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Demographics of cardiac arrest: association with residence in a low-income area.

OBJECTIVE: To report cardiac arrest demographics and assess whether arrest rate is associated with differences in intracity regional population densities, incomes, or race distributions. METHODS: One-year retrospective review of out-of-hospital cardiac arrests in a city with a two-tier emergency medical service (EMS) system. Associations of population density, median income, and race data with age- and gender-adjusted cardiac arrest rates for seven city regions and groupings of high- and low-income census tracts were made. RESULTS: Median income, but not race or population density, was associated with sex- and age-adjusted intracity regional cardiac arrest rates (p = 0.034). This association of cardiac arrest rate with income status was magnified when the 20 lowest and the 20 highest income census tracts were compared. Cardiac arrest victims in these two income groups did not differ in regard to rate of witnessed arrest, bystander-administered CPR, or previous cardiac disease. Rates of survival to hospital discharge were not significantly different between the two groups. CONCLUSION: The association of lower income with cardiac arrest suggests that cardiac health promotion and EMS intervention measures, including CPR instruction, should be targeted to lower-income neighborhoods. These findings may help explain previous studies suggesting a racial or population density association with cardiac arrest rates.

Cardiopulmonary Resuscitation↗

Diagnosis of unexplained cardiac arrest: role of adrenaline and procainamide infusion.

BACKGROUND: Cardiac arrest with preserved left ventricular function may be caused by uncommon genetic conditions. Although these may be evident on the ECG, long-term monitoring or provocative testing is often necessary to unmask latent primary electrical disease. METHODS AND RESULTS: Patients with unexplained cardiac arrest and no evident cardiac disease (normal left ventricular function, coronary arteries, and resting corrected QT) underwent pharmacological challenge with adrenaline and procainamide infusions to unmask subclinical primary electrical disease. Family members underwent noninvasive screening and directed provocative testing on the basis of findings in the proband. Eighteen patients (mean+/-SD age, 41+/-17 years; 11 female) with unexplained cardiac arrest were assessed. The final diagnosis was catecholaminergic ventricular tachycardia (CPVT) in 10 patients (56%), Brugada syndrome in 2 patients (11%), and unexplained (idiopathic ventricular fibrillation) in 6 patients (33%). Of 55 family members (mean+/-SD age, 27+/-17 years; 33 female), 9 additional affected family members were detected from 2 families, with a single Brugada syndrome patient and 8 CPVT patients. CONCLUSIONS: Provocative testing with adrenaline and procainamide infusions is useful in unmasking the etiology of apparent unexplained cardiac arrest. This approach helps to diagnose primary electrical disease, such as CPVT and Brugada syndrome, and provides the opportunity for therapeutic intervention in identified, asymptomatic family members who harbor the same disease.

Anti-Arrhythmia Agents↗

Turkey slaughtering procedures: time to loss of brain responsiveness after exsanguination or cardiac arrest.

The effect of inducing a cardiac arrest or severing both carotid arteries on the spontaneous and visual evoked electrical activity in the brain were examined in anaesthetised turkeys. The time to loss of evoked activity was greater following the cardiac arrest. It was concluded that the potential humanitarian advantages of inducing a cardiac arrest at stunning are less pronounced in the turkey than for other poultry species.

Abattoirs↗

THE CHEMOTHERAPY OF CARDIAC ARREST.

Direct-air ventilation, external cardiac compression, and external defibrillation are established techniques for patients who unexpectedly develop cardiac arrest. The proper use of drugs can increase the incidence of successful resuscitation. Intracardiac adrenaline (epinephrine) acts as a powerful stimulant during cardiac standstill and, in addition, converts fine ventricular fibrillation to a coarser type, more responsive to electrical defibrillation. Routine use of intravenous sodium bicarbonate is recommended to combat the severe metabolic acidosis accompanying cardiac arrest. Lidocaine is particularly useful when ventricular fibrillation or ventricular tachycardia tends to recur. Analeptics are contraindicated, since they invariably increase oxygen requirements of already hypoxic cerebral tissues. The following acrostic is a useful mnemonic for recalling the details of the management of cardiac arrest in their proper order: A (Airway), B (Breathing), C (Circulation), D (Diagnosis of underlying cause), E (Epinephrine), F (Fibrillation), G (Glucose intravenously), pH (Sodium bicarbonate), I (Intensive care).

Acidosis↗

Cardiac arrest calls in a general hospital.

