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To blow or not to blow: a randomised controlled trial of compression-only and standard telephone CPR instructions in simulated cardiac arrest.

This randomised controlled trial used a manikin model of cardiac arrest to compare skill performance in untrained lay persons randomised to receive either compression-only telephone CPR (Compression-only tel., n=29) or standard telephone CPR instructions (Standard tel., n=30). Performance was evaluated during standardised 10 min cardiac arrest simulations using a video recording and data from a laptop computer connected to the training manikin. A number of subjects in both groups did not open the airway. More than 75% in the Standard tel. group failed to deliver two effective initial rescue breaths, and only 17% provided an adequate inflation volume for subsequent breaths, delivering a median of only five inflations during the entire scenario. Most subjects in both groups gave chest compressions that were too shallow and at an inappropriately rapid rate. Hand position was also poor, but was worse in the group given simplified instructions. There was a significant delay to first compression in both groups, although this interval was shortened by over a minute when ventilations were eliminated from the telephone instruction algorithm (245 vs. 184 s, P<0.001). Over two-and-a-half times as many chest compressions were delivered during an average ambulance response time with compression-only telephone directions compared with standard CPR (461 vs. 186, P<0.001). These variables may be critical in predicting survival from out-of-hospital cardiac arrest. Further research is necessary to establish if modifications to scripted telephone instructions can remedy the identified performance deficiencies. Eliminating instructions for rescue breaths from scripted telephone directions will have little impact on the ventilation of most patients. Research is required to determine if the consequent reduction in the delay to starting chest compressions and the significant increase in the number of compressions delivered can increase survival from out-of-hospital cardiac arrest.

Adult↗

The effect of bystander CPR on survival of out-of-hospital cardiac arrest victims.

The effect of bystander cardiopulmonary resuscitation (CPR) was studied in 2142 emergency medical service (EMS) cardiac arrest runs. When bystander CPR was administered to cardiac arrest victims, 22.9% of the victims survived until they were admitted to the hospital and 11.9% were discharged alive. In comparison, the statistics for cardiac arrest victims who did not receive bystander CPR were 14.6% and 4.7%, respectively (p less than 0.001). A critical factor in patient survival was the amount of time that elapsed before the EMS personnel arrived and administered CPR. Patients who received bystander CPR were more likely to have ventricular fibrillation when the EMS arrived. Other factors relating to patient survival were the location of the victim at the time of the cardiac arrest and the age of the victim. Understanding these factors is important in developing community strategies to treat patients with cardiac arrest out of hospital.

Adult↗

Risk indicators for, and symptoms associated with, death among patients hospitalized after out-of-hospital cardiac arrest.

BACKGROUND: An increasing proportion of patients who have an out-of-hospital cardiac arrest are initially successfully resuscitated and thus hospitalized. AIMS: To define risk indicators for, and to describe the mode of, in-hospital death among patients hospitalized after an out-of-hospital cardiac arrest. SETTING: Göteborg, Sweden. PATIENTS: All patients hospitalized after out-of-hospital cardiac arrest between 1980 and 1992. RESULTS: A total of 707 out of 3434 patients were hospitalized after out-of-hospital cardiac arrest, of whom 278 (39%) were discharged alive. Independent risk indicators for in-hospital death were: type of initial arrhythmia on the scene, age, interval between cardiac arrest and arrival of first ambulance, bystander-initiated cardiopulmonary resuscitation and history of diabetes mellitus. Of the patients who died in hospital, 88% had brain damage and 43% myocardial damage. CONCLUSION: Risk indicators for hospital death can be defined. The majority of in-hospital deaths were associated with brain damage.

Aged↗

Cell membrane trans-fatty acids and the risk of primary cardiac arrest.

