Overall Performance Category Research Articles

Neuroprotection with hypothermic reperfusion and extracorporeal cardiopulmonary resuscitation - A randomized controlled animal trial of prolonged ventricular fibrillation cardiac arrest in rats.

Extracorporeal cardiopulmonary resuscitation (ECPR) facilitates resuscitation with immediate and precise temperature control. This study aimed to determine the optimal reperfusion temperature to minimize neurological damage after ventricular fibrillation cardiac arrest (VFCA). Twenty-four rats were randomized (n = 8 per group) to normothermia (NT = 37°C), mild hypothermia (MH = 33°C) or moderate hypothermia (MOD = 27°C). The rats were subjected to 10 minutes of VFCA, before 15 minutes of ECPR at their respective target temperature. After ECPR weaning, rats in the MOD group were rapidly rewarmed to 33°C, and temperature maintained at 33°C (MH/MOD) or 37°C (NT) for 12 hours before slow rewarming to normothermia (MH/MOD). The primary outcome was 30-day survival with overall performance category (OPC) 1 or 2 (1 = normal, 2 = slight disability, 3 = severe disability, 4 = comatose, 5 = dead). Secondary outcomes included awakening rate (OPC ≤ 3) and neurological deficit score (NDS, from 0 = normal to 100 = brain dead). The survival rate did not differ between reperfusion temperatures (NT = 25%, MH = 63%, MOD = 38%, p = 0.301). MH had the lowest NDS (NT = 4[IQR 3-4], MH = 2[1-2], MOD = 5[3-5], p = 0.044) and highest awakening rate (NT = 25%, MH = 88%, MOD = 75%, p = 0.024). In conclusion, ECPR with 33°C reperfusion did not statistically significantly improve survival after VFCA when compared with 37°C or 27°C reperfusion but was neuroprotective as measured by awakening rate and neurological function.

Vagus Nerve Stimulation Improves Mitochondrial Dysfunction in Post–cardiac Arrest Syndrome in the Asphyxial Cardiac Arrest Model in Rats

Cerebral mitochondrial dysfunction during post–cardiac arrest syndrome (PCAS) remains unclear, resulting in a lack of therapeutic options that protect against cerebral ischemia–reperfusion injury. We aimed to assess mitochondrial dysfunction in the hippocampus after cardiac arrest and whether vagus nerve stimulation (VNS) can improve mitochondrial dysfunction and neurological outcomes. In an asphyxial cardiac arrest model, male Sprague–Dawley rats were assigned to the vagus nerve isolation (CA) or VNS (CA + VNS) group. Cardiopulmonary resuscitation was performed 450 s after pulseless electrical activity. After the return of spontaneous circulation (ROSC), left cervical VNS was performed for 3 h in the CA + VNS group. Mitochondrial respiratory function was evaluated using high-resolution respirometry of the hippocampal tissue. The neurologic deficit score (NDS) and overall performance category (OPC) were assessed at 24, 48, and 72 h after resuscitation. The leak respiration and oxidative phosphorylation capacity of complex I (OXPHOS CI) at 6 h after ROSC were significantly higher in the CA + VNS group than in the CA group (p = 0.0308 and 0.0401, respectively). Compared with the trends of NDS and OPC in the CA group, the trends of those in the CA + VNS group were significantly different, thus suggesting a favorable neurological outcome in the CA + VNS group (p = 0.0087 and 0.0064 between times × groups interaction, respectively). VNS ameliorated mitochondrial dysfunction after ROSC and improved neurological outcomes in an asphyxial cardiac arrest rat model.

Neurological outcome in adult out-of-hospital cardiac arrest – Not all doom and gloom!

