Ventricular Fibrillation Arrest Research Articles

140 The diagnostic yield of brugada syndrome in families affected by sudden arrhythmic death syndrome; the impact of higher intercostal V1 and V2 leads

<h3>Introduction</h3> Brugada syndrome is an established cause of sudden arrhythmic death syndrome (SADS). The use of higher (2nd-intercostal space) intercostal V1 and V2 leads has been associated with increased surface electrocardiogram (ECG) sensitivity in the detection of the Brugada phenotype, either on the baseline ECG or following provocation using sodium ion channel blocking agents, without compromising specificity. Despite the potential implications, there is a paucity of data relating to the efficacy of this simple methodology in the diagnostic yield of Brugada syndrome in victims of ventricular fibrillation (VF) or 1st-degree relatives of SADS victims. <h3>Methods</h3> We identified 34 families diagnosed with Brugada syndrome based on the presence of a type-1 ECG in ¡Ý1 family members in the context of an unexplained VF arrest or a SADS death in a 1st-degree relative. The 12-lead ECGs of 139 individuals, who underwent comprehensive cardiac investigations including an Ajmaline provocation test, when appropriate, were reviewed. Electrocardiograms were performed with leads V1 and V2 placed in both the conventional 4th and the higher 2nd intercostal space. Family members not genetically related to the individuals diagnosed with Brugada syndrome were used as controls. <h3>Results</h3> Fifty-two of the 139 family members (37%) were diagnosed with Brugada syndrome. Only 6 (12%) individuals exhibited a diagnostic baseline ECG, while the great majority required an Ajmaline provocation test to unmask the Brugada phenotype. Of the 111 individuals who received Ajmaline, 22 (20%) developed the Brugada phenotype in the conventional ECG. The diagnostic Brugada phenotype was observed in 48 (43%) individuals by raising V1 and V2 leads at the 2nd-intercostal space (p&lt;0.001). None of the controls exhibited the Brugada phenotype in either the conventional or higher intercostal leads. Only 18 (53%) of the families were diagnosed on the basis of the standard ECG lead whereas all 34 (100%) families had at least one member with a positive type-1 ECG in the higher intercostal leads (p&lt;0.001). <h3>Conclusion</h3> Utilising higher intercostal leads for the detection of Brugada phenotype increases the diagnostic yield when screening families of SADS victims. This is primarily due to increased sensitivity of the Ajmaline provocation test. In our cohort almost 50% of the families and the majority (56%) of 1st-degree family relatives harbouring the Brugada gene would have remained undetected based on the standard 12-lead ECG alone.

Minimizing pre- and post-defibrillation pauses increases the likelihood of return of spontaneous circulation (ROSC)

Background The three-phase model of ventricular fibrillation (VF) arrest suggests a period of compressions to “prime” the heart prior to defibrillation attempts. In addition, post-shock compressions may increase the likelihood of return of spontaneous circulation (ROSC). The optimal intervals for shock delivery following cessation of compressions (pre-shock interval) and resumption of compressions following a shock (post-shock interval) remain unclear. Objective To define optimal pre- and post-defibrillation compression pauses for out-of-hospital cardiac arrest (OOHCA). Methods All patients suffering OOHCA from VF were identified over a 1-month period. Defibrillator data were abstracted and analyzed using the combination of ECG, impedance, and audio recording. Receiver–operator curve (ROC) analysis was used to define the optimal pre- and post-shock compression intervals. Multiple logistic regression analysis was used to quantify the relationship between these intervals and ROSC. Covariates included cumulative number of defibrillation attempts, intubation status, and administration of epinephrine in the immediate pre-shock compression cycle. Cluster adjustment was performed due to the possibility of multiple defibrillation attempts for each patient. Results A total of 36 patients with 96 defibrillation attempts were included. The ROC analysis identified an optimal pre-shock interval of <3 s and an optimal post-shock interval of <6 s. Increased likelihood of ROSC was observed with a pre-shock interval <3 s (adjusted OR 6.7, 95% CI 2.0–22.3, p = 0.002) and a post-shock interval of <6 s (adjusted OR 10.7, 95% CI 2.8–41.4, p = 0.001). Likelihood of ROSC was substantially increased with the optimization of both pre- and post-shock intervals (adjusted OR 13.1, 95% CI 3.4–49.9, p < 0.001). Conclusions Decreasing pre- and post-shock compression intervals increases the likelihood of ROSC in OOHCA from VF.

