Post Return Of Spontaneous Circulation Research Articles

Valproic Acid Combined With Postcardiac Arrest Hypothermic-Targeted Temperature Management Prevents Delayed Seizures and Improves Survival in a Rat Cardiac Arrest Model

High-dose valproic acid in combination with hypothermic-targeted temperature management has been reported to synergistically improve neurologic outcomes after cardiac arrest. This study investigated the potential synergistic mechanisms. Prospective, randomized, experimental study. University research institution. Male Long Evans rats. Rats resuscitated from asphyxial cardiac arrest were randomized to one of the three groups: normothermic-targeted temperature management (37°C ± 1°C), hypothermic-targeted temperature management (33° ± 1° × 24 hr + placebo infusion), hypothermic-targeted temperature management plus high-dose valproic acid (300 mg/kg IV × 1 initiated 5 min post return of spontaneous circulation and infused over 20 min) (hypothermic-targeted temperature management + valproic acid). Seventy-two-hour survival was significantly greater with hypothermic-targeted temperature management + valproic acid, compared to hypothermic-targeted temperature management and normothermic-targeted temperature management (p < 0.05). Survival with good neurologic function, neurodegeneration, expression of HSP70, phosphorylation of Akt and Erk1/2 were not significantly different between hypothermic-targeted temperature management and hypothermic-targeted temperature management + valproic acid. The prevalence of seizures during the first 72-hour postcardiac arrest was significantly lower with hypothermic-targeted temperature management + valproic acid compared to hypothermic-targeted temperature management and normothermic-targeted temperature management (p = 0.01). High-dose valproic acid combined with hypothermic-targeted temperature management prevents postcardiac arrest seizures and improves survival. It remains to be determined if the mechanism of seizure prevention is through the antiepileptic effect of valproic acid or direct neuroprotection. Overall, the combination of high-dose valproic acid and hypothermic-targeted temperature management remains a promising strategy to improve cardiac arrest outcomes.

A CONTEMPORARY REVIEW OF EXTRACORPOREAL MEMBRANE OXYGENATION FOR CARDIAC ARRESTS IN THE CARDIAC CATHETERIZATION LABORATORY

Patients who sustain refractory in-hospital cardiac arrest (IHCA) with severe cardiopulmonary compromise in the cardiac catheterization laboratory have an extremely low survival. Despite early revascularization to infarct-related coronary artery, mortality rates vary between 80-90%. Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) can be lifesaving and is increasingly used in patients with reversible conditions who sustain refractory cardiac arrest or profound cardiogenic shock. The primary objective was to determine the characteristics and outcomes of patients receiving VA-ECMO in cardiac catheterization laboratory following IHCA or hemodynamic collapse. Secondary objectives included determination of 30-day mortality and identification of univariate predictors of 30-day survival. Between 2010 and 2016, all consecutive adults who received VA-ECMO in the cardiac catheterization laboratory at a single tertiary care center were retrospectively reviewed. Refractory cardiac arrest was defined as those who required ECMO cannulation during active cardiopulmonary resuscitation or those with profound cardiogenic shock post return of spontaneous circulation (ECPR-ROSC). Data collection information included baseline demographics, comorbid cardiovascular risk factors, referral diagnosis, etiology of cardiac arrest, procedural characteristics and in and out of hospital outcomes. A total of 41 ECMO cannulations (57-66, 18 males) occurred in the cardiac catheterization laboratory between July 2010 and April 2016. The baseline cardiovascular risk factors between survivors and non-survivors were relatively similar (Table 1). Overall, the majority of cases were related to cardiogenic shock secondary to an acute coronary syndrome (Table 1). None of the patients who suffered a mechanical complication secondary to an ACS survived. Procedural complications such as aortic dissections, pulmonary artery and atrial rupture accounted for 10% of the ECMO cannulations and had a 75% (n=3) associated mortality. 30-day survival for the entire cohort was 43.9% (Figure 1). There was no difference from time to cannulation between those that survived 30 days and those that did not survive. There was no difference in the complications rate between those that survived and those that did not survive ECMO cannulation. However, ECMO site bleeding was increased in those that did not survive. In the evolving field of mechanical support, VA-ECMO is becoming increasingly available as a temporizing measure for patients with refractory shock or cardiac arrest. Our study shows that patients with ACS or procedural complication in the catheterization lab who develop IHCA or profound cardiogenic shock benefit from VA-ECMO. VA-ECMO cannulation demonstrates an impressive 30-day survival in a patient cohort which has extremely high mortality.View Large Image Figure ViewerDownload Hi-res image Download (PPT)

