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PubMed2001

A comparison of myocardial function after primary cardiac and primary asphyxial cardiac arrest.

Although myocardial dysfunction after resuscitation from ventricular fibrillation (VF) has been extensively investigated, less is known of the function of the myocardium after asphyxial cardiac arrest. The present experimental study was designed to compare postresuscitation left ventricular (LV) function after cardiac arrest caused by asphyxia with that of cardiac arrest induced by dysrhythmia. Four groups of Sprague-Dawley rats, which included eight animals in each group, were investigated. In the first two groups, cardiac arrest followed asphyxia produced by neuromuscular blockade with and without airway obstruction. In a third group, cardiac arrest was induced by electrical fibrillation of the ventricle. The fourth group represented animals in which the duration of asphyxial cardiac arrest was maintained for a time interval corresponding to that of the VF group. The fourth group received approximately the same number of electrical shocks as the third (VF) group. All animals were successfully resuscitated with precordial compression and mechanical ventilation. Postresuscitation measurements, including cardiac output, LV end-diastolic pressure (LVEDP), rate of pressure rise at LV pressure of 40 mm Hg (LV dP/dt40), and negative LV dP/dt, demonstrated decreased myocardial function in each group. No differences in cardiac function were observed between the animals with primary respiratory arrest whether or not the airway was obstructed. However, disproportionate and consistently greater impairment in myocardial function followed primary cardiac arrest due to VF when compared with equal duration of asphyxial cardiac arrest. We conclude that in this healthy animal model, asphyxial cardiac arrest resulted in significantly lesser impairment of postresuscitation myocardial function when compared with cardiac arrest caused by VF.

Animals↗

PubMed2002

The identification of risk factors for cardiac arrest and formulation of activation criteria to alert a medical emergency team.

AIM: (1) To identify risk factors for in-hospital cardiac arrest; (2) to formulate activation criteria to alert a clinical response culminating in attendance by a Medical Emergency Team (MET); (3) to evaluate the sensitivity and specificity of the scoring system. METHODS: Quasi-experimental design to determine prevalence of risk factors for cardiac arrest in the hospitalised population. Weighting of risk factors and formulation of activation criteria to alert a graded clinical response. ROC analysis of weighted cumulative scores to determine their sensitivity and specificity. SETTING: An acute 700 bed district general hospital with 32,348 adult admissions in 1999 and a catchment population of around 365,000. SUBJECTS: 118 consecutive adult patients suffering primary cardiac arrest in-hospital and 132 non-arrest patients, randomly selected according to stratified randomisation by gender and age. RESULTS: Risk factors for cardiac arrest include: abnormal respiratory rate (P = 0.013), abnormal breathing indicator (abnormal rate or documented shortness of breath) (P < 0.001), abnormal pulse (P < 0.001), reduced systolic blood pressure (P < 0.001), abnormal temperature (P < 0.001), reduced pulse oximetry (P < 0.001), chest pain (P < 0.001) and nurse or doctor concern (P < 0.001). Multivariate analysis of cardiac arrest cases identified three positive associations for cardiac arrest: abnormal breathing indicator (OR 3.49; 95% CI: 1.69-7.21), abnormal pulse (OR 4.07; 95% CI: 2.0-8.31) and abnormal systolic blood pressure (OR 19.92; 95% CI: 9.48-41.84). Risk factors were weighted and tabulated. The aggregate score determines the grade of clinical response. ROC analysis determined that a score of 4 has 89% sensitivity and 77% specificity for cardiac arrest; a score of 8 has 52% sensitivity and 99% specificity. All patients scoring greater than 10 suffered cardiac arrest. CONCLUSION: Risk factors for cardiac arrest have been identified, quantified and formulated into a table of activation criteria to help predict and avert cardiac arrest by alerting a clinical response. A graded clinical response has resulted in a tool that has both sensitivity and specificity for cardiac arrest.

Adolescent↗

PubMed2006

Vasopressin or epinephrine for out-of-hospital cardiac arrest.

