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PubMed2005

Incidence of EMS-treated out-of-hospital cardiac arrest in Europe.

BACKGROUND: The potential impact of efforts in Europe to improve survival from out-of-hospital cardiac arrest is unclear, in part, because estimates of incidence and survival are uncertain. The aim of the investigation was to determine a representative European incidence and survival from cardiac arrest in all-rhythms and in ventricular fibrillation treated by the emergency medical services (EMS). METHODS AND RESULTS: We used Medline to identify peer-reviewed articles published between 1 January 1980 and 30 June 2004 that reported a European community's EMS cardiac arrest experience. Inclusion criteria required the study to include at least 25 cases, report of the total number of all-rhythm and/or ventricular fibrillation arrests, and information about population size and study duration. The incidence was computed by dividing the total number of events by the product of the community's population and the study duration. Reports from 37 communities met the inclusion criteria. A total of 18,105 all-rhythm EMS-treated cardiac arrests occurred during 48 million person-years of observation, resulting in an overall incidence for all-rhythm arrests of 37.72 per 100,000 person-years. Incidence of ventricular fibrillation arrest was 16.84 per 100,000 person-years. Survival was 10.7% for all-rhythm and 21.2% for ventricular fibrillation cardiac arrest. Applying these results to the European population, approximately, 275,000 persons would experience, all-rhythm cardiac arrest treated by the EMS with 29,000 persons surviving to hospital discharge. CONCLUSION: The results provide a framework to assess opportunities and limitations of EMS care with regard to the public health burden of cardiac arrest in Europe.

Cardiopulmonary Resuscitation↗
PubMed1991

Increased risk of death and cardiac arrest from encainide and flecainide in patients after non-Q-wave acute myocardial infarction in the Cardiac Arrhythmia Suppression Trial. CAST Investigators.

This report examines whether in the Cardiac Arrhythmia Suppression Trial death and cardiac arrest from encainide, flecainide and moricizine during the titration phase and from encainide and flecainide during the follow-up phase were related to presence (Q-wave acute myocardial infarction [Q-AMI]) or absence (non-Q-AMI) of pathologic Q waves. In all, 2,371 patients (70% with Q-AMI, 26% with non-Q-AMI, and 4% unknown) entered the titration phase, starting 117 +/- 163 days after index AMI and lasting for an average of 21 days. For the titration phase, no significant differences existed between Q-AMI and non-Q-AMI patients for death and cardiac arrest rate, ventricular premature complex suppression rate, and nonrandomization rate. A total of 1,498 patients entered the follow-up phase of an average of 10 months (starting 129 +/- 158 days after the index AMI), and were randomized to encainide or flecainide, or their matching placebos. In the placebo group, non-Q-AMI patients had a significantly lower rate of death and cardiac arrest than Q-AMI patients (1.0 and 4.6%, respectively; p = 0.04). Encainide and flecainide significantly elevated death and cardiac arrest rate in both non-Q-AMI patients (8.7%, p less than 0.01) and Q-AMI patients (7.8%, p = 0.04). The relative risk for encainide or flecainide over placebo in the non-Q-AMI patients was 8.7, which was significantly higher than 1.7 observed for the Q-AMI patients (p = 0.03). None of the baseline characteristics had any significant interaction with encainide or flecainide.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Complexes, Premature↗
PubMed2005

In-hospital cardiac arrest.