In Situ Simulation Comparing In-Hospital First Responder Sudden Cardiac Arrest Resuscitation Using Semiautomated Defibrillators and Automated External Defibrillators

Multifaceted approaches using simulation and human factors methods may optimize in-hospital sudden cardiac arrest (SCA) response. The Arrhythmia Simulation/Cardiac Event Nursing Training-Automated External Defibrillator phase (ASCENT-AED) study used in situ medical simulation to compare traditional and AED-supplemented SCA first-responder models. The study was conducted at an academic 719-bed hospital with institutional review board approval. Two simulation scenarios were developed and featured either respiratory arrest with perfusing bradycardia or ventricular fibrillation (VF) arrest. Study floors were equipped with either a semiautomated defibrillator (SD) only (control) or with both SD and AED (experimental); subjects functioned as solitary first responders and did not receive resuscitation training. Fifty nurses were enrolled on control (n=25) and experimental (n=25) floors. The groups' nonblinded performances exhibited the following differences during VF scenario: slower calls for help by the control group [mean time to completion of 25+/-17 seconds versus 18+/-11 seconds for the experimental group (P<0.05)] and fewer subjects in the control group performing chest compressions [44.0% versus experimental group's 95.8% (P<0.001)]. Eighty-eight percent of the control group defibrillated the manikin at an average of 155+/-59 seconds, with 32.0% of those subjects using semiautomated rhythm analysis; 100% (not significant [NS]) of experimental group defibrillated at 154+/-72 seconds (NS) with 100% AED analysis (P<0.001). Fewer control group subjects (28.0%) were observed during the bradycardia scenarios to perform inappropriate chest compressions than the AED-supplemented subjects [69.6% (P=0.01)]; nonindicated defibrillation was delivered during these scenarios by a single subject in the control group. Twenty-eight percent and 72% of VF scenarios were managed appropriately by control and experimental groups, respectively; bradycardia scenarios were managed without severe adverse event by 64% of control group and 28% of experimental group. In situ simulation can provide useful information, both anticipated and unexpected, to guide decisions about proposed defibrillation technologies and SCA response models for in-hospital resuscitation system design and education before implementation.

Extending the Use of the Pacing Pulmonary Artery Catheter for Safe Minimally Invasive Cardiac Surgery

In this study, the therapeutic use of pacing pulmonary artery catheters in association with minimally invasive cardiac surgery was evaluated. A retrospective study. A single institutional university hospital. Two hundred twenty-four consecutive patients undergoing minimally invasive cardiac surgery through a small (5-cm) right anterolateral thoracotomy using fibrillatory arrest without aortic cross-clamping. Two hundred eighteen patients underwent mitral valve surgery (97%) alone or in combination with other procedures. Six patients underwent other cardiac operations. In all patients, the pacing pulmonary artery catheter was used intraoperatively to induce ventricular fibrillation during the cooling period, and in the postoperative period it also was used in 37 (17%) patients who needed to be paced, mainly for bradyarrhythmias (51%). There were no complications related to the insertion of the catheters. Six (3%) patients experienced a loss of pacing capture, and 2 (1%) experienced another complication requiring the surgical removal of the catheter. Seven (3%) patients needed postoperative implantation of a permanent pacemaker. In combination with minimally invasive cardiac surgery, pacing pulmonary artery catheters were therapeutically useful to induce ventricular fibrillatory arrest intraoperatively and for obtaining pacing capability in the postoperative period. Their use was associated with a low number of complications.

