Cerebral energy failure following experimental cardiac arrest: Hypothermia treatment reduces secondary lactate/pyruvate-ratio increase

AimThis was an experimental study performed to investigate cerebral metabolism during hypothermia treatment and rewarming after resuscitation from cardiac arrest (CA).Materials and methodsSixteen pigs underwent CA followed by cardiopulmonary resuscitation (CPR). After randomisation into one hypothermic (n = 8) and one normothermic group (n = 8) the animals received infusion of 4 or 38 °C saline, respectively. Following restoration of spontaneous circulation (ROSC) both groups were observed for 360 min. The hypothermic group was cooled for 180 min and then rewarmed. Temperature was not modulated in the normothermic group.Cerebral microdialysis was conducted and lactate/pyruvate (L/P)-ratio and glutamate were analysed. Intracranial pressure probe was inserted. Oxygen saturation in venous jugular bulb blood (SjO₂) was analysed.ResultsAll animals initially had increased L/P-ratio (>30). A total of nine animals developed secondary increase. In the hypothermic group this was observed in 2/7 animals and in the normothermic group in 7/8 (p = 0.04). Glutamate increased initially in all animals with secondary increases in two animals in each group. No differences in L/P-ratio or glutamate were detected during the rewarming phase compared to the hypothermic phase. The hypothermic group had higher SjO₂ (p = 0.04). In both groups intracranial pressure increased after ROSC.ConclusionAfter resuscitation from CA there was a risk of cerebral secondary energy failure (reflected as an increased L/P-ratio) but hypothermia treatment seemed to counteract this effect. Cerebral oxygen extraction, measured by SjO_2, was increased in the hypothermic group probably due to reduced metabolism. Rewarming did not reveal any obvious harmful events.     

Mechanical active compression–decompression cardiopulmonary resuscitation (ACD-CPR) versus manual CPR according to pressure of end tidal carbon dioxide (PETCO2) during CPR in out-of-hospital cardiac arrest (OHCA)

AimIn animal and human studies, measuring the pressure of end tidal carbon dioxide (P_ETCO₂) has been shown to be a practical non-invasive method that correlates well with the pulmonary blood flow and cardiac output (CO) generated during cardiopulmonary resuscitation (CPR). This study aims to compare mechanical active compression–decompression (ACD) CPR with standard CPR according to P_ETCO₂ among patients with out-of-hospital cardiac arrest (OHCA), during CPR and with standardised ventilation.MethodsThis prospective, on a cluster level, pseudo-randomised pilot trial took place in the Municipality of Göteborg. During a 2-year period, all patients aged >18 years suffering an out-of-hospital cardiac arrest (OHCA) of presumed cardiac etiology were enrolled. The present analysis included only tracheally intubated patients in whom P_ETCO₂ was measured for 15 min or until the detection of a pulse-giving rhythm.ResultsIn all, 126 patients participated in the evaluation, 64 patients in the mechanical chest compression group and 62 patients in the control group. The group receiving mechanical ACD-CPR obtained the significantly highest P_ETCO₂ values according to the average (p = 0.04), initial (p = 0.01) and minimum (p = 0.01) values. We found no significant difference according to the maximum value between groups.ConclusionIn this hypothesis generating study mechanical ACD-CPR compared with manual CPR generated the highest initial, minimum and average value of P_ETCO₂. Whether these data can be repeated and furthermore be associated with an improved outcome after OHCA need to be confirmed in a large prospective randomised trial.     

An investigation of thrust,depth and the impedance cardiogram as measures of cardiopulmonary resuscitation efficacy in a porcine model of cardiac arrest