Abstract 12123: Periodicity-Analysis of a Photoplethysmography Signal May Support Pulse Detection in a Few-Second Compression-Pause During Cardiopulmonary Resuscitation

Introduction: Pulse checks during cardiopulmonary resuscitation (CPR) are typically performed by manual palpation, which is unreliable and can interrupt compressions for longer than the recommended 10 s. Hypothesis: Presence of a spontaneous pulse can be detected in a compression-free photoplethysmography (PPG) signal within 5 s, by assessing the periodicity of the signal. Methods: We measured nasal PPG signals in 11 pigs during periods of 10-min baseline, arrest induction, 20-min 30:2 CPR, defibrillation, and 20-min post return of spontaneous circulation (ROSC), with aortic pressure and thoracic impedance as references. We annotated pulse presence and obtained compression-free windows of PPG signals from the ventilation pauses and by segmenting the baseline and post-ROSC phases in 4-s non-overlapping windows. Pulse presence was detected by assessing signal periodicity in the autocorrelation function (ACF), which compared a window of the PPG signal to time shifts of this window. Windows with pulse had local maxima in the ACF when a time shift aligned the pulses in both windows (Fig. 1a). Pulseless windows had unstructured ACFs (Fig. 1b). We assessed periodicity via the maximum prominence of all peaks at non-zero shift in the ACF. Prominence is the amplitude relative to the largest surrounding minimum (Fig. 1a,b). We used the prominence and related features in a logistic regression classifier to quantify pulse absence and presence on a continuous scale from 0 to 1 (Fig. 1c). We trained and validated the classifier via five-fold cross-validation, regarding a classifier output of ≥0.5 as indicative of pulse presence. Results: Sensitivity was 97.1% and specificity was 96.2%. Conclusions: Periodicity analysis allows for pulse detection in PPG signals within 5 s. This could be used during existing ventilation pauses to prepare for a faster pulse check or avoid an unnecessary pulse check. Fig. 1: (a) ACF for pulse presence. (b) ACF for pulse absence. (c) Classifier output.

Effect of Splenic Regulatory T-cell Apoptosis on the Postresuscitation Immune Dysfunction in a Porcine Model.

Background:Postresuscitation immune dysfunction contributes to the low survival rate after successful resuscitation, but its mechanism remains poorly understood. The purpose of this study was to investigate whether splenic regulatory T-cell (Treg) apoptosis was involved in the postresuscitation immune dysfunction.Methods:Thirty-eight pigs were randomly divided into sham-operated group (SHAM group, n = 8), 12 h post return of spontaneous circulation (ROSC) group, 24 h post-ROSC group, and 48 h post-ROSC group (n = 10 per group). A Wuzhishan miniature porcine model of 8-min ventricular fibrillation cardiac arrest (CA) was established. The apoptosis rates of Treg in the spleen were tested by flow cytometry; the expressions of forkhead/winged helix transcription factor (Foxp3) of Treg in the spleen were detected by real-time polymerase chain reaction; and the levels of interleukin-4 (IL-4), IL-10, and interferon gamma (IFN-γ) of Treg in the spleen were detected by enzyme-linked immunosorbent assay.Results:The apoptosis rates of Treg in all post-ROSC groups were significantly lower than that of SHAM group (7.7% ± 1.9%, 7.1% ± 1.8%, 6.2% ± 0.4% vs. 13.1% ± 1.6%; P < 0.05); the expression levels of Foxp3 and IL-10 were also decreased with the increase of apoptosis rates of Treg. Helper T-cells CD4+ lymphocyte subsets were significantly lower in the post-ROSC groups compared with SHAM group (29.1% ± 2.2%, 24.3% ± 2.2%, 24.1% ± 2.5% vs. 43.8% ± 4.5%; P < 0.01) at 12, 24, and 48 h after ROSC. Compared with SHAM group, the levels of IFN-γ (161.0 ± 12.9, 167.7 ± 10.5, 191.2 ± 7.7 vs. 7.6 ± 0.9 ng/L) and IL-4 (27.7 ± 6.2, 35.9 ± 3.5, 50.6 ± 6.1 vs. 13.3 ± 2.3 ng/L) and the ratio of IFN-γ/IL-4 (8.6 ± 2.3, 4.9 ± 0.4, 4.5 ± 0.9 vs. 0.8 ± 0.2) were all greatly elevated in all post-ROSC groups (P < 0.05).Conclusions:Apoptosis rate of Treg was significantly decreased after CA, and thus the proportion of Treg was increased and the inhibitory effects were enhanced, which further led to the decrease of the amount of CD4+ T-cells. In addition, the T helper type 2/T helper type 1 (Th2/Th1) cell drift of Treg in the spleen caused postresuscitation immune dysfunction.

