[On the incidence of cardiac arrest in our changing times. With special reference to autopsy by police inspectors in sudden cardiac arrest].
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Autopsy↗
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Results for “CARDIAC ARREST”
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[Cardiac arrest and external cardiac massage].
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Adolescent↗
The location of collapse and its effect on survival from cardiac arrest.
Survival from cardiac arrest is higher when the collapse occurs outside the home. Of 781 patients collapsing at home, 101 (13%) survived to hospital discharge. This compared with 66 survivors among 248 (27%) patients arresting outside the home (P less than .001). Patients collapsing outside the home were younger and more frequently were men. Cardiac arrests outside the home were more often witnessed, more likely to have bystander CPR, less often preceded by symptoms, and the collapsing rhythm was more frequently ventricular fibrillation. Mean time to CPR was shorter. Multivariate logistic regression showed that the effect of location on survival was still statistically significant, although diminished, after adjusting for the above variables (P less than .01). We speculate that comorbidity, underlying etiology, and activity level may explain the remaining difference. Because 76% of arrests occur in the home, efforts to increase the frequency of bystander-CPR through targeted and dispatcher-assisted CPR programs are warranted.
Aged↗
[Cardiac arrest in 2 cardiac intensive therapy unit].
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Adult↗
Rational use of drugs for cardiac arrest and after cardiac resuscitation.
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Adams-Stokes Syndrome↗
Prevention of deterioration of ventricular fibrillation by basic life support during out-of-hospital cardiac arrest.
Survival of cardiac arrest is improved by basic life support (BLS). This study investigated the relationship between ventricular fibrillation (VF) characteristics and survival. In a 2-year prospective study out-of-hospital witnessed non-traumatic cardiac arrests were observed. The probabilities of recording VF, asystole or other rhythms in relation to BLS and the time to the rhythm recording were analyzed with logistic regression. Amplitude and baseline crossings of VF were related to survival, using linear regression analysis. In 873 patients, the probability to record VF decreased per minute (OR 0.92, 95%CI 0.89-0.95) and of asystole increased (OR 1.13, 95%CI 1.09-1.18) as time from collapse elapsed. BLS reduced these trends significantly for VF (OR 0.97, 95%CI 0.94-0.99) and asystole (OR 1.09, 95%CI 1.05-1.13). This effect was not observed for other rhythms. The amplitude of VF decreased in time; significantly less for patients who received BLS than for those who did not (p=0.009). Survival significantly decreased with lower amplitude of VF (OR 0.23 per mV, 95%CI 0.07-0.79) and with less baseline crossings (OR 0.80 per baseline crossings per second, 95%CI 0.71-0.91). Our study demonstrated that BLS and VF as initial rhythm, considered being "baseline" predictors in survival models, were proved not independent of each other. The decrease of VF amplitude and increase in prevalence of asystole is slowed significantly by BLS. Predicting survival from VF amplitude and baseline crossings alone is limited.
Cardiopulmonary Resuscitation↗
Cardiac arrest during pregnancy.
Cardiac arrest occurs rarely in pregnancy. Nevertheless, the practicing obstetrician stands a likely chance of encountering this acute condition at least once over the course of a busy career. A basic understanding of maternal-fetal physiology and the acute management of cardiac arrest are of key importance. ECC is not significantly changed from that administered to the nonpregnant patient. Factors unique to pregnancy, however, such as lateral uterine displacement, effects of drugs on the mother and the fetus, and the issues of perimortem cesarean section should be understood by the consulting obstetrician. The critical period in management of these patients is within the first several minutes of the event. In many situations, the obstetrician may be the first to arrive and initiate therapy before the arrival of multidisciplinary assistance. Prompt initial management will give the mother and fetus the best chances for survival.
Cardiopulmonary Resuscitation↗
Understanding the drugs used during cardiac arrest response.
During cardiac arrest the survival of the patient depends on a rapid response that provides high-quality treatment based on the latest guidelines. Administration of the correct drugs is an important aspect of this process and one in which nurses are taking an increasingly important role. This article will help nurses to understand the use of drugs in cardiac arrest resuscitation, explaining the rationale for their use, the dosage and any significant problems likely to be encountered.
Amiodarone↗
End-tidal carbon dioxide and outcome of out-of-hospital cardiac arrest.