ObjectiveOptimising the depth and rate of applied chest compressions following out of hospital cardiac arrest is crucial in maintaining end organ perfusion and improving survival. The impedance cardiogram (ICG) measured via defibrillator pads produces a characteristic waveform during chest compressions with the potential to provide feedback on cardiopulmonary resuscitation (CPR) and enhance performance. The objective of this pre-clinical study was to investigate the relationship between mechanical and physiological markers of CPR efficacy in a porcine model and examine the strength of correlation between the ICG amplitude, compression depth and end-tidal CO₂ (ETCO₂).MethodsTwo experiments were performed using 24 swine (12 per experiment). For experiment 1, ventricular fibrillation (VF) was induced and mechanical CPR commenced at varying thrusts (0–60 kg) for 2 min intervals. Chest compression depth was recorded using a Philips QCPR device with additional recording of invasive physiological parameters: systolic blood pressure, ETCO2, cardiac output and carotid flow. For experiment 2, VF was induced and mechanical CPR commenced at varying depths (0–5 cm) for 2 min intervals. The ICG was recorded via defibrillator pads attached to the animal's sternum and connected to a Heartsine 500P defibrillator. ICG amplitude, chest compression depth, systolic blood pressure and ETCO₂ were recorded during each cycle. In both experiments the within-animal correlation between the measured parameters was assessed using a mixed effect model.ResultsIn experiment 1 moderate within-animal correlations were observed between physiological parameters and compression depth (r = 0.69–0.77) and thrust (r = 0.66–0.82). A moderate correlation was observed between compression depth and thrust (r = 0.75). In experiment 2 a strong within-animal correlation and moderate overall correlations were observed between ICG amplitude and compression depth (r = 0.89, r = 0.79) and ETCO₂ (r = 0.85, r = 0.64).ConclusionIn this porcine model of induced cardiac arrest moderate within animal correlations were observed between mechanical and physiological markers of chest compression efficacy demonstrating the challenge in utilising a single mechanical metric to quantify chest compression efficacy. ICG amplitude demonstrated strong within animal correlations with compression depth and ETCO₂ suggesting its potential utility to provide CPR feedback in the out of hospital setting to improve performance.     

Increased serum brain-derived neurotrophic factor with high-intensity interval training in stroke patients: A randomized controlled trial

BackgroundPhysiological adaptations of stroke patients after high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) remain unclear.ObjectiveThis study determined the HIIT and MICT effects on aerobic capacity, cerebral oxygenation, peak cardiac output (CO), and serum brain-derived neurotrophic factor (BDNF) in stroke patients.MethodsWe included 23 stroke patients with age about 55 years and stroke duration > 24 months; participants completed 36 sessions of exercise training for 30 min; 13 were randomly assigned to perform MICT at 60% of peak oxygen consumption (VO_2peak) and 10 to perform HIIT at alternating 80% (3 min) and 40% (3 min) VO_2peak. Before and after interventions, we evaluated VO_2peak, peak CO, arteriovenous oxygen difference (AV O_2diff), bilateral frontal cortex oxygenation (relative changes of oxyhemoglobin Δ[O₂Hb], deoxyhemoglobin Δ[HHb], and total hemoglobin Δ[THb] levels), serum brain-derived neurotrophic factor (BDNF) level, and fluorescent cell staining for neuron morphology and percentage of cell-bearing neurites (% neurites).ResultsHIIT induced significant increases in VO_2peak (P = 0.008), CO (P = 0.038), Δ[HHb] (P = 0.046), Δ[THb] (P = 0.046), and serum BDNF level (P = 0.012). The improvement in VO_2peak was significantly greater with HIIT than MICT (20.7% vs. 9.8%, P = 0.031), as was AV O_2diff (P = 0.041), Δ[HHb] (P = 0.027), and serum BDNF level (P < 0.001). HIIT facilitated neuron dendritic protrusions (greater % neurites, P = 0.012) with prominent redistribution of mitochondria.ConclusionAs compared with MICT, HIIT-improved aerobic capacity by increasing systemic tissue O₂ extraction in stroke patients. Increased cerebral O₂ utilization in the involved hemisphere was also identified after HIIT. These physiological adaptations may be associated with increased serum BDNF level. In vitro dendritic growth in neurons treated with serum from HIIT participants may imply significant effects on neuron activities as compared with MICT.ClinicalTrials.gov identifierNCT04135391.     

The association of gasping and outcome,in out of hospital cardiac arrest: A systematic review and meta-analysis

ObjectiveGasping is common after cardiac arrest, and its frequency decreases over time. The aim of this study was to conduct a meta-analysis to evaluate the association of gasping and survival to discharge in patients who suffered out-of-hospital cardiac arrest.MethodsRelevant studies were identified by searching in PubMed, Medline, Embase, OVID, Web of Science and Google Scholar. Risk ratios (RR) and 95% confidence intervals (CI) were calculated to assess the association of gasping and on out-of-hospital cardiac arrest outcomes. Heterogeneity, subgroup analysis, sensitivity analysis and publication bias were explored.ResultsIndividual patient data was obtained from 10,797 participants suffered out-of-hospital cardiac arrest in five cohort studies of 4 articles. A fixed effects model suggested that patients with gasping were 3.525 times (95% CI: 3.028–4.104; P < 0.01) more likely to survive to discharge than those without gasping, and there was no heterogeneity among studies (P = 0.564). Also it may be a favorable factor for return of spontaneous circulation (RR: 2.170; 95% CI: 1.691, 2.785) with high heterogeneity (Q = 5.26; P = 0.022).ConclusionsFindings of this meta-analysis demonstrated that gasping is common after cardiac arrest, and is associated with increased survival to discharge. Patients who are cardiac arrest with gasping should be promptly resuscitated.     