BACKGROUND: The relation of trans-fatty acid intake to life-threatening arrhythmias and primary cardiac arrest is unknown. METHODS AND RESULTS: We investigated the association of trans-fatty acid intake, assessed through a biomarker, with the risk of primary cardiac arrest in a population-based case-control study. Cases, aged 25 to 74 years, were out-of-hospital cardiac arrest patients attended by paramedics in Seattle, Washington from 1988 to 1999 (n=179). Controls, matched to cases by age and sex, were randomly identified from the community (n=285). Participants were free of previous clinically diagnosed heart disease. Blood was obtained at the time of cardiac arrest (cases) or at the time of an interview (controls) to assess trans-fatty acid intake. Higher total trans-fatty acids in red blood cell membranes was associated with a modest increase in the risk of primary cardiac arrest after adjustment for medical and lifestyle risk factors (odds ratio for interquintile range, 1.5; 95% CI, 1.0 to 2.1). However, trans isomers of oleic acid were not associated with risk (odds ratio for interquintile range, 0.8; 95% CI, 0.5 to 1.2), whereas higher levels of trans isomers of linoleic acid were associated with 3-fold increase in risk (odds ratio for interquintile range, 3.1; 95% CI, 1.7 to 5.4). CONCLUSIONS: These findings suggest that dietary intake of total trans-fatty acids is associated with modest increase and trans isomers of linoleic acid with a larger increase in the risk of primary cardiac arrest. These associations need to be confirmed in future studies that distinguish between trans isomers of linoleic acid and trans isomers of oleic acid.

Adult↗

Comparison of heart rate variability in survivors and nonsurvivors of sudden cardiac arrest.

Imbalances in autonomic nervous system function have been posed as a possible mechanism that produces ventricular fibrillation and sudden cardiac arrest in patients with cardiovascular disease. Heart rate (HR) variability is described in survivors and nonsurvivors of sudden cardiac arrest within 48 hours after resuscitation using time and frequency domain analytic approaches. HR data were collected using 24-hour ambulatory electro-cardiograms in 16 survivors and 5 nonsurvivors of sudden cardiac arrest, and 5 control subjects. Survivors of sudden cardiac arrest were followed for 1 year, with recurrent cardiac events occurring in 4 patients who died within that year. Analysis of 24-hour electrocardiograms demonstrated that control subjects had the highest HR variability (standard deviation of all RR intervals = 155.2 +/- 54 ms), with nonsurvivors demonstrating the lowest HR variability (standard deviation of all RR intervals = 52.3 +/- 6.1 ms) and survivors of sudden cardiac arrest falling between the other 2 groups (standard deviation of all RR intervals = 78 +/- 25.5 ms, p less than or equal to 0.0000). Two other indexes of HR variability (mean number of beat to beat differences in RR intervals greater than 50 ms/hour and root-mean-square of successive differences in RR intervals) did not demonstrate the expected pattern in this sample, indicating that perhaps patterns of HR variability differ between groups of patients with cardiovascular disorders. Spectral analytic methods demonstrated that survivors of sudden cardiac arrest had reduced low- and high-frequency spectral power, whereas nonsurvivors demonstrated a loss of both low- and high-frequency spectral power.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Risk factors for out-of-hospital cardiac arrest: the Reykjavik Study.

AIMS: To examine risk factors for out-of-hospital cardiac arrest in the Reykjavik Study, a long-term, prospective, population-based cohort study that started in 1967. METHODS AND RESULTS: From 1987 to 1996, 137 men and 44 women out of the 8006 men and 9435 women in the study sustained out-of-hospital cardiac arrest due to cardiac causes. Determinants included coronary artery disease (CAD), its classical risk factors, and age, body mass index (BMI), heart rate, cardiomegaly, and erythrocyte sedimentation rate. Electrocardiograms (ECGs) were examined for various abnormalities. Significance was determined by Cox regression analysis. In multivariable analysis, the risk in men was significantly associated with age, diastolic blood pressure, cholesterol, current smoking, and previous diagnosis of myocardial infarction (MI). In women, the risk was associated with diastolic blood pressure, elevated levels of cholesterol and triglycerides, and increased voltage on ECG. Increased BMI was inversely related to women's risk of out-of-hospital cardiac arrest. CONCLUSION: In this prospective, population-based cohort study previous MI and the classical risk factors for CAD significantly increased the risk of out-of-hospital cardiac arrest, the endpoint of this study. Increased voltage on ECG additionally increased women's risk.