BACKGROUND: Survival after cardiac arrest occurring outside the hospital averages less than 3 percent. Unfortunately, the outcome of prolonged resuscitative attempts cannot be predicted. End-tidal carbon dioxide levels reflect cardiac output during cardiopulmonary resuscitation. We prospectively determined whether death could be predicted by monitoring end-tidal carbon dioxide during resuscitation after cardiac arrest. METHODS: We performed a prospective observational study in 150 consecutive victims of cardiac arrest outside the hospital who had electrical activity but no pulse. The patients were intubated and evaluated by mainstream end-tidal carbon dioxide monitoring. Our hypothesis was that an end-tidal carbon dioxide level of 10 mm Hg or less after 20 minutes of standard advanced cardiac life support would predict death. RESULTS: There was no difference in the mean age or initial end-tidal carbon dioxide level between patients who survived to hospital admission (survivors) and those who did not (nonsurvivors). After 20 minutes of advanced cardiac life support, end-tidal carbon dioxide (+/-SD) averaged 4.4+/-2.9 mm Hg in nonsurvivors and 32.8+/-7.4 mm Hg in survivors (P< 0.001). A 20-minute end-tidal carbon dioxide value of 10 mm Hg or less successfully discriminated between the 35 patients who survived to hospital admission and the 115 nonsurvivors. When a 20-minute end-tidal carbon dioxide value of 10 mm Hg or less was used as a screening test to predict death, the sensitivity, specificity, positive predictive value, and negative predictive value were all 100 percent. CONCLUSIONS: An end-tidal carbon dioxide level of 10 mm Hg or less measured 20 minutes after the initiation of advanced cardiac life support accurately predicts death in patients with cardiac arrest associated with electrical activity but no pulse. Cardiopulmonary resuscitation may reasonably be terminated in such patients.
Adult↗
The ethics of cardiac arrest research.
In cardiac arrest research, prior informed consent is not available to resolve the conflict between the rights and well-being of subjects and the possible benefit to future patients. The right to autonomy is the fundamental right that is protected by the legal doctrine of informed consent. As a fundamental right, it cannot be balanced against other goods. Rather, it is a constraint, or trump, on the balancing of goods and can be overridden only for a narrow range of reasons: its recognition in a given case conflicts with another basic right, infringing the right will prevent great harm to others, and excluding a particular case from its scope will recognize and advance the right in the long run. Proxy consent, deferred consent, and presumed consent to cardiac arrest research are examined to determine if they qualify as justified infringements of the right to autonomy. The conclusion is that only presumed consent can be used, provided that the researcher can honestly say that outside of the randomized clinical trial of two or more treatments, a physician would have no basis for choosing one over the others.
Ethics, Medical↗
The neurological and cognitive sequelae of cardiac arrest.
BACKGROUND: Although cardiac arrest (CA) is commonly cited as a cause of amnesia, patients referred to the authors' center with a diagnosis of "amnesia" after CA rarely have isolated memory deficits. OBJECTIVE: To determine whether CA is a cause of pure amnesia and to assess patterns of cognitive deficits after CA. METHODS: The authors used cognitive assessment of 11 consecutive patients referred for memory deficits after CA, targeted at deficit domains identified in the literature reviews, and analysis of specific case reports and prospective studies of cognition after CA. RESULTS: The most common pattern of impairment in their patients was a combination of memory and motor deficits with variable executive impairment. No patient had isolated memory impairment. The case reports do not support the claim that isolated amnesia is a residual of CA; most cases of isolated amnesia are caused by subacute episodes of anoxia or excitotoxic injury. The prospective reports identify highly variable patterns of impairment, but isolated amnesia remains rare. CONCLUSIONS: Diffuse, sudden ischemic-hypoxic injury caused by cardiac arrest (CA) does not preferentially damage memory systems. Subacute or stepwise hypoxic or excitotoxic injury may cause isolated hippocampal injury and amnesia. The common pattern of impairment in the postacute phase after CA is a combination of memory, subtle motor, and variable executive deficits.
Adolescent↗
Spinal cord ischemia after cardiac arrest.