To review the current management of in-hospital cardiac arrest and to identify variables that influence outcomes, OLDMEDLINE from 1950 to 1966 and MEDLINE from 1966 to March 2005 were searched using the keywords cardiopulmonary resuscitation, cardiac arrest, in hospital, and adult. Secondary sources were derived from review publications and personal communications by one of the authors. There is no secure evidence that the ultimate outcomes after cardiopulmonary resuscitation in settings of in-hospital cardiac arrest have improved in the >40 yrs that followed the landmark report by Kouwenhoven, Jude, and Knickerbocker, which launched the modern era of cardiopulmonary resuscitation. A paucity of objective measurements preclude secure protocols for sequencing of interventions and, even more, when to initiate and discontinue cardiopulmonary resuscitation. The preparedness of both physicians and nursing professionals to implement the published guidelines has itself been questioned. Whereas early access defibrillation with automated external defibrillators may be of benefit in out-of-hospital settings, there has as yet been no secure evidence that automated external defibrillators have had a favorable impact on in-hospital cardiopulmonary resuscitation when used on infrequent occasions by first responders. This contrasts with the much greater success of advanced life support providers and especially when electrical defibrillation is promptly performed by expertly trained personnel after onset of cardiac arrest. Outcomes are therefore improved in critical care settings and especially in coronary care units in which patients are continuously monitored.

Cardiopulmonary Resuscitation↗
PubMed2001

Astroglial protein S-100 is an early and sensitive marker of hypoxic brain damage and outcome after cardiac arrest in humans.

BACKGROUND: The results of early conventional tests do not correlate with cerebral outcome after cardiac arrest. We investigated the serum levels of astroglial protein S-100 as an early marker of brain damage and outcome after cardiac arrest. METHODS AND RESULTS: In 66 patients undergoing cardiopulmonary resuscitation after nontraumatic cardiac arrest, blood samples for the evaluation of S-100 were drawn immediately after and 15, 30, 45, and 60 minutes; 2, 8, 24, 48, and 72 hours; and 7 days after initiation of cardiopulmonary resuscitation. Moreover, the serum levels of neuron-specific enolase were determined between 2 hours and 7 days. If patients survived for >48 hours, brain damage was assessed by a combination of neurological, cranial CT, and electrophysiological examinations. Overall, 343 blood samples were taken for the determination of S-100. Maximum S-100 levels within 2 hours after cardiac arrest were significantly higher in patients with documented brain damage (survivors and nonsurvivors, 3.70+/-0.77 microg/L) than in patients without brain damage (0.90+/-0.29 microg/L). Significant differences between these 2 groups were observed from 30 minutes until 7 days after cardiac arrest. In addition, the positive predictive value of the S-100 test at 24 hours for fatal outcome within 14 days was 87%, and the negative predictive value was 100% (P<0.001). With regard to neuron-specific enolase, significant differences between patients with documented brain damage and those with no brain damage were found at 24, 48, and 72 hours and 7 days. CONCLUSIONS: Astroglial protein S-100 is an early and sensitive marker of hypoxic brain damage and short-term outcome after cardiac arrest in humans.

Adult↗
PubMedDate not supplied

Hippocampal damage in the human brain after cardiac arrest.