Early Electroencephalographic Findings Correlate With Neurologic Outcome in Children Following Cardiac Arrest.

To determine the clinical and electroencephalographic findings associated with prognosis in nonneonate children following cardiac arrest. Retrospective observational study. PICU and cardiac ICU. Nonneonate children with a history of cardiac arrest more than 2 minutes. Electroencephalographic monitoring within 72 hours of return of spontaneous circulation. Clinical and features, neurophysiologic data, and Pediatric Cerebral Performance Category scores were collected. Electroencephalographic traces were reviewed in a blinded manner, all seizures and electroencephalographic findings noted, and the electroencephalography was scored at 1 hour, 24 hours, and continuous electroencephalographic end. Discrete data regarding specific characteristics of the electroencephalographic background and seizures were studied. Univariate and multivariate analyses were performed to identify associations between clinical variables, electroencephalographic findings, and Pediatric Cerebral Performance Category score at hospital discharge. Multivariate analysis of 73 children revealed duration of cardiac arrest less than 20 minutes or continuous electroencephalographic background activity within 12 hours postreturn of spontaneous circulation were associated with good short term neurologic outcome. Change in electroencephalographic background score over time and electroencephalographic data collected after the initial hour were not associated with outcome. Following pediatric cardiac arrest, an initially normal electroencephalography or generalized slowing of the electroencephalographic background was associated with good neurologic outcome at hospital discharge.

Reperfusion injury protection during Basic Life Support improves circulation and survival outcomes in a porcine model of prolonged cardiac arrest

ObjectiveIschemic postconditioning (PC) using three intentional pauses at the start of cardiopulmonary resuscitation (CPR) improves outcomes after cardiac arrest in pigs when epinephrine (epi) is used before defibrillation. We hypothesized PC, performed during basic life support (BLS) in the absence of epinephrine, would reduce reperfusion injury and enhance 24h functional recovery. DesignProspective animal investigation. SettingAnimal laboratory SubjectsFemale farm pigs (n=46, 39±1kg). InterventionsProtocol A: After 12min of ventricular fibrillation (VF), 28 pigs were randomized to four groups: (A) Standard CPR (SCPR), (B) active compression-decompression CPR with an impedance threshold device (ACD-ITD), (C) SCPR+PC (SCPR+PC) and (D) ACD-ITD CPR+PC. Protocol B: After 15min of VF, 18 pigs were randomized to ACD-ITD CPR or ACD-ITD+PC. The BLS duration was 2.75min in Protocol A and 5min in Protocol B. Following BLS, up to three shocks were delivered. Without return of spontaneous circulation (ROSC), CPR was resumed and epi (0.5mg) and defibrillation delivered. The primary end point was survival without major adverse events. Hemodynamic parameters and left ventricular ejection fraction (LVEF) were also measured. Data are presented as mean±SEM. Measurements and Main ResultsProtocol A: ACD-ITD+PC (group D) improved coronary perfusion pressure after 3min of BLS versus the three other groups (28±6, 35±7, 23±5 and 47±7 for groups A, B, C, D respectively, p=0.05). There were no significant differences in 24h survival between groups. Protocol BLVEF 4h post ROSC was significantly higher with ACD-ITD+PC vs ACD-ITD alone (52.5±3% vs. 37.5±6.6%, p=0.045). Survival rates were significantly higher with ACD-ITD+PC vs. ACD-ITD alone (p=0.027). ConclusionsBLS using ACD-ITD+PC reduced post resuscitation cardiac dysfunction and improved functional recovery after prolonged untreated VF in pigs. Protocol number12-11.