AimsTo describe neurological and functional outcomes among out-of-hospital cardiac arrest (OHCA) patients who survived to hospital discharge; to determine the association between neurological outcome at hospital discharge and 12-month survival. MethodsOur cohort comprised adult OHCA patients (≥18 years) attended by St John WA (SJWA) paramedics in Perth, Western Australia (WA), who survived to hospital discharge, between 1st January 2004 and 31st December 2019. Neurological and functional status at hospital discharge (and before the arrest) was determined by medical record review using the five-point ‘Cerebral Performance Category (CPC)’ and ‘Overall Performance Category (OPC)’ scores. Adjusted multivariable logistic regression analysis was used to estimate the association of CPC score at hospital discharge with 12-month survival, adjusted for prognostic variables. ResultsOver the study period, SJWA attended 23,712 OHCAs. Resuscitation was attempted in 43.4% of cases (n = 10,299) with 2171 subsequent admissions, 99.4% (n = 2158) of these were admitted to a study hospital. Of the 1062 hospital survivors, 71.3% (n = 757) were CPC1 (highest category of neurological performance), 21.4% (n = 227) CPC2, 6.3% (n = 67) CPC3 and 1.0% (n = 11) CPC4. OPC scores followed a similar distribution. Of the 1,011 WA residents who survived to hospital discharge, 92.3% (n = 933) survived to 12-months. A CPC1-2 at hospital discharge was significantly associated with 12-month survival (adjusted odds ratio 3.28, 95% confidence interval 1.69–6.39). ConclusionWhilst overall survival is low, most survivors of OHCA have a good neurological outcome at hospital discharge and are alive at 12-months.

Mortality and Neurological Outcomes in Out-of-Hospital Cardiac Arrest Patients With and Without Targeted Temperature Management in a Multiethnic Asian Population

The use of targeted temperature management (TTM) is increasing although adoption is still variable. We describe our 6-year experience and compare the mortality and neurological outcomes of out-of-hospital cardiac arrest (OHCA) patients with and without the use of TTM in a multiethnic Asian population. We performed a retrospective observational study at a tertiary academic medical centre. OHCA survivors admitted to our hospital between April 2010‒December 2016 were included. Outcomes of interest were 30-day mortality postresuscitation, Cerebral Performance Category (CPC) and Overall Performance Category (OPC) scores. A total of 121 of 261 patients (46.3%) underwent TTM. TTM patients were younger (TTM 60.0 years old vs no TTM 63.7 years old, P = 0.047). There was no difference in the initial arrest rhythm of shockable origin between the 2 groups (P = 0.289). There was suggestion of lower 30-day mortality (TTM 24.3% vs no TTM 31.4%, P = 0.214), higher and good CPC/OPC scores (TTM 19.0% vs no TTM 15.7%, P = 0.514) with TTM although this did not reach statistical significance. On multivariable logistic regression analysis, TTM was not associated with 30-day mortality (P = 0.07). However, older age, initial non-shockable rhythm and increased duration from arrest to return of spontaneous circulation were associated with increased mortality. Malay ethnicity was associated with a poorer CPC/ OPC score. Adoption and outcomes of TTM postresuscitation is variable and there is still a need to optimise management of the identified predictors of survival and good neurological outcomes while TTM is being used.

Effect of Electrical Vagus Nerve Stimulation on Cerebral Blood Flow and Neurological Outcome in Asphyxial Cardiac Arrest Model of Rats.

Vagus nerve stimulation (VNS) during post-resuscitation may increase recovery of cerebral blood flow (CBF) and reduce neurological injury. This study was designed to investigate the effect of electrical VNS on neurological outcomes following cardiac arrest (CA). Male Sprague-Dawley rats (n = 48) were subjected to the asphyxial CA model and blindly allocated to the VN isolation (CA + VN isolation) or VNS group (CA + VNS group). Cardiopulmonary resuscitation was initiated 450s after pulseless electrical arrest, and the left cervical vagus nerve was electrically stimulated (0.05mA, 1Hz) for 3h in the CA + VNS group. The neurological deficit score (NDS) and overall performance category (OPC) were assessed at 24h after resuscitation, and histological injury of the hippocampus was evaluated. Independent experiments were performed to evaluate the effect of VNS on global cortical CBF after resuscitation using laser speckle Doppler imaging through a thinned skull window from pre-arrest to 6h after resuscitation. The baseline characteristics were not significantly different between the two groups. The NDS was significantly higher, and the OPC was substantially lower in the CA + VNS group (p = 0.022 and p = 0.049, respectively) supported by decrease in histological injury of the hippocampal CA1 region. CBF in the early period of post-return of spontaneous circulation (ROSC) was significantly higher in the CA + VNS group (p < 0.05 at post-ROSC 2h and 4h), and 4-hydroxynonenal was significantly lower in the CA + VNS group (p = 0.026). VNS improved cerebral perfusion and neurological outcomes at 24h after ROSC in an asphyxial CA model of rats.

Establishing a Rodent Model of Ventricular Fibrillation Cardiac Arrest With Graded Histologic and Neurologic Damage With Different Cardiac Arrest Durations.

