The use of 100% compared to 50% oxygen during ineffective experimental cardiopulmonary resuscitation improves brain oxygenation.

INTRODUCTION: Perfusion pressure and chest compression quality are generally considered key determinants of brain oxygenation during cardiopulmonary resuscitation (CPR) and the impact of oxygen administration is less clear. We compared ventilation with 100% and 50% oxygen during ineffective manual chest compressions and hypothesized that 100% oxygen would improve brain oxygenation. METHODS: Ventricular fibrillation (VF) was induced electrically in anaesthetized pigs and left untreated for 5 minutes, followed by randomization to ineffective manual CPR with ventilation of 50% or 100% oxygen. The first defibrillation was performed 10 minutes after induction of VF, and CPR continued with mechanical chest compressions (LUCAS2™) and defibrillation every 2 minutes until 36 minutes or return of spontaneous circulation (ROSC). Brain oxygenation was measured with near-infrared spectroscopy (rSO2) and invasive brain tissue oxygen (PbtO2) with a probe (NEUROVENT-PTO, RAUMEDIC) inserted into frontal brain tissue. Cerebral oxygenation was compared between groups with Mann-Whitney U tests and linear mixed models. RESULTS: Twenty-eight pigs were included in the study: 14 subjects in each group. During ineffective chest compressions relative PbtO2 was higher in the group ventilated with 100% compared to 50% oxygen (5.2 mmHg [1.4-20.5] vs 2.2 [0.8-6.8], p = 0.001), but there was no difference in rSO2 (22% [16-28] vs 18 [15-25], p = 0.090). The use of 50% or 100% oxygen showed no difference in relative PbtO2 (p = 1.00) and rSO2 (p = 0.206) during mechanical CPR. CONCLUSIONS: The use of 100% compared to 50% oxygen during ineffective manual CPR improved brain oxygenation measured invasively in brain tissue, but there was no difference in rSO2.

Incidence of hyperoxia and factors associated with cerebral oxygenation during cardiopulmonary resuscitation.

BACKGROUND: High oxygen levels may worsen cardiac arrest reperfusion injury. We determined the incidence of hyperoxia during and immediately after successful cardiopulmonary resuscitation and identified factors associated with intra-arrest cerebral oxygenation measured with near-infrared spectroscopy (NIRS). METHODS: A prospective observational study of out-of-hospital cardiac arrest patients treated by a physician-staffed helicopter unit. Collected data included intra-arrest brain regional oxygen saturation (rSO2) with NIRS, invasive blood pressures, end-tidal CO2 (etCO2) and arterial blood gas samples. Moderate and severe hyperoxia were defined as arterial oxygen partial pressure (paO2) 20.0-39.9 and ≥40 kPa, respectively. Intra-arrest factors correlated with the NIRS value, rSO2, were assessed with the Spearman's correlation test. RESULTS: Of 80 recruited patients, 73 (91%) patients had rSO2 recorded during CPR, and 46 had an intra-arrest paO2 analysed. ROSC was achieved in 28 patients, of whom 20 had paO2 analysed. Moderate hyperoxia was seen in one patient during CPR and in four patients (20%, 95% CI 7-42%) after ROSC. None had severe hyperoxia during CPR, and one patient (5%, 95% 0-25%) immediately after ROSC. The rSO2 during CPR was correlated with intra-arrest systolic (r = 0.28, p < 0.001) and diastolic blood pressure (p = 0.32, p < 0.001) but not with paO2 (r = 0.13, p = 0.41), paCO2 (r = 0.18, p = 0.22) or etCO2 (r = 0.008, p = 0.9). CONCLUSION: Hyperoxia during or immediately after CPR is rare in patients treated by physician-staffed helicopter units. Cerebral oxygenation during CPR appears more dependent, albeit weakly, on hemodynamics than arterial oxygen concentration.

Point-of-care laboratory analyses of intraosseous, arterial and central venous samples during experimental cardiopulmonary resuscitation.

INTRODUCTION: Screening and correcting reversible causes of cardiac arrest (CA) are an essential part of cardiopulmonary resuscitation (CPR). Point-of-care (POC) laboratory analyses are used for screening pre-arrest pathologies, such as electrolyte disorders and acid-base balance disturbances. The aims of this study were to compare the intraosseous (IO), arterial and central venous POC values during CA and CPR and to see how the CPR values reflect the pre-arrest state. METHODS: We performed an experimental study on 23 anaesthetised pigs. After induction of ventricular fibrillation (VF), we obtained POC samples from the IO space, artery and central vein simultaneously at three consecutive time points. We observed the development of the values during CA and CPR and compared the CPR values to the pre-arrest values. RESULTS: The IO, arterial and venous values changed differently from one another during the course of CA and CPR. Base excess and pH decreased in the venous and IO samples during untreated VF, but in the arterial samples, this only occurred after the onset of CPR. The IO, arterial and venous potassium values were higher during CPR compared to the pre-arrest arterial values (mean elevations 4.4 mmol/l (SD 0.72), 3.3 mmol/l (0.78) and 2.8 mmol/l (0.94), respectively). CONCLUSIONS: A dynamic change occurs in the common laboratory values during CA and CPR. POC analyses of lactate, pH, sodium and calcium within IO samples are not different from analyses of arterial or venous blood. Potassium values in IO, arterial and venous samples during CPR are higher than the pre-arrest arterial values.

