Ventricular Fibrillation Cardiac Arrest Research Articles

Beau's Lines After Cardiac Arrest

A 34-year-old man with uncontrolled hypertension suffered a ventricular fibrillation cardiac arrest from an obstructive left anterior descending artery occlusion. He was defibrillated more than 10 times before achieving return of spontaneous circulation. He was comatose after his arrest and was treated with therapeutic hypothermia, and a bare metal stent was placed in his obstructed coronary artery with restoration of excellent postobstruction blood flow. His postarrest course was complicated by cardiogenic shock; prolonged ventilator-dependent respiratory failure requiring tracheostomy; tracheobronchitis, with cultures positive for methicillin-resistant Staphylococcus aureus (MRSA); and an extended period of agitation and delirium. Thirty-four days after his arrest, his mental status started to improve rapidly. His delirium resolved, he became oriented and lucid, and he was able to be discharged to a rehabilitation facility on hospital day 41, with an excellent prognosis and close follow-up in primary care, cardiology, tracheostomy, and coumadin clinics. He returned to the emergency department 65 days later with the complaint of intermittent chest pain of 4 days' duration. Upon physical examination he was found to have Beau's lines on his fingernails. He was admitted to the hospital for a rule-out myocardial infarction workup, which was uneventful. He was discharged to home in good condition 2 days later.

Abstract 181: Relation between Electrocardiographic Changes and Neurologic Outcomes in Patients Treated with Hypothermia after Out-of-hospital Ventricular Fibrillation Cardiac Arrest: J-PULSE-Hypo Registry

Background: The 2010 American Heart Association Guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) recommend that comatose adult patients with return of spontaneous circulation (ROSC) after out-of-hospital ventricular fibrillation (VF) cardiac arrest should receive therapeutic hypothermia (Class I). However, it remains unclear whether therapeutic hypothermia is effective for cardiac arrest patients whose have VF initially, but not at hospital arrival. Methods: We conducted a multicenter retrospective study at 14 institutions to evaluate the effect of therapeutic hypothermia on out-of-hospital cardiac arrest between January 2005 and March 2011. The study committee entrusted each hospital with the timing of cooling, cooling methods, target temperature, duration, and rewarming rate. Patients were divided into the VF-VF group, VF-PEA (pulseless electrical activity) group, and VF-Asystole group according to the pre-hospital initial rhythm and the hospital arrival rhythm, and neurologic outcomes at 90 days after cardiac arrest were compared. A favorable outcome was defined as a Cerebral Performance Category (CPC) of 1-2. Results: A total of 135 patients were studied. There were no significant differences among the VF-VF group (n=83), the VF-PEA group (n=35), and the VF-Asystole group (n=17) in age, sex, frequency of witnessed cardiac arrest, the presence of bystander CPR, time to achieving target temperature, or duration of therapeutic hypothermia. The rate of favorable outcomes was higher in the VF-VF group (46%) than in the VF-PEA group (23%; p<0.01) and the VF-Asystole group (6%; p<0.01). Multivariate analysis showed that VF rhythm at hospital arrival was an independent predictor of favorable outcomes at 90 days after cardiac arrest. Conclusions: Our results suggest that therapeutic hypothermia after ROSC most effectively improves neurologic outcomes in patients who have VF initially as well as at hospital arrival, with no ROSC by the time of hospital arrival. Additional therapeutic strategies are needed to improve neurologic outcomes in patients who have VF initially with no ROSC and a rhythm other than VF at hospital arrival.

Abstract 232: Temperature Profile of Esophageal, Rectal and Tympanic Temperature Probes in a Rodent Model of Cardiopulmonary Bypass Resuscitation from Ventricular Fibrillation Cardiac Arrest