ABSTRACTPurpose:The aim of the study was to establish a ventricular fibrillation (VF) cardiac arrest (CA) resuscitation model with consistent neurologic and neuropathologic damage as potential therapeutic target.Methods:Prospectively randomized groups of experiments in two phases. In phase 1 four groups of male Sprague–Dawley rats (n = 5) were resuscitated after 6 min VFCA with 2 and 6 min basic life support durations (BLS) with and without adrenaline. In phase 2 the most promising group regarding return of spontaneous circulation (ROSC) and survival was compared with a group of 8 min CA. Resuscitability, neurologic deficit scores (NDS), and overall performance category (OPC) were assessed daily; histolopathology of the hippocampal CA1 region [hematoxylin and eosin- (viable neurons), Fluoro-Jade- (dying neurons), and Iba-1 immunostaining (microglial activation–semiquantitative)] on day 14.Results:Two minutes BLS and with adrenaline as most promising group of phase 1 compared with an 8 min group in phase 2 exhibited ROSC in 8 (80%) vs. 9 (82%) animals and survivors till day 14 in 7 (88%) (all OPC 1, NDS 0 ± 0) vs. 6 (67%) (5 OPC 1, 1 OPC 2, NDS 0.83 ± 2.4) animals. OPC and NDS were only significantly different at day 1 (OPC: P = 0.035; NDS: P = 0.003). Histopathologic results between groups were not significantly different; however, a smaller variance of extent of lesions was found in the 8 min group. Both CA durations caused graded neurologic, overall, such as histopathologic damage.Conclusions:This dynamic global ischemia model offers the possibility to evaluate further cognitive and novel neuroprotective therapy testing after CA.

Cognitive function and quality of life after successful resuscitation from cardiac arrest

BackgroundStudies on out-of-hospital cardiac arrest (OHCA) use overall performance category (OPC)/cerebral performance category (CPC) as outcome. We studied quality of life, neuro-cognitive functioning and independency in daily life of patients and strain of caregivers 6–12 months after cardiac arrest. MethodsTwo hundred and twenty patients (>18 year) who survived 6–12 months after OHCA and relatives were interviewed by telephone with validated questionnaires (Short-form Health Survey) (SF-12), Modified Rankin Scale (MRS), telephonic interview cognitive status (TICS) and Caregiver Strain Index (CSI) and compared with OPC and CPC at discharge. SF-12 of elderly (≥80 years) was compared to an open Dutch population of ≥80 years. ResultsOf all patients, 45% had normal physical and 90% had normal mental SF-12. Eighty-one percent had a normal MRS (MRS≤2). Eighty-four percent had normal TICS. Compared to the reference population, elderly scored 40.5 on the physical and 53.2 on the mental SF-12, while the reference population scored 38.1 (θ=0.20) and 54.4 (θ=−0.15), respectively, (n.s.) Of the patients with OPC≤2 and CPC≤2 at discharge 15% scored MRS 3–5 and 15% abnormal TICS at follow-up, respectively. Ninety-two percent of all patients gave their quality of life a value of ≥6 (maximum 10). Patients treated with hypothermia scored on most health outcomes similar to those who did not need such treatment. Sixteen percent of caregivers experienced strain, correlating significantly with TICS of patients. ConclusionThe great majority of survivors have normal functioning and cognition 6–12 months after OHCA. Functional and neuro-cognitive telephonic tests 6–12 months after OHCA are simple and better reflect patients functioning at home than OPC/CPC at discharge.

The Overall Performance Category and Cerebral Performance Category to assess neurologic intact survival at discharge from a cardiac arrest. A good estimate of patients’ functioning?

Purpose: Most studies on out-of-hospital cardiac arrest (OHCA) use the Overall Performance Category (OPC)/Cerebral Performance Category (CPC) as outcome at discharge. We studied the neurocognitive functioning (NCF) and level of independence (LoI) of patients (pts) 6–12 months after OHCA and compared the results with the OPC/CPC at discharge.

Abstract 85: The Overall Performance Category and Cerebral Performance Category to Assess Neurologically Intact Survival at Discharge from Cardiac Arrest: A Good Estimate of Patients’ Functioning?