Early administration of xenon or isoflurane may not improve functional outcome and cerebral alterations in a porcine model of cardiac arrest

BackgroundXenon (Xe) is neuroprotective when given 1 h after cardiopulmonary resuscitation (CPR). Here, we investigated if an earlier administration of Xe or isoflurane (Iso) would also reduce neurological dysfunction.Methods10 min after CPR from 8 min of cardiac arrest 21 pigs were randomized to three groups (n = 7/group) and then ventilated for 1 h with gas mixtures as follows: (1) control: 30% O₂ + 70% N₂; (2) Iso: 30% O₂ + 69% N₂ + 1% Iso; (3) Xe: 30% O₂ + 70% Xe. Physiological variables were obtained before cardiac arrest and 10, 60 and 240 min post-CPR including cardiac output (CO) and mean arterial pressure (MAP). Four days after CPR we assessed functional performance using an established neurocognitive test and overall neurological status using a neurologic deficit score (NDS). On day 5, brains of the re-anaesthetized pigs were harvested for neurohistopathological analyses.ResultsPrior to CPR there were no differences in hemodynamics and neurological status between groups. CO and MAP were significantly reduced after starting Iso administration. Both variables were also significantly lower in comparison to Xe and control animals. Control animals presented severe neurological dysfunction as measured by the NDS and the neurocognitive tests. Although Xe and Iso animals showed slightly better functional outcome this trend was not significant. Histopathological evaluation revealed ischaemic damage of neurons predominantly in the CA1 sector of the hippocampus with no differences between groups.ConclusionsIn this study early administration of Xe and Iso did not significantly reduce neurological dysfunction and histopathological alterations induced by cardiac arrest and CPR.     

Sinus bradycardia during hypothermia in comatose survivors of out-of-hospital cardiac arrest – A new early marker of favorable outcome?

BackgroundBradycardia is a common finding in patients undergoing therapeutic hypothermia (TH) following out-of-hospital cardiac arrest (OHCA), presumably as a normal physiological response to low body temperature. We hypothesized that a normal physiological response with sinus bradycardia (SB) indicates less neurological damage and therefore would be associated with lower mortality.MethodsWe studied 234 consecutive comatose survivors of OHCA with presumed cardiac etiology and shockable primary rhythm, who underwent a full 24-h TH-protocol (33 °C) at a tertiary heart center (years: 2004–2010). Primary endpoint was 180-day mortality; secondary endpoint was favorable neurological outcome (180-day cerebral performance category: 1–2).ResultsSB, defined as sinus rhythm <50 beats per minute during TH, was present in 115 (49%) patients. Baseline characteristics including sex, witnessed arrest, bystander cardiopulmonary resuscitation and time to return of spontaneous circulation were not different between SB- and no-SB patients. However, SB-patients were younger, 57 ± 14 vs. 63 ± 14 years, p < 0.001 and less frequently had known heart failure (7% vs. 20%, p < 0.01).Patients experiencing SB during the hypothermia phase of TH had a 17% 180-day mortality rate compared to 38% in no-SB patients (p < 0.001), corresponding to a 180-day hazard ratio (HR_adjusted = 0.45 (0.23–0.88, p = 0.02)) in the multivariable analysis. Similarly, SB during hypothermia was directly associated with lower odds of unfavorable neurological outcome (OR_unadjusted = 0.42 (0.23–0.75, p < 0.01).ConclusionSinus bradycardia during therapeutic hypothermia is independently associated with a lower 180-day mortality rate and may thus be a novel, early marker of favorable outcome in comatose survivors of OHCA.     