A randomized comparison of cardiocerebral and cardiopulmonary resuscitation using a swine model of prolonged ventricular fibrillation

Background Cardiocerebral resuscitation (CCR) is reportedly superior to cardiopulmonary resuscitation (CPR) for primary cardiac arrest in the prehospital setting. This study was done using a swine model of prolonged ventricular fibrillation (VF) to quantify the effect of the emergency medical services component of CCR with intraosseous access (CCR-IO) compared with standard CPR with intravenous access (CPR-IV) as it is typically performed during out-of-hospital cardiac arrest (OHCA) resuscitation in a prospective randomized fashion. Methods Fifty-three animals were instrumented under anesthesia and VF was electrically induced. After 10 min of untreated VF, baseline characteristics were recorded, and animals were block randomized to one of two resuscitation schemes. The controls had mechanical chest compressions at 100/min with ventilations at a ratio of 30:2. Consistent with clinical practice, two 30-s pauses in chest compressions occurred to simulate attempts to accomplish endotracheal intubation at minutes 1 and 3 of CPR and successful IV access was simulated to occur three additional minutes after endotracheal intubation. The CCR group had continuous uninterrupted mechanical chest compressions at 100/min. No active ventilations were provided. A tibial IO needle was placed in real time for vascular access. Both groups received epinephrine (0.1 mg/kg) as soon as access became available followed by 2.5 min of chest compressions before the first 120J rescue shock attempt. After successful rescue shock, standardized post-resuscitative care was provided to a 20-min endpoint. Failed rescue shock was followed by continued chest compressions with positive pressure ventilation in both groups, repeat doses of epinephrine (0.01 mg/kg) every 3 min, and rescue shock every minute as long as a shockable rhythm persisted. Group comparisons were assessed using descriptive statistics. Proportions with 95% confidence intervals were calculated for VF termination, ROSC, and survival. Results Baseline characteristics and chemistries between the two groups at VF induction and after 10 min of non-treatment were mathematically the same. The proportions of VF termination (0.50 vs. 0.82), ROSC (0.30 vs. 0.59), and 20-min survival (0.19 vs. 0.40) all strongly favored the CCR-IO group. Conclusion In this swine model of witnessed VF arrest with no bystander-initiated resuscitation, CCR-IO resulted in substantial improvement in all three outcomes relative to typical emergency medical services provided CPR-IV.

Successful treatment using PCPS and IABP in a fluminant myocarditis case with 7 days of intractable ventricular fibrillation and cardiac arrest

Successful treatment using PCPS and IABP in a fluminant myocarditis case with 7 days of intractable ventricular fibrillation and cardiac arrest

Sudden Cause of Cardiac Death—Be Aware of Me: A Case Report and Short Review on Brugada Syndrome

Introduction. Brugada syndrome accounts for about 4% of sudden cardiac deaths (SCD). It is characterized by an ST-segment elevation in the right precordial electrocardiogram (EKG) leads. Case Presentation. We describe a 39-year-old healthy Caucasian man who was admitted to the intensive care unit after being cardioverted from ventricular fibrillation (VF) arrest. His past history was significant for an episode of syncope one month prior to this presentation for which he was admitted to an outlying hospital. EKG during that admission showed ST elevations in V1 and V2 leads, a pattern similar to Type 1 Brugada. A diagnosis of Brugada syndrome was missed and the patient had a cardiac arrest a month later. We discuss a short review of Brugada syndrome and emphasize the need to look for it in patients presenting with SCD and malignant arrhythmias. Conclusion. Physicians should always consider Brugada syndrome in the differential diagnosis of ST-segment elevation in anterior precordial leads of EKG and associated VT/VF. Although more than 17 years have passed since the first case was reported, increased awareness of this syndrome is needed to identify patients with EKG changes and treat them accordingly to prevent incidence of (SCD) and its deleterious complications.