All acute hospitals have a cardiac arrest team. A retrospective study of cardiac arrest calls prospectively recorded over a 24-month period was performed. 174 cardiac arrest calls were analyzed with 76 of these calls being false alarms. Only 16.5% of patients survived to discharge. Median age of patients suffering a cardiopulmonary arrest was 71.5 years (range 22-96 years) with an arrest occurring a median of 2 days post admission (range 0-83 days). A pilot study to determine physiological deterioration in the 24 hours prior to cardiac arrest was also performed. 45% of patients demonstrated a physiological deterioration over this time. Recommendations are made regarding the management of in-hospital cardiac arrests.

Adult↗

Leisure-time physical activity and the risk of primary cardiac arrest.

BACKGROUND: Because the risks of sudden cardiac death and myocardial infarction are transiently increased during acute bouts of high-intensity activity, it is an important question from the public health perspective whether regular participation in moderate-intensity activity confers overall protection from sudden cardiac death. PARTICIPANTS AND METHODS: We used data from a population-based case-control study to assess the associations of regular high-intensity and moderate-intensity leisure-time physical activity with primary cardiac arrest. Cases were patients with primary cardiac arrest, aged 25 to 74 years, attended by paramedics between 1988 and 1994 in King County, Washington (n = 333). Controls were randomly identified from the same community (n = 503), matched for age and sex. All case patients and controls were free of prior clinical heart disease, major comorbidity, and self-reported poor health. Spouses of case patients and controls were interviewed to assess participation in 15 high-intensity and 6 moderate-intensity physical activities during the prior year. RESULTS: Compared with subjects who performed none of the activities, the odds ratio for primary cardiac arrest from matched analyses was 0.34 (95% confidence interval, 0.13-0.89) among subjects who performed only gardening activities for more than 60 minutes per week; 0.27 (95% confidence interval, 0.11-0.67) among subjects who walked for exercise for more than 60 minutes per week; and 0.34 (95% confidence interval, 0.16-0.75) among subjects who engaged in any high-intensity activities, after adjustment for age, smoking, education, diabetes, hypertension, and health status. CONCLUSIONS: The results suggest that regular participation in moderate-intensity activities, such as walking and gardening, are associated with a reduced risk of PCA and support current exercise recommendations.

Adult↗

Survival after sudden cardiac arrest in hospital.

Although there are many reports on sudden cardiac arrest occurring outside the hospital, little is known about the precise prognostic factors that determine the outcome after cardiopulmonary resuscitation. Clinical information before and immediately after sudden cardiac arrest is frequently incomplete because the event occurs outside the hospital. We studied 90 consecutive patients with sudden and unexpected cardiac arrest who were resuscitated in the general ward of our hospital. Twenty-five (28%) were discharged from the hospital. Multivariate analysis revealed that the promptness of initiation of CPR, age, severity of cardiac dysfunction, time and the type of arrhythmia are of significance in relation to survival. To evaluate long-term survival after hospital cardiac arrest, we analyzed long-term follow-up data accumulated during a 16 year period. In the group of 25 patients in our study, there have been a total of 10 deaths (40%). Five of the 10 deaths resulted from recurrent cardiac arrest and 1 was a noncardiac death. There was a high rate of recurrence of cardiac arrest in the first year following resuscitation, especially among the cardiomyopathy patients.

Adolescent↗

Characteristics of the resuscitated out-of-hospital cardiac arrest victim with coronary heart disease.

The clinical entry characteristics and medical history of 142 resuscitated out-of-hospital cardiac arrest victims with coronary heart disease were studied in order to identify factors that affect their long-term survival. The cardiac arrest event was classified as being secondary to an acute myocardial infarction (AMI) in 44% (62 of 142), an ischemic event (IE) in 34% (49 of 142) and a primary arrhythmic event (PAE) in 22% (31 of 142). The majority of patients in all groups had a history of angina pectoris. Twenty-seven percent of the AMI, 55% of the IE, and 71% of the PAE patients had a history of infarction. Ten percent of the AMI, 31% of the IE, and 55% of the PAE had used digitalis before their cardiac arrest. Cardiac arrest was the first cardiac event in 35% of the AMI, 16% of the IE and 6% of the PAE patients. One year after arrest, 89% of the AMI, 80% of the IE and 71% of the PAE were alive (p less than 0.01). Covariate analysis for more than 40 variables indicates that a high-risk group included 22% (31 of 142) of the cardiac arrest victims had 1- and 2-year survival rates of 71% and 55%, respectively, and was characterized as having used digitalis before arrest, experiencing blood urea nitrogen elevation and pulmonary congestion during the hospitalization for the event, and classification of the cardiac arrest event as a PAE. A low-risk group comprised 78% (111 of 142) of the survivors and had 1- and 2-year survival rates of 85% and 69%, respectively. These data indicate that cardiac arrest due to coronary heart disease is secondary to several mechanisms related to subsequent survival.