BACKGROUND: Exact and valid temperature measurement is crucial to assess the effects of temperature levels on outcome after cardiac arrest (CA). In this study, we assessed the temperature profile in different body locations in our rat ventricular fibrillation (VF) CA model with emergency cardiopulmonary bypass (ECPB) resuscitation. METHODS: Adult Sprague-Dawley rats (400g) were equipped with esophagus (Tes), tympanic (Ttym) and rectal (Trec) temperature probes along standard instrumentation. Following 10 min of VF CA, rats were randomized to normothermic control (NT, 37±0.5°C), mild hypothermic (MH, 33±0.5°C) or deep hypothermic (DH, 27±0.5°C) reperfusion and put on ECPB for 15 min. On ECPB rats were rapidly cooled to and maintained at target temperature. After ECPB and return of spontaneous circulation (ROSC), MH and DH were maintained mild hypothermic with surface cooling/warming. Temperature profiles for the first five rats in the DH group are presented as mean±SD, variances tested by ANOVA and post-hoc Tukey analysis. Results: Before CA, all rats were normothermic with all three probes and cooled passively by 0.8±0.6°C during CA. In the MH and NT group, no differences in temperature measurements were found during the entire experiment, whereas in the DH group, temperature profile of the three probes significantly differed, which is presented below. With start of ECPB, cooling rate was significantly higher according to Tes (2.5±0.7°C/min) versus Ttym (1.4±0.6, p=0.44) or Trec (0.6±0.2, p=0.002) and target temperature reached by Tes within 2.8±1.0 min, but only in two animals by Ttym (4.5±0.7 min) and not at all by Trec. Rewarming rate to mild hypothermia at the end of ECPB did not vary significantly between probes (0.12±0.02) and was reached by 33±4 min. CONCLUSION: Even in a small animal model, temperature differs significantly in measurement locations. But what is true brain temperature? In future studies, measurement of brain temperature might be indicated.

Abstract 270: Developing a Ventricular Fibrillation Cardiac Arrest Rat Model - Pitfalls and Challenges

Introduction: The ideal rodent model of ventricular fibrillation (VF) cardiac arrest (CA) produces consistent histologic and neurologic damage as target for novel therapies and shows a high survival rate to minimize animal use and allow for long term outcome. VF induction, chest compressions and ventilation are crucial techniques and published in many variants in literature. We report our experiences during model development. Materials and Methods: A non-randomized cohort study evaluating different methods of VF induction, chest compressions techniques, mechanical ventilation and defibrillation was performed with regards to it’s feasibility, complications, ROSC rate and survival. Results: Male Sprague-Dawley rats (350g, anesthetised, instrumented) underwent VF induction with 2 min endocardial fibrillation via a transjugular neonatal pacing catheter with minimal current use, low incidence of autodefibrillation and good resuscitability. Mechanical chest compressions with approx. 30% of thorax diameter depth were applied with a pneumatic thumper 200/min placed mid-sternally, tilted upwards. Strong fixation with tapes avoided throrax-instability. Epinephrine (20μg/kg) and NaHCO3 (1mmol/ kg) were administered before CPR start and epinephrine repeatedly given after defibrillations every 2min. For defibrillations (5J, biphasic) modified paediatric defi pads were used. ROSC was achieved in 7/10 animals in a 6 min CA group and 6/11 in a 8 min CA group. CPR time was 2.6±1.0 min (mean±SD), number of defibrillations needed 2±1 and a cumulative epinephrine dose of 46±10 μg/kg with no differences between groups. Conclusions: Researchers developing a VF CA model are facing a multitude of difficulties, a lack of data on model development and many variations published in literature, often without detailed description. We developed a CPR rat model for VF CA with graded cognitive deficits and long-term survival. We propose detailed description of model development, including ineffective methods, to facilitate experience exchange between research groups, to avoid that future experimental groups repeat possible mistakes.

Abstract 362: Behavioral Testing With Morris Water Maze in Rats Resuscitated With Emergency Cardiopulmonary Bypass From 10 Min Ventricular Fibrillation Cardiac Arrest

Background: Rodent models of cardiac arrest help to investigate detailed pathophysiologic mechanisms of cerebral ischemia and reperfusion. Sensitive neurologic and behavioral tests would enhance the ability of such models to evaluate possible beneficial effects of protective therapies. The Morris Water Maze (MWM) is a procedure to study spatial learning and memory. The aim of this study was to investigate behavioral testing with the MWM in rats resuscitated from ventricular fibrillation (VF) cardiac arrest (CA) via emergency cardiopulmonary bypass (ECPB). Methods: Sprague-Dawley rats (450g, male, anesthetized) were put into VF CA. After 10 min of CA the animals were resuscitated with ECPB, epinephrine and defibrillations and cooled to mild hypothermia (33°C) . Ten surviving animals with favorable neurologic recovery were compared to 8 healthy rats. MWM was performed in each animal 2 times on 4 consecutive days for maximal 60 s with a hidden platform in a 22°C cold water tank and on day 7 and 14 with the platform removed for memory testing. Results: The latency time to find the hidden platform decreased in the CPB group and the control group from 60(IQR 39-60) s and 60(IQR 60-60) s to 9(IQR 6-29) s and 10(IQR 6-19) s respectively (p=0.46). After removal of the platform the time within the target sector on day 7 in 60 s was 17±6 s and 22±5 s (p=0.08) and on day 14 12±4 s and 13±4 s (p=0.76) respectively. Conclusions: Spatial learning and memory in clinical neurologically intact animals resuscitated from a 10 min VF CA cooled to mild hypothermia was comparable to normal healthy controls. With this MWM setup learning was performed well, the remembrance of platform position was kept for one week in both groups equally.