Impact of Prior Statin Therapy on Arrhythmic Events in Patients With Acute Coronary Syndromes (from the Global Registry of Acute Coronary Events [GRACE

Animal models of myocardial ischemia have demonstrated reduction in arrhythmias using statins. It was hypothesized that previous statin therapy before hospitalization might be associated with reductions of in-hospital arrhythmic events in patients with acute coronary syndromes. In this multinational, prospective, observational study (the Global Registry of Acute Coronary Events [GRACE]), data from 64,679 patients hospitalized for suspected acute coronary syndromes (from 1999 to 2007) were analyzed. The primary outcome of interest was in-hospital arrhythmic events in previous statin users compared with nonusers. The 2 primary end points were atrial fibrillation and the composite end point of ventricular tachycardia, ventricular fibrillation, and/or cardiac arrest. In-hospital death was also examined. Of the 64,679 patients, 17,636 (27%) had received previous statin therapy. Those taking statins had higher crude rates of histories of angina (69% vs 46%), diabetes (34% vs 22%), heart failure (15% vs 8.4%), hypertension (74% vs 58%), atrial fibrillation (9.3% vs 7.0%), and dyslipidemia (85% vs 35%). Patients previously taking statins were less likely to have in-hospital arrhythmias. In propensity-adjusted multivariable models, previous statin use was associated with a lower risk for ventricular tachycardia, ventricular fibrillation, or cardiac arrest (odds ratio 0.81, 95% confidence interval 0.72 to 0.96, p = 0.002); atrial fibrillation (odds ratio 0.81, 95% confidence interval 0.73 to 0.89, p <0.0001); and death (odds ratio 0.82, 95% confidence interval 0.70 to 0.95, p = 0.010). In conclusion, patients previously taking statins had a lower incidence of in-hospital arrhythmic events after acute coronary syndrome than those not previously taking statins. Our study suggests another possible benefit from appropriate primary and secondary prevention therapy with statins.

Ethyl pyruvate enhances intra-resuscitation hemodynamics in prolonged ventricular fibrillation arrest

Aims As the duration of untreated cardiac arrest increases, the effectiveness of standard therapies declines, and may be more harmful than helpful. We investigated the hemodynamic, metabolic and anti-inflammatory effects of Ringer's ethyl pyruvate solution (REPS) versus Ringer's solution (RS) in the acute model of prolonged porcine arrest. Methods Seventeen mixed-breed swine were induced into ventricular fibrillation (VF) and left untreated for 8 min. CPR was begun using a mechanical chest compression device at a rate of 100 per minute. At the onset of CPR, animals were randomly assigned to treatment with either 25 mL/kg of RS or 25 mL/kg of REPS containing 40 mg/kg of ethyl pyruvate, infused over 5 min in blinded fashion. CPR continued with administration of a drug cocktail at 2 min and the first rescue shock was delivered at minute 13 of VF. Animals having ROSC were supported with standardized care for 2 h. Results Both groups had 100% ROSC and 100% 2-h survival. The REPS group exhibited higher median CPP (27.3 mmHg) than the control group (16.5 mmHg) by 3 min of CPR, which continued throughout the duration of CPR ( p = 0.02). The median time to hypotension following ROSC was 9.64 min in the REPS group and 7.25 min in controls ( p = 0.04) and there was a non-significant trend of decreased use of vasopressors for the duration of resuscitation. There was no difference in systemic or cerebral metabolism between groups. There were non-significant trends of decreased IL-6, increased Il-10 and decreased mesenteric bacterial colony growth in those treated with REPS when compared to RS. Conclusions The administration of REPS with CPR significantly improved intra- and post-resuscitation hemodynamics in this swine model of prolonged cardiac arrest, but did not definitely change the metabolic or inflammatory profile during the acute resuscitation period.