Subsequent to cardiac arrest, a 58-year-old man with intractable dysrhythmia and severe arteriosclerosis developed flaccid paraplegia, depressed deep tendon reflexes, and showed no pain or temperature sensation caudal to Th-7 in spite of completely intact proprioception and vibration sensation. An echocardiogram showed no clots or vegetation on the prosthetic valve and no thrombus in the left atrium or left ventricle. The patient's paraplegia was permanent, at least through a follow-up period of 2 years. These findings suggest that the etiology was spinal cord ischemia due to blood supply in the area of the anterior spinal artery (ASA); however, magnetic resonance T2-weighted imaging demonstrated signal abnormalities throughout the gray matter and in the adjacent center white matter. Somatosensory-evoked potentials (SEP) measure neural transmission in the afferent spinal cord pathway, which is located in the lateral and posterior columns of the white matter; these showed a delay in latency between Th-6 and Th-7. The spinal cord is as vulnerable to transient ischemia as the brain. Spinal cord ischemia after cardiac arrest results from principal damage in the anterior horn of the gray matter, the so-called ASA syndrome; however, the pathways of SEP and pathogenesis of the spinal cord ischemia need further investigation.
Evoked Potentials, Somatosensory↗
Pulmonary and left ventricular decompression by artificial pulmonary valve incompetence during percutaneous cardiopulmonary bypass support in cardiac arrest.
BACKGROUND: In cardiac arrest, use of percutaneous cardiopulmonary bypass support (PCPS) may lead to left ventricular loading, with deleterious effects on the myocardium, and is often accompanied by an increase in pulmonary artery pressure. The present study was designed to assess the potential of artificially induced pulmonary valve incompetency to retrogradely decompress the left ventricle during PCPS in ventricular fibrillation. METHODS AND RESULTS: Studies were performed using a standardized experimental animal model in sheep (n = 12; body weight, 77 to 112 kg). When PCPS was used during fibrillation, an increase in left ventricular pressure (from 21.4 +/- 5.0 mm Hg after 1 minute to 28.4 +/- 9.5 mm Hg after 10 minutes of fibrillation) was observed in all animals, with a simultaneous increase in pulmonary artery pressure in 6 animals, from 15.5 +/- 3.8 to 24.3 +/- 5.4 mm Hg (group A). In these animals, artificial pulmonary valve incompetency, which was induced by a special "pulmonary valve spreading catheter," led to effective decompression of both the pulmonary circulation (decrease in pulmonary artery pressure from 24.3 to 11.3 mm Hg) and the left ventricle (decrease in left ventricular pressure from 30.5 to 17.7 mm Hg). We simultaneously measured a decrease in the myocardial release of lactate (increase in arterial coronaryvenous difference in lactate content from -0.01 to 0.14 mmol/L), demonstrating the myocardial protective effect of the procedure. In contrast, in 6 animals without an increase in pulmonary artery pressure during PCPS (group B), artificial pulmonary valve incompetency did not reduce left ventricular loading, which was probably because of competent mitral valves in these animals. CONCLUSIONS: In case of increasing pulmonary artery pressure during PCPS in cardiac arrest, artificial pulmonary valve incompetency might be a useful tool for effective pulmonary and retrograde left ventricular decompression.
Animals↗
Emergency cardiopulmonary bypass support in patients with cardiac arrest in the catheterization laboratory.
Cardiac arrest in the catheterization laboratory is fatal if unresponsive to advanced cardiac life support (ACLS). Seven patients not responding to ACLS following cardiac arrest in the catheterization laboratory underwent percutaneously instituted cardiopulmonary bypass support. Cardiac arrest occurred following abrupt closure postcoronary angioplasty in three patients, during cardiogenic shock in three patients, and during diagnostic angiography in one patient. Cardiopulmonary bypass was instituted 10-45 min (mean, 21 min) following the onset of cardiac arrest. Flows on bypass ranged from 4.0 to 5.2 liter/min. Mean blood pressure ranged from 70 to 110 mm Hg on bypass. Six of the seven patients regained consciousness after the institution of bypass. Acid-base balance was normalized in all patients. Coronary bypass surgery was subsequently performed in three patients and coronary angioplasty in two. Four patients survived. One patient died following coronary bypass surgery. Two patients, who were not suitable candidates for revascularization, expired. Total bypass time was 1.5-8.5 hr (mean, 2.7 hr). At a mean follow-up of 6 months, all four survivors are alive and asymptomatic or NYHA class 1. We conclude that cardiopulmonary bypass support 1) can stabilize patients following cardiac arrest in the catheterization laboratory, 2) can facilitate emergency coronary angioplasty or transfer to the operating room for coronary bypass surgery, and (3) can improve survival in patients unresponsive to ACLS when instituted early following cardiac arrest in the catheterization laboratory.