A feasibility study evaluating the role of cerebral oximetry in predicting return of spontaneous circulation in cardiac arrest

To date there has been no reliable noninvasive real time monitoring available to determine cerebral perfusion during cardiac arrest.ObjectivesTo investigate the feasibility of using a commercially available cerebral oximeter during in-hospital cardiac arrest, and determine whether this parameter predicts return of spontaneous circulation (ROSC).MethodsCerebral oximetry was incorporated in cardiac arrest management in 19 in-hospital cardiac arrest cases, five of whom had ROSC. The primary outcome measure was the relationship between rSO₂ and ROSC.ResultsThe use of cerebral oximetry was found to be feasible during in hospital cardiac arrest and did not interfere with management. Patients with ROSC had a significantly higher overall mean ± SE rSO₂ (35 ± 5 vs. 18 ± 0.4, p < 0.001). The difference in mean rSO₂ between survivors and non-survivors was most pronounced in the final 5 min of cardiac arrest (48 ± 1 vs. 15 ± 0.2, p < 0.0001) and appeared to herald imminent ROSC. Although spending a significantly higher portion of time with an rSO₂ > 40% was found in survivors (p < 0.0001), patients with ROSC had an rSO₂ above 30% for >50% of the duration of cardiac arrest, whereas non-survivors had an rSO₂ that was below 30% > 50% of their cardiac arrest. Patients with ROSC also had a significantly higher change in rSO₂ from baseline compared to non-survivors (310% ± 60% vs. 150% ± 27%, p < 0.05).ConclusionCerebral oximetry may have a role in predicting ROSC and the optimization of cerebral perfusion during cardiac arrest.     

Bundled postconditioning therapies improve hemodynamics and neurologic recovery after 17 min of untreated cardiac arrest

ObjectiveIschemic postconditioning (stutter CPR) and sevoflurane have been shown to mitigate the effects of reperfusion injury in cardiac tissue after 15 min of ventricular fibrillation (VF) cardiac arrest. Poloxamer 188 (P188) has also proven beneficial to neuronal and cardiac tissue during reperfusion injury in human and animal models. We hypothesized that the use of stutter CPR, sevoflurane, and P188 combined with standard advanced life support would improve post-resuscitation cardiac and neurologic function after prolonged VF arrest.MethodsFollowing 17 min of untreated VF, 20 pigs were randomized to Control treatment with active compression/decompression (ACD) CPR and impedance threshold device (ITD) (n = 8) or Bundle therapy with stutter ACD CPR + ITD + sevoflurane + P188 (n = 12). Epinephrine and post-resuscitation hypothermia were given in both groups per standard protocol. Animals that achieved return of spontaneous circulation (ROSC) were evaluated with echocardiography, biomarkers, and a blinded neurologic assessment with a cerebral performance category score.ResultsBundle therapy improved hemodynamics during resuscitation, reduced need for epinephrine and repeated defibrillation, reduced biomarkers of cardiac injury and end-organ dysfunction, and increased left ventricular ejection fraction compared to Controls. Bundle therapy also improved rates of ROSC (100% vs. 50%), freedom from major adverse events (50% vs. 0% at 48 h), and neurologic function (42% with mild or no neurologic deficit and 17% achieving normal function at 48 h).ConclusionsBundle therapy with a combination of stutter ACD CPR, ITD, sevoflurane, and P188 improved cardiac and neurologic function after 17 min of untreated cardiac arrest in pigs.All studies were performed with approval from the Institutional Animal Care Committee of the Minneapolis Medical Research Foundation (protocol #12-11).     

Association of presence and timing of invasive airway placement with outcomes after pediatric in-hospital cardiac arrest

BackgroundLittle data exist regarding the association of presence of an invasive airway before cardiac arrest or early placement of an invasive airway after cardiac arrest with outcomes in children who experience in-hospital cardiac arrest.MethodsWe conducted a retrospective review of patients aged 1 day to 18 years who received cardiopulmonary resuscitation (CPR) for ≥1 min in any of the three intensive care units (ICUs) at a tertiary care, academic children's hospital between 2002 and 2010. Specific outcomes evaluated included survival to hospital discharge, return of spontaneous circulation (ROSC), 24-h survival, and good neurological status at hospital discharge. We fitted multivariable logistic regression models to evaluate the association between the presence of an invasive airway prior to cardiac arrest and timing of placement of an invasive airway with these outcomes.ResultsThree hundred and ninety-one patients were included. Of these, 197 (51%) patients were already tracheally intubated before the occurrence of cardiac arrest. Median time to intubation was 6 min [interquartile range (IQR): 2, 12] among the 194 patients tracheally intubated following cardiac arrest. We found lower survival to hospital discharge among patients intubated prior to cardiac arrest (intubated vs. non-intubated group, 43% vs. 61%, p < 0.001). After adjusting for patient and event characteristics, presence of an invasive airway prior to cardiac arrest was not associated with a significant improvement in survival to hospital discharge [odds ratio (OR): 0.70, 95% confidence interval (CI): 0.42–1.16, p = 0.17], or good neurological outcomes (OR: 0.60, 95% CI: 0.34–1.05, p = 0.07). Similarly, early placement of an invasive airway after cardiac arrest was also not associated with an improvement in survival to hospital discharge (OR: 1.05, 95% CI: 0.78–1.42, p = 0.73), or good neurological outcomes (OR: 1.08, 95% CI: 0.77–1.53, p = 0.65).ConclusionsOur study demonstrates that presence of an invasive airway prior to cardiac arrest or early placement of an invasive airway after cardiac arrest is not associated with an improvement in survival to hospital discharge or good neurological outcomes. Further study of the relationship between invasive airway management and survival following cardiac arrest is warranted.     