Age Factors↗

Therapeutic hypothermia-induced pharmacokinetic alterations on CYP2E1 chlorzoxazone-mediated metabolism in a cardiac arrest rat model.

OBJECTIVES: Therapeutic hypothermia has demonstrated considerable benefit in patients experiencing cardiac arrest. Despite increasing clinical use, there is a paucity of information regarding the effect of hypothermia on the disposition of medications, specifically cytochrome P450-mediated drug metabolism. The objective was to determine the effect of hypothermia after cardiac arrest on the in vivo kinetics of a cytochrome P450 (CYP2E1) probe drug, chlorzoxazone, and to investigate the mechanism of these alterations. DESIGN: Laboratory investigation. SETTING: University pharmacy school and animal research facility. SUBJECTS: Sixteen male Sprague-Dawley rats. INTERVENTIONS: An asphyxial arrest rat model was used and moderate hypothermia was induced immediately postinsult via surface cooling. Chlorzoxazone was administered as an intravenous bolus, and plasma concentrations were analyzed using high-performance liquid chromatography methods. Protein binding was analyzed using rat control plasma, and Michaelis-Menten enzyme kinetic analysis was performed at 37 degrees C and 30 degrees C using control rat microsomes at varying concentrations of chlorzoxazone. MEASUREMENTS AND MAIN RESULTS: Moderate hypothermia after cardiac arrest in rats markedly decreased the systemic clearance of the CYP2E1 substrate, chlorzoxazone, when compared with normothermia after cardiac arrest, 1.26+/-0.34 mL/min vs. 0.580+/-0.37 mL/min (p<.001). No changes in chlorzoxazone protein binding were observed at 37 degrees C and 30 degrees C, and CYP2E1 enzyme capacity (maximum velocity) was not altered at these different incubation temperatures. However, Michaelis-Menten constant was significantly increased at 30 degrees C (551+/-150 microM) compared with incubations at 37 degrees C (255+/-52 microM, p<.01). CONCLUSIONS: Moderate hypothermia markedly reduces the systemic clearance of chlorzoxazone in cardiac arrest rats. This results from hypothermia-induced decreases in the CYP2E1 enzyme affinity for the substrate chlorzoxazone. This is the first systematic mechanistic investigation of the effect of hypothermia on CYP2E1-mediated metabolism.

Analysis of Variance↗

Adherence to CPR guidelines during perioperative cardiac arrest in a developing country.

UNLABELLED: BACKGROUND AND GOAL OF STUDY: Cardiopulmonary resuscitation (CPR) is an integral part of anaesthetic training. In Nigeria, these skills are taught mainly during medical school and postgraduate training. International guidelines were introduced in 2000 and new guidelines were produced in November 2005. The study sought to assess how closely anaesthetists in a Nigerian teaching hospital abide by the 2000 guidelines. MATERIALS AND METHODS: All perioperative cardiac arrests in adults that occurred in a 1-year-period were studied prospectively. All patients <15 years and cardiac arrests occurring outside the direct supervision of the anaesthetists were excluded. Time and duration of arrest, cardiac arrest rhythm and management were documented along with immediate outcome. RESULTS: Thirteen cardiac arrests occurred in 2147 perioperative cases (incidence: 6/1000). Seven patients had non ventricular fibrillation/pulseless ventricular tachycardia (VF/VT) rhythms. The mean age of patients was 30.23+/-11.06 years. Orotracheal intubation, manual ventilation with 100% O(2) and external chest compressions were instituted in all cases. The mean duration of arrest was 25.66+/-13.34 min. All patients received adrenaline (epinephrine) and atropine. The median interval between adrenaline doses was 7.5 min. Only one cycle of defibrillation was given to patients in VF/VT. Immediate survival occurred in five patients (38.46%). CONCLUSION: Anaesthetists in our hospital are not applying proper resuscitation guidelines. The lack of organised simulation practice resulted in deficient knowledge and skills. There is a need for continuing training in basic and advanced resuscitation for all anaesthetists according to the guidelines.