STUDY OBJECTIVE: The use of vasopressin in patients with cardiac arrest presenting with specific rhythms is controversial. We performed an evidence-based emergency medicine review of evidence comparing vasopressin to epinephrine in structured cardiac arrest protocols. METHODS: We searched MEDLINE, EMBASE, the Cochrane Library, and other databases for randomized trials or systematic reviews comparing vasopressin to epinephrine for adults with cardiac arrest and measuring survival to hospital discharge and neurologic function in survivors. We used standard criteria to appraise the quality of published trials and systematic reviews. We used the random effects model in supplementary analyses to summarize results and to test for significant differences across subgroups of patients presenting with different arrest rhythms. RESULTS: We found 3 high-quality well-reported randomized trials and 1 rigorous meta-analysis. The evidence does not confirm a consistent benefit of vasopressin over epinephrine in increasing survival or improving neurologic outcome in survivors. Subgroup analysis reveals a large difference in effect of vasopressin over epinephrine in cardiac arrest patients with asystole, compared to other arrest rhythms, coming from within-trial comparisons. The difference is not consistent across otherwise similar trials, is not statistically significant, may reflect the application of multiple unplanned subgroup analyses, and is not supported by a plausible biological hypothesis. CONCLUSION: Evidence from randomized trials does not establish a benefit of vasopressin over epinephrine in increasing survival to discharge or improving neurologic outcomes in adult patients with nontraumatic cardiac arrest.

Brain Damage, Chronic↗

PubMed1990

Hyperkalaemia during rapid blood transfusion and hypovolaemic cardiac arrest in children.

A morbidity and mortality review documented a high occurrence of hyperkalaemia in cardiac arrests associated with rapid blood transfusion, which resulted in further study. In order to stimulate events during rapid blood transfusion and cardiac arrest, the central circulation was modeled as a linear one compartment, and used to stimulate a child who suffered a hypovolaemic cardiac arrest and was resuscitated with rapid blood transfusion (RBT). The simulation suggested that the combination of RBT and a low cardiac output state could be associated with hyperkalaemia, if the potassium concentration in the plasma fraction of the transfused blood was greater than or equal to 10 mmol.L-1. In an associated clinical study the plasma potassium concentration during cardiac arrest was documented from a retrospective review of 138 cardiac arrests in a paediatric population. Patients were divided into two groups. The RBT-group received a rapid blood transfusion during resuscitation. The non-RBT group did not receive blood during resuscitation. During cardiac arrest the plasma [K] in the non-RBT group was 5.63 +/- 2.39 mmol.L-1 compared with 8.23 +/- 1.99 mmol.L-1 in the RBT-group (P less than 0.05). The hyperkalaemia during cardiac arrest in the RBT-group could be explained as a consequence of RBT to a hypovolaemic child with a low cardiac output.

Adolescent↗

PubMed1983

Intellectual and social function of patients surviving cardiac arrest outside the hospital.

Thirteen survivors of cardiac arrest outside the hospital were examined by clinical and psychological tests 1-3 years after the incidence, and compared to a matched control group of 13 patients with acute myocardial infarction without cardiac arrest. Psychological tests revealed that 7 patients with previous cardiac arrest and 4 control patients had mild-moderate to moderate-severe dementia. The demential symptoms were not detectable by a clinical interview. Four patients in each group exhibited pronounced anxiety symptoms. There were no clear differences between the two groups in respect of changes in cardiac function and social status after the incidence.

Adult↗

PubMed2006

Out-of-hospital cardiac arrest in Victoria: rural and urban outcomes.