Acute ischemic heart disease alters ventricular fibrillation waveform characteristics in out-of hospital cardiac arrest

BackgroundAlthough ventricular fibrillation waveform characteristics (VFWC) correlate with coronary perfusion pressure and may predict defibrillation outcome, recent animal data indicate that these waveform characteristics are altered in both acute myocardial infarction (AMI) and chronic coronary heart disease (CHD). We wanted to confirm these recent animal data in humans and explore the possibility for such characteristics to identify acute ischemia during cardiac arrest.MethodsData from all adult patients admitted to hospital after out-of-hospital VF cardiac arrest in Oslo between May 2003 and July 2007 were prospectively collected. Patients were categorized into one of four pre-defined etiologic groups: patients with AMI (AMI only), patients with AMI and CHD (AMI and CHD), patients with previous CHD without evidence for a new AMI (CHD only), and patients with primary arrhythmia (PA). VFWC were analyzed from prehospital ECG tracings, and the different etiologic groups compared using ANOVA.ResultsOne-hundred-and-one patients with ECG recordings usable for VF analysis could confidently be categorized; 16 with AMI only, 34 with AMI and CHD, 41 with CHD only and 10 with PA. The two VFWC median slope (MS) and amplitude spectral area (AMSA) were significantly depressed in patients with AMI only compared to both PA (MS p = 0.008, AMSA p = 0.035) and CHD only patients (MS p = 0.008, AMSA p = 0.006).ConclusionsAMI patients have depressed MS and AMSA compared to patients without AMI during VF cardiac arrest. VFWC might be helpful in identifying patients with AMI during cardiac arrest, but prospective clinical studies are warranted to assess its feasibility and clinical benefit.     

Managing cardiac arrest with refractory ventricular fibrillation in the emergency department: Conventional cardiopulmonary resuscitation versus extracorporeal cardiopulmonary resuscitation

AimRefractory ventricular fibrillation, resistant to conventional cardiopulmonary resuscitation (CPR), is a life threatening rhythm encountered in the emergency department. Although previous reports suggest the use of extracorporeal CPR can improve the clinical outcomes in patients with prolonged cardiac arrest, the effectiveness of this novel strategy for refractory ventricular fibrillation is not known. We aimed to compare the clinical outcomes of patients with refractory ventricular fibrillation managed with conventional CPR or extracorporeal CPR in our institution.MethodThis is a retrospective chart review study from an emergency department in a tertiary referral medical center. We identified 209 patients presenting with cardiac arrest due to ventricular fibrillation between September 2011 and September 2013. Of these, 60 patients were enrolled with ventricular fibrillation refractory to resuscitation for more than 10 min. The clinical outcome of patients with ventricular fibrillation received either conventional CPR, including defibrillation, chest compression, and resuscitative medication (C-CPR, n = 40) or CPR plus extracorporeal CPR (E-CPR, n = 20) were compared.ResultsThe overall survival rate was 35%, and 18.3% of patients were discharged with good neurological function. The mean duration of CPR was longer in the E-CPR group than in the C-CPR group (69.90 ± 49.6 min vs 34.3 ± 17.7 min, p = 0.0001). Patients receiving E-CPR had significantly higher rates of sustained return of spontaneous circulation (95.0% vs 47.5%, p = 0.0009), and good neurological function at discharge (40.0% vs 7.5%, p = 0.0067). The survival rate in the E-CPR group was higher (50% vs 27.5%, p = 0.1512) at discharge and (50% vs 20%, p = 0. 0998) at 1 year after discharge.ConclusionsThe management of refractory ventricular fibrillation in the emergency department remains challenging, as evidenced by an overall survival rate of 35% in this study. Patients with refractory ventricular fibrillation receiving E-CPR had a trend toward higher survival rates and significantly improved neurological outcomes than those receiving C-CPR.     