BACKGROUND AND PURPOSE: Very few reports are available on changes in the human hippocampus after cardiac arrest. The objective of this study was to investigate if specific hippocampal volume losses can be demonstrated in the human brain following reperfusion after cardiac arrest. METHODS: We assessed the volumes of the hippocampal formation (HF) and temporal lobe excluding HF (TL) as the contrast using magnetic resonance (MR)-imaging-based volumetry in 11 vegetative patients after cardiac arrest and in 22 healthy controls of similar age, sex and body size distribution. The measured volumes were normalized for differences in the head size among subjects by dividing by the total intracranial volume (TICV). The MR images of the 11 patients were obtained between days 8 and 21 after cardiac arrest. RESULTS: The observed volumes of HFs and TLs of both patient and control groups were as follows: right HF volume (HFV): 2.67 +/- 0.19 (mean +/- SD, cm(3)) in patients versus 3.89 +/- 0.44 in controls; left HFV: 2.72 +/- 0.17 versus 3.74 +/- 0.35; right TL volume (TLV): 73.37 +/- 6.54 versus 80.08 +/- 7.62, and left TLV: 72. 45 +/- 6.77 versus 78.59 +/- 6.68. The normalized indices (HFV/TICV and TLV/TICV) were as follows: right HF: 0.0021 +/- 0.0002 (mean +/- SD) in patients versus 0.0031 +/- 0.0001 in controls, p < 0.0001, left HF: 0.0022 +/- 0.0002 versus 0.0030 +/- 0.0001, p < 0.0001, right TL: 0.058 +/- 0.002 versus 0.064 +/- 0.004, p = 0.0007, and left TL: 0.058 +/- 0.002 versus 0.062 +/- 0.004, p = 0.0014. The HFV-TLV ratios (HFV/TICV divided by TLV/TICV) of both groups were: right HFV-TLV ratio: 0.037 +/- 0.004 in patients versus 0.049 +/- 0. 004 in controls, p < 0.0001, left HFV-TLV ratio: 0.038 +/- 0.004 versus 0.048 +/- 0.004, p < 0.0001. CONCLUSIONS: The patient group had HFs that were 26.8-30.6% smaller than those of the control group, but in the patient group, the TLs slightly decreased in size by only 7.8-8.2% of the volume of those in the control group within 21 days after cardiac arrest. The volume reductions in the bilateral HFs of patients after cardiac arrest were significantly larger than those in the bilateral TLs. We speculate that this specific rapid hippocampal shrinkage reflects its greater vulnerability to global brain ischemia.

Aged↗
PubMed2004

In-hospital cardiac arrest: survival depends mainly on the effectiveness of the emergency response.

OBJECTIVES: To evaluate the factors affecting the outcome of in-hospital cardiac arrest. SETTING: A 1400-bed tertiary care teaching hospital with a dedicated cardiac arrest team (CAT). The CAT was immediately available in monitored areas (intensive care unit and emergency room). In the wards the staff had only BLS skills and automated external defibrillation was not available. METHODS: A 2-year prospective audit according to the Utstein style. RESULTS: A total of 114 cardiac arrests (37 with VF/VT and 77 with non-VF/VT) were included. Fifty-two cardiac arrests (46%) occurred in monitored areas, 62 (54%) occurred in non-monitored areas. The CAT arrival time in non-monitored areas was 3.98+/-1.73 min. Thirty-seven patients (32%) survived to hospital discharge. Cardiac arrests occurring in monitored areas had a significantly better outcome than those occurring in the wards. Patient survival in the wards was significantly higher when the CAT arrival time was less than 3 min. No patient whose CAT arrival time was longer than 6 min survived. CAT arrival time was significantly shorter (1.30+/-1.70) in survivors than in non-survivors (2.51+/-2.37; P<0.005). Sex, age and presence of bystanders were not significantly associated with survival. CONCLUSIONS: In our setting, where bystander defibrillation was not available, the survival of patients having cardiac arrest in non-monitored areas strongly depends on advanced life support provided by the CAT. A faster CAT response and early defibrillation from the ward staff are the most important improvements necessary to increase cardiac arrest survival in our setting.

Adult↗
PubMed1983

Prolonged hypoperfusion in the cerebral cortex following cardiac arrest and resuscitation in dogs.

Increasing cerebral vascular resistance and brain perfusion failure occur within 90 minutes following cardiac arrest and resuscitation. This study followed cortical perfusion for 18 hours after a 15-minute cardiac arrest. Six dogs were anesthetized with ketamine and gallamine and then mechanically ventilated. They were instrumented for arterial pressure, central venous pressure, and regional cerebral cortical blood flow (rCCBF) determined by thermodilution. A left thoracotomy and pericardiotomy were done. Two dogs served as non-arrest controls. Cardiac arrest was produced in four dogs with an intravenous bolus of KCl at 1 mEq/kg. After 15 minutes of cardiac arrest, the animals were resuscitated with internal massage, NaHCO3, epinephrine, and internal defibrillation. Cortical blood flow was followed for 18 hours. Arterial core temperature was never less than 35 C. Pre-arrest cortical blood flows were 0.86 cc/min/g (+/- 0.11). The two control animals had stable rCCBF (0.74 +/- 0.17) for all determinations during the 18-hour follow-up period. Determinations of rCCBF from 6 to 18 hours in post-arrest animals were 7% to 14% of pre-arrest values. We conclude that the post-resuscitation perfusion failure in the cortex is prolonged. Any potential for neuronal recovery, unless perfusion is protected, would not be realized given this phenomenon.