Cost-Effectiveness of Therapeutic Hypothermia After Cardiac Arrest

Therapeutic hypothermia can improve survival and neurological outcomes in cardiac arrest survivors, but its cost-effectiveness is uncertain. We sought to evaluate the cost-effectiveness of treating comatose cardiac arrest survivors with therapeutic hypothermia. A decision model was developed to capture costs and outcomes for patients with witnessed out-of-hospital ventricular fibrillation arrest who received conventional care or therapeutic hypothermia. The Hypothermia After Cardiac Arrest (HACA) trial inclusion criteria were assumed. Model inputs were determined from published data, cooling device companies, and consultation with resuscitation experts. Sensitivity analyses and Monte Carlo simulations were performed to identify influential variables and uncertainty in cost-effectiveness estimates. The main outcome measures were quality-adjusted survival after cardiac arrest, cost of hypothermia implementation, cost of posthospital discharge care, and incremental cost-effectiveness ratios. In our model, postarrest patients receiving therapeutic hypothermia gained an average of 0.66 quality-adjusted life years compared with conventional care, at an incremental cost of $31,254. This yielded an incremental cost-effectiveness ratio of $47,168 per quality-adjusted life year. Sensitivity analyses demonstrated that poor neurological outcome postcooling and costs associated with posthypothermia care (in-hospital and long term) were the most influential variables in the model. Even at extreme estimates for costs, the cost-effectiveness of hypothermia remained less than $100,000 per quality-adjusted life year. In 91% of 10,000 Monte Carlo simulations, the incremental cost-effectiveness ratio was less than $100,000 per quality-adjusted life year. In cardiac arrest survivors who meet HACA criteria, therapeutic hypothermia with a cooling blanket improves clinical outcomes with cost-effectiveness that is comparable to many economically acceptable health care interventions in the United States.

Multisite Vancomycin Intermediate-Sensitive Staphylococcus Aureus Infective Endocarditis With Giant Vegetations on Implantable Cardioverter-Defibrillator Lead