Acute Disease↗

Cardiac arrests in skilled nursing facilities: continuing room for improvement?

OBJECTIVES: To characterize the care received by skilled nursing facility (SNF/NF) patients suffering cardiac arrest and to evaluate the outcome of SNF/NF patients experiencing cardiac arrest. DESIGN: A retrospective analysis of an existing cardiac arrest registry to characterize SNF/NF cardiac arrest patients and to compare them to community-dwelling cardiac arrest patients was performed. SETTING: The study took place in Rochester, NY, an urban city in upstate New York with approximately 220,000 residents. PARTICIPANTS: All patients for whom emergency medical services (EMS) assistance was requested via the 911 system and who were treated for cardiac arrest between January 1998 and December 2001 were included. MEASUREMENTS: Demographic characteristics such as age, gender, race; clinical characteristics and interventions such as cardiopulmonary resuscitation (CPR), defibrillation, initial cardiac rhythm, and call response interval; outcomes measures such as return of spontaneous circulation and 1-year survival were obtained. RESULTS: Forty-two (8%) of cardiac arrest patients resided in an SNF/NF. Sixteen (38%) of the events were witnessed arrests. Only 28 (67%) patients received CPR and none were defibrillated prior to EMS arrival. One (2%) patient was alive 1 year after the event, a survival rate similar to the community-dwelling population (5%). CONCLUSION: SNF/NF patients suffering cardiac arrest often did not receive CPR or defibrillation while awaiting EMS arrival. SNF/NF patients suffering cardiac arrest have a very low survival rate, similar to the community-dwelling population. The impact of not providing CPR and defibrillation on the survival rate is unclear, but needs to be evaluated prior to any decisions regarding the medical futility of resuscitating SNF/NF patients.

Aged↗

Electron microscopic investigation of rat brain after brief cardiac arrest.

Rats were submitted to 10-min cardiac arrest, followed by resuscitation and survival for 1 day, 3 days or 1 week. Five regions of interest (CA1 and CA3 sector of hippocampus, dentate gyrus, reticular nucleus of thalamus and parietal cortex) where studied by light and electron microscopy at each of the survival times, and compared with non-ischemic control rats. Cell counts revealed delayed neuronal loss of about 30% after 3 days in both CA1 and CA3 sectors. Ischemic cell changes consisting of cytoplasmic condensation and nuclear pyknosis appeared in these regions on day 7 and --to a lesser degree-- also affected dentate gyrus, the reticular nucleus of thalamus and cerebral cortex. Ultrastructural alterations were evaluated using an ultrastructural injury catalogue. In all brain regions similar, although quantitatively differently expressed, changes occurred except ribosomal disaggregation, which was restricted to neurons of hippocampal CA1 sector on the first day after cardiac arrest. Progressive alterations included swelling of mitochondria and endoplasmic reticulum, which was most pronounced in CA1 and CA3 sectors of hippocampus, as well as chromatin aggregation and alterations of neuronal volume, which affected mainly the granule cells of dentate gyrus. Other alterations, such as osmiophilic inclusions or the formation of nuclear pore complexes, were transient with a maximum on the first day after cardiac arrest. Treatment with the free-radical scavenger alpha-phenyl-N-tert-butyl nitrone (PBN) suppressed the formation of nuclear pores but otherwise did not markedly change the morphological outcome. In comparison to previous studies of global brain ischemia induced by arterial inflow occlusion of the same duration, the present data demonstrate remarkable preservation of tissue integrity in CA1 sector but also distinct changes in brain regions considered to be resistant to ischemic injury. Morphological alterations of brain after cardiac arrest do not follow the established pattern of selective vulnerability.

Animals↗

Arterial blood pressure after human cardiac arrest and neurological recovery.