Animals↗
PubMed1991

Brain nuclear DNA survives cardiac arrest and reperfusion.

Iron-mediated peroxidation of brain lipids is known to occur during reperfusion following cardiac arrest. Since in vitro damage to DNA is caused by similar iron-dependent peroxidation, we tested whether free radical damage to genomic DNA also develops during reperfusion following cardiac arrest and resuscitation. Genomic DNA was isolated from the cerebral cortex in (i) normal dogs, (ii) dogs subjected to a 20-min cardiac arrest, and (iii) dogs resuscitated from a 20-min cardiac arrest and then allowed to reperfuse for 2 or 8 h. DNA strand nicks were evaluated by in vitro labeling of newly created 3' and 5' termini. DNA base damage was evaluated utilizing reaction with piperidine prior to labeling of 5' termini. The 3' DNA termini were labeled before and after digestion with exonuclease III, and the 5' DNA termini were labeled before and after treatment with piperidine. In vitro experiments with genomic DNA damaged by oxygen radicals verified that these labeling methods identified radical damage. In the experimental animal groups, terminal incorporation and electrophoretic mobility of brain nuclear DNA are not significantly changed either by 20 min of complete brain ischemia or during the first 8 h of reperfusion. We conclude that genomic DNA is not extensively damaged during cardiac arrest and early reperfusion, and therefore such DNA damage does not appear to be an important early aspect of the neurologic injury that accompanies cardiac arrest and resuscitation.

Animals↗
PubMed2006

Percutaneous coronary intervention for cardiac arrest secondary to ST-elevation acute myocardial infarction. Influence of immediate paramedical/medical assistance on clinical outcome.

BACKGROUND: Patients with cardiac arrest have been excluded from most randomized trials on percutaneous coronary intervention (PCI) for acute myocardial infarction (AMI). OBJECTIVE: The aim of the study was to evaluate the outcome of patients undergoing primary PCI for acute myocardial infarction who suffered from cardiac arrest prior to the procedure, focusing the study on the influence of immediate paramedical-medical assistance on the outcome. METHODS AND RESULTS: Sixty-three patients with ST-elevation AMI and previous cardiac arrest underwent primary PCI within 12 hours after symptom onset. Three groups of patients were defined: Group 1: Cardiac arrest before hospital admission, without immediate (< 1 minute) initiation of resuscitation maneuvers (n = 13); Group 2: Pre-hospital cardiac arrest with immediate initiation of resuscitation maneuvers (n = 14); Group 3: Cardiac arrest after hospital admission. The proportion of patients with ventricular tachycardia or fibrillation as documented initial rhythm was similar among the groups (77%, 79% and 83%, respectively), as well as the rate of angiographic success (92%, 93% and 86%, respectively). However, the incidence of cardiac events at 30 days was significantly higher in Group 1 than in Groups 2 or 3 (54%, 29% and 17%, respectively; p = 0.03), as well as the mortality rate at 30 days (46%, 21% and 18%, respectively; p = 0.06). Interestingly, the outcomes were not statistically different between Groups 2 and 3. In multivariate analysis, the independent predictors for mortality at 30 days for Group 1 were: multivessel disease, angiographic failure and cardiogenic shock. CONCLUSIONS: Combining immediate initiation of resuscitation maneuvers and primary PCI yields a very good clinical outcome in patients with AMI suffering from cardiac arrest.

Adult↗
PubMed2006

Traumatic cardiac arrest: who are the survivors?

