeal membrane oxygenation cardiopulmonary resuscitation (ECPR) and conventional CPR (CCPR) were utilised. The independence of effect of hyperoxia in this setting is not clear. Study-objective was to examine the association between hyperoxia and 30-day mortality in a mixed cohort of ECPR and CCPR patients.Methods and designThis was a retrospective cohort study of CA patients admitted to a tertiary level cardiac arrest centre in Australia from 1st January 2013 to 31st August 2018. Mean arterial oxygen levels (PaO2) and episodes of extreme hyperoxia (PaO2 ≥ 300mmHg) were analysed over the first 8 days. The primary outcome was 30-day mortality.ResultsA total of 169 post CA patients were assessed over a 6.5-year time period: 79 patients undergoing ECPR vs 90 patients undergoing CCPR. The mean age of the cohort was 54 (±...
Resuscitation, 2018
Recent studies suggest the administration of 100% oxygen to hyperoxic levels following return-of-spontaneous-circulation (ROSC) post-cardiac arrest may be harmful. However, the feasibility and safety of oxygen titration in the prehospital setting is unknown. We conducted a multi-centre, phase-2 study testing whether prehospital titration of oxygen results in an equivalent number of patients arriving at hospital with oxygen saturations SpO2 ≥ 94%. We enrolled unconscious adults with: sustained ROSC; initial shockable rhythm; an advanced airway; and an SpO2 ≥ 95%. Initially (Sept 2015-March 2016) patients were randomised 1:1 to either 2 litres/minute (L/min) oxygen (titrated) or >10 L/min oxygen (control) via a bag-valve reservoir. However, one site experienced a high number of desaturations (SpO2 < 94%) in the titrated arm and this arm was changed (April 2016) to an initial reduction of oxygen to 4 L/min then, if tolerated, to 2 L/min, and the desaturation limit was decreased t...
Resuscitation, 2013
Aim: As recent clinical data suggest a harmful effect of arterial hyperoxia on patients after resuscitation from cardiac arrest (CA), we aimed to investigate this association during cardiopulmonary resuscitation (CPR), the earliest and one of the most crucial phases of recirculation. Methods: We analysed 1015 patients who from 2003 to 2010 underwent out-of-hospital CPR administered by emergency medical services serving 300,000 inhabitants. Inclusion criteria for further analysis were nontraumatic background of CA and patients >18 years of age. One hundred and forty-five arterial blood gas analyses including oxygen partial pressure (paO2) measurement were obtained during CPR. Results: We observed a highly significant increase in hospital admission rates associated with increases in paO2 in steps of 100 mmHg (13.3 kPa). Subsequently, data were clustered according to previously described cutoffs (≤60 mmHg [8 kPa]], 61-300 mmHg [8.1-40 kPa], >300 mmHg [>40 kPa]). Baseline variables (age, sex, initial rhythm, rate of bystander CPR and collapse-to-CPR time) of the three compared groups did not differ significantly. Rates of hospital admission after CA were 18.8%, 50.6% and 83.3%, respectively. In a multivariate analysis, logistic regression revealed significant prognostic value for paO2 and the duration of CPR. Conclusion: This study presents novel human data on the arterial paO2 during CPR in conjunction with the rate of hospital admission. We describe a significantly increased rate of hospital admission associated with increasing paO2. We found that the previously described potentially harmful effects of hyperoxia after return of spontaneous circulation were not reproduced for paO2 measured during CPR. Clinical trial registration: n/a.