Adrenergic Agonists↗

Description of time- and frequency- domain-based measures of heart rate variability in individuals taking antiarrhythmics, beta blockers, calcium channel blockers, and/or antihypertensive drugs after sudden cardiac arrest.

Concomitant drug therapies after sudden cardiac arrest and their potential effect of altering heart rate variability (HRV) represent confounding factors in interpreting the outcome of nonpharmacologic therapies on HRV. The purpose of this study is to describe a broad spectrum of time-domain and frequency-domain measurements of HRV in 50 individuals after sudden cardiac arrest. Some of the individuals were taking antiarrhythmics (n = 9), beta blockers (n = 13), calcium channel blockers (n = 10), nitrates (n = 8), cardiac glycosides (n = 10), and/or antihypertensives (n = 12). Heart rate variability was measured using a Holter recorder for 24 hours and the SpaceLabs FT2000 Monitoring System (Redmond, WA). In those individuals taking antiarrhythmic drugs, the power density within the low-frequency range (.016-.04 Hz) was significantly decreased (P = .001) compared to those not taking antiarrhythmics (n = 41). However, 78% of the people taking antiarrhythmics also had congestive heart failure (New York Heart Association functional classes II and III), which also decreased HRV. Those individuals taking beta blockers tended to have slower heart rates (P < .01). The association between beta blocker use and HRV was positive, but not statistically significant except for the increased power density in the low-frequency range (P < .05). In general, the relationships between HRV and drug therapy--calcium channel blockers, antihypertensives, cardiac glycosides, or nitrates--were not statistically significant.

Adrenergic beta-Antagonists↗

Manual chest compression vs use of an automated chest compression device during resuscitation following out-of-hospital cardiac arrest: a randomized trial.

CONTEXT: High-quality cardiopulmonary resuscitation (CPR) may improve both cardiac and brain resuscitation following cardiac arrest. Compared with manual chest compression, an automated load-distributing band (LDB) chest compression device produces greater blood flow to vital organs and may improve resuscitation outcomes. OBJECTIVE: To compare resuscitation outcomes following out-of-hospital cardiac arrest when an automated LDB-CPR device was added to standard emergency medical services (EMS) care with manual CPR. DESIGN, SETTING, AND PATIENTS: Multicenter, randomized trial of patients experiencing out-of-hospital cardiac arrest in the United States and Canada. The a priori primary population was patients with cardiac arrest that was presumed to be of cardiac origin and that had occurred prior to the arrival of EMS personnel. Initial study enrollment varied by site, ranging from late July to mid November 2004; all sites halted study enrollment on March 31, 2005. INTERVENTION: Standard EMS care for cardiac arrest with an LDB-CPR device (n = 554) or manual CPR (n = 517). MAIN OUTCOME MEASURES: The primary end point was survival to 4 hours after the 911 call. Secondary end points were survival to hospital discharge and neurological status among survivors. RESULTS: Following the first planned interim monitoring conducted by an independent data and safety monitoring board, study enrollment was terminated. No difference existed in the primary end point of survival to 4 hours between the manual CPR group and the LDB-CPR group overall (N = 1071; 29.5% vs 28.5%; P = .74) or among the primary study population (n = 767; 24.7% vs 26.4%, respectively; P = .62). However, among the primary population, survival to hospital discharge was 9.9% in the manual CPR group and 5.8% in the LDB-CPR group (P = .06, adjusted for covariates and clustering). A cerebral performance category of 1 or 2 at hospital discharge was recorded in 7.5% of patients in the manual CPR group and in 3.1% of the LDB-CPR group (P = .006). CONCLUSIONS: Use of an automated LDB-CPR device as implemented in this study was associated with worse neurological outcomes and a trend toward worse survival than manual CPR. Device design or implementation strategies require further evaluation. TRIAL REGISTRATION: clinicaltrials.gov Identifier: NCT00120965.