STUDY OBJECTIVE: Survival from traumatic cardiac arrest is poor, and some consider resuscitation of this patient group futile. This study identified survival rates and characteristics of the survivors in a physician-led out-of-hospital trauma service. The results are discussed in relation to recent resuscitation guidelines. METHODS: A 10-year retrospective database review was conducted to identify trauma patients receiving out-of-hospital cardiopulmonary resuscitation. The primary outcome measure was survival to hospital discharge. RESULTS: Nine hundred nine patients had out-of-hospital cardiopulmonary resuscitation. Sixty-eight (7.5% [95% confidence interval 5.8% to 9.2%]) patients survived to hospital discharge. Six patients had isolated head injuries and 6 had cervical spine trauma. Eight underwent on-scene thoracotomy for penetrating chest trauma. Six patients recovered after decompression of tension pneumothorax. Thirty patients sustained asphyxial or hypoxic insults. Eleven patients appeared to have had "medical" cardiac arrests that occurred before and was usually the cause of their trauma. One patient survived hypovolemic cardiac arrest. Thirteen survivors breached recently published guidelines. CONCLUSION: The survival rates described are poor but comparable with (or better than) published survival rates for out-of-hospital cardiac arrest of any cause. Patients who arrest after hypoxic insults and those who undergo out-of-hospital thoracotomy after penetrating trauma have a higher chance of survival. Patients with hypovolemia as the primary cause of arrest rarely survive. Adherence to recently published guidelines may result in withholding resuscitation in a small number of patients who have a chance of survival.

Cardiopulmonary Resuscitation↗
PubMed1995

In-hospital mortality after out-of-hospital cardiac arrest.

In-hospital management of out-of-hospital cardiac arrest is complicated by uncertainty about prognosis and the need to identify markers of adverse outcome in individuals surviving initial resuscitation. We sought to identify factors that predict in-hospital death among patients who initially survive out-of-hospital cardiac arrest. We investigated 346 consecutive cases of out-of-hospital cardiac arrest received by a single centre in Edinburgh, UK (270 cases examined retrospectively, 76 prospectively). Of the retrospective cohort, 246 cases were thought to be of cardiac origin. There were associations between in-hospital mortality and pre-arrest variables, resuscitation variables, and factors measured during admission. Crew-witnessed arrests were associated with low mortality; arrest rhythm (p < 0.001), resuscitation by a health professional (p < 0.05), conscious level on admission (p < 0.001), and requirement for ventilation (p < 0.05) independently predicted in-hospital mortality. A weighted prognostic scoring system based on three of these variables accurately predicted the likelihood of in-hospital death in the prospective test group. Further assessment of conscious level during admission with the Glasgow coma score predicted mortality rates in the study population, but coma did not predict a hopeless prognosis in individual cases unless it persisted for 72 h or more. Accurate prognostic assessment of out-of-hospital cardiac arrest survivors can be made from information available on admission. Of factors that independently predicted outcome, the skill of the resuscitator is most readily modified. This suggests that public training in resuscitation may reduce mortality rates.

Adult↗
PubMed2005

Survival from in-hospital cardiac arrest: the potential impact of infection.

OBJECTIVE: The aim of this study was to examine the relationship between outcome from cardiac arrest and infection status at the time of in-hospital cardiac arrest. DESIGN: This was a retrospective database review from a single resuscitation service supporting two major hospitals. SETTING: Two urban University Hospitals in London. PATIENTS: Data from 1436 in-patient cardiac arrest were available for analysis. INTERVENTIONS: Nil. MEASUREMENTS AND RESULTS: Patients were classified into infected or non-infected groups by the resuscitation audit process and the hospitals diagnostic coding unit. Survival was followed according to the in-hospital Utstein timepoints. In addition, the data were examined by presenting the cardiac rhythm. Age and length of prior hospitalisation were recorded. Infection associated diagnoses appear to be increasing in prevalence. Initial survival from cardiac arrest was not affected by infection status, but this did have a substantial impact on chance of leaving the initial hospital (odds ratio 0.52, confidence intervals 0.3-0.8), or being discharged to home (odds ratio 0.48, confidence intervals 0.4-0.8). The outcome from ventricular fibrillation/pulseless ventricular tachycardia was worse for infected patients (odds ratio for home discharge 0.37, confidence intervals 0.2-0.9), although initial survival was not significantly different. CONCLUSIONS: Infection may be becoming an increasingly important association with cardiac arrest in the hospitalised population. Initial survival from cardiac arrest is the same as for non-infected patients, but longer term survival is much poorer. Long-term survival from ventricular fibrillation or pulseless ventricular tachycardia is relatively poor, in spite of similar initial success.

