Time for primary review 29 days. When sudden death (SD) occurs in adults and elderly persons, coronary atherosclerosis is the usual cause [1,2]. On the. Cardiac arrest is a sudden loss of blood flow resulting from the failure of the heart to effectively pump. Symptoms include loss of consciousness and abnormal or. Main · Videos; Sudden death definition and epidemiologic considerations when dating. Ms&l will correlate workaholism errata than favorability outreach.
This commentary is intended to assess potentials for progress in developing improved approaches to SCD prediction and prevention through new clinical and basic research on the fundamental causes of ventricular arrhythmias, the development of new markers of electrical instability, and better understanding of the role of genetic variability in their origin.
Time for primary review 3 days. Strategies for prevention depend heavily on risk profiling in population studies that have, for the most part, focused on the presence and extent of underlying coronary artery disease CADeven though the power of these approaches in individual patients remains low.
Therapeutic interventions for primary or secondary prevention of cardiac arrest have not to date successfully targeted specific mechanisms of sudden cardiac death except for the use of implantable defibrillators ICDs for some subsets of patients. ICD use for more general segments of the population remains unrealistic. Further, community-based programs using automatic external defibrillators AEDs have been limited by a lack of knowledge regarding the effectiveness of such strategies in the hands of expanded types of first responders, and information on the efficacy of various distribution strategies.
Even in more focused populations, data have only recently become available to support the benefits hypothesized for the use of these devices. Predicting and preventing sudden cardiac death remains a major challenge for which new strategies are needed and understanding its causes represents an enormous challenge for clinical and basic cardiovascular science.
However, since then, two factors have come into play that could influence the reliability of that estimate. The first is a change in age-adjusted mortality from coronary heart disease, with present estimates indicating that deaths due to this category are occurring later, but not necessarily that the actual incidences of death or prevalence of disease are decreasing . In addition, an improvement in short-term mortality from acute myocardial infarction experienced during the second half of the 20th century, in conjunction with an increased older population, has established a large population of older patients with chronic heart disease, resulting in an epidemiologic cohort at increased risk for events .Prevalence and Causes of Sudden Cardiac Arrest in the Young
Whether these two factors have increased, decreased, or had no effect on the actual incidence of sudden cardiac death needs to be identified through contemporary prospective observations, designed to quantify the current sudden death burden.
For many years, clinicians have depended upon epidemiologic profiling of risk of development of coronary heart disease as a surrogate for sudden cardiac death prediction . It follows that the epidemiology of evolution of coronary heart disease is a general indicator of risk.
Unfortunately, while this strategy applies generally to the population, it does not have sufficient power to identify individual total mortality risk, and even less so for sudden death specifically. The limitations experienced in predicting sudden cardiac death due to coronary heart disease are even more confounding for sudden cardiac deaths due to other causes, such as the acquired myopathies, a diffuse array of other structural disorders and entities in which genetically heritable mechanisms have been implicated [7,8].
Numerically, and particularly in the middle aged-to-older adult population, these figures are dominated by dilated cardiomyopathies. Unfortunately, this category is poorly defined etiologically, including undefined acquired mechanisms among the idiopathic dilated cardiomyopathies, and various acquired causes such as myocarditis, alcohol-induced disorders, and other rare causes.
The epidemiology for this cluster of disorders is not well understood, and risk factors and other specific etiologic characteristics remain unknown. A different kind of epidemiologic problem exists for those cases that display a strong familial pattern, including the long QT-interval syndromes, familial hypertrophic cardiomyopathies, right ventricular dysplasia, Brugada's syndrome and idiopathic ventricular fibrillation .
Among these subgroups, epidemiologic considerations migrate into new territory, namely possible genetic predictors of cardiac arrest as a manifestation of disorders that may affect channels, contractile elements and other cellular proteins.
However, it is also clear that risks of SCD due to mutations at a given gene locus and among members of families in which a specific mutation has been identified, are not necessarily uniform. This variance in disease expression may indicate mutation-specific variations in functional alterations, involvement of secondary linkages to other genes, environmental inducers or comorbidity.
This area of clinical epidemiology is in its infancy and is hampered by the relatively small number of patients and families identified to date. Nevertheless, the potential ability to associate a specific genetic mutation with a specific risk of sudden death offers the hope of improved identification of susceptibility among affected families. Understanding genetic determinism in such small populations might ultimately provide road maps for risk identification in the more common entities such as coronary artery disease or the cardiomyopathies [2,9].
The magnitude of sudden cardiac death risk is age-dependent and cause-related Fig.
A generally assumed risk of 0. However, the risk of sudden cardiac death is strongly age-related with the most marked increase occurring between the ages of 40 and 65 years, with causation dominated largely by coronary artery disease. However, among the subgroup of patients with far-advanced structural heart disease, the extent of disease rather than age, influences risk more strongly and therefore, age-related risk curves blunt in that subgroup of population Fig.
There is also an inverse relationship between the incidence of sudden cardiac death and absolute number of events in the various epidemiologic or clinical categories of coronary artery disease [3,10,11]. The probable etiologies of a cardiac arrest are dominated by coronary artery disease and the cardiomyopathies at age 35 and beyond and by a diverse group of acquired and inherited disorders in the younger age groups modified from Fig.
Among the general adult population beyond the age of 35 years, overall sudden death risk is 0.
Cardiac arrest - Wikipedia
These subgroups progress from multiple high-risk markers through prior myocardial infarction, low ejection fraction and congestive heart failure, to survivors of out-of-hospital cardiac arrest and highly specific very-high-risk subgroups in post-myocardial infarction patients.
There is as much as a fold increase in risk across this sequence. However, the increase is accompanied by a progressive and steep decrease in the absolute number of victims in that risk category. The highest risk subgroups account for a minority of the sudden death victims, and the lowest risk groups have such a large denominator relative to event rates that they are impractical for specific therapeutic interventions.
Thus, one of the most important challenges is to identify specific individuals at risk for sudden cardiac death within the large population pools that constitute the categories with lower overall incidence. This challenge will be met only by understanding the fundamental causes of lethal arrhythmias, through new basic, clinical and population studies.
After a conditioning state is established as a result of various structural or functional disorders, or for example in individuals who develop coronary artery disease, a sequence of events leading to severe alterations in cellular electrophysiology may occur, that results in increased risk of ventricular arrhythmogenesis. This is followed by gradual rewarming over the next 12 to 24 hrs.
Sudden death--definition and epidemiologic considerations.
A do not resuscitate order DNR in the form of an advance health care directive makes it clear that in the event of cardiac arrest, the person does not wish to receive cardiopulmonary resuscitation. The chain consists of the following "links": Early recognition — If possible, recognition of illness before the person develops a cardiac arrest will allow the rescuer to prevent its occurrence.
In particular, by keeping the brain supplied with oxygenated blood, chances of neurological damage are decreased.
Early defibrillation — is effective for the management of ventricular fibrillation and pulseless ventricular tachycardia  Early advanced care Early post-resuscitation care which may include percutaneous coronary intervention  If one or more links in the chain are missing or delayed, then the chances of survival drop significantly.
These protocols are often initiated by a code bluewhich usually denotes impending or acute onset of cardiac arrest or respiratory failurealthough in practice, code blue is often called in less life-threatening situations that require immediate attention from a physician.
This reflects an overall survival following cardiac arrest of 6. Thus one can hear mentions of "prior episodes of sudden cardiac death" in a living person.
If corrective measures are not taken rapidly, this condition progresses to sudden death.