Aged↗

Serum neuron-specific enolase and S-100B protein in cardiac arrest patients treated with hypothermia.

BACKGROUND AND PURPOSE: High serum levels of neuron-specific enolase (NSE) and S-100B protein are known to be associated with ischemic brain injury and poor outcome after cardiac arrest. Therapeutic hypothermia has been shown to improve neurological outcome after cardiac arrest. The aim of this study was to evaluate the effect of therapeutic hypothermia on levels of serum NSE and S-100B protein, their time course, and their prognostic value in predicting unfavorable outcome after out-of-hospital cardiac arrest. METHODS: Seventy patients resuscitated from ventricular fibrillation were randomly assigned to hypothermia of 33+/-1 degrees C for 24 hours or to normothermia. Serum NSE and S-100B were sampled at 24, 36, and 48 hours after cardiac arrest. Neurological outcome was dichotomized into good or poor at 6 months after cardiac arrest. RESULTS: The levels of NSE (P=0.007 by analysis of variance for repeated measurements) but not S-100B were lower in hypothermia- than normothermia-treated patients. A decrease in NSE values between 24 and 48 hours was observed in 30 of 34 patients (88%) in the hypothermia group and in 16 of 32 patients (50%) in the normothermia group (P<0.001). The decrease in NSE values was associated with good outcome at 6 months after cardiac arrest (P=0.005), recovery of consciousness (P<0.001), and survival for at least 6 months after cardiac arrest (P=0.012). CONCLUSIONS: Decreasing levels of serum NSE but not S-100B over time may indicate selective attenuation of delayed neuronal death by therapeutic hypothermia in victims of cardiac arrest.

Adolescent↗

Long term survival and costs per life year gained after out-of-hospital cardiac arrest.

PURPOSE: To study long-term survival and estimate the costs per year of survival after out-of-hospital cardiac arrest of cardiac origin. MATERIALS AND METHODS: Cardiac arrest patients treated by the physician-manned ambulance in Oslo from January 1971 to June 1992. The condition of the patient when discharged from hospital was noted and survival followed until June 2002. Costs of the Emergency Medical Service (EMS), hospital treatment, rehabilitation and nursing homes and psychiatric institutions after discharge from hospital were included in a cost-effectiveness analysis. RESULTS: 1300 (42%) of 3065 patients receiving ALS were admitted to hospital after return of spontaneous circulation (ROSC). 1066 of these patients had a cardiac cause of the arrest, full hospital report and were found in the National Registry. Median age was 68 years (60-74) and 802 (75%) were men. 269 of the 1066 patients were discharged from hospital alive, 239 to their homes and 30 patients to rehabilitation/nursing homes or psychiatric institutions. The mean survival of the 1066 patients was 532 days. They spent mean 3.4 days in a CCU, 6.8 days in a general ward and 11.2 days in nursing/rehabilitation homes or psychiatric institutions. 30 patients were discharged to rehabilitation/nursing homes or psychiatric institutions. The mean survival time for the 269 patients discharged from hospital alive was 6.13 years. 110 patients were alive after five and 61 after 10 years. The cost per patient discharged alive was 40,642 or 6,632 per life year gained. CONCLUSIONS: Cardiac arrest patients do not occupy intensive care beds too long, and few end up in a vegetative state. Methodological differences in different studies makes meaningful comparisons of costs difficult, but the costs per life year saved are not high compared to other publications.

Advanced Cardiac Life Support↗

Non-invasive continuous haemodynamic and PETCO2 monitoring during peroperative cardiac arrest.