Adolescent↗
PubMed2000

Chronicity of memory impairment in long-term out-of-hospital cardiac arrest survivors.

As a result of out-of-hospital defibrillation initiatives, many cities have an increasing population of out-of-hospital cardiac arrest survivors. We previously identified that one third of these patients suffer memory problems in the months after resuscitation. The pattern of memory impairment (impaired recall memory and intact recognition memory) is suggestive of hippocampal damage. In this study we followed up ten subjects who had previously been found to have memory impairment after their cardiac arrest. To assess the chronicity of this memory impairment, we re-tested memory function approximately 3 years after the index events. These subjects were compared with age and sex matched control subjects with previous myocardial infarction and no cardiac arrest. Memory was assessed using the Rivermead Behavioural Memory test (RBMT). To further assess recall and recognition memory we used the Doors and People test (DPT), which is specifically designed to identify deficits in these functions. RBMT scores declined significantly in both groups compared with the original assessment 8 months after cardiac arrest, possibly an effect of ageing-control group: mean (S.D.) 22.2 (1. 4)-18.4 (2.9); cardiac arrest group: 16.1 (2.7)-14.6 (4.4). The inter-group difference in RBMT score remained significant (P=0.001). DPT scores were poor in the cardiac arrest group (mean (S.D.) total 5.8 (2.8)), compared with the control group (10.8 (3.4)) who scored normally. Both recall and recognition memory were poor in the cardiac arrest group. We conclude that the memory deficits that we previously observed in cardiac arrest victims are persistent. Both recall and recognition memory are affected, implying that non-selective brain injury may be the mechanism.

Aged↗
PubMed1997

The association between blood lactate concentration on admission, duration of cardiac arrest, and functional neurological recovery in patients resuscitated from ventricular fibrillation.

OBJECTIVE: To assess the association between arterial lactate concentration on admission and the duration of human ventricular fibrillation cardiac arrest, and to what degree the arterial lactate concentration on admission is an early predictor of functional neurological recovery in human cardiac arrest survivors. DESIGN: Cohort study. Arterial lactate concentrations and out-of-hospital data concerning cardiac arrest and cardiopulmonary resuscitation were collected retrospectively according to a standardized protocol. Functional neurological recovery was assessed prospectively at regular intervals for 6 months. SETTING: Emergency department of an urban tertiary care hospital. PATIENTS: A total of 167 primary survivors of witnessed out-of-hospital ventricular fibrillation cardiac arrest. MEASUREMENTS: The association between arterial lactate concentration on admission, the duration of cardiac arrest, and functional neurological recovery was assessed. Further, we assessed whether admission concentrations of arterial lactate and duration of cardiac arrest can predict unfavorable functional neurological recovery. Functional neurological recovery was measured in cerebral performance categories (CPC). No or minimal functional impairment (CPC 1 and 2) was defined as favorable outcome; the remaining categories (CPC 3, 4 and 5) were defined as unfavorable functional neurological recovery. RESULTS: In 167 patients, a weak association between total duration of cardiac arrest and admission levels of lactate (r = 0.49, P < 0.001) could be shown. With increasing admission concentrations of arterial lactate functional neurological recovery was more likely to be unfavorable (OR 1.15 per mmol/l increase, 95% CI 1.04-1.27). Nevertheless, only at very high levels of lactate (16.3 mmol/l) could unfavorable neurological recovery be detected with 100% specificity, yielding a very low sensitivity of 16%. CONCLUSIONS: The arterial admission lactate concentration after out-of-hospital ventricular fibrillation cardiac arrest is a weak measure of the duration of ischemia. High admission lactate levels are associated with severe neurological impairment. However, this parameter has poor prognostic value for individual estimation of the severity of subsequent functional neurological impairment.