Microdialysis Assessment of Cerebral Perfusion during Cardiac Arrest, Extracorporeal Life Support and Cardiopulmonary Resuscitation in Rats – A Pilot Trial

Cerebral metabolic alterations during cardiac arrest, cardiopulmonary resuscitation (CPR) and extracorporeal cardiopulmonary life support (ECLS) are poorly explored. Markers are needed for a more personalized resuscitation and post—resuscitation care. Aim of this study was to investigate early metabolic changes in the hippocampal CA1 region during ventricular fibrillation cardiac arrest (VF-CA) and ECLS versus conventional CPR. Male Sprague-Dawley rats (350g) underwent 8min untreated VF-CA followed by ECLS (n = 8; bloodflow 100ml/kg), mechanical CPR (n = 18; 200/min) until return of spontaneous circulation (ROSC). Shams (n = 2) were included. Glucose, glutamate and lactate/pyruvate ratio were compared between treatment groups and animals with and without ROSC. Ten animals (39%) achieved ROSC (ECLS 5/8 vs. CPR 5/18; OR 4,3;CI:0.7–25;p = 0.189). During VF-CA central nervous glucose decreased (0.32±0.1mmol/l to 0.04±0.01mmol/l; p<0.001) and showed a significant rise (0.53±0.1;p<0.001) after resuscitation. Lactate/pyruvate (L/P) ratio showed a 5fold increase (31 to 164; p<0.001; maximum 8min post ROSC). Glutamate showed a 3.5-fold increase to (2.06±1.5 to 7.12±5.1μmol/L; p<0.001) after CA. All parameters normalized after ROSC with no significant differences between ECLS and CPR. Metabolic changes during ischemia and resuscitation can be displayed by cerebral microdialysis in our VF-CA CPR and ECLS rat model. We found similar microdialysate concentrations and patterns of normalization in both resuscitation methods used.Institutional Protocol Number: GZ0064.11/3b/2011

The association between post resuscitation hemoglobin level and survival with good neurological outcome following Out Of Hospital cardiac arrest

Aimsto explore the association between post return of spontaneous circulation (ROSC) hemoglobin level and survival with good neurological outcome following out-of-hospital cardiac arrest. MethodsWe studied adults with non-traumatic out-of-hospital cardiac arrest who achieved ROSC within 50min of collapse. We quantified the association between post ROSC hemoglobin level and good neurological outcome (defined as Cerebral Performance Category score of 1or 2), using multivariate logistic regression analyses. The impact of Post ROSC hemoglobin level ≥10gdl−1 and time varying hemoglobin level ≥10gdl−1 on time to Survival with good outcome was assessed using Cox proportional hazard models. ResultsOf 931 cardiac arrest patients, 146 (16%) achieved ROSC and 30 survived to discharge with a good neurological outcome. Of those with post ROSC hemoglobin level ≥10gdl−1, 28% (27/98) had good outcome, whereas of those with level <10mgdl−1 only 6% (3/48) had good outcome (CPC<3, P=0.003). The use of blood transfusions and therapeutic hypothermia were comparable in both good and bad outcome groups. An immediate post ROSC hemoglobin level ≥10gdl−1 was significantly associated with good neurological outcome (AOR 8.31 95% CI 1.89–36.52 P=0.005). Patients with post ROSC hemoglobin ≥10gdl−1 were more likely to achieve good outcome earlier (HR 6.02 95% CI 1.75–20.72 P=0.004). ConclusionsPost ROSC hemoglobin level ≥10gdl−1 is associated with survival with good neurological outcome. The importance of time to achieve such level and the role of blood transfusion warrants further investigation.

Abstract 13162: Post-Cardiac Arrest Serum TNF-α Levels Are Associated With Short-Term Survival in a Swine Model of Ventricular Fibrillation

Introduction: Most resuscitated victims of out-of-hospital cardiac arrest who survive to hospital expire due to the post-resuscitation syndrome. This syndrome is characterized by a sepsis-like pro-inflammatory state. Hypothesis: We hypothesized that a relationship exists between the rise of TNF-α, a pro-inflammatory cytokine, following return of spontaneous circulation (ROSC) and early post-arrest survival in a clinically relevant animal model of spontaneous VF. Methods: Mixed-breed Yorkshire swine (n=20), weighing 39 + 5 kg, were anesthetized and catheters placed in the right atrium and left ventricle/ascending aorta for continuous pressure monitoring. VF was induced by occluding the LAD with an angioplasty balloon. After 7 min of untreated VF, ALS resuscitation attempts were made for up to 20 min. Animals achieving ROSC were monitored for 3 hrs and fluid and pressor support was administered as needed. TNF-α levels were measured prior to VF and at 0, 15, and 30 min after ROSC using quantitative sandwich ELISA. Exact logistic regression and binomial proportions were used for analysis. Results: Twelve (60%) animals experienced early death, expiring during the 3-hour post-arrest period (9 PEA, 2 VF, and 1 asystole). The TNF-α level at 15 minutes post-ROSC was significantly associated with death within the first 3 hours post ROSC with a univariate odds ratio (OR) of 1.4 (95% confidence interval [CI] 1.05-2.2, p=0.01). Using a cutoff TNF-α level of 525 pg/mL at 15 min post ROSC had 100% negative predictive value (95% CI 0-37%) and 67% positive predictive value (95% CI 35-90%) for early death. Conclusions: The pro-inflammatory cytokine TNF-α increases shortly after ROSC and is predictive of early death. Early identification of resuscitated victims at greatest risk for hemodynamic collapse and recurrent arrest might facilitate the use of early hospital-based interventions to decrease the likelihood of a poor outcome.