Abstract 226: Relation Between Glasgow Coma Scale Motor Score Immediately After ROSC and Neurologic Outcomes in Patients Treated With Hypothermia After Out-of-Hospital Cardiac Arrest: J-PULSE-Hypo Registry

Background: The 2010 American Heart Association Guidelines for cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) recommend that comatose adult patients with return of spontaneous circulation (ROSC) after out-of-hospital ventricular fibrillation (VF) cardiac arrest should receive therapeutic hypothermia (Class I). However, it remains unclear whether Glasgow Coma Scale (GCS) immediately after ROSC predicts neurologic outcome in patients treated with hypothermia after out-of-hospital cardiac arrest. Methods: We conducted a multicenter retrospective study at 14 institutions to evaluate the effect of therapeutic hypothermia on out-of-hospital cardiac arrest between January 2005 and March 2011 (505 patients). The study committee entrusted each hospital with the timing of cooling, cooling methods, target temperature, duration, and rewarming rate. In the patients with ROSC at hospital arrivals, the relationship between GCS score at hospital arrivals and neurological outcomes were analyzed. Neurologic outcomes at 90 days after cardiac arrest were examined. A favorable outcome was defined as a Cerebral Performance Category (CPC) of 1-2. Results: A total of 100 patients were studied. GCS score at hospital arrivals was distributed from 3 to 10. GCS motor scale at hospital arrivals was distributed from M1 (n=64), M2 (n=9), M3 (n=10), M4 (n=15), to M5 (n=2). Time interval between ROSC and hospital arrivals was distributed from 0 to 51 min (median 10 min, IQR: 5 - 17). A favorable outcome at 90 days after cardiac arrest was observed in 89 patients (89 %). All patients with GCS M4 and M5 (n=17) in which examined within 22 min after ROSC predict favorable outcome. Among the patients with GCS M1-3 (n=83) in which examined within 51 min after ROSC, favorable outcome was observed in 87 % (n=72) patients. Conclusions: Our results suggest that GCS motor scale at hospital arrivals after ROSC before induction of therapeutic hypothermia predict favorable outcomes.

Abstract 241: Amplitude Spectrum Area as a Tool to Identify the Circulatory Phase of Ventricular Fibrillation

Background: Ventricular fibrillation (VF) cardiac arrest (CA) is characterized by 3 time dependent phases: electrical (shorter than 4min), circulatory (4-10min), and metabolic (longer than 10min). These phases reflect the progressive increase of myocardial ischemia and suggest the potentially optimal treatment. During the electrical phase, immediate defibrillation is likely to be successful, while during the circulatory phase, the success of defibrillation diminishes without CPR. In the metabolic phase, there is low likelihood of successful resuscitation and probably a longer CPR interval prior to defibrillation is necessary. In the out-of-hospital (OH) setting, most patients may have passed the electrical phase when EMS arrives. Identification of the VF phase may therefore facilitate the proper CPR treatment. We used AMSA to determine if patients were in circulatory or in metabolic phase at EMS arrival. Methods: Data from an Utstein-compliant registry along with electronic ECG records were collected on consecutive adult OHCA patients treated by 2 EMS agencies over a 2 year period. Patients with bystander witnessed CA and with VF as initial CA rhythm were included (n=41). AMSA was calculated in earliest pause without compression artifacts, using a 2 sec ECG with a Tukey (0.2) FFT window. VF duration was calculated as the sum of the time interval from collapse to defibrillator on and the time interval from defibrillator on to first CPR interruption for defibrillation delivery. Results: VF duration ranged between 6.5 and 29.6 min (11.3+4.1 min), with a corresponding AMSA between 2.1 and 16.4 mV-Hz (9.4+4.2 mV-Hz). AMSA measured in the circulatory phase (N=19) was significantly higher than that in the metabolic phase (N=22) (8.14+3.17 vs. 5.98+2.88, p=0.03). Linear regression revealed that AMSA decreases by 0.22 mV-Hz for every min of VF. AMSA was able to predict circulatory phase with an accuracy of 0.7 in ROC area. An AMSA threshold of 10 mV-Hz was able to predict the circulatory phase with sensitivity of 32%, specificity of 95%, PPV of 86%, NPV of 62% and overall accuracy of 66%. Conclusions: AMSA is a good indicator of downtime in OHCA with initial rhythm of VF. AMSA could be used to identify VF phase and thereby suggest for the proper CPR intervention.