OBJECTIVE: To compare the survival rate from out-of-hospital cardiac arrest in rural and urban areas of Victoria, and to investigate the factors associated with these differences. DESIGN: Retrospective case series using data from the Victorian Ambulance Cardiac Arrest Registry. SETTING: All out-of-hospital cardiac arrests occurring in Victoria that were attended by Rural Ambulance Victoria or the Metropolitan Ambulance Service. PARTICIPANTS: 1790 people who suffered a bystander-witnessed cardiac arrest between January 2002 and December 2003. RESULTS: Bystander cardiopulmonary resuscitation was more likely in rural (65.7%) than urban areas (48.4%) (P = 0.001). Urban patients with bystander-witnessed cardiac arrest were more likely to arrive at an emergency department with a cardiac output (odds ratio [OR], 2.92; 95% CI, 1.65-5.17; P < 0.001), and to be discharged from hospital alive than rural patients (urban, 125/1685 [7.4%]; rural, 2/105 [1.9%]; OR, 4.13; 95% CI, 1.09-34.91). Major factors associated with survival to hospital admission were distance of cardiac arrest from the closest ambulance branch (OR, 0.87; 95% CI, 0.82-0.92), endotracheal intubation (OR, 3.46; 95% CI, 2.49-4.80), and the presence of asystole (OR, 0.50; 95% CI, 0.38-0.67) or pulseless electrical activity (OR, 0.73; 95% CI, 0.56-0.95) on arrival of the first ambulance crew. CONCLUSIONS: Survival rates differ between urban and rural cardiac arrest patients. This is largely due to a difference in ambulance response time. As it is impractical to substantially decrease response times in rural areas, other strategies that may improve outcome after cardiac arrest require investigation.

Aged↗

PubMed1984

Abnormal quinidine binding in survivors of prehospital cardiac arrest.

Quinidine binding was studied in 15 survivors of prehospital cardiac arrest and was compared to 18 normal individuals and 20 patients with coronary artery disease. The unbound quinidine fraction was 6.3 +/- 2.8% in the survivors of prehospital cardiac arrest, a value significantly lower than normal individuals (unbound quinidine fraction = 9.9 +/- 3.0%, p less than 0.005). Furthermore, unbound quinidine fraction correlated with interdose quinidine half-life in the six survivors of prehospital cardiac arrest where this could be measured (r = 0.79, p less than 0.05). The resultant quinidine interdose half-life was significantly prolonged (10 +/- 3 hours) when compared to normal (6 +/- 2 hours, p less than 0.02). The reduction in free drug fraction in cardiac arrest survivors was a nonspecific finding in that free drug fraction was also reduced in the patients with coronary artery disease (unbound quinidine fraction = 7.4 +/- 3%) and was independent of the alpha-1-glycoprotein concentration. Therefore survivors of prehospital cardiac arrest have a mean 40% reduction in free quinidine drug fraction which results in less free drug at any given total drug concentration and may relate to quinidine pharmacokinetics and pharmacodynamics in this patient group.

Blood Proteins↗

PubMedDate not supplied

Estimating cost-effectiveness of mass cardiopulmonary resuscitation training strategies to improve survival from cardiac arrest in private locations.

INTRODUCTION: Most cardiopulmonary resuscitation (CPR) trainees are young, and most cardiac arrests occur in private residences witnessed by older individuals. OBJECTIVE: To estimate the cost-effectiveness of a CPR training program targeted at citizens over the age of 50 years compared with that of current nontargeted public CPR training. METHODS: A model was developed using cardiac arrest and known demographic data from a single suburban zip code (population 36,325) including: local data (1997-1999) regarding cardiac arrest locations (public vs. private); incremental survival with CPR (historical survival rate 7.8%, adjusted odds ratio for CPR 2.0); arrest bystander demographics obtained from bystander telephone interviews; zip code demographics regarding population age and distribution; and 12.50 dollars per student for the cost of CPR training. Published rates of CPR training programs by age were used to estimate the numbers typically trained. Several assumptions were made: 1) there would be one bystander per. arrest; 2) the bystander would always perform CPR if trained; 3) cardiac arrest would be evenly distributed in the population; and 4) CPR training for a proportion of the population would proportionally increase CPR provision. Rates of arrest, bystanders by age, number of CPR trainees needed to result in increased arrest survival, and training cost per life saved for a one-year study period were calculated. RESULTS: There were 24.3 cardiac arrests per year, with 21.9 (90%) occurring in homes. In 66.5% of the home arrests, the bystander was more than 50 years old. To yield one additional survivor using the current CPR training strategy, 12,306 people needed to be trained (3,510 bystanders aged < or = 50 years and 8,796 bystanders aged > 50 years), which resulted in CPR provision to 7.14 additional patients. The training cost per life saved for a bystander aged < or = 50 years was 313,214 dollars, and that for a bystander aged > 50 years was 785,040 dollars. Using a strategy of training only those < or = 50 years, 583 elders per cardiac arrest would need to be trained, with a cost of 53,383 dollars per life saved. CONCLUSION: Using these assumptions, current CPR training strategy is not a cost-effective intervention for home cardiac arrests. The high rate of elders witnessing CPR mandates focused CPR interventions for this population.