Abstract 10134: Potassium Cardioplegia During CPR for Porcine VF Arrest: A Blinded Randomized Controlled Trial

Introduction: Potassium cardioplegia-induced transient asystole may conserve myocardial energy and improve outcome in ventricular fibrillation (VF) cardiac arrest. Hypothesis: We hypothesized potassium infusion during VF arrest would lead to an increase in intra-arrest amplitude spectrum area (AMSA) prior to defibrillation, and improved hemodynamic parameters in those animals that attained return of spontaneous circulation (ROSC). Methods: Twelve swine were randomized to KCl or placebo in a randomized controlled trial, and 10 were included in an amended protocol. After initiation of monitoring, induction of anesthesia, and instrumentation of the aorta and right atrium, VF was electrically induced. After 4 minutes, 1.5 meq/kg KCl or placebo was infused in blinded fashion in a peripheral ear vein and mechanical chest compressions and ventilations were begun. Initial defibrillation was performed 10 minutes post VF induction, as appropriate. Animals without ROSC received continued resuscitation per Advanced Cardiac Life Support(ACLS) guidelines for 10 more minutes. Animals that achieved ROSC were monitored for 30 more minutes. The primary outcome, change in AMSA from just before study drug infusion to 5 minutes post infusion, was compared using nonparametric statistics. Results: Six animals were randomized to KCl and 4 to Placebo. KCl infusion induced approximately 1 minute of transient asystole at the dosage used. The mean change in normalized AMSA was -0.24 in the KCl and 0.21 in the Placebo group, with a median difference of -0.50 (95%CI -0.79 to -0.09), p=0.038, favoring Placebo. Five of 6 (83%) animals in the KCl group and 2 of 4 (50%) in the Placebo group developed an organized, though not necessarily, perfusing rhythm with the difference in proportion 33% (95% CI -33 to 86). One of 6 (17%) animals in the KCl and 2 of 4 (50%) in the Placebo group achieved ROSC with the difference in proportion -33% (95%CI -93 to 33). Hemodynamics were not quantitatively compared post ROSC due to limited survivors. One animal in each group required norepinephrine infusion. Conclusions: Potassium as a single agent did not benefit AMSA or ROSC in this porcine model of VF arrest.

The significance of diarrhea after cardiac arrest – A retrospective analysis

Introduction: In post Resuscitation care there are just a few parameters that can help physicians in the first 24 h post ROSC (Return of spontaneous circulation) to evaluate the patients prognosis. 1 Nürnberger A. Sterz F. et al. Out of hospital cardiac arrest in Vienna: incidence and outcome. Resuscitation. 2013; 84: 42-47 Abstract Full Text Full Text PDF PubMed Scopus (54) Google Scholar , 2 Grimaldi et al. Short- and long-term outcome in elderly patients. After out-of-hospital cardiac arrest: a cohort study. Crit Care Med. 2014; 42 Crossref PubMed Scopus (54) Google Scholar

Abstract 282: Poloxamer 188 Improves Intra-CPR Hemodynamics and Post-Resuscitation LV Function in a Pig Model of Prolonged Cardiac Arrest