Acute kidney injury after cardiac arrest of ventricular fibrillation and asphyxiation swine model

PurposesThe purposes of the study are to investigate the renal function in ventricular fibrillation (VF) and asphyxiation cardiac arrest in a swine model and to estimate the value of novel biomarkers in the acute kidney injury (AKI) after cardiac arrest. MethodThirty-two healthy inbred Wu-Zhi-Shan miniature piglets were randomized into 2 groups (n = 16 per group). Cardiac arrest was induced by programmed electric stimulation and clamping the endotracheal tube in the VF group and asphyxiation group, respectively. Cardiopulmonary resuscitation was done for return of spontaneous circulation (ROSC). ResultsOne hundred percent (16/16) ROSC was observed in the VF group, and 50% (8/16) in the asphyxiation group (P < .01). All AKI biomarkers elevated significantly after ROSC. The novel biomarkers changed much earlier than the creatinine. The concentration of novel biomarkers in the asphyxiation group was higher than the VF group. Live animals had an oliguria and developed AKI. Characteristic morphological injuries in renal tissues were observed under light microscope and transmission electron microscope and were more serious in the asphyxiation group. ConclusionsAcute kidney injury at early stage of postresuscitation is common in different causes of cardiac arrest. Asphyxiation has more severe kidney injury and gets worse prognosis.

Epinephrine reduces carotid blood flow during cardiopulmonary resuscitation in a porcine model of cardiac arrest

Introduction: Epinephrine (epi) administered during CPR improves return of spontaneous circulation. However, its effect on long term outcome is still controversial. Moreover, decreases in cerebral microcirculation after epinephrine have been earlier reported in a model of ventricular fibrillation (VF) cardiac arrest. We sought to investigate the effects of epi on carotid blood flow (CBF) during CPR in a porcine model of post shock pulseless electrical activity (PEA) cardiac arrest.

No-flow time CPR in different situations. Mouth to mouth, pocket mask and Lund university cardiac arrest system

Purpose: Immediate cardiopulmonary resuscitation (CPR) is the recommended treatment for ventricular fibrillation cardiac arrest. Quality CPR increases the chances of survival of the victim who suffers a cardiac arrest. It is very important to reduce the no-flow time, The rescuer does not take more than five seconds to realize two rescue breaths. The aim of this study was to evaluate the quality and no-flow time on the CPR in different situations.

Differences of postresuscitation myocardial dysfunction in ventricular fibrillation versus asphyxiation

PurposeThis study aims to characterize postresuscitation myocardial dysfunction in 2 porcine models of cardiac arrest (CA): ventricular fibrillation cardiac arrest (VFCA) and asphyxiation cardiac arrest (ACA). MethodsThirty-two pigs were randomized into 2 groups. The VFCA group (n = 16) were subject to programed electrical stimulation, and the ACA group (n = 16) underwent endotracheal tube clamping to induce CA. Once induced, CA remained untreated for 8 minutes. Two minutes after initiation of cardiopulmonary resuscitation (CPR), defibrillation was attempted until return of spontaneous circulation (ROSC) was achieved or animals died. ResultsReturn of spontaneous circulation was 100% successful in VFCA and 50% successful in ACA. Cardiopulmonary resuscitation duration in VFCA was about half as short as in ACA. The survival time of VFCA was significantly longer than that of ACA. Ventricular fibrillation cardiac arrest had better mean arterial pressure, cardiac output, and left ventricular ± dp/dtmax after ROSC than ACA. Echocardiography revealed significantly lower left ventricular ejection fraction in ACA than in VFCA. Myocardial perfusion imaging using single-photon emission computed tomography demonstrated that myocardial injuries after ACA were more severe and widespread than after VFCA. Under a transmission electron microscope, the overall heart morphologic structure and the mitochondrial crista structure were less severely injured in the VFCA group than in the ACA group. Moreover, the percentage of apoptotic cardiomyocytes was higher in ACA than in VFCA. ConclusionsCompared with VFCA, ACA causes more severe cardiac dysfunction associated with less successful resuscitation and shorter survival time.