Aged↗

PubMed2003

Cardiac arrest in dialysis patients: approaches to alter an abysmal outcome.

Cardiac disease is the major cause of death in dialysis patients, accounting for 45% of all-cause mortality. Sudden cardiac death may be implicated in 60% of these cardiac deaths in dialysis patients. The combination of obstructive coronary artery disease, electrolyte shifts (in hemodialysis patients), left ventricular hypertrophy, and abnormal myocardial ultrastructure and function may contribute to the vulnerability of ESRD patients to sudden death. In this review, the epidemiology of cardiac arrest in dialysis patients is presented, including the high lethality associated with cardiac arrest. Clinical strategies to reduce the likelihood of fatal cardiac arrest include the identification of high-risk patients, alteration of dialysis prescription to avoid large volume and electrolyte shifts, and reduction of myocardial ischemic burden. Implantable cardioverter defibrillators may potentially reduce the risk of fatal cardiac arrest in dialysis patients and improve long-term cardiac survival.

Heart Arrest↗

PubMed1995

Epinephrine and high-flow reperfusion after cardiac arrest in a canine model.

STUDY OBJECTIVES: Epinephrine has been used in cardiac arrest to increase the low blood flow generated by standard CPR methods. Reperfusion with high flow such as that obtained with cardiopulmonary bypass (CPB) may obviate the need for or alter the dose of epinephrine after cardiac arrest. The objective of this study was to evaluate the effect of high-flow reperfusion after cardiac arrest with and without epinephrine on coronary perfusion pressure, defibrillation energy, restoration of spontaneous circulation (ROSC), and 2-hour survival after prolonged cardiac arrest. DESIGN: Prospective, randomized, double-blind, placebo-controlled study using a canine model. INTERVENTIONS: Thirty mongrel dogs were randomized to receive, after ventricular fibrillation cardiac arrest of 12 minutes' duration without CPR, placebo (n = 10), standard-dose epinephrine (.02 mg/kg) (n = 10), or high-dose epinephrine (.2 mg/kg) (n = 10) during reperfusion with CPB. Epinephrine or placebo was given with the start of CPB and then every 5 minutes, followed by countershock until ROSC or crossover at the fourth dose to high-dose epinephrine. RESULTS: ROSC was achieved in the first 15 minutes of bypass in 10 of 10 dogs given high-dose epinephrine, in 9 of 10 given standard-dose epinephrine, and in 1 of 10 given placebo. After the crossover to high-dose epinephrine, ROSC was achieved in 8 of 10 dogs originally given placebo and the remaining animal given the standard dose of epinephrine. During early reperfusion, the high-dose group had a higher mean coronary perfusion pressure (high dose, 153 + 62 mm Hg; standard dose, 81 +/- 18 mm Hg; placebo, 51 +/- 15 mm Hg; P < .002) and a shorter mean ROSC time (high dose, 16.2 +/- 8 minutes; standard dose, 20.3 +/- 3.6 minutes; placebo, 27.9 +/- 3.2; P < .02) and required less defibrillation energy. CPB flow during ventricular fibrillation was 63% of baseline cardiac output in all three groups. Two-hour survival was 5 of 10 in the high-dose group, 8 of 10 in the standard-dose group, and 5 of 10 in the placebo group. CONCLUSION: Restoration of high blood flow alone is insufficient to restore spontaneous circulation after prolonged cardiac arrest. Epinephrine, when administered early under high-flow conditions, increases coronary perfusion pressure, decreases defibrillation energy, and decreases time elapsed before ROSC. Higher doses of epinephrine under conditions of high-flow reperfusion do not improve 2-hour survival compared with standard-dose epinephrine.

Animals↗

PubMed2005

Clinical investigation: thyroid function test abnormalities in cardiac arrest associated with acute coronary syndrome.