HomeCirculationVol. 119, No. 19Multisite Vancomycin Intermediate-Sensitive Staphylococcus Aureus Infective Endocarditis With Giant Vegetations on Implantable Cardioverter-Defibrillator Lead Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissionsDownload Articles + Supplements ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toSupplemental MaterialFree AccessReview ArticlePDF/EPUBMultisite Vancomycin Intermediate-Sensitive Staphylococcus Aureus Infective Endocarditis With Giant Vegetations on Implantable Cardioverter-Defibrillator Lead Henry W. Huang, Sherri Pontes and Sally B. Slome Henry W. HuangHenry W. Huang From the Permanente Medical Group Inc. Search for more papers by this author , Sherri PontesSherri Pontes From the Permanente Medical Group Inc. Search for more papers by this author and Sally B. SlomeSally B. Slome From the Permanente Medical Group Inc. Search for more papers by this author Originally published19 May 2009https://doi.org/10.1161/CIRCULATIONAHA.108.795971Circulation. 2009;119:2643–2644A 50-year-old woman was admitted to the hospital with shortness of breath, fever to 102.8°F, and leukocytosis. She had a history of nonischemic cardiomyopathy with ejection fraction of 25% to 35% and prior ventricular fibrillation arrest for which she had received a single-chamber implantable cardioverter-defibrillator about 18 months previously. She also had a history of end-stage renal disease requiring hemodialysis, diabetes mellitus, and hypertension. Over the preceding 5 months, she had experienced recurrent S. aureus dialysis catheter infections with bacteremia, for which she had received intravenous antibiotic therapy, including vancomycin.On admission to the hospital, ECG showed sinus tachycardia at 108 bpm, left atrial abnormality, and left ventricular hypertrophy with secondary repolarization abnormality (Figure 1). The initial blood cultures grew out methicillin-resistant S. aureus, and she was placed on an intravenous antibiotic regimen of daptomycin and gentamycin. Despite treatment, she continued to have persistently positive blood cultures, fevers, and leukocytosis. Download figureDownload PowerPointFigure 1. Twelve-lead ECG on admission showed sinus tachycardia at 108 bpm, left atrial abnormality, and left ventricular hypertrophy with secondary repolarization abnormality.Transesophageal echocardiography was performed to evaluate for evidence of endocarditis. Multiple large vegetations coated the defibrillator lead from the right atrium to the right ventricle (Online-only Data Supplement Movies I and II), with a giant vegetation at the level of the tricuspid valve measuring approximately 2.6×1.8 cm (online-only Data Supplement Movie III). Smaller vegetations involved the native mitral valve, with a coating of bacterial growth seen over the leaflets and annulus, invading the tissue. There appeared to be a heterogeneous mix of older calcified vegetation and newer superimposed layers of bacterial growth (online-only Data Supplement Movies IV and V). Moderate mitral regurgitation with 2 regurgitant jets, one through each leaflet, was seen (online-only Data Supplement Movie VI). The aortic valve also appeared to have a vegetation (online-only Data Supplement Movie VII).The diagnosis of multisite infective endocarditis, with primary involvement of the defibrillator lead, was made. The patient underwent emergent percutaneous lead extraction without complications. Cultures of the defibrillator lead vegetation grew out vancomycin intermediate-sensitive S. aureus. Afterward, she received a prolonged intravenous antibiotic course of linezolid, daptomycin, and gentamycin. She remained afebrile, and surveillance blood cultures were negative. However, follow-up transesophageal echocardiography showed persistent valve vegetations, and involvement of the mitral-aortic intervalvular fibrosa could not be ruled out. Cardiovascular surgery was consulted and recommended operative treatment, but the patient refused. A new defibrillator was deferred because of the risk of reinfection and could not have been accomplished via a transvenous approach because of a complete occlusion of the right innominate vein. After a prolonged hospital course, the patient died from a ventricular fibrillation arrest.This case was unusual because of the presence of concomitant left- and right-sided endocarditis affecting multiple valves and an endovascular lead. Also unusual were the size of the vegetations observed and the virulence and resistance of the microorganism involved. It is likely that the route of initial S. aureus infection was via a hemodialysis catheter in the venous circulation, leading to the development of right-sided endocarditis, followed by subsequent hematogenous spread to the left-sided valves. Repeated courses of antibiotics probably led to the high-grade resistance of the S. aureus microorganism, a sobering illustration of a problem that the medical community faces.The online-only Data Supplement is available with this article at http://circ.ahajournals.org/cgi/content/full/119/19/2643/DC1.DisclosuresNone.FootnotesCorrespondence to Henry W. Huang, MD, Kaiser Permanente Oakland, 280 W MacArthur Blvd., Oakland, CA 94611. E-mail [email protected] Previous Back to top Next FiguresReferencesRelatedDetailsCited By Xie J, Liu S, Yang J, Xu J and Zhu G (2014) Inaccuracy of transthoracic echocardiography for the identification of right‐sided vegetation in patients with no history of intravenous drug abuse or cardiac device insertion, Journal of International Medical Research, 10.1177/0300060513505498, 42:3, (837-848), Online publication date: 1-Jun-2014. May 19, 2009Vol 119, Issue 19 Advertisement Article InformationMetrics https://doi.org/10.1161/CIRCULATIONAHA.108.795971PMID: 19451366 Originally publishedMay 19, 2009 PDF download Advertisement SubjectsCatheter Ablation and Implantable Cardioverter-DefibrillatorEchocardiographyInfectious EndocarditisValvular Heart Disease

Short QT Syndrome in a Pediatric Patient

Short QT syndrome (SQTS) is a recently described genetic syndrome characterized by abnormally brisk ventricular repolarization. Similar to long QT syndrome, SQTS might result in ventricular arrhythmias, syncope, and sudden death. The clinical diagnosis of SQTS is supported by the finding of an abnormally short QT interval on the resting electrocardiogram in combination with a suggestive clinical or family history. To date, few pediatric cases have been reported and the ideal therapy is unknown. We report a teenage boy who suffered a witnessed ventricular fibrillation arrest and was subsequently diagnosed with SQTS. Additional data from nine other pediatric patients diagnosed with SQTS are presented.