Amplitude spectrum area to guide resuscitation—A retrospective analysis during out-of-hospital cardiopulmonary resuscitation in 609 patients with ventricular fibrillation cardiac arrest

IntroductionThe capability of amplitude spectrum area (AMSA) to predict the success of defibrillation (DF) was retrospectively evaluated in a large database of out-of-hospital cardiac arrests. MethodsElectrocardiographic data, including 1260 DFs, were obtained from 609 cardiac arrest patients due to ventricular fibrillation. AMSA sensitivity, specificity, accuracy, and positive and negative predictive values (PPV, NPV) for predicting DF success were calculated, together with receiver operating characteristic (ROC) curves. Successful DF was defined as the presence of spontaneous rhythm ≥40bpm starting within 60s from the DF. In 303 patients with chest compression (CC) depth data collected with an accelerometer, changes in AMSA were analyzed in relationship to CC depth. ResultsAMSA was significantly higher prior to a successful DF than prior to an unsuccessful DF (15.6±0.6 vs. 7.97±0.2mV-Hz, p<0.0001). Intersection of sensitivity, specificity and accuracy curves identified a threshold AMSA of 10mV-Hz to predict DF success with a balanced sensitivity, specificity and accuracy of almost 80%. Higher AMSA thresholds were associated with further increases in accuracy, specificity and PPV. AMSA of 17mV-Hz predicted DF success in two third of instances (PPV of 67%). Low AMSA, instead, predicted unsuccessful DFs with high sensitivity and NPV >97%. Area under the ROC curve was 0.84. CC depth affected AMSA value. When depth was <1.75in., AMSA decreased for consecutive DFs, while it increased when the depth was >1.75in. (p<0.05). ConclusionsAMSA could be a useful tool to guide CPR interventions and predict the optimal timing of DF.

Establishment and evaluation of a swine model of acute myocardial infarction and reperfusion–ventricular fibrillation–cardiac arrest using the interventional technique

BackgroundVentricular fibrillation is the main cause of sudden cardiac death among patients with acute myocardial infarction (AMI). Substantial benefits could be obtained by both researchers and practitioners if an AMI reperfusion-ventricular fibrillation-cardiac arrest model were established. MethodsTwenty swine were anesthetized and underwent occlusion of the left anterior descending branch for 90 minutes prior to blood reperfusion. Throughout this process, continuous 12-lead electrocardiography (ECG) was used to monitor heart rate, rhythm, and electrocardiogram alteration. Thereafter, AMI was confirmed by ECG and left ventricular angiography. Heart tissue was collected for pathological analysis, and for evaluation of the establishment of a model of AMI reperfusion. ResultsSeven swine died during the model establishment, and the 13 surviving swine were proven to have myocardial infarction; nine of those survivors had ventricular fibrillation–cardiac arrest after reperfusion based on the electrocardiograph and pathological examination. ConclusionBlocking the left anterior descending branch by inflation of an over-the-wire coronary balloon catheter in swine can result in successful establishment of a swine model of AMI and reperfusion–ventricular fibrillation–cardiac arrest, with good reproducibility and a high survival rate.

Prophylactic lidocaine for post resuscitation care of patients with out-of-hospital ventricular fibrillation cardiac arrest