Two minutes CPR versus five cycles CPR prior to reanalysis of the cardiac rhythm: A prospective,randomized simulator-based trial

Aim of the studyWhile the 2005 cardiopulmonary resuscitation (CPR) guidelines recommended to provide CPR for five cycles before the next cardiac rhythm check, the current 2010 guideline now recommend to provide CPR for 2 min. Our aim was to compare adherence to both targets in a simulator-based randomized trial.Methods119 teams, consisting of three to four physicians each, were randomized to receive a graphical display of the simplified circular adult BLS algorithm with the instruction to perform CPR for either 2 min or five cycles 30:2. Subsequently teams had to treat a simulated unwitnessed cardiac arrest. Data analysis was performed using video-recordings obtained during simulations. The primary endpoint was adherence, defined as being within ±20% of the instructed target (i.e. 96–144 s in the 2 min teams and 4–6 cycles in the fivex30:2 teams).Results22/62 (35%) of the “two minutes” teams and 48/57 (84%) of the “five × 30:2″ teams provided CPR within a range of ± 20% of their instructed target (P < 0.0001). The median time of CPR prior to rhythm check was 91 s and 87 s, respectively, (P = 0.59) with a significant larger variance (P = 0.023) in the “two minutes” group.ConclusionsThis randomized simulator-based trial found better adherence and less variance to an instruction to continue CPR for five cycles before the next cardiac rhythm check compared to continuing CPR for 2 min. Avoiding temporal targets whenever possible in guidelines relating to stressful events appears advisable.     

Oxygen requirement during cardiopulmonary resuscitation (CPR) to effect return of spontaneous circulation

BackgroundRecent scientific evidence has demonstrated the importance of good quality chest compressions without interruption to improve cardiac arrest resuscitation rates, and suggested that a de-emphasis on minute ventilation is needed. However, independent of ventilation, the role of oxygen and the optimal oxygen concentration during CPR is not known. Previous studies have shown that ventilation with high oxygen concentration after CPR is associated with worse neurologic outcome. We tested the hypothesis that initial ventilation during CPR without oxygen improves resuscitation success.MethodsSprague–Dawley rats were anesthetized with ketamine/xylazine (IP), intubated and ventilated with room air. A KCl bolus (0.04 mg/g) was given (IV) to induce asystolic cardiac arrest and ventilation was stopped. At 6 min, CPR was started with an automated chest compressor at a rate of 200–240/min and epinephrine (0.01 mg/kg) was given 1 min later. During CPR, the ventilation rate was 50% of baseline with one of three oxygen concentrations: (1) 0% O₂ (100% N₂), (2) 21% O₂, or (3) 100% O₂. The prescribed oxygen concentration was continued for 2 min after return of spontaneous circulation (ROSC) and then all animals were switched to 100% oxygen for 1 h prior to extubation. Blood gases were measured at baseline, 2 min and 1 h after ROSC. Group comparisons were done using Fisher's exact test and ANOVA.ResultsROSC was achieved in 1/10 (0% O₂), 9/11 (21% O₂) and 10/12 (100% O₂, p < 0.001). ROSC times after starting CPR were 80 s in the 0% O₂, 115 ± 87 s in the 21% O₂ group and 95 ± 33 s in the 100% O₂ group (mean ± SD, p = 0.5). Aortic end-diastolic pressure before ROSC was not different among groups. 100% oxygen ventilation in the first 2 min resulted in higher PaO₂ at ROSC 2 min (109 ± 44 mm Hg vs. 33 ± 8 mm Hg, p < 0.001). Survival to 72 h was 0/1 (0% O₂), 7/9 (21% O₂) and 8/10 (100% O₂) with a low neurologic deficit score in both O₂ groups (NDS range 5–25).ConclusionsIn a mild cardiac arrest model with generally good neurologic recovery, initial CPR ventilation with no O₂ did not allow for ROSC. In contrast, CPR coupled with room air or higher oxygen levels result in a high rate of ROSC with good neurologic recovery. During CPR, the level of oxygenation must be considered, which if too low may preclude initial ROSC.     