INTRODUCTION: It is known that thyroid homeostasis is altered during the acute phase of cardiac arrest. However, it is not clear under what conditions, how and for how long these alterations occur. In the present study we examined thyroid function tests (TFTs) in the acute phase of cardiac arrest caused by acute coronary syndrome (ACS) and at the end of the first 2 months after the event. METHOD: Fifty patients with cardiac arrest induced by ACS and 31 patients with acute myocardial infarction (AMI) who did not require cardioversion or cardiopulmonary resuscitation were enrolled in the study, as were 40 healthy volunteers. The patients were divided into three groups based on duration of cardiac arrest (<5 min, 5-10 min and >10 min). Blood samples were collected for thyroid-stimulating hormone (TSH), tri-iodothyronine (T3), free T3, thyroxine (T4), free T4, troponin-I and creatine kinase-MB measurements. The blood samples for TFTs were taken at 72 hours and at 2 months after the acute event in the cardiac arrest and AMI groups, but only once in the control group. RESULTS: The T3 and free T3 levels at 72 hours in the cardiac arrest group were significantly lower than in both the AMI and control groups (P < 0.0001). On the other hand, there were no significant differences between T4, free T4 and TSH levels between the three groups (P > 0.05). At the 2-month evaluation, a dramatic improvement was observed in T3 and free T3 levels in the cardiac arrest group (P < 0.0001). In those patients whose cardiac arrest duration was in excess of 10 min, levels of T3, free T3, T4 and TSH were significantly lower than those in patients whose cardiac arrest duration was under 5 min (P < 0.001, P < 0.001, P < 0.005 and P < 0.05, respectively). CONCLUSION: TFTs are significantly altered in cardiac arrest induced by ACS. Changes in TFTs are even more pronounced in patients with longer periods of resuscitation. The changes in the surviving patients were characterized by euthyroid sick syndrome, and this improved by 2 months in those patients who did not progress into a vegetative state.

Cardiopulmonary Resuscitation↗

PubMed1991

Potential complications of high-dose epinephrine therapy in patients resuscitated from cardiac arrest.

Adults resuscitated from nontraumatic cardiac arrest who received intravenous epinephrine in doses chosen by the treating physician and who survived at least 6 hours were studied to determine if high-dose epinephrine produced more complications than standard-dose. A total of 68 patients were enrolled and evaluated for postresuscitation complications attributable to epinephrine, using a two-tailed t test, and contingency analysis. The 33 patients receiving high-dose epinephrine and 35 patients receiving standard-dose epinephrine were similar in demographics and variables known to affect outcome. There was no difference in potential complications between groups except serum calcium, which was 1.97 mmol/L (SD, 0.20) in the high-dose epinephrine group and 2.10 (SD, 0.20) in the standard-dose group. Hospital discharge rates (18% in the high-dose vs 30% in the standard-dose group) and neurological status on discharge were not significantly different. High-dose epinephrine did not produce increased direct complications in this cardiac arrest population compared with standard-dose epinephrine.

Aged↗

PubMedDate not supplied

Characteristics and outcome among patients with a suspected in-hospital cardiac arrest.

AIM: To describe the characteristics and outcome among patients with a suspected in-hospital cardiac arrest. METHODS: All the patients who suffered from a suspected in-hospital cardiac arrest during a 14-months period, where the cardiopulmonary resuscitation (CPR) team was called, were recorded and described prospectively in terms of characteristics and outcome. RESULTS: There were 278 calls for the CPR team. Of these, 216 suffered a true cardiac arrest, 16 a respiratory arrest and 46 neither. The percentage of patients who were discharged alive from hospital was 42% for cardiac arrest patients, 62% for respiratory arrest and 87% for the remaining patients. Among patients with a cardiac arrest, those found in ventricular fibrillation/ventricular tachycardia had a survival rate of 64%, those found in asystole 24% and those found in pulseless electrical activity 10%. Among patients who were being monitored at the time of arrest, the survival rate was 52%, as compared with 27% for non-monitored patients (P= 0.001). Among survivors of cardiac arrest, a cerebral performance category (CPC) of 1 (no major deficit) was observed in 81% at discharge and in 82% on admission to hospital prior to the arrest. CONCLUSION: We conclude that, during a 14-month period at Sahlgrenska University Hospital in Göteborg, almost half the patients with a cardiac arrest in which the CPR team was called were discharged from hospital. Among survivors, 81% had a CPC score of 1 at hospital discharge. Survival seems to be closely related to the relative effectiveness of the resuscitation organisation in different parts of the hospital.