Objective- It is known that recovery from neurologic damage takes 6-12 months. However, most studies on out of hospital cardiac arrest (OHCA) use the Overall Performance Category (OPC)/Cerebral Performance Category (CPC) as outcome at discharge from hospital. We studied the neurocognitive functioning and level of independence (LoI) of patients (pts) 6-12 months after OHCA and compared the results with the OPC/CPC at discharge. Materials and methods- The study population comprises all pts (&gt;18 year) who survived 6-12 months after OHCA from mid-2010 to mid-2011. Pts were interviewed by telephone with questionnaires validated for telephonic application. We used a validated cut-off score. Neurocognitive functioning was measured with the Telephonic Interview Cognitive Status (TICS) and LoI with the Modified Rankin Scale (MRS). If needed, the IQ-code was used as proxy-questionnaire to measure the neurocognitive functioning of the pt. Neurological outcome at discharge was assessed from hospital records estimating OPC/CPC (figure). Results- Comparison between OPC at discharge and MRS at 6-12 months is shown in the figure. Of all pts, 93% was classified as having a good outcome (OPC 1-2) at discharge. At 6-12 months only 76% had a good outcome (MRS 0-2). Thirty of the 218 (13%) pts seemed to be cognitively impaired (TICS &lt;31) at 6-12 months while they were classified as having a good outcome (CPC 1-2) at discharge. Conclusion- MRS and other tests 6-12 months after discharge better reflect pts’ functioning at home than OPC/CPC at the moment of discharge. OPC/CPC cannot measure impairments that manifest themselves only in the home environment.

Abstract 78: Modified Rankin Score at Hospital Discharge Is Predictive of 1-Year Neurological Function in Survivors After Cardiac Arrest

Background: A randomized multicenter clinical trial compared standard CPR (S-CPR) with active compression decompression CPR plus an inspiratory impedance threshold device (ACD+ITD) in patients with non-traumatic, out-of- hospital cardiac arrest (OHCA) from a presumed cardiac cause. Survival to hospital discharge (HD) with favorable neurologic function, defined as a modified Rankin Score (MRS) ≤3, and one year survival were greater in the ACD+ITD group. We evaluated the concordance of the primary endpoint, HD with MRS ≤3, with multiple secondary neurologic endpoints assessed at one year. Methods: A total of 813 patients were enrolled in the S-CPR group and 842 in the ACD+ITD group. MRS at HD, and Cerebral Performance Category (CPC), Overall Performance Category (OPC), Health Utilities Index (HUI) and Cognitive Abilities Screening Instrument (CASI) assessments were based on responses from consented survivors and known deaths at one year. Neurologic assessments were administered by research staff blinded to the CPR treatment. Survival data were available for 98% of subjects. Fisher’s Exact Test, Pearson Chi-Square test, Mann-Whitney U test, and t-test for Equality of Means were used, as applicable, for comparisons. All statistical tests were 2-sided and p-values &lt; 0.05 were regarded as significant. Results: The MRS (≤3 vs. &gt;3) neurological assessment at HD was highly predictive of whether or not a patient would be alive with favorable neurological function in both study groups, assessed using the CPC score (&lt;3 vs. ≥3) at one year (98.0% observed agreement, kappa = 0.800, p &lt; 0.001). Similar concordance was also shown with overall survival, OPC, HUI, CASI. Table shows data for MRS and CPC comparisons. Conclusion: Neurological status at the time of HD, as measured by MRS, is highly predictive of long-term neurological function at one year. This is the first time that the MRS at the time of HD has demonstrated the ability to predict long-term outcomes for patients with OHCA.

Prehospital Epinephrine Use and Survival among Patients with Out-of-Hospital Cardiac Arrest: Hagihara A, Hasegawa M, Abe T, Nagata T, Wakata Y, Miyazaki S. JAMA 2012; 307:1161–8.

Epinephrine is widely used as an adjuvant to cardiopulmonary resuscitation in the setting of cardiac arrest. There is, however, little evidence to support its efficacy. Recent studies on its use have noted improved likelihood of return of spontaneous circulation (ROSC) in resuscitation, though no statistical difference in survival to hospital discharge. This Japanese study sought to determine if the use of epinephrine in the prehospital cardiac arrest setting was associated with immediate and 1-month survival. A prospective observational model was used to evaluate data on all out-of-hospital cardiac arrests (OHCA) in Japan from 2005 through 2008. There were 417,188 OHCAs meeting criteria in the time frame. Data were collected on ROSC, survival rates, and, in those who survived, neurological outcome, as measured by the Glasgow-Pittsburgh Performance Category (CPC) and the Overall Performance Category (OPC). The four primary endpoints were ROSC before hospital arrival, 1-month survival, CPC category 1 or 2, and OPC category 1 or 2 at 1-month follow-up. Epinephrine use before hospital arrival was not randomized, so a propensity score was used to control for confounding and selection bias. There were 15,030 patients matched in each group. Data were abstracted from propensity-matched patients, and multiple conditional logistic regression models were fit with endpoints as dependent variables. Crude analysis of the data revealed a positive association between prehospital epinephrine and 1-month survival (odds ratio [OR] 1.15; p < 0.001), though adjustment for propensity score and all confounding variables revealed a significant negative association (OR 0.54, p < 0.001). Epinephrine use was, however, a significant positive predictor of ROSC before hospital arrival (OR 2.51, p < 0.001). Data for CPC and OPC yielded odds ratios < 1 in all analyses for association between prehospital epinephrine use and long-term neurological outcome (OR 0.21–0.41 and 0.23–0.43 respectively, p < 0.001 for all). The authors concluded that epinephrine in the prehospital setting was strongly predictive of short-term survival, though associated with decreased 1-month survival and neurological outcome.