Cardiac arrest survival after implementation of automated external defibrillator technology in the in-hospital setting

Survival from ventricular tachycardia (VT) or ventricular fibrillation (VF) arrest is inversely related to delay to defibrillation. The automated external defibrillator (AED) has improved survival after out-of-hospital VT/VF arrest by decreasing time to defibrillation. The purpose of this study was to determine whether survival to discharge after in-hospital cardiac arrest caused by VT/VF could be improved via an institution-wide change from a standard monophasic defibrillator to a biphasic defibrillator with AED capability. After extensive staff education, all standard defibrillators were replaced by AEDs at a single institution. Outcomes were analyzed for 1 year before the change and 1 year after the change using a prospective database. In patients whose initial rhythm was VT/VF, AEDs were not associated with improvement in time to first shock (median 1 minute for both cohorts, p = 0.79) or survival to discharge (31% vs. 29%, p = 0.8) compared with standard defibrillators. In patients whose initial rhythm was asystole or pulseless electrical activity, AEDs were associated with a significant decrease in survival (15%) compared with standard defibrillators (23%, p = 0.04). The overall AED cohort showed no difference in survival to discharge compared with the standard cohort (18% vs. 23%, p = 0.09). Replacement of standard monophasic defibrillators with biphasic AEDs was associated with unchanged survival after in-hospital VT/VF arrest and decreased survival after in-hospital asystole or pulseless electrical activity arrest.

Protozoal Hepatitis Associated with Immunosuppressive Therapy in a Dog

Protozoal Hepatitis Associated with Immunosuppressive Therapy in a Dog

Introduction of an external noninvasive cooling device for effective implementation of Intensive Care Society standards post cardiac arrest

Despite cardiac arrests accounting for 5.8% of admissions to intensive care, there is significant variation in the management and outcome of these patients in different units [1]. Randomised controlled trials have demonstrated that active cooling to 32 to 34°C for 12 to 24 hours after return of spontaneous circulation (ROSC) significantly improves the outcome of patients who have an out-of-hospital ventricular fibrillation arrest [2]. However there are a range of cooling techniques employed, and no trials have demonstrated that any particular system is superior [3].

Nasopharyngeal cooling during resuscitation: randomized study

Nasopharyngeal cooling during cardiopulmonary resuscitation has been shown to ease the resuscitation effort and to improve the resuscitation rate, survival and neurologic outcome in porcine models of both prolonged ventricular fibrillation and pulseless electrical activity arrest. The aim of this study was to determine whether nasopharyngeal cooling initiated during resuscitation improves the resuscitation rate (return of spontaneous circulation (ROSC)), survival and neurologic outcome.

Advanced Cardiac Life Support and Defibrillation in Severe Hypothermic Cardiac Arrest

The application of Advanced Cardiac Life Support (ACLS) in severe hypothermic cardiac arrest remains controversial. While the induction of mild hypothermia has been shown to improve outcomes in patients already resuscitated from cardiac arrest, it is unknown whether ACLS protocols are effective during the resuscitation of the severely hypothermic cardiac arrest patient. We describe a case of a 47-year-old man who was successfully resuscitated from a ventricular fibrillation (VF) arrest with a core body temperature of 26.4°C. The patient had been found unresponsive in a bathtub of cold water following an apparent suicide attempt. An incorrect pronouncement of death by the fire department delayed his transport to the hospital by more than four hours. Once in the emergency department (ED), the patient sustained a VF cardiac arrest and was successfully defibrillated using ACLS protocols. He ultimately survived his hospitalization with near-complete neurologic recovery. In this case report, we discuss the application of ACLS to the resuscitation of the hypothermic cardiac arrest patient as well as the issues involved in the prehospital determination of death.