The effect of 50% compared to 100% inspired oxygen fraction on brain oxygenation and post cardiac arrest mitochondrial function in experimental cardiac arrest.

BACKGROUND AND AIM: We hypothesised that the use of 50% compared to 100% oxygen maintains cerebral oxygenation and ameliorates the disturbance of cardiac mitochondrial respiration during cardiopulmonary resuscitation (CPR). METHODS: Ventricular fibrillation (VF) was induced electrically in anaesthetised healthy adult pigs and left untreated for seven minutes followed by randomisation to manual ventilation with 50% or 100% oxygen and mechanical chest compressions (LUCAS®). Defibrillation was performed at thirteen minutes and repeated if necessary every two minutes with 1mg intravenous adrenaline. Cerebral oxygenation was measured with near-infrared spectroscopy (rSO2, INVOS™5100C Cerebral Oximeter) and with a probe (NEUROVENT-PTO, RAUMEDIC) in the frontal brain cortex (PbO2). Heart biopsies were obtained 20min after the return of spontaneous circulation (ROSC) with an analysis of mitochondrial respiration (OROBOROS Instruments Corp., Innsbruck, Austria), and compared to four control animals without VF and CPR. Brain rSO2 and PbO2 were log transformed and analysed with a mixed linear model and mitochondrial respiration with an analysis of variance. RESULTS: Of the twenty pigs, one had a breach of protocol and was excluded, leaving nine pigs in the 50% group and ten in the 100% group. Return of spontaneous circulation (ROSC) was achieved in six pigs in the 50% group and eight in the 100% group. The rSO2 (p=0.007) was lower with FiO2 50%, but the PbO2 was not (p=0.93). After ROSC there were significant interactions between time and FiO2 regarding both rSO2 (p=0.001) and PbO2 (p=0.004). Compared to the controls, mitochondrial respiration was decreased, with adenosine diphosphate (ADP) levels of 57 (17)pmols-1mg-1 compared to 92 (23)pmols-1mg-1 (p=0.008), but there was no difference between different oxygen fractions (p=0.79). CONCLUSIONS: The use of 50% oxygen during CPR results in lower cerebral oximetry values compared to 100% oxygen but there is no difference in brain tissue oxygen. Cardiac arrest disturbs cardiac mitochondrial respiration, but it is not alleviated with the use of 50% compared to 100% oxygen (Ethical and hospital approvals ESAVI/1077/04.10.07/2016 and HUS/215/2016, §7 30.3.2016, Funding Helsinki University and others).

Prevalence and factors correlating with hyperoxia exposure following cardiac arrest--an observational single centre study.

PURPOSE OF THE STUDY: Arterial hyperoxia during care in the intensive care unit (ICU) has been found to correlate with mortality after cardiac arrest (CA). We examined the prevalence of hyperoxia following CA including pre-ICU values and studied differences between those exposed and those not exposed to define predictors of exposure. MATERIALS AND METHODS: A retrospective analysis of a prospectively collected cohort of cardiac arrest patients treated in an Australian tertiary hospital between August 2008 and July 2010. Arterial blood oxygen values and used fractions of oxygen were recorded during the first 24 hours after the arrest. Hyperoxia was defined as any arterial oxygen value greater than 300 mmHg. Chi-square test was used to compare categorical data and Mann-Whitney U-test to continuous data. Statistical methods were used to identify predictors of hyperoxia exposure. RESULTS: Of 122 patients treated in the ICU following cardiac arrest 119 had one or several arterial blood gases taken and were included in the study. Of these, 49 (41.2%) were exposed to hyperoxia and 70 (58.8%) were not during the first 24 hours after the CA. Those exposed had longer delays to return of spontaneous circulation (26 minutes vs. 10 minutes) and a longer interval to ICU admission after the arrest (4 hours compared to 1 hour). Location of the arrest was an independent predictor of exposure to hyperoxia (P-value = 0,008) with out-of-hospital cardiac arrest patients being more likely to have been exposed (65%), than those with an in-hospital (21%) or ICU (30%) cardiac arrest. Out-of-hospital cardiac arrest patients had higher oxygen concentrations to the fraction of inspired oxygen ratios. CONCLUSIONS: Hyperoxia exposure was more common than previously reported and occurred more frequently in association with out-of-hospital cardiac arrest, longer times to ROSC and delays to ICU admission.