New conventional long-term survival normovolemic cardiac arrest pig model

Aim of the studyA reproducible long-term intensive care and outcome cardiac arrest model for exploring new cerebral preservation strategies is needed. We tried to determine effects and limitations of current therapies after different ‘no-flow’ times. MethodsThirty-five female Large White Breed pigs (26–37kg) were included in the study. Three pigs served as sham animals without cardiac arrest (CA). Ventricular fibrillation (VF) CA was induced in 32 animals for 0, 7, 10 and 13min (each group consisting of 8 animals), followed by 8min of chest compressions, mechanical ventilation and vasopressors. Thereafter, up to 3 defibrillations were delivered. After restoration of spontaneous circulation (ROSC), the animals underwent intensive care for 20h. Neurologic examination was performed at designated time points using a neurologic deficit (ND) and an overall performance category (OPC) score. ResultsRestoration of spontaneous circulation was achieved in 8 of 8 animals in the 0min-group, 6 of 8 in the 7min-group, 7 of 8 in the 10min-group and 0 of 8 in the 13min-group. All animals of the sham-group and 0min-group were neurologically intact survivors; the 7 and 10min-groups showed a median ND of 55%(26;94) and 73%(58;78), respectively. There were no significant differences between the 7 and 10min-groups regarding OPC and NDS. Coronary perfusion pressure during CPR decreased concordantly with ‘no-flow’ times with a tendency towards significance. ConclusionThis study established a reproducible cardiac arrest and resuscitation model in pigs which will be used to test novel resuscitation strategies to improve neurologic outcome after cardiac arrest.

Protein nitration and poly-ADP-ribosylation in brain after rapid exsanguination cardiac arrest in a rat model of emergency preservation and resuscitation

Emergency preservation and resuscitation (EPR) of 60 min in rats is achievable with favorable outcome, while 75 min is associated with substantial mortality and impaired neurological outcome in survivors. We hypothesized that 75 min but not 60 min of EPR would be associated with activation of two potential secondary injury cascades in brain as reflected by protein nitration and poly (ADP-ribose) polymerase (PARP) activation. Rats were rapidly exsanguinated over 5 min. After 1 min of cardiac arrest (CA), rats were cooled to a target tympanic temperature of 15 degrees C. After either 60 min or 75 min of CA, resuscitation was achieved via cardiopulmonary bypass (CPB). Rats subjected to CPB only served as controls. Overall performance category (OPC) and neurologic deficit score (NDS) were assessed at 24 h. Protein nitration and poly-ADP-ribosylation were assessed by Western blotting and immunohistochemistry for 3-nitrotyrosine and poly-ADP ribose polymers, respectively, in multiple brain regions. Neurologic outcome was better in the 60 min vs. the 75 min EPR group (OPC, P<0.001; NDS, P=0.001). Densitometric analysis of the major 64 kD band showed that nitration and PARP activation were significantly increased in hippocampus, cortex and striatum in the 75 min EPR group vs. other groups. However, there were no differences in cerebellum. Analysis of the full protein spectrum showed significantly increased PARP activation only in hippocampus in the 75 min EPR group vs. other groups. Extending the duration of EPR beyond the limit that can yield favorable recovery in rats was associated with increased nitration and ribosylation of selected proteins in selectively vulnerable brain regions. The impact of these mechanisms on the outcome remains to be determined.

Who survives from out-of-hospital pulseless electrical activity?