BackgroundAntiarrhythmic drugs like lidocaine are usually given to promote return of spontaneous circulation (ROSC) during ongoing out-of-hospital cardiac arrest (OHCA) from ventricular fibrillation/tachycardia (VF/VT). Whether administering such drugs prophylactically for post-resuscitation care after ROSC prevents re-arrest and improves outcome is unstudied. MethodsWe evaluated a cohort of 1721 patients with witnessed VF/VT OHCA who did (1296) or did not receive prophylactic lidocaine (425) at first ROSC. Study endpoints included re-arrest, hospital admission and survival. ResultsProphylacic lidocaine recipients and non-recipients were comparable, except for shorter time to first ROSC and higher systolic blood pressure at ROSC in those receiving lidocaine. After initial ROSC, arrest from VF/VT recurred in 16.7% and from non-shockable arrhythmias in 3.2% of prophylactic lidocaine recipients, 93.5% of whom were admitted to hospital and 62.4% discharged alive, as compared with 37.4%, 7.8%, 84.9% and 44.5%, of corresponding non-recipients (all p<0.0001). Adjusted for pertinent covariates, prophylactic lidocaine was independently associated with reduced odds of re-arrest from VF/VT, odds ratio, (95% confidence interval) 0.34 (0.26–0.44) and from nonshockable arrhythmias (0.47 (0.29–0.78)); a higher hospital admission rate (1.88, (1.28–2.76)) and improved survival to discharge (1.49 (1.15–1.95)). However in a propensity score-matched sensitivity analysis, lidocaine's only beneficial association with outcome was in a lower incidence of recurrent VF/VT arrest. ConclusionsAdministration of prophylactic lidocaine upon ROSC after OHCA was consistently associated with less recurrent VF/VT arrest, and therapeutic equipoise for other measures. The prospect of a promising association between lidocaine prophylaxis and outcome, without evidence of harm, warrants further investigation.

P35: Nitrite as a novel resuscitation adjunct after ventricular fibrillation cardiac arrest in rats: A preliminary report

Background Beside therapeutic hypothermia no novel therapies have been developed to improve outcomes of patients suffering cardiac arrest (CA). In rat models, nitrite NO 2 - has the theoretical advantage of being converted locally to nitric oxide (NO) in ischemic regions improving microcirculation. Nitrite reduced neurological damage after asphyxial CA in rats. Whether nitrite is protective in CA due to ventricular fibrillation (VF) is unclear. Therefore, we developed a novel VF rat CA model to test this hypothesis and characterize nitrite’s pharmacokinetics in this disease model. Methods In this pilot randomized blinded trial, adult male Sprague–Dawley rats were anesthetized, intubated and catheterized (arterial and venous). VF was induced using a bipolar pacing catheter and left untreated for 5 min. Manual cardiopulmonary resuscitation (CPR) with drugs (epinephrine/sodium bicarbonate) and defibrillation was initiated using a predefined protocol simulating current practice. After return of spontaneous circulation (ROSC), rats were randomized to 500 μL placebo (Plasmalyte), low-dose (2 μM) or high-dose (8 μM) intravenous nitrite given as a 5 min infusion at 5 min and 50 min after CPR-start. Nitrite whole blood levels were measured at baseline, before and after each of 2 drug infusions. Hemodynamics and temperature were measured over 60 min after CPR-start; temperature was controlled (37 °C) for 12 h post-arrest. Neurologic Deficit Score (NDS) was assessed on post-arrest days 1–2 and fear-conditioning (a hippocampal-mediated behavior) on days 7–8. On day 8, rats were perfused with formalin and surviving hippocampal CA1 neurons were quantified using HE Fig. 1 ) There were no significant differences between the treatment groups and placebo in regards to baseline nitrite levels, hemodynamics, temperature, NDS, fear conditioning, or CA1 neuronal survival, which was approximately 99 (51–133) cells/mm. Conclusion In this feasibility study, nitrite can be safely administered early after ROSC in a novel though mild model of VF CA. The clearance of the first nitrite dose was faster than the second dose suggesting either alteration in the volume of distribution, perhaps due to tissue saturation with higher doses, or in the half-life. These results are guiding present studies of nitrite in more lethal VF. Disclosure Supported by research grants from the Max Kade Foundation Inc. and the Laerdal Foundation for Acute Medicine.

Early onset of cooling catheter–related right atrial thrombus following cardiac arrest

Catheter-related right atrial thrombus (RAT) is an uncommon life-threatening complication. Few cases of endovascular cooling catheter–related complications have been reported. We report the first case of endovascular cooling catheter–related RAT. A 17-year-old adolescent boy was treated with therapeutic hypothermia using an endovascular cooling catheter following ventricular fibrillation cardiac arrest. He became alert, but RAT was found 3 days after the placement of the cooling catheter. Anticoagulation with enoxaparin for 2 weeks completely resolved the RAT, and he was consequently treated with radiofrequency ablation and received an implanted cardiac defibrillator. This case report highlights the occurrence of endovascular cooling catheter–related RAT early after the placement of a catheter. Physicians should monitor whether RAT occurs during and following therapeutic hypothermia with a cooling catheter.