Left-Dominant Arrhythmogenic Cardiomyopathy: An Under-Recognized Clinical Entity

We sought to investigate the clinical-genetic profile of left-dominant arrhythmogenic cardiomyopathy (LDAC). In the absence of coronary disease and left ventricular (LV) systolic dysfunction, lateral T-wave inversion and arrhythmia of LV origin are often considered benign. Similarly, chest pain with enzyme release might be attributed to viral myocarditis. We hypothesized that these abnormalities might be manifestations of the "left-dominant" subtype of arrhythmogenic right ventricular cardiomyopathy. The 42-patient cohort was established through clinical evaluation of individuals with unexplained (infero)lateral T-wave inversion, arrhythmia of LV origin, and/or proven LDAC/idiopathic myocardial fibrosis in the family. Patients presented from adolescence to age >80 years with arrhythmia or chest pain but not heart failure. Desmosomal mutations were identified in 8 of 24 families (15 of 33 patients). Magnetic resonance findings included LV late-enhancement in a subepicardial/midwall distribution, corresponding to fibrofatty replacement and fibrosis on histopathology. Fifty percent had previously been misdiagnosed with viral myocarditis, dilated cardiomyopathy (DCM), hypertrophic cardiomyopathy, or idiopathic ventricular tachycardia. Arrhythmic events included presentation with ventricular fibrillatory arrest in 1 patient and 2 instances of sudden cardiac death during follow-up. Arrhythmogenic cardiomyopathy is distinguished from DCM by a propensity towards arrhythmia exceeding the degree of ventricular dysfunction. The left-dominant subtype is under-recognized owing to misattribution to other disorders and lack of specific diagnostic criteria. Clinicians are alerted to the possibility of LDAC in patients of any age with unexplained arrhythmia of LV origin, (infero)lateral T-wave inversion, apparent DCM (with arrhythmic presentation), or myocarditis (chest pain and enzyme rise with unobstructed coronary arteries).

Cardiac catheterization is underutilized after in-hospital cardiac arrest

Indications for immediate cardiac catheterization in cardiac arrest survivors without ST elevation myocardial infarction (STEMI) are uncertain as electrocardiographic and clinical criteria may be challenging to interpret in this population. We sought to evaluate rates of early catheterization after in-hospital ventricular fibrillation (VF) arrest and the association with survival. Using a billing database we retrospectively identified cases with an ICD-9 code of cardiac arrest (427.5) or VF (427.41). Discharge summaries were reviewed to identify in-hospital VF arrests. Rates of catheterization on the day of arrest were determined by identifying billing charges. Unadjusted analyses were performed using Chi-square, and adjusted analyses were performed using logistic regression. One hundred and ten in-hospital VF arrest survivors were included in the analysis. Cardiac catheterization was performed immediately or within 1 day of arrest in 27% (30/110) of patients and of these patients, 57% (17/30) successfully received percutaneous coronary intervention. Of those who received cardiac catheterization the indication for the procedure was STEMI or new left bundle branch block (LBBB) in 43% (13/30). Therefore, in the absence of standard ECG data suggesting acute myocardial infarction, 57% (17/30) received angiography. Patients receiving cardiac catheterization were more likely to survive than those who did not receive catheterization (80% vs. 54%, p<.05). In patients receiving cardiac catheterization, more than half received this procedure for indications other than STEMI or new LBBB. Cardiac catheterization was associated with improved survival. Future recommendations need to be established to guide clinicians on which arrest survivors might benefit from immediate catheterization.

Magnitude and Prognosis Associated With Ventricular Arrhythmias in Patients Hospitalized With Acute Coronary Syndromes (from the GRACE Registry)

The incidence, prognosis, and factors associated with ventricular arrhythmia (VA) in acute coronary syndrome are unknown. We sought to examine the magnitude, predictors, and outcomes of in-hospital VA in patients with acute coronary syndrome. The population comprised 52,380 patients enrolled in the Global Registry of Acute Coronary Events from 1999 to 2005. The proportion who developed VA during hospitalization was 6.9% (1.8% with ventricular tachycardia, 5.1% with ventricular fibrillation or cardiac arrest). The incidence of in-hospital VA decreased over time (8.0% in 1999, 7.0% in 2002, 5.8% in 2005, p <0.001). In-hospital case-fatality rates were higher in patients with versus those without VA (52% vs 1.6%). Several demographic and clinical variables were associated with the occurrence of VA including ST deviation, Killip class, age, initial cardiac markers, serum creatinine and heart rate, and history of selected co-morbidities. Six-month postdischarge mortality was higher in survivors of in-hospital VA versus those who did not develop VA during hospitalization (odds ratio 1.57, 95% confidence interval 1.27 to 1.95). In conclusion, development of VA during hospitalization for acute coronary syndrome was associated with higher in-hospital and 6-month mortalities.