STUDY - Technical - New Dacian's Medicine
Cardiovascular
Collapse, Cardiac Arrest and Sudden Cardiac Death (1)
Translation Draft
Cardiovascular disease is the leading cause for the vast majority of sudden natural deaths. The severity of the problem of heart causes is reflected in the fact that millions of sudden heart deaths (CSIs) occur annually in the world and that about 50% of all heart deaths are sudden and unexpected.
MSC is the direct consequence of cardiac arrest, which can be reversible if prompt intervention is taken. Since resuscitation technique and emergency system are able to save patients who go into cardiac arrest outside hospital units, always fatal in the past, understanding the problem of MSC is of considerable practical importance.
MSC should be carefully defined. From a chronological point of view, the term "sudden" is defined, for clinical and epidemiological purposes, as the time period of 1 hour or less elapsed since the onset of the terminal clinical event and death. An exception is death without witnesses, in this situation anatomologists can extend the time period to 24 hours after the victim was seen alive and in a stable clinical condition.
Due to rapid community interventions, the victim may remain biologically alive for days or weeks after cardiac arrest which caused irreversible damage to the central nervous system. Confusion of terms can be avoided by strictly referring to the definition of death, cardiac arrest and cardiovascular collapse. Thus, death represents the irreversible cessation of all biological functions, without any exception whatsoever.
Cardiac arrest is the brutal stopping of the heart pump function, reversible by prompt intervention, but leading, in its absence to exitus (there are some exceptions represented by a rare spontaneous reversibility and possible successful interventions related to the stop mechanism and clinical condition).
Cardiovascular collapse is a sudden loss of actual blood flow due to peripheral cardiac and/ or vascular factors, which can be spontaneously reversible (e.g. vasodrepressor syncope) or only by interventions (e.g. cardiac arrest). There is here at cardiovascular collapse some specificities related to the use of nonspecific term, which includes cardiac arrest and its consequences and also incidents that, characteristically, are spontaneously reversible.
So death is, biologically, forensically and literally, an absolute and irreversible event. Death may be delayed to a survivor of a cardiac arrest, but "survival after sudden death" is contradictory.
Currently, the accepted definition of MSC is "natural death due to cardiac causes", announced by sudden loss of consciousness within one hour of the onset of acute symptoms, in an individual who may have a history of heart disease, but at which the time and manner of death are unexpected. When the biological death of the cardiac arrest victim is delayed due to interventions, the relevant physiopathological element remains sudden and unexpected cardiac arrest, which ultimately leads to existus, even if it is delayed by artificial methods. Thus, the terminology used must reflect the fact that the key event was cardiac arrest and that death was due to its delayed consequences.
Intensive epidemiological studies have identified populations at high risk for MSCs. In addition, a number of pathological data provide information about pre-existing structural abnormalities in MSC victims and clinical/physiological studies have begun to identify a group of transient factors that can turn a long-lasting, clinically stable structural abnormality into a clinically unstable one.
These are represented by: 1. coronary heart disease (a. coronary abnormalities represented by: i. chronic atherosclerotic lesions, ii. acute active lesions such as plaque cracking, platelet aggregation or acute thrombosis and iii. anatomical abnormalities of the coronary arteries and b. myocardial infarction either cured or acutely), 2. myocardial hypertrophy (which may be secondary a. or b. obstructive or non-obstructive hypertrophic cardiomyopathy), 3. dilatative cardiomyopath (primary muscle disease), 4. inflammatory and infiltrating diseases (a. myocarditis, b. non-infectious inflammatory diseases or c. infiltrating diseases), 5. heart valve disease, 6. structural electrophysiological abnormalities (such as a. abnormal beams in Wolff-Parkinson-White syndrome, b. driving system disease or c. membrane channel structure such as the case of prolonged, congenital QT syndrome).
Of course there are also associated functional factors such as: 1. alterations in coronary blood flow (a. transient ischemia or b. reperfusion after ischemia), 2. low heart rate (such as a. chronic or acute decompensated heart failure or b. shock), 3. systemic metabolic abnormalities (a. electrolyte imbalances such as hypopotasemia and b. hypoxemia or acidosis), 4. neurophysiological disturbances (such as a. central, nerve and/ or humoral autonomic fluctuations or b. receptor functions), 5. toxic responses (such as a. proarrhythmic effects of medication, b. cardiac toxins such as cocaine or digital intoxication and c. drug interactions). This information leads to an understanding of the causes and mechanisms of the MSC.
Heart disorders are the most common cause of sudden natural death. The incidence of sudden death peaks initially between birth and the age of 6 months (sudden infant death syndrome), and then drops sharply/ steeply, remaining at a low level throughout childhood and adolescence. The incidence begins to increase in young adults, reaching a second peak between 45 and 75 years of age. Moreover, aging is an important risk factor for sudden cardiac death and the proportion of heart disease, of all types of natural sudden deaths, increases dramatically with age.
From 1 to 13 years, only one in five sudden natural deaths are due to cardiac causes. Between the ages of 14 and 21 the proportion increases to 30% and then to 88% in middle-aged and elderly people. Young and middle-aged men and women have different susceptibility to MSCs, but gender differentiation disappears with advancing age. The total ratio of men to women is approximately 4:1, but in the 45-64 age group, MSC in men increases and the proportion is almost 7:1. This percentage drops to about 2:1 between 65 and 74 years of age. The difference in the risk of MSC goes parallel to the risk for other manifestations of coronary heart disease in men and women.
As the range of other manifestations of coronary heart disease closes in the seven and eight months of life, the risk of MSC decreases. Despite the lower incidence in women, coronary risk factors are still present in this category (smoking, diabetes, hyperlipidemia, hypertension) and MSC remains an important clinical and epidemiological problem. hereditary factors contribute to the risk to MSCs, but in a non-specific manner. They represent the expression of hereditary predisposition to coronary heart disease.