We describe a cardiac arrest which occurred during general anaesthesia in the prone position for surgical correction of lumbar kyphosis in a patient with Marfan's syndrome. Peroperative monitoring was routine with ECG, non-invasive arterial pressure, oximetry, PETCO2 and central venous pressure, plus aortic blood flow and and systolic time intervals via an oesophageal echo-Doppler device. Forty-five minutes after the start of surgery, a sudden decrease in aortic blood flow followed by a decrease in PETCO2 suggested acute cardiac failure despite continuation of the ECG signal. Initial CPR in the prone position produced a slight increase in PETCO2. When the patient was turned to the supine position and the legs elevated, chest compression was more efficient and spontaneous circulation was rapidly restored. Circulatory arrest could be explained by incompletely treated hypovolaemia, or by myocardial depression (decrease in aortic blood flow and lengthened pre-ejection period) combined with excessive hypotension in a patient with Marfan's syndrome, thus compromising coronary blood flow producing ST segment depression. Continuous non-invasive aortic blood flow and PETCO2 monitoring proved valuable in the early detection and treatment of circulatory arrest and in the evaluation of the efficiency of peroperative CPR.

Adolescent↗

A short delay from out of hospital cardiac arrest to call for ambulance increases survival.

AIM: To describe the relative impact on survival of the delay from estimated time of collapse to call for an ambulance among patients who suffer from a bystander witnessed out of hospital cardiac arrest of a cardiac aetiology. METHODS: A majority of all ambulance organizations in Sweden (covering 85% of Sweden inhabitants) participate in a National survey of out of hospital cardiac arrest. RESULTS: In all there were 9340 patients with a bystander witnessed cardiac arrest of a cardiac aetiology in whom cardiopulmonary resuscitation (CPR) was attempted participating in this survey. Survival at one month among patients with a delay between estimated time of collapse and call for ambulance of < or =4 min (median) was 6.9% versus 2.8% among patients with a median of >4 min (P<0.0001). When adjusting for age, sex, initial rhythm, estimated interval between collapse and start of CPR, place of arrest and the interval between call for ambulance and arrival of the rescue team, the odds ratio for survival was 0.70 (0.95% CI. 0.58-0.84) per unit increase of the natural logarithm of delay in minutes between collapse and call. CONCLUSION: Among patients with a bystander witnessed out of hospital cardiac arrest of a cardiac aetiology increased delay from estimated time of collapse to call for an ambulance decreased the chance of survival.

Age Distribution↗

Antimyoclonic and neuroprotective effects of lamotrigine in an animal model of cardiac arrest.

A major consequence of severe cardiac arrest is impairment of neurological functions. Posthypoxic myoclonus and seizures are two of the major neurological problems following ischemic and hypoxic insults. This condition affects motor function to different degrees of severity ranging from mild to serious debilitation. The pathophysiological mechanism(s) associated with these neurological conditions remain elusive. Glutamate-mediated neuronal overexcitation is thought to play a major role in the neuronal damage and in the neurological consequences of the posthypoxic state. Therefore, lamotrigine, a new anticonvulsant that indirectly modulates glutamatergic neurotransmission by interfering with voltage-dependent sodium channels, was tested for its effectiveness in controlling the neurological and histopathological changes in the animal model of cardiac arrest-induced myoclonus. Lamotrigine dose-dependently attenuated the audiogenic seizures and action myoclonus seen in this rat model. Histological analysis using Nissl staining and the novel Fluoro-Jade histochemistry in cardiac-arrested rats showed an extensive neuronal degeneration in the hippocampus and cerebellum. Lamotrigine treatment significantly attenuated the neuronal degeneration in these brain areas. The neuroprotective effect was more pronounced in hippocampal pyramidal and cerebellar Purkinje neurons. The therapeutic window of lamotrigine in this model was 8 hours. These results suggest that lamotrigine can be viewed as a potential antimyoclonic and neuroprotective agent for the treatment of posthypoxic myoclonus and seizures. The study also suggests that neuronal hyperexcitability may play a role in the etiology of posthypoxic myoclonus and seizure.

Journal Article↗

Outcome model of asphyxial cardiac arrest in rats.