BACKGROUND AND PURPOSE: In animal cardiac arrest studies, outcome has been improved by inducing arterial hypertension early after return of spontaneous circulation. The aim of our study was to evaluate whether arterial blood pressure within the first minutes and hours after return of spontaneous circulation influences neurological recovery in human cardiac arrest survivors. METHODS: Of 136 retrospectively evaluated patients after sudden cardiac death, two groups were defined: group 1, mean arterial blood pressure (MABP) within 5 minutes after return of spontaneous circulation above 100 mm Hg; group 2, MABP of 100 mm Hg or less. Thereafter MABP was measured every 5 minutes until 2 hours after return of spontaneous circulation. The groups were compared in regard to age, sex, in/out of hospital, witnessed/not witnessed, first electrocardiographic rhythm, time from cardiac arrest to beginning of life support and to return of spontaneous circulation, cumulative epinephrine dose administered, and best neurological outcome within 6 months. RESULTS: In group 1 (n = 54) good neurological recovery was observed in 63% and in group 2 (n = 82) in 55% (chi 2 = 0.87, P = NS). Both groups exhibited comparable baseline values except that time intervals from beginning of life support to return of spontaneous circulation were shorter in group 1. After we controlled for this difference with Spearman's partial rank correlation (rs), there was no association between MABP measured within the first 5 minutes and outcome (rs = -.023; P = NS). Good neurological recovery was independently and directly related to MABP measured during 2 hours after return of spontaneous circulation (rs = .26; P < .01). CONCLUSIONS: In human cardiac arrest survivors, good functional neurological recovery was independently and positively associated with arterial blood pressure during the first 2 hours after human cardiac arrest but not with hypertensive reperfusion within the first minutes after return of spontaneous circulation.

Aged↗

Antioxidant Tempol enhances hypothermic cerebral preservation during prolonged cardiac arrest in dogs.

The authors are systematically exploring pharmacologic preservation for temporarily unresuscitable exsanguination cardiac arrest in dogs. They hypothesized that the antioxidant Tempol improves cerebral outcome when added to aortic saline flush at the start of cardiac arrest. In study A, no drug (n = 8), Tempol 150 mg/kg (n = 4), or Tempol 300 mg/kg (n = 4) was added to 25 mL/kg saline flush at 24 degrees C (achieving mild cerebral hypothermia) at the start of 20-minute cardiac arrest. In study B, no drug (n = 8) or Tempol 300 mg/kg (n = 7) was added to 50 mL/kg saline flush at 2 degrees C (achieving moderate cerebral hypothermia) at the start of 40-minute cardiac arrest. Cardiac arrest was reversed with cardiopulmonary bypass. Mild hypothermia lasted for 12 hours, controlled ventilation was sustained to 24 hours, and intensive care was provided for up to 72 hours. In study A, overall performance category 1 or 2 (good outcome) was achieved in all eight dogs treated with Tempol compared with three of eight dogs in the control group ( P = 0.03). In study B, good outcome was achieved in all seven dogs treated with Tempol versus only two of 8 dogs in the control group ( P = 0.007). In both studies, neurologic deficit scores were significantly better in the Tempol group, but not total histologic damage scores. At 72 hours, electron paramagnetic resonance spectroscopy of Tempol revealed direct evidence for its presence in the brain. Single- and double-strand DNA damage, nitrotyrosine immunostaining, total antioxidant reserve, and ascorbate acid levels were similar between groups, and thiol levels were decreased after Tempol in study B. The authors conclude that when added to aortic saline flush at the start of prolonged cardiac arrest, the antioxidant Tempol can enhance mild or moderate hypothermic cerebral preservation in terms of improved functional outcome. The mechanisms involved in this beneficial effect need further clarification.

Animals↗

Adult cardiac arrest in general practice.

BACKGROUND: Out of hospital cardiac arrest victims contribute significantly to adult mortality figures but are encountered infrequently by most general practitioners and their staff. A number of scientific organisations produce guidelines for the basic and advanced management of cardiac arrest. OBJECTIVE: To review the management principles for basic and advanced adult cardiac life support measures for cardiac arrest. DISCUSSION: General practitioners are required to manage cardiac arrest victims infrequently. The initiation of bystander cardiopulmonary resuscitation and the rapid defibrillation of suitable cardiac rhythms determine a favourable outcome. All staff working at a surgery must be skilled in basic life support. The GP needs an understanding of advanced life support principles.

Adult↗

Out-of-hospital cardiac arrests in Helsinki: Utstein style reporting.