A case of vasospastic angina diagnosed by emergency acetylcholine provocation test after out-of-hospital ventricular fibrillation cardiac arrest

A case of vasospastic angina diagnosed by emergency acetylcholine provocation test after out-of-hospital ventricular fibrillation cardiac arrest

Therapeutic Hypothermia on Its 10th Anniversary

It has been 10 years since 2 seminal articles reported a dramatic improvement in survival and neurological outcome of comatose survivors from out-of-hospital ventricular fibrillation cardiac arrest (CA) with postresuscitative therapeutic hypothermia (TH).1,2 These exciting findings came after many years of resuscitation research that failed to yield a breakthrough therapy substantially advancing the outcome of CA victims. The results sparked a new enthusiasm in resuscitation research and launched multiple initiatives to bring this method to practice. Surprisingly, the protocol used in these studies was very simple: induce TH to between 32°C and 34°C and maintain it for 12 to 24 hours. The obvious simplicity and the apparent lack of need for sophisticated equipment made the technique very appealing. It was readily adopted in the both 2005 and 2010 resuscitation guidelines and soon started to be implemented worldwide. Article see p 2826 These findings were not surprising to those who closely followed resuscitation literature. In fact, hypothermia has been used for CA survivors and other critically ill patients for decades.3 To our knowledge, the initial series of TH applied to victims of CA of various origins (anaphylactic shock, respiratory failure, and trauma) was published in 1958.4 Surprisingly, the target temperatures and duration of cooling (30–34°C for 24–72 hours) closely resembled current recommendations (32–34°C for 12–24 hours). In 1959, Benson et al5 reported the first case series of in-hospital CA patients. Their data revealed favorable neurological recovery in 50% of patients treated with hypothermia versus 14% in those treated with normothermia. In 1964, TH was already endorsed by Safar in his first “ABCs of resuscitation.”6 However, variable use of hypothermia, being implemented at levels ≤30°C or for prolonged durations, was associated with adverse effects that stalled the future developments.7 On the other hand, experimental …

AMSA and Slope Are Predictive of Shock Success and Return of Spontaneous Circulation but Not Arrest Duration Following Ventricular Fibrillation Cardiac Arrest

AMSA and Slope Are Predictive of Shock Success and Return of Spontaneous Circulation but Not Arrest Duration Following Ventricular Fibrillation Cardiac Arrest

Abstract 28: Administration of Intravenous Ascorbic Acid Following Return of Spontaneous Circulation, with and Without Hypothermia, Improved Both Myocardial Dysfunction and Survival from Ventricular Fibrillation Cardiac Arrest

Background Our previous studies disclosed intravenous administration of ascorbic acid (AA) during CPR facilitates resuscitation and improves outcomes in VF cardiac arrest. However, the effect of AA administrated after ROSC and the interaction with hypothermia has not been clarified. Hypothesis Intravenous administration of AA after ROSC, with and without hypothermia, both can improve myocardial dysfunction and survival in VF cardiac arrest. Methods The animals were equally randomized to AA, hypothermia, AA+hypothermia and control groups. VF was induced and untreated for 5 minutes, followed by 1 minutes of CPR, and then one electrical shock of 5 J. After ROSC, the AA and AA+hypothermia group received intravenous administration of AA (100 mg/kg), and the hypothermia and control group received saline as placebo. In the hypothermia and AA+hypothermia groups, therapeutic hypothermia of 32°C was applied for 2 hours following ROSC. Malondialdehyde(MDA) of myocardium was assessed to determine oxidative stress. Results Within the first 2 hours, the control and the AA groups had higher heart rates than the hypothermia and AA+hypothermia groups. At the 4 th hour, the AA, hypothermia and AA+hypothermia groups had significant lower MDA concentration than the control group ( p &lt;0.05). The AA, hypothermia and AA+hypothermia groups had better dp/dt 40 and -dp/dt max than the control group, within 4 hours following ROSC (Table 1). Histological exam showed less myocytolysis in the AA, hypothermia and AA+hypothermia groups than in the control group. The AA, hypothermia and AA+hypothermia groups had better survival than the control group ( p &lt;0.05), but there was no difference between the AA, hypothermia and AA+hypothermia groups. Conclusion Intravenous administration of AA after ROSC, with and without hypothermia, both may improve myocardial dysfunction and survival in VF cardiac arrest.