Regional cerebral oxygen saturation monitoring for predicting interventional outcomes in patients following out-of-hospital cardiac arrest of presumed cardiac cause: A prospective,observational, multicentre study

AimThis study investigated the value of regional cerebral oxygen saturation (rSO₂) monitoring upon arrival at the hospital for predicting post-cardiac arrest intervention outcomes.MethodsWe enrolled 1195 patients with out-of-hospital cardiac arrest of presumed cardiac cause from the Japan-Prediction of Neurological Outcomes in Patients Post-cardiac Arrest Registry. The primary endpoint was a good neurologic outcome (cerebral performance categories 1 or 2 [CPC1/2]) 90 days post-event.ResultsA total of 68 patients (6%) had good neurologic outcomes. We found a mean rSO₂ of 21% ± 13%. A receiver operating characteristic curve analysis indicated an optimal rSO₂ cut-off of ≥40% for good neurologic outcomes (area under the curve 0.92, sensitivity 0.81, specificity 0.96). Good neurologic outcomes were observed in 53% (55/103) and 1% (13/1092) of patients with high (≥40%) and low (<40%) rSO₂, respectively. Even without return of spontaneous circulation (ROSC) upon arrival at the hospital, 30% (9/30) of patients with high rSO₂ had good neurologic outcomes. Furthermore, 16 patients demonstrating ROSC upon arrival at the hospital and low rSO₂ had poor neurologic outcomes. Multivariate analyses indicated that high rSO₂ was independently associated with good neurologic outcomes (odds ratio = 14.07, P < 0.001). Patients with high rSO₂ showed favourable neurologic prognoses if they had undergone therapeutic hypothermia or coronary angiography (CPC1/2, 69% [54/78]). However, 24% (25/103) of those with high rSO₂ did not undergo these procedures and exhibited unfavourable neurologic prognoses (CPC1/2, 4% [1/25]).ConclusionrSO₂ is a good indicator of 90-day neurologic outcomes for post-cardiac arrest intervention patients.     

Initial end-tidal carbon dioxide as a prognostic indicator for inpatient PEA arrest

AimInvestigate the relationship of initial PetCO2 values of patients during inpatient pulseless electrical activity (PEA) cardiopulmonary arrest with return of spontaneous circulation (ROSC) and survival to discharge.MethodsThis study was performed in two urban, academic inpatient hospitals. Patients were enrolled from July 2009 to July 2013. A comprehensive database of all inpatient resuscitative events is maintained at these institutions, including demographic, clinical, and outcomes data. Arrests are stratified by primary etiology of arrest using a priori criteria. Inpatients with PEA arrest for whom recorded PetCO2 was available were included in the analysis. Capnography data obtained after ROSC and/or more than 10 min after initiation of CPR were excluded. Multivariable logistic regression was used to explore the association between initial PetCO2 >20 mmHg and both ROSC and survival-to-discharge.ResultsA total of 50 patients with PEA arrest and pre-ROSC capnography were analyzed. CPR continued an average of 11.8 min after initial PetCO2 was recorded confirming absence of ROSC at time of measurement. Initial PetCO2 was higher in patients with versus without eventual ROSC (25.3 ± 14.4 mmHg versus 13.4 ± 6.9 mmHg, P = 0.003). After adjusting for age, gender, and arrest location (ICU versus non-ICU), initial PetCO2 >20 mmHg was associated with increased likelihood of ROSC (adjusted OR 4.8, 95% CI 1.2–19.2, P = 0.028). Initial PetCO2 was not significantly associated with survival-to-discharge (P = 0.251).ConclusionsInitial PetCO2 >20 mmHg during CPR was associated with ROSC but not survival-to-discharge among inpatient PEA arrest victims. This analysis is limited by relatively small sample size.     

Correlation between initial serum levels of lactate after return of spontaneous circulation and survival and neurological outcomes in patients who undergo therapeutic hypothermia after cardiac arrest

ObjectivesWe analysed the relationship between serum levels of lactate within 1 h of return of spontaneous circulation (ROSC) and survival and neurological outcomes in patients who underwent therapeutic hypothermia (TH).MethodsThis was a multi-centre retrospective and observational study that examined data from the first Korean Hypothermia Network (KORHN) registry from 2007 to 2012. The inclusion criteria were out-of-hospital cardiac arrest (OHCA) and examination of serum levels of lactate within 1 h after ROSC, taken from KORHN registry data. The primary endpoint was survival outcome at hospital discharge, and the secondary endpoint was poor neurological outcome (Cerebral Performance Category, CPC, 3–5) at hospital discharge. Initial lactate levels and other variables collected within 1 h of ROSC were analysed via multivariable logistic regression.ResultsData from 930 cardiac arrest patients who underwent TH were collected from the KORHN registry. In a total of 443 patients, serum levels of lactate were examined within 1 h of ROSC. In-hospital mortality was 289/443 (65.24%), and 347/443 (78.33%) of the patients had CPCs of 3–5 upon hospital discharge. The odds ratios of lactate levels for CPC and in-hospital mortality were 1.072 (95% confidence interval (CI) 1.026–1.121) and 1.087 (95% CI = 1.031–1.147), respectively, based on multivariate ordinal logistic regression analyses.ConclusionHigh levels of lactate in serum measured within 1 h of ROSC are associated with hospital mortality and high CPC scores in cardiac arrest patients treated with TH.     