To study factors associated with short-term and long-term survival after out-of-hospital cardiac arrest presenting with pulseless electrical activity (PEA). This was a retrospective observational study. All out-of-hospital cardiac arrests in Helsinki, Finland during 1 January 1997-31 December 2005 were prospectively registered in the cardiac arrest database. Of 3291 arrests 984 had PEA as the first registered rhythm. The use of adrenaline was the only factor associated with long-term survival, by increasing mortality. Increasing delay to the return of spontaneous circulation (ROSC) was the only factor associated with survival among patients that survived to admission, also by increasing mortality. There were no survivors that were discharged in overall performance category (OPC) 1-2 after a bystander-witnessed arrest (excluding cases of hypothermia and/or near-drowning) with first responding unit (FRU)-delay over 14 min, or that were resuscitated for more than 20 min. There were no survivors who were discharged in OPC 1-2 after an unwitnessed arrest with the duration of advanced life support (ALS) exceeding 5.5 min. The use of adrenaline during resuscitation was the only significant factor which was found to decrease the long-term survival. Among admitted patients, short delay to ROSC was the only factor associated with increased survival. Bystander-CPR and delays to the arrival of the FRU or to the initiation of ALS were not associated with survival. Therefore, it seems difficult to increase survival rates of PEA by improving the chain of survival. More effort should be put to education of the public to call for an ambulance before the cardiac arrest occurs.

Prolonged deep hypothermic circulatory arrest in rats can be achieved without cognitive deficits

Cardiopulmonary bypass (CPB) and deep hypothermic circulatory arrest (DHCA) enable surgical repair of cardiovascular defects. However, neurological complications can result after both CPB and DHCA. We sought to investigate if 75 min of CPB or DHCA caused motor, cognitive or histological deficits in rats. Three groups were studied: DHCA, CPB, and sham. Rats in the DHCA group were subjected to 75 min DHCA at 15 °C, with a total CPB duration of 75 min. Rats in the CPB group were subjected to 75 min of normothermic CPB. Shams received the same anesthesia, cannulations and infusions. Motor function was assessed using beam testing on days 3–13. Cognitive performance was evaluated using Morris water maze tasks on days 7–13. Overall Performance Category (OPC) and Neurologic Deficit Score (NDS) were assessed daily. Histological Damage Score (HDS) was assessed in survivors on day 14. Sustained deficits on beam testing were seen only in the CPB group. Rats in the CPB and DHCA groups exhibited similar cognitive performance vs. sham. There were no differences in OPC or NDS between groups. Neuronal degeneration was present only in small foci in rats after DHCA ( n = 4/7). However, HDS was not different in individual brain regions or viscera between DHCA or CPB vs. sham. Surprisingly, CPB, but not DHCA was associated with motor deficits vs. sham, and no cognitive deficits were seen in either group vs. sham. Future studies with longer DHCA duration will be necessary to provide targets to assess novel preservation strategies.

Evolution of a community-wide early defibrillation programme: Experience over 13 years using police/fire personnel and paramedics as responders

Background: In November 1990, a 2-year trial period was initiated in which police officers in the city of Rochester, Minnesota, were trained in the operation of automated external defibrillators (AEDs). Following the trial, the program was expanded as the city grew in population and area. In 1998 firefighters also were equipped with AEDs, bringing to a total 18 AEDs with police and fire personnel, in addition to paramedic capability. Methods: From November 1990 to December 2003, all adult patients with atraumatic cardiac arrest with ventricular fibrillation (VF) as the presenting rhythm were included for analysis. Call-to-shock time intervals, restoration of spontaneous circulation after defibrillation shocks only (without need for vasoactive or inotropic drug administration), and neurologically intact survival (overall performance category (OPC) 1 or 2) were study end-points. Results: One hundred and ninety-three patients presented in VF. Of these, 80 (41%) were discharged neurologically intact. Of the 159 VF patients whose arrest was bystander-witnessed 73 (46%) were discharged. Survival from non-VF arrest was very low (5%). Assessment of VF survivors demonstrated a quality of life, adjusted for age, gender, and disease, similar to that of the general population. Conclusions: These data demonstrate that a relatively high survival can be obtained in a city of this size and area employing a non-tiered community-wide approach within the emergency medical services (EMS) system.