OBJECTIVE: To determine the epidemiology of out-of-hospital cardiac arrests and survival after resuscitation and to apply the Utstein style of reporting to data collection. DESIGN: Prospective cohort study. SETTING: A middle-sized urban city (population 516,000) served by a single emergency medical services system. PATIENTS: Consecutive prehospital cardiac arrests occurring between 1 January and 31 December 1994. INTERVENTION: Advanced cardiac life support according to the recommendations of American Heart Association. MAIN OUTCOME MEASURES: Survival from cardiac arrest to hospital discharge, and factors associated with survival. RESULTS: Four hundred and twelve patients were considered for resuscitation. The overall incidence of out-of-hospital cardiac arrest was 79.8/100,000 inhabitants/year. Fifty seven patients (16.6%) survived to discharge when resuscitation was attempted. 32.5% survived when cardiac arrest was bystander witnessed and was of cardiac origin with ventricular fibrillation as the initial rhythm. When asystole or pulseless electrical activity was the first rhythm recorded, discharge rates were 6.2 and 2.7% respectively. The cause of cardiac arrest was cardiac in 66.5%, and ventricular fibrillation was the initial rhythm in 65.0% of bystander witnessed cardiac arrests of cardiac origin. 22.1% of patients received bystander initiated cardiopulmonary resuscitation. The mean time intervals from the receipt of the call to the arrival of a first response advanced life support unit and mobile intensive care unit at the patient's side and to the return of spontaneous circulation were 7.0 and 10.3 and 12.6 and 16.7 min respectively. In the logistic regression model bystander witnessed arrest, age, ventricular fibrillation as initial rhythm, and the call-to-arrival interval of the first response unit were independent factors relating to survival. Utstein style reporting with modification of time zero was found to be an appropriate form of data collection in this emergency medical services system. CONCLUSIONS: After implementation of major changes in the emergency medical services system during the 1980s survival from out-of-hospital cardiac arrest markedly increased. However, early access, which has turned out to be the weakest link in the chain of survival, should receive major attention in the near future. Utstein style reporting with a modified time zero was found to be appropriate, although laborious, protocol for data collection.

Aged↗

Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest.

OBJECTIVE: Spontaneous subarachnoid haemorrhage as a cause of out-of-hospital cardiac arrest is poorly evaluated. We analyse disease-specific and emergency care data in order to improve the recognition of subarachnoid haemorrhage as a cause of cardiac arrest. DESIGN: We searched a registry of cardiac arrest patients admitted after primarily successful resuscitation to an emergency department retrospectively and analysed the records of subarachnoid haemorrhage patients for predictive features. RESULTS: Over 8.5 years, spontaneous subarachnoidal haemorrhage was identified as the immediate cause in 27 (4%) of 765 out-of-hospital cardiac arrests. Of these 27 patients, 24 (89%) presented with at least three or more of the following common features: female gender (63%), age under 40 years (44%), lack of co-morbidity (70%), headache prior to cardiac arrest (39%), asystole or pulseless electric activity as the initial cardiac rhythm (93%), and no recovery of brain stem reflexes (89%). In six patients (22%), an intraventricular drain was placed, one of them (4%) survived to hospital discharge with a favourable outcome. CONCLUSIONS: Subarachnoid haemorrhage complicated by cardiac arrest is almost always fatal even when a spontaneous circulation can be restored initially. This is due to the severity of brain damage. Subarachnoid haemorrhage may present in young patients without any previous medical history with cardiac arrest masking the diagnosis initially.

Adult↗

Frequency of hypokalemia after successfully resuscitated out-of-hospital cardiac arrest compared with that in transmural acute myocardial infarction.

To evaluate the prevalence of hypokalemia in out-of-hospital cardiac arrest, the initial serum potassium and arterial pH values were reviewed from 138 consecutive patients resuscitated from cardiac arrest. For comparison, the same variables were reviewed for 62 consecutive patients who had transmural acute myocardial infarction (AMI) without cardiac arrest. The mean serum potassium level was lower after resuscitation from cardiac arrest (3.6 +/- 0.6 mEq/liter) than during AMI (3.9 +/- 0.5 mEq/liter) (p less than 0.005). The incidence of hypokalemia (potassium less than 3.5 mEq/liter) was greater in patients sustaining cardiac arrest (41%) than in patients who had AMI without cardiac arrest (11%) (p less than 0.001). Hypokalemia was common after cardiac arrest regardless of the occurrence of AMI at the time of arrest. Hypokalemia after cardiac arrest was independent of arterial pH, epinephrine or bicarbonate therapy during resuscitation, or prior therapy with diuretic drugs, digoxin or propranolol. In 10 patients with marked hypokalemia, the serum potassium level returned to normal rapidly (16 hours) during the hospitalization even though only 29% of the predicted potassium requirement was infused before its normalization. Thus, hypokalemia is prevalent immediately after out-of-hospital cardiac arrest, whereas it is uncommon in AMI in the absence of cardiac arrest. The cause and electrophysiologic consequences of this hypokalemia are unknown; in most cases, it is apparently caused by a shift of potassium from the intravascular compartment rather than a total body depletion of potassium.

Acute Disease↗