Introduction: Poloxamer 188 (P188) is a copolymer surfactant that has been shown to protect against ischemia/reperfusion injury. We hypothesized that P188 administration at the initiation of cardiopulmonary resuscitation (CPR) would improve post-resuscitation LV function. Methods: Following 15 min of untreated ventricular fibrillation (VF), 12 pigs received 4 minutes of CPR with automated active compression/decompression and an impedance threshold device. Six animals received an IV bolus (250 mg/kg) at the initiation of CPR and infusion of 120 ml of 150 mg/ml of P188 for 4 hours after return of spontaneous circulation (ROSC). Six other animals received no P188 (CTL). Aortic systolic (AoS), diastolic (AoD), and right atrial diastolic (RAD) pressures were recorded continuously. Coronary perfusion pressure (CPP) was calculated as the difference between AoD and RAD. All animals received 0.5 mg of epinephrine 1 min prior to defibrillation. Left ventricular ejection fraction (LVEF) was obtained with echocardiography 1 and 4 hours after return of spontaneous circulation (ROSC). Unpaired t-tests were used for statistical analysis; significance assumed at p&lt;0.05 (two-tailed). Results: 5/6 animals treated with P188 and 6/6 CTL animals had ROSC. P188 significantly increased intra-CPR hemodynamics (table) and eliminated post resuscitation LV ventricular dysfunction. LVEF at 1 and 4 hours post ROSC with P188 vs. CTL was 58±7 and 62±11% versus 36±12 and 38±9 %, respectively (p&lt;0.05). Conclusion: Poloxamer 188, when administered at the initiation of CPR as a bolus and as an infusion post ROSC, improved intra-CPR hemodynamics and post-ROSC LVEF after 15 minutes of untreated VF in an animal model. The mechanism of action is thought to be membrane stabilization and this will be the aim of future studies.

Niacin Suppresses the Mitogen-Activated Protein Kinase Pathway and Attenuates Brain Injury After Cardiac Arrest in Rats*

To determine whether niacin attenuates brain injury and improves neurological outcome after cardiac arrest in rats and if its therapeutic benefits are associated with suppression of the mitogen-activated protein kinase pathway. Prospective laboratory study. University laboratory. Male Sprague-Dawley rats (n=77). After 6 minutes of no flow time induced by ventricular fibrillation, cardiopulmonary resuscitation was provided and return of spontaneous circulation was achieved. Animals were then administered vehicle, single low dose (360 mg/kg; at 1 hr postreturn of spontaneous circulation), single high dose (1080 mg/kg; at 1 hr), or repeated low dose of niacin (360 mg/kg/d for 3 d; at 1, 24, and 48 hr) through an orogastric tube. Neurologic deficit scales were scored at 24 hours, 72 hours, and 7 days postreturn of spontaneous circulation. Single high dose of niacin improved neurologic deficit scales at 48 hours and 7 days, and repeated low dose of niacin improved neurologic deficit scales at 7 days. Then, a separate set of animals were killed at 72 hours postreturn of spontaneous circulation, and brain tissues were harvested. Single high dose and repeated low dose of niacin attenuated cellular apoptosis and neuronal damage in hippocampal cornu ammonis 1 and decreased axonal injury and microglial activation in corpus callosum. They increased nicotinamide adenine dinucleotide, reduced nicotinamide adenine dinucleotide phosphate and reduced glutathione levels, and decreased malondialdehyde level in brain tissues. Furthermore, they suppressed the phosphorylations of p38 and c-Jun N-terminal kinase/stress-activated protein kinase and the cleavage of caspase 3. However, they failed to enhance extracellular signal-regulated kinases 1/2 phosphorylation. Single high dose and repeated low dose of niacin attenuated brain injury and improved neurological outcome after cardiac arrest in rats. Their therapeutic benefits were associated with suppressions of the phosphorylations of p38 and c-Jun N-terminal kinase/stress-activated protein kinase and the cleavage of caspase 3.

029 PREDICTORS OF SURVIVAL AND NEUROLOGICAL RECOVERY IN ST-ELEVATION MYOCARDIAL INFARCTION COMPLICATED BY OUT OF HOSPITAL CARDIAC ARREST