Aged↗
PubMed1999

A cumulative meta-analysis of the effectiveness of defibrillator-capable emergency medical services for victims of out-of-hospital cardiac arrest.

STUDY OBJECTIVE: More than 1,000 patients experience sudden cardiac arrest each day. Treatment for this includes cardiopulmonary resuscitation (CPR) and emergency medical services (EMS) that provide CPR-basic life support (BLS), BLS with defibrillation (BLS-D), or advanced life support (ALS). Our previous systematic review of treatments for sudden cardiac arrest was limited by suboptimal data. Since then, debate has increased about whether bystander CPR is effective or whether attention should focus instead on rapid defibrillation. Therefore a cumulative meta-analysis was conducted to determine the relative effectiveness of differences in the defibrillation response time interval, proportion of bystander CPR, and type of EMS system on survival after out-of-hospital cardiac arrest. METHODS: A comprehensive literature search was performed by using a priori exclusion criteria. We considered EMS systems that provided BLS-D, ALS, BLS plus ALS, or BLS-D plus ALS care. A generalized linear model was used with dispersion estimation for random effects. RESULTS: Thirty-seven eligible articles described 39 EMS systems and included 33,124 patients. Median survival for all rhythm groups to hospital discharge was 6.4% (interquartile range, 3.7 to 10.3). Odds of survival were 1.06 (95% confidence interval [CI], 1.03 to 1.09; P <.01) per 5% increase in bystander CPR. Survival was constant if the defibrillation response time interval was less than 6 minutes, decreased as the interval increased from 6 to 11 minutes, and leveled off after 11 minutes (P <.01). Compared with BLS-D, odds of survival were as follows: ALS, 1. 71 (95% CI, 1.09 to 2.70; P =.01); BLS plus ALS, 1.47 (95% CI, 0.89 to 2.42; P =.07); and BLS with defibrillation plus ALS, 2.31 (95% CI, 1.47 to 3.62; P <.01.) CONCLUSION: We confirm that greater survival after sudden cardiac arrest is associated with provision of bystander CPR, early defibrillation, or ALS. More research is required to evaluate the relative benefit of early defibrillation versus early ALS.

Electric Countershock↗
PubMed2001

Improving survival from sudden cardiac arrest: the role of the automated external defibrillator.

CONTEXT: Sudden cardiac death is a major public health problem in the United States, and improving survival after out-of-hospital cardiac arrest has been the subject of intense study. Early defibrillation has been shown to be critical to improving survival. Use of automated external defibrillators (AEDs) has become an important component of emergency medical systems, and recent advances in AED technology have allowed expansion of AED use to nontraditional first responders and the lay public. OBJECTIVES: To examine advancements in AED technology, review the impact of AEDs on time to defibrillation and survival, and explore the future role of AEDs in the effort to improve survival following sudden cardiac arrest. DATA SOURCES: MEDLINE was searched for articles from 1966 through December 2000 (Medical Subject Headings: electric countershock, heart arrest, resuscitation, emergency medical services; keywords: automatic external defibrillator, automated external defibrillator, public access defibrillation). Reference lists of relevant articles, news releases, and product information from manufacturers were also reviewed. STUDY SELECTION: Initial MEDLINE search produced 4816 articles, from which 101 articles were selected for referencing based on having been published in a peer-reviewed journal and on relevance to the subject of the manuscript as determined by all 5 authors. DATA EXTRACTION: All studies were critically reviewed for relevance, accuracy, and quality of data and study design by all authors. DATA SYNTHESIS: Recent advances in AED technology and design have resulted in marked simplification of AED operation, improvements in accuracy and effectiveness, and reductions in cost. Use of AEDs by first responders and laypersons has reduced time to defibrillation and improved survival from sudden cardiac arrest in several communities. Initial studies of the cost-effectiveness of AED use in comparison with other commonly used treatments are favorable. CONCLUSION: The AED represents an efficient method of delivering defibrillation to persons experiencing out-of-hospital cardiac arrest and its use by both traditional and nontraditional first responders appears to be safe and effective. The rapidly expanding role of AEDs in traditional emergency medical systems is supported by the literature, and initial studies of public access to defibrillation offer hope that further improvements in survival after sudden cardiac death can be achieved.