Adolescent↗

PubMed2005

Back from irreversibility: extracorporeal life support for prolonged cardiac arrest.

BACKGROUND: The survival of patients after prolonged cardiac arrest is still inadequate. Extracorporeal life support (ECLS) represents an alternative therapeutic method for patients who do not respond to conventional cardiopulmonary cerebral resuscitation. This technology is used to support the circulation of a patient with severe cardiac failure. METHODS: Between June 1997 and January 2003, 40 ECLS procedures were performed in patients who presented with refractory cardiac arrest. During external cardiac massage, the patient was connected to an extracorporeal circuit by the insertion of an arterial and venous cannula through the femoral vessels. The extracorporeal circuit included a centrifugal pump and an oxygenator. Mean age was 42 +/- 15 years; the average time of external cardiac massage was 105 +/- 44 minutes. RESULTS: Once the circulation was restored, 22 patients were disconnected from the extracorporeal circulation because of brain death or multiorgan failure; after 24 hours, among the 18 survivors, 6 were weaned off the pump, 9 were bridged to a ventricular assist device, and 2 patients were directly bridged to cardiac transplantation. Eight patients are alive and without any sequelae at 18 month's follow-up. CONCLUSIONS: In prolonged cardiac arrest with failing conventional measures, rescue by extracorporeal support provides an ultimate therapeutic option with a good outcome in survivors. Our results encourage the wider application of ECLS for refractory cardiocirculatory arrest in selected patients. The high rate of neurologic death needs further improvements in the early phase of resuscitation maneuvers.

Adult↗

PubMed2006

Allelic variants of SCN5A and risk of sudden cardiac arrest in patients with coronary artery disease.

BACKGROUND: Most sudden cardiac arrests occur in patients who have associated significant coronary artery disease (CAD), but current methods of risk stratification are inadequate. OBJECTIVES: The purpose of this study was to evaluate whether allelic variation of SCN5A could determine risk of sudden cardiac arrest among patients with CAD. METHODS: This case-control study was conducted as part of the ongoing Oregon Sudden Unexpected Death Study (Ore-SUDS). Cases of sudden cardiac arrest with associated CAD were identified among residents of Multnomah County, Oregon (population 660,486). Geographically matched control subjects had significant CAD but no history of cardiac arrest, ventricular arrhythmia, or syncope. DNA was extracted from blood samples, and all 28 exons of SCN5A were screened for allelic variants using denaturing high-performance liquid chromatography. All identified variants were confirmed by direct sequencing. RESULTS: Sixty-seven cases (mean age 65 +/- 13 years, 18% female) and 91 controls (mean age 66 +/- 12 years, 30% female) were compared. Race was known in 94% of all patients; 92% of case subjects and 89% of control subjects were Caucasian. No patient had clinically manifest familial long QT syndrome. Nonsynonymous nucleotide changes were found in 4% of cases and 1% of controls (P = .31), with one novel mutation (G1291A) identified in one case subject. Synonymous nucleotide changes were found in 27% of cases and 21% of controls (P = .45). CONCLUSION: The overall prevalence of amino acid-altering polymorphisms of the SCN5A gene was relatively low in both groups. Allelic variants of SCN5A did not contribute to risk of sudden cardiac arrest in this primarily Caucasian population with significant CAD.

Aged↗

PubMed1989

Long-term outcome of patients with hypertrophic cardiomyopathy successfully resuscitated after cardiac arrest.