Cerebral effects of three resuscitation protocols in uncontrolled haemorrhagic shock: A randomised controlled experimental study

BackgroundTo compare haemodynamic and cerebral variables during aggressive fluid resuscitation vs. administration of a hypertonic starch solution (HS) combined with either noradrenaline [norepinephrine] or arginine vasopressin in an animal model of uncontrolled haemorrhagic shock.MethodsAfter Animal Investigational Committee approval, 24 anaesthetised pigs underwent a liver trauma. At haemodynamic decompensation, animals were randomly assigned to receive fluid resuscitation (6% HES 130/0.4, 20 mL/kg, and Ringer, 40 mL/kg; FR group, n = 8), or noradrenaline (bolus 20 μg/kg, continuously 1 μg/kg/min) combined with HS (7.2% NaCl/6% HES 200/0.5; 4 mL/kg) (n = 8; NA/HS group), or vasopressin (bolus 0.2 U/kg, continuously 0.04 U/kg/min) combined with HS (4 mL/kg) (n = 8; AVP/HS group), respectively. Thirty minutes after drug administration, bleeding was controlled manually.ResultsMean arterial blood pressure (MAP), cerebral perfusion pressure (CPP), and brain tissue oxygen pressure (P_btO₂) decreased significantly with haemorrhage in all groups (p < 0.05). AVP/HS resulted in a faster and higher increase of MAP and CPP compared to both NA/HS and FR (p < 0.001 vs. FR; p < 0.01 vs. NA/HS). Compared to FR, P_btO₂ increased faster with AVP/HS and NA/HS (p < 0.05) after therapy, and ICP was lower at the end of the study period (p < 0.05). All animals (8/8) of the AVP/HS group survived, compared to 4/8 and 4/8 in the NA/HS and FR group, respectively (p = 0.07).ConclusionsFollowing uncontrolled haemorrhagic shock in this animal model, combination of HS with arginine vasopressin increased CPP and cerebral oxygenation faster than aggressive fluid resuscitation, without re-increasing ICP.     

Association between early arterial blood gas tensions and neurological outcome in adult patients following in-hospital cardiac arrest

ObjectiveThe early partial pressures of arterial O₂ (PaO₂) and CO₂ (PaCO₂) have been found in animal studies to be correlated with neurological outcome after brain injury. However, the relationship of early PaO₂ and PaCO₂ to the neurological outcomes of resuscitated patients after cardiac arrest was still not clear.MethodsThis was a retrospective observational cohort study in a single medical center. Adult patients who had in-hospital cardiac arrest between 2006 and 2012 and achieved sustained return of spontaneous circulation (ROSC) (ROSC > 20 min without resumption of chest compression) were included. Multivariable logistic regression analysis was used to identify factors associated with favorable neurological outcome at hospital discharge. The first PaO₂ and PaCO₂ values measured after first sustained ROSC were used for analysis.ResultsOf the 550 included patients, 154 (28%) survived to hospital discharge and 74 (13.5%) achieved favorable neurological outcome. The mean time from sustained ROSC to the measurement of PaO₂ and PaCO₂ was 136.8 min. The mean PaO₂ and PaCO₂ were 167.4 mmHg and 40.3 mmHg, respectively. PaO₂ between 70 and 240 mmHg (odds ratio [OR] 1.96, 95% confidence interval [CI] 1.08–3.64) and PaCO₂ levels (OR 0.98, 95% CI 0.95–0.99) were positively and inversely associated with favorable neurological outcome, respectively.ConclusionsThe early PaO₂ and PaCO₂ levels obtained after ROSC might be correlated with neurological outcome of patients with in-hospital cardiac arrest. However, because of the inherent limitations of the retrospective design, these results should be further validated in future studies.