Cost-Benefit Analysis↗
PubMed2006

Therapeutic hypothermia after cardiac arrest.

PURPOSE OF REVIEW: Patients who are successfully resuscitated following cardiac arrest often have a significant medical condition termed postresuscitation disease. This includes myocardial stunning, metabolic abnormalities and neurologic injury from global ischemia. There are no clinical signs or diagnostic tests for 24-72 h to distinguish patients who will and will not recover neurologic function. RECENT FINDINGS: Therapeutic hypothermia had been advocated for decades as a treatment to improve neurologic outcome after cardiac arrest. The early studies focused on moderate hypothermia, which was associated with complications and was not clearly beneficial. Over the past decade, studies have focused on mild hypothermia with target temperatures of 32-34 degrees C. Two recent multicentered, randomized, controlled trials have demonstrated improved neurologic outcome with mild therapeutic hypothermia applied to comatose survivors after cardiac arrest compared with a normothermic control group. SUMMARY: As a result of these studies the International Liaison Committee on Resuscitation recommends that 'Unconscious adult patients with spontaneous circulation after out-of-hospital cardiac arrest should be cooled to 32 degrees C to 34 degrees C for 12 to 24 hours when the initial rhythm was ventricular fibrillation'. Mild therapeutic hypothermia should also be considered for patients with in-hospital arrest and asystole and pulseless electrical activity who are comatose after return of spontaneous circulation.

Cardiopulmonary Resuscitation↗
PubMed2000

The incidence of pulmonary embolism in unexplained sudden cardiac arrest with pulseless electrical activity.

PURPOSE: The cause of many cases of sudden cardiac arrest from pulseless electrical activity is unknown. We hypothesized that pulmonary embolism was responsible for a substantial proportion of these cases and used transesophageal echocardiography to identify pulmonary embolism among patients with sudden cardiac arrest. SUBJECTS AND METHODS: We performed a prospective study at a tertiary care, university-operated county hospital, with a level 1 trauma center. Consecutive patients (n = 36) who were admitted with (n = 20) or unexpectedly developed (n = 16) sudden cardiac arrest of unknown cause were studied with transesophageal echocardiography during cardiopulmonary resuscitation. We determined the presence of central pulmonary embolism, right ventricular enlargement, and other causes of sudden cardiac arrest (such as myocardial infarction and aortic dissection) using prospectively defined criteria. RESULTS: Of the 25 patients with pulseless electrical activity as the initial event, 9 (36%) had pulmonary emboli (8 seen with transesophageal echocardiography and 1 diagnosed at autopsy) compared with none of the 11 patients with other rhythms, such as asystole or ventricular tachycardia or fibrillation (P = 0.02). Of the 8 patients who had pulmonary embolism diagnosed by transesophageal echocardiography, 2 survived to hospital discharge. CONCLUSIONS: Mortality from massive pulmonary embolism is high, particularly if patients present with sudden cardiac arrest. Earlier diagnosis of pulmonary embolus may permit wider use of thrombolytic agents or other interventions and may potentially increase survival.

Aged↗