<h3>Background</h3> Recent UK epidemiological data suggests that while incidence and mortality of myocardial infarction (MI) is in decline, mortality associated with out of hospital cardiac arrest (OOHCA) in the setting of MI is still a significant problem now constituting 70% of its total fatality. Small studies have shown survival benefit with primary percutaneous coronary intervention (pPCI) in OOHCA in the setting of ST elevation myocardial infarction (STEMI). There is little contemporary outcome data in this population. We sought to identify predictors of survival in STEMI complicated by OOHCA in a large, contemporary cohort in the era of pPCI. <h3>Methods</h3> Between January 2008 and October 2011, 1836 consecutive STEMI admissions to a high volume pPCI centre were retrospectively analysed. 132 patients were identified as having OOHCA. Clinical and procedural data was collected from the UK Myocardial Ischaemia National Audit Project (MINAP) database and patient notes. Endpoints were all cause mortality to 4 years (mean: 559 days, median: 380 days) and neurological recovery at discharge (Cerebral Performance Score/CPS 1). Mortality data was collected using the Office of National Statistics mortality database. <h3>Results</h3> 132 out of 1836 consecutive STEMI patients were identified with OOHCA (7.2%). The mean age of patients was 59.4±14years, 78.8% were male and 55% were directly conveyed to the pPCI centre; the remaining were transferred from district hospitals. Survival to discharge was 76.5% (101/132 patients). 86 patients had full neurological recovery (65% of the whole cohort). Long term follow-up revealed only one further death making the overall survival rate 75.8%. Survivors had significantly higher incidence of witnessed arrest (p&lt;0.0001) and immediate cardiopulmonary resuscitation (CPR)/advanced life support (ALS) (p&lt;0.0001), a shorter time to return of spontaneous circulation (ROSC) (p&lt;0.0001) and were more likely to be alert post ROSC (p&lt;0.0001). Shorter call to balloon time (p=0.0117) and time from arrest to arrival at pPCI centre (p&lt;0.0001) were strongly associated with improved survival as was successful pPCI (p=0.0004) defined as TIMI 2–3 flow. Patient factors associated with poor outcome included three-vessel disease (p=0.0007), severe left ventricular impairment (p=0.0179), cardiogenic shock (p=0.0023) and renal dysfunction (p&lt;0.0001) on admission. Improved neurological outcome in survivors was strongly associated with witnessed arrest (p&lt;0.0001), immediate CPR/ALS (p=0.0186), shorter time to ROSC (p&lt;0.0001), patient being alert post ROSC (p&lt;0.0001) and shorter call to balloon (p=0.0028) and arrest to arrival times (p&lt;0.0001). <h3>Conclusions</h3> To our knowledge, this is the first reported series of STEMI complicated by OOHCA of this size in UK contemporary practice. This data shows a 76% survival rate, 65% rate of full neurological recovery and supports the emergent transfer of this patient group to a cardiac centre for pPCI.

Abstract 218: Cerebral Oximetry as a Post-ROSC Predictor of Neurologic Outcome After OOHCA

No reliable early predictors of neurological outcome exist for patients resuscitated from an OOHCA. Objectives: We investigated the prognostic utility of cerebral oximetry (rSO2) obtained after Return of Spontaneous Circulation (ROSC) on neurological outcome after OOHCA. Methods: This IRB approved, observational trial collected data on a convenience sample of patients presenting to an academic, urban Emergency Department with OOHCA. Cerebral Oximetry uses near infrared spectroscopy to measure oxygen in the brain independent of pulse using adhesive rSO2sensors that were placed on patient’s forehead upon ED arrival and data recorded for at least 4 hours post ROSC. We followed Utstein criteria for demographics and data recording. Blinded investigators abstracted CPC scores for all patients. Outcome measure defined as good CPC (≤ 2) at hospital discharge. We analyzed data with descriptive statistics and logistic regression. Results: We analyzed 32 patients: 69% were male, mean age 62.5 years (52 to 75), 30 (93.8%) witnessed and 23 (71.9%) had bystander CPR. Initial rhythm was VF/VT 19%, PEA 40%, Asystole 34% and 2 unknown. There were 7 (22%) with good CPC at hospital discharge. Univariate analysis showed only the average rSO2 during first 4-hours post ROSC predictive of good outcome (p&lt;0.003). Initial Mean Arterial Pressure (MAP) was a good prognosticator (p&lt;0.087). Logistic regression revealed only average rSO2 4-hours post ROSC as indicative of good outcome (p&lt;0.086). Conclusion: The average cerebral oximetry in the first 4 hours post ROSC was an excellent predictor of good neurological outcome at hospital discharge. This study is limited by small sample size and observational nature.