Influence of early defibrillation on the survival rate and quality of life after CPR in prehospital emergency medical service in a German metropolitan area

Early defibrillation by emergency medical personnel has been shown to improve survival in patients suffering from out-of-hospital cardiac arrest with ventricular fibrillation. Due to organisational differences it is difficult to compare results in various studies. Comparison of studies has been simplified by introduction of the Utstein template. After introduction of an early defibrillation program in Hamburg, we compared the patients being treated with early defibrillation by emergency medical technicians (EMTs) with patients being defibrillated by physicians in an out-of-hospital emergency service in a prospective study. All patients suffered from non EMT-witnessed ventricular fibrillation of cardiac origin. During 1 year, 103 patients were analyzed with respect to survival rate and quality of life. Of the 53 patients in the early defibrillation group (G1) 11 regained a palpable pulse at physicians’ arrival, whereas all patients of the control group (G2) showed ventricular fibrillation. More patients treated with early defibrillation regained sinus rhythm without antiarrhythmics in the prehospital phase (G1: n=43 (86%); G2: n=32 (60%); P<0.05) and had a shorter in-hospital stay (G1: median, 23 days; range 5–51 days; G2: median 39, range 15–88 days; P<0.05). Twelve patients in G1 and 16 in G2 were discharged from hospital. The survival rate was similar in both groups (after 6 months G1: n=12; G2: n=14, after 12 months G1: n=10; G2: n=13 and after 24 months G1: n=9; G2: n=10), and the quality of life according to Glasgow–Pittsburgh Cerebral Performance Category (CPC) and Overall Performance Category (OPC) scores also was comparable between groups. We conclude that early defibrillation provides a higher incidence of return of a spontaneous circulation, a reduced need for antiarrhythmics and shorter in-hospital treatment times in patients with out-of-hospital ventricular fibrillation.

Rapid Induction of Mild Cerebral Hypothermia by Cold Aortic Flush Achieves Normal Recovery in a Dog Outcome Model with 20‐minute Exsanguination Cardiac Arrest

Resuscitation attempts in trauma victims who suffer cardiac arrest (CA) from exsanguination almost always fail. The authors hypothesized that an aortic arch flush with cold normal saline solution (NSS) at the start of exsanguination CA can preserve cerebral viability during 20-minute no-flow. Twelve dogs were exsanguinated over 5 minutes to CA of 20-minute no-flow, resuscitated by cardiopulmonary bypass, followed by post-CA mild hypothermia (34 degrees C) continued to 12 hours, controlled ventilation to 20 hours, and intensive care to 72 hours. At CA 2 minutes, the dogs received a 500-mL flush of NSS at either 24 degrees C (group 1, n = 6) or 4 degrees C (group 2, n = 6), using a balloon-tipped catheter inserted via the femoral artery into the descending thoracic aorta. The flush at 24 degrees C (group 1) decreased tympanic membrane temperature [mean (+/-SD)] from 37.5 degrees C (+/-0.1) to 35.7 degrees C (+/-0.2); the flush at 4 degrees C (group 2) to 34.0 degrees C (+/-1.1) (p = 0.005). In group 1, one dog achieved overall performance category (OPC) 2 (moderate disability), one OPC 3 (severe disability), and four OPC 4 (coma). In group 2, four dogs achieved OPC 1 (normal), one OPC 2, and one OPC 3 (p = 0.008). Neurologic deficit scores (0-10% normal, 100% brain death) [median (25th-75th percentile)] were 62% (40-66) in group 1 and 5% (0-19) in group 2 (p = 0.01). Total brain histologic damage scores were 130 (62-137) in group 1 and 24 (10-55) in group 2 (p = 0.008). Aortic arch flush of 4 degrees C at the start of CA of 20 minutes rapidly induces mild cerebral hypothermia and can lead to normal functional recovery with minimal histologic brain damage. The same model with aortic arch flush of 24 degrees C results in survival with brain damage in all dogs, which makes it suitable for testing other (e.g., pharmacologic) preservation potentials.

Rapid hypothermic aortic flush can achieve survival without brain damage after 30 minutes cardiac arrest in dogs.