An outcome model with asphyxial cardiac arrest in rats has been developed for quantifying brain damage. Twenty-two rats were randomized into three groups. Control group I was normal, was conscious, and had no asphyxia (n = 6). Sham group II had anesthesia and surgery but no asphyxia (n = 6). All 12 rats in groups I and II survived to 72 h and were functionally and histologically normal. Arrest group III (the model; n = 10) had light anesthesia and apneic asphyxia of 8 min, which led to cessation of circulation at 3-4 min of apnea, resulting in cardiac arrest (no flow) of 4-5 min. All 10 rats had spontaneous circulation restored by standard external cardiopulmonary resuscitation. Nine rats survived controlled ventilation for 1 h and observation to 72 h, while one rat died before extubation. All nine survivors were conscious at 72 h, with neurologic deficit scores (0% = best; 100% = worst) of 7 +/- 6% (2-16%). All brain regions at five coronal levels were examined for ischemic neurons. The prevalence of ischemic neurons in five regions was categorically scored. The average total brain histopathologic damage score in group III (n = 9) was 2.1 (p < 0.05 vs. group I or II). A reproducible outcome model of cardiac arrest in rats was documented. It provides a tool for investigating pathophysiological mechanisms of neuronal death caused by a transient global hypoxic-ischemic brain insult.

Animals↗

Left ventricular myotomy and myectomy in patients with obstructive hypertrophic cardiomyopathy and previous cardiac arrest.

Left ventricle myotomy and myectomy was carried out in nine patients with obstructive hypertrophic cardiomyopathy solely because of a previously documented episode of cardiac arrest. Before cardiac arrest, each patient had either no or only minimal functional limitation and therefore would not have met the usual criteria for operation, namely, severe symptoms unresponsive to medical therapy. Of the nine patients, one died in the perioperative period, and one died suddenly and unexpectedly 9 months postoperatively. The remaining seven patients have survived 9 months to 5.5 years after operation; six of the seven are asymptomatic and one has only mild symptoms. Operation resulted in a marked decrease or abolition of the left ventricular outflow gradient under basal conditions in seven of the eight patients studied postoperatively. Significant residual outflow obstruction was demonstrated after operation in the patient who later died. Sudden death in patients with obstructive hypertrophic cardiomyopathy appears usually to result from ventricular arrhythmia, and prevention of recurrent fatal arrhythmia is the goal of treatment in patients who have had cardiac arrest and have been resuscitated. Such patients should be treated indefinitely with antiarrhythmic drugs. In addition, when severe outflow obstruction is present, we postulate that effective operative relief of obstruction and consequent reduction of left ventricular systolic pressure will provide additional protection.

Adolescent↗

Age and sex analyses of out-of-hospital cardiac arrest in Osaka, Japan.

OBJECTIVE: To determine effective interventional targets for out-of-hospital cardiac arrests by analyzing the distribution characteristics of arrest patients according to age and sex with special emphasis on ventricular fibrillation (VF). METHODS: All patients who suffered out-of-hospital cardiac arrest in Osaka Prefecture, Japan during 2 years, were prospectively recorded based on the Utstein style. The number and the incidence rate of cases of arrest, witnessed arrest, and witnessed VF were evaluated according to age and sex. The percentage of resuscitation attempts in arrest cases was also calculated. RESULTS: We recorded 10139 consecutive out-of-hospital cardiac arrest cases. Resuscitation was attempted in 97.0% of 10139 and showed no significant differences by age and sex. The incidence rate of cardiac arrests increased exponentially with age. Men showed a significantly higher incidence rate of out-of-hospital arrests than women in every age group. Most of the witnessed VF cases showed cardiac a aetiology and were predominantly observed in men in their 50s, 60s and 70s. The incidence rates of witnessed VF were also greater in them. CONCLUSION: Our study provides evidence that there are significant age and sex related epidemiological differences in cardiac arrests and we need to understand them better. Strategies that focus on high yielded patients, those in witnessed VF, should be pursued. These efforts should be expected to yield sex and age related differences in survivors.

Age Distribution↗