Abstract 40: Tissue Oximetry During Out-of-Hospital Cardiopulmonary Resuscitation

Introduction: Coronary perfusion pressure is a common surrogate marker for myocardial perfusion and the effectiveness of CPR. Peripheral perfusion is far less studied. We sought to evaluate tissue oxygen saturation (StO 2 ) as a surrogate marker for peripheral perfusion during CPR and after return of spontaneous circulation (ROSC) during out-of-hospital cardiac arrest (OOHCA). Methods: This study was approved by our IRB. EMS physicians responded to cases of cardiac arrest and placed a continuous near infrared tissue oximeter on the thenar eminence of the patient to measure StO 2 , which was recorded continuously during the resuscitation. Each case was then broken down into 30-second epochs classified as ongoing CPR or post-ROSC. The mean StO 2 for each epoch was calculated. A two-sample T test was used to compare the two conditions. Results: 16 patient encounters were analyzed with a total of 390 epochs, 175 with pulses and 215 during CPR. Patients ranged in age from 34-88 and 10 were male (62.5%). The StO 2 average for the epochs during CPR was 50.04 (SD 18.5) and 66.74 (24.6) after ROSC in patients with pulses. A difference of 16.7 was seen between the two conditions (p&lt;0.001). Conclusion: In this cohort of patients, there was a lower average StO 2 reading in patients with CPR being performed when compared to the post ROSC group. While the cause of this difference may be multifactorial, lower tissue oxygen saturation may imply worse peripheral perfusion. Future studies will need to evaluate the cause of this difference and potential impacts it may have on cardiac arrest outcome in the prehospital setting.

367 Post Resuscitative Factors Influencing Survival after In-Hospital Pediatric Cardiac Arrest

Background and AimsIn-hospital pediatric cardiac arrest (CA) achieves high return of spontaneous circulation (ROSC) rates but survival to hospital discharge is low. The aim of this study was to determine...

Abstract 200: Temporal Relationship Between Left Ventricular Dysfunction and Plasma High-Sensitivity Cardiac Troponin T Levels in a Rat Model of Cardiac Arrest and Resuscitation

Introduction. Post resuscitation left ventricular (LV) dysfunction is one of the leading causes of death after return of spontaneous circulation (ROSC). Impairment in cardiac myofilament cross-bridge cycling and the associated degradation and release of cardiac troponins (cTn) concur to depressed contractile function. We hypothesized that the severity of myocardial dysfunction would be associated with plasma cTn levels following cardiac arrest in rats. Methods. Ventricular fibrillation was induced in 17 rats and was untreated for 6 min. CPR, including mechanical chest compressions, ventilation, and epinephrine, was then initiated and continued for additional 6 min prior to defibrillations. Two, 4, and 72 hr following ROSC, LV morphology, systolic and diastolic function were assessed by echocardiography. Animals were then sacrificed, plasma collected and high sensitivity cTnT (hs-cTnT) assayed. Additional 5 rats were not subjected to cardiac arrest and served as controls. Results. At 2 and 4 hr post ROSC, LV end-diastolic volume was enlarged compared to controls (+22% and +25%, respectively) but similar at 72 hr. LVEF was lower than in control rats at 2 and 4 hr following ROSC (Fig., left pannel), but similar at 72 hr. Post ROSC deceleration time (DT) of the E wave showed similar trends (Fig., middle pannel). Plasma release of hs-cTnT increased at 2 and 4 hr post ROSC compared to controls, but was similar at 72 hr (Fig., right pannel). LVEF and DT were significantly inversely correlated with hs-cTnT (r=-0.89, p&lt;0.0001 and r=-0.53, p=0.014). Conclusions. A strong relationship between LVEF and circulating hs-cTnT was observed at different time points following ROSC. Normal LV function at 72 hr post ROSC indicates that myocardial viability was preserved even after remarkable TnT release.

Temperature post out-of-hospital cardiac arrest: the TOPCAT study

IntroductionOut-of-hospital cardiac arrest (OHCA) is a significant cause of death and severe neurological disability. The only postreturn of spontaneous circulation (ROSC) therapy shown to increase survival is mild therapeutic hypothermia...

The Role of Oxygen in Cardiac Arrest Resuscitation

The heart is incapable of storing significant oxygen or substrates and thus is entirely dependent on a continuous delivery of flow in order to support its high metabolic state.&nbsp;Following cardiac arrest, myocardial tissue oxygen tension falls rapidly and aerobic production of ATP ceases.&nbsp;Without re-oxygenation of the ischemic myocardium, return of spontaneous circula-tion (ROSC)&nbsp;cannot be achieved.&nbsp;The oxygen paradox which has been described regarding other ischemia-reperfusion conditions seems to have application in cardiac arrest.&nbsp;It is clear that some level of oxygenation is necessary to achieve ROSC, however post ROSC there appears to be increased toxicity associated with hyperoxia.&nbsp;The optimal conditions for re-oxygenation in the setting of cardiac arrest remain ill defined at present.