This study describes the long-term outcome of 33 patients with hypertrophic cardiomyopathy who experienced a cardiac arrest but were successfully resuscitated. Cardiac arrest occurred at ages 9 to 62 years (mean 32); five patients survived multiple (two or three) arrests. A variety of treatments were administered; 18 patients with left ventricular outflow tract obstruction underwent ventricular septal myotomy-myectomy or mitral valve replacement and also received drug therapy; 15 patients received medical therapy alone. To date, 22 (67%) of the 33 patients have survived after the initial cardiac arrest for periods of 17 months to 22 years (mean 7 years); 12 patients have survived for greater than or equal to 5 and 6 for greater than or equal to 10 years. Of the 22 survivors, 16 have remained asymptomatic or only mildly symptomatic over the period of follow-up; 6 others have become severely symptomatic with heart failure, including 3 with evidence of left ventricular wall thinning and cavity enlargement. Eight patients ultimately died of natural cardiac causes (suddenly or of progressive heart failure) 7 months to 8.4 years (mean 4 years) after their initial cardiac arrest. Actuarial patient survival was 97 +/- 3%, 74 +/- 9% and 61 +/- 11% after 1, 5 and 10 years, respectively. Event-free rate (defined as actuarial survival without recurrent cardiac arrest of death) was 83 +/- 7%, 65 +/- 9% and 53 +/- 11%, respectively. For this group of patients with hypertrophic cardiomyopathy who were treated in a nonsystematic fashion with a variety of therapeutic strategies, the long-term outcome after surviving a cardiac arrest was variable.(ABSTRACT TRUNCATED AT 250 WORDS)

Actuarial Analysis↗

PubMed1992

Influence of coronary bypass surgery on subsequent outcome of patients resuscitated from out of hospital cardiac arrest.

The effect of coronary bypass surgery on recurrent cardiac arrest was estimated in 265 patients resuscitated from out of hospital cardiac arrest between 1970 and 1988. From this cohort, 85 patients (32%) underwent coronary bypass surgery after recovery from cardiac arrest and 180 patients (68%) were treated medically. A multivariate Cox analysis was used to estimate the effect of coronary bypass surgery on subsequent survival after adjusting for effects of age, prior cardiac history, ejection fraction, year of the event, history of angina, antiarrhythmic drug use and whether the arrest was related to acute myocardial infarction. The use of coronary bypass surgery had a significant effect in reducing the incidence of subsequent cardiac arrest during follow-up study (risk ratio [RR] 0.48, 95% confidence interval [CI] 0.24 to 0.97, p less than 0.04). There was also a trend consistent with a reduction in total cardiac mortality (RR 0.65, 95% CI 0.39 to 1.10, p = 0.10). These findings suggest that coronary bypass surgery may reduce the incidence of sudden death in suitable patients resuscitated from an episode of ventricular fibrillation.

Cohort Studies↗

PubMed2001

Fatal and non fatal cardiac arrests related to anesthesia.

PURPOSE: The aim of this study was to assess the incidence and causes of cardiac arrests related to anesthesia. METHODS: All patients undergoing anesthesia over a six year period were included in a prospective study. The cardiac arrests encountered during anesthesia and the first twelve postoperative hours in the PACU or ICU were analysed. For each arrest, partially or totally related to anesthesia, the sequence of events leading to the accident was evaluated. RESULTS: Eleven cardiac arrests related to anesthesia were identified among the 101,769 anesthetic procedures (frequency: 1.1/10,000 [0.44-1.72]). Mortality related to anesthesia was 0.6/10,000 [0.12-1.06]. Age over 84 yr and an ASA physical status > 2 were found to be risk factors of cardiac arrest related to anesthesia. The main causes of anesthesia related cardiac arrest were anesthetic overdose (four cases), hypovolemia (two cases) and hypoxemia due to difficult tracheal intubation (two cases). No cardiac arrests due to alveolar hypoventilation were noted during the postoperative periods in either PACU or ICU. At least one human error was noted in ten of the eleven cardiac arrests cases, due to poor preoperative evaluation in seven. All cardiac arrests totally related to anesthesia were classified as avoidable. CONCLUSION: Efforts must be directed towards improving preoperative patient evaluation. Anesthetic induction doses should be titrated in all ASA 3 and 4 patients. The prediction of difficult tracheal intubation, and if required, the use of awake tracheal intubation techniques, should remain a priority when performing general anesthesia.

Adolescent↗