Aged↗
[Early defibrillation in the treatment of sudden cardiac arrest].
Recovery from nontraumatic cardiac arrest depends on the presence of all the elements in the chain of survival. "Early defibrillation" is critical because ventricular fibrillation is the most common initial dysrhythmia of sudden cardiac arrest. Defibrillation is the only treatment, and survival from ventricular fibrillation is determined by time. Out-of-hospital studies have demonstrated that defibrillation provided by first responders improves survival. Technologic advances have simplified defibrillation delivery through the development of automated external defibrillators (AEDs). Early defibrillation programs with AEDs are quickly becoming a standard of care for emergency medical service systems throughout the United States. Improvement in in-hospital survival rates from cardiac arrest is not as evident as in the emergency medical service community. Medical centers need to assess response times to cardiac arrest and implement AED programs. All the nurses should learn to use an AED as part of basic life support training.
Clinical Competence↗
Management of cardiac arrest by ambulance technicians and paramedics. Paramedics have other uses beside attending cardiac arrests.
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Allied Health Personnel↗
Hypothermia for cardiac arrest.
Therapeutic hypothermia for cardiac arrest survivors has emerged as a highly effective means of improving neurologic outcome. There are a number of purported mechanisms by which it is felt to be effective, but the exact mechanism is unknown. This article reviews the biochemical mechanisms of injury occurring in cardiac arrest, as well as the avenues that hypothermia takes to combat this injury. It also reviews the animal model data in support of this, as well as the newer animal studies that may help to improve the field. Several human studies of hypothermia in cardiac arrest have been performed, and this article reviews these for their methods and shortcomings. Our currently recommended guidelines for performing therapeutic hypothermia are presented. With therapeutic hypothermia comes potential risks to the patient, primarily affecting cardiac, metabolic, and hematologic systems, and these risks and their management are discussed. Multiple methods of cooling exist, including selective cranial as well as systemic cooling by internal or external approaches. Finally, the article discusses the current research in the field of hypothermia for cardiac arrest and implications for future practice.
Animals↗
Cerebral resuscitation potentials for cardiac arrest.
Permanent brain damage after cardiac arrest and resuscitation is determined by many factors, predominantly arrest (no-flow) time, cardiopulmonary resuscitation (low-flow) time, and temperature. Research since around 1970 into cardiopulmonary-cerebral resuscitation has attempted to mitigate the postischemic-anoxic encephalopathy. These efforts' results have recently shown outcome benefits as documented in clinically relevant outcome models in dogs and in clinical trials. Pharmacologic strategies have so far yielded relatively disappointing results. In a recent exploration of 14 drugs in dogs, only the antioxidant tempol administered at the start of prolonged cardiac arrest improved functional outcome in dogs. Cerebral blood flow promotion by hypertensive reperfusion and hemodilution has resulted in improved outcome in dogs, and brief hypertension after restoration of spontaneous circulation is associated with improved outcome in patients. Postarrest hypercoagulability of blood seems to yield to therapeutic thrombolysis, which is associated with improved cerebral outcome in animals and patients. In a clinically relevant dog outcome model, mild postarrest cerebral hypothermia (34 degrees C), initiated with reperfusion and continued for 12 hrs, combined with cerebral blood-flow promotion increased from 5 to >10 mins the previously longest normothermic no-flow time that could be reversed to complete cerebral recovery. Mild hypothermia by surface cooling after prolonged cardiac arrest in patients has been found effective in recent clinical studies in Australia and Europe. Preliminary data on the recent randomized study in Europe have been reported. For presently unresuscitable cardiac arrests, research since the 1980s in dog outcome models of prolonged exsanguination cardiac arrest has culminated in brain and organism preservation during cardiac arrest (no-flow) durations of up to 90 mins, perhaps 120 mins, at a tympanic temperature of 10 degrees C and complete recovery of function and normal histology. This "suspended animation for delayed resuscitation" strategy includes use of an aortic flush of cold saline (or preservation solution) within the first 5 mins of no flow. This strategy should also be explored for the larger number of patients with unresuscitable out-of-hospital cardiac arrests. Suspended animation for prolonged preservation of viability could buy time for transport and repair during hypothermic no flow followed by resuscitation, or it could serve as a bridge to prolonged cardiopulmonary bypass.
Animals↗