Neither exsanguination to pulselessness nor cardiac arrest of 30 min duration can be reversed with complete neurologic recovery using conventional resuscitation methods. Techniques that might buy time for transport, surgical hemostasis, and initiation of cardiopulmonary bypass or other resuscitation methods would be valuable. We hypothesized that an aortic flush with high-volume cold normal saline solution at the start of exsanguination cardiac arrest could rapidly preserve cerebral viability during 30 min of complete global ischemia and achieve good outcome. Sixteen dogs weighing 20-25 kg were exsanguinated to pulselessness over 5 min, and circulatory arrest was maintained for another 30 min. They were then resuscitated using closed-chest cardiopulmonary bypass and had assisted circulation for 2 h, mild hypothermia (34 degrees C) for 12 h, controlled ventilation for 20 h, and intensive care to outcome evaluation at 72 h. Two minutes after the onset of circulatory arrest, the dogs received a flush of normal saline solution at 4 degrees C into the aorta (cephalad) via a balloon catheter. Group I (n = 6) received a flush of 25 ml/kg saline with the balloon in the thoracic aorta; group II (n = 7) received a flush of 100 ml/kg saline with the balloon in the abdominal aorta. The aortic flush decreased mean tympanic membrane temperature (Tty) in group I from 37.6 +/- 0.1 to 33.3 +/- 1.6 degrees C and in group II from 37.5 +/- 0.1 to 28.3 +/- 2.4 degrees C (P = 0.001). In group 1, four dogs achieved overall performance category (OPC) 4 (coma), and 2 dogs achieved OPC 5 (brain death). In group II, 4 dogs achieved OPC 1 (normal), and 3 dogs achieved OPC 2 (moderate disability). Median (interquartile range [IQR]) neurologic deficit scores (NDS 0-10% = normal; NDS 100% = brain death) were 69% (56-99%) in group I versus 4% (0-15%) in group II (P = 0.003). Median total brain histologic damage scores (HDS 0 = no damage; > 100 = extensive damage; 1,064 = maximal damage) were 144 (74-168) in group I versus 18 (3-36) in group II (P = 0.004); in three dogs from group II, the brain was histologically normal (HDS 0-5). A single high-volume flush of cold saline (4 degrees C) into the abdominal aorta given 2 min after the onset of cardiac arrest rapidly induces moderate-to-deep cerebral hypothermia and can result in survival without functional or histologic brain damage, even after 30 min of no blood flow.

Adenosine by aortic flush fails to augment the brain preservation effect of mild hypothermia during exsanguination cardiac arrest in dogs — an exploratory study

Most trauma cases with rapid exsanguination to cardiac arrest (CA) in the field, as well as many cases of normovolemic sudden cardiac death are ‘unresuscitable’ by standard cardiopulmonary–cerebral resuscitation (CPCR). We are presenting a dog model for exploring pharmacological strategies for the rapid induction by aortic arch flush of suspended animation (SA), i.e. preservation of cerebral viability for 15 min or longer. This can be extended by profound hypothermic circulatory arrest of at least 60 min, induced and reversed with (portable) cardiopulmonary bypass (CPB). SA is meant to buy time for transport and repair during pulselessness, to be followed by delayed resuscitation to survival without brain damage. This model with exsanguination over 5 min to CA of 15-min no-flow, is to evaluate rapid SA induction by aortic flush of normal saline solution (NSS) at room temperature (24°C) at 2-min no-flow. This previously achieved normal functional recovery, but with histologic brain damage. We hypothesized that the addition of adenosine would achieve recovery with no histologic damage, because adenosine delays energy failure and helps repair brain injury. This dog model included reversal of 15-min no-flow with closed-chest CPB, controlled ventilation to 20 h, and intensive care to 72 h. Outcome was evaluated by overall performance, neurologic deficit, and brain histologic damage. At 2 min of CA, 500 ml of NSS at 24°C was flushed (over 1 min) into the brain and heart via an aortic balloon catheter. Controls ( n=5) received no drug. The adenosine group ( n=5) received 2-chloro-adenosine (long acting adenosine analogue), 30 mg in the flush solution, and, after reperfusion, adenosine i.v. over 12 h (210 μg/kg per min for 3 h, 140 μg/kg per min for 9 h). The 24°C flush reduced tympanic membrane temperature ( T ty) within 2 min of CA from 37.5 to ≈36.0°C in both groups. At 72 h, final overall performance category (OPC) 1 (normal) was achieved by all ten dogs of the two groups. Final neurologic deficit scores (NDS; 0–10% normal, 100% brain death) were 5±3% in the control group versus 6±5% in the adenosine group (NS). Total brain histologic damage scores (HDS) at 72 h were 74±9 (64–80) in the control group versus 68±19 (40–88) in the adenosine group (NS). In both groups, ischemic neurons were as prevalent in the basal ganglia and neocortex as in the cerebellum and hippocampus. The mild hypothermic aortic flush protocol is feasible in dogs. The adenosine strategy used does not abolish the mild histologic brain damage.