With the exception of a few specific syndromes, such as genetic hyperlipoproteinemia, congenital prolonged QT interval syndrome and a number of myopathic and dysplastic syndromes, there are no specific hereditary risk factors for MSC. As for the major categories of structural causes and functional factors contributing to MSC syndrome (previously presented), in the world and especially in the West, coronary atherosclerotic disease is the most common structural abnormality associated with MSC, up to 80% of all MSIs due to its consequences.
Cardiomyopathy is involved in 10-15% of cases of MSC, and all other etiological factors cause only 5-10% of these incidents. Transient ischemia of the heart with scarring or hypertrophy, hemodynamic and hydroelectrolytic disorders, fluctuations in the autonomic nervous system and transient electrophysiological changes (e.g. proarrhythmia) caused by drugs and other chemicals, were involved as mechanisms responsible for the transition from stability to electrophysiological instability. In addition, spontaneous reperfusion of ischemic myocardium, caused by vasomotor changes in the coronary vessels and/ or spontaneous thrombolysis, may cause transient electrophysiological instability and arrhythmia.
Let's move on to anatomology! Data obtained through necropsy of MSC victims are added to clinical observations on the prevalence of coronary heart disease as a major structural factor. More than 80% of MSC victims have anatomological sequelae of coronary heart disease. These sequelae usually associate extensive, chronic atherosclerotic lesions of epicardial coronarys and acute coronary lesions, the latter being a combination of cracked or broken plaques, platelet aggregates, hemorrhages and thrombosis.
In one of the studies, chronic coronary atherosclerosis, present in two or more vessels with a minimum of 75% stenosis, was found in 75% of the victims. In another study, cracked atherosclerotic plaques, platelet aggregates and/ or acute thrombosis were observed in 95% of cases of necropsy individuals after MSC. Many of these acute changes overlapped with pre-existing chronic lesions. Then, 70-75% of men with sudden death had a history of myocardial infarction (MI), but only 20-30% had recently suffered an acute infarction. An increased incidence of left ventricular hypertrophy (VS) coexists with a history of IM.
I will complete this post with some elements about the clinical definition of forms of cardiovascular collapse. Cardiovascular collapse is a general term that denotes decreased actual blood flow due to cardiac dysfunction and/ or peripheral vascularity. Cardiovascular collapse can be caused by vasopressor syncope (vasovagal syncope, postural hypotension with syncope or neurocardiogenic syncope), a severe transient bradycardia or cardiac arrest.
The latter is different from transient forms of cardiovascular collapse in that it requires an intervention for resuscitation. In contrast, vasodepressor syncope and several of the primary bradyarrhythmic syncopes are transient and the patient regains consciousness spontaneously. The most common electrical mechanism of cardiac arrest is ventricular fibrillation (VF), responsible for 65-80% of cardiac arrests. Persistent severe bradyarithmias, asystolia, electromechanical dissociation (organized electrical activity is present, but there is no mechanical response) are trigger inghering causes in another 20-30% of cases.
Ventricular tachycardia (TV) supported with hypotension is uncommon. Acute cardiac rate-lowering states, suddenly installed, may also be clinically present as cardiac arrest. Causes include massive acute pulmonary embolism, internal bleeding by rupture of an aortic aneurysm, intense anaphylaxis, heart tear after myocardial infarction and sudden, fatal arrhythmia due to electrolyte disturbances.
I'm done! I'm going to continue on the 6th with the presentation of the clinical characteristics of cardiac arrest...
Cardiovascular disease is the leading cause for the vast majority of sudden natural deaths. The severity of the problem of heart causes is reflected in the fact that millions of sudden heart deaths (CSIs) occur annually in the world and that about 50% of all heart deaths are sudden and unexpected.
MSC is the direct consequence of cardiac arrest, which can be reversible if prompt intervention is taken. Since resuscitation technique and emergency system are able to save patients who go into cardiac arrest outside hospital units, always fatal in the past, understanding the problem of MSC is of considerable practical importance.
MSC should be carefully defined. From a chronological point of view, the term "sudden" is defined, for clinical and epidemiological purposes, as the time period of 1 hour or less elapsed since the onset of the terminal clinical event and death. An exception is death without witnesses, in this situation anatomologists can extend the time period to 24 hours after the victim was seen alive and in a stable clinical condition.
Due to rapid community interventions, the victim may remain biologically alive for days or weeks after cardiac arrest which caused irreversible damage to the central nervous system. Confusion of terms can be avoided by strictly referring to the definition of death, cardiac arrest and cardiovascular collapse. Thus, death represents the irreversible cessation of all biological functions, without any exception whatsoever.
Cardiac arrest is the brutal stopping of the heart pump function, reversible by prompt intervention, but leading, in its absence to exitus (there are some exceptions represented by a rare spontaneous reversibility and possible successful interventions related to the stop mechanism and clinical condition).
Cardiovascular collapse is a sudden loss of actual blood flow due to peripheral cardiac and/ or vascular factors, which can be spontaneously reversible (e.g. vasodrepressor syncope) or only by interventions (e.g. cardiac arrest). There is here at cardiovascular collapse some specificities related to the use of nonspecific term, which includes cardiac arrest and its consequences and also incidents that, characteristically, are spontaneously reversible.
So death is, biologically, forensically and literally, an absolute and irreversible event. Death may be delayed to a survivor of a cardiac arrest, but "survival after sudden death" is contradictory.
Currently, the accepted definition of MSC is "natural death due to cardiac causes", announced by sudden loss of consciousness within one hour of the onset of acute symptoms, in an individual who may have a history of heart disease, but at which the time and manner of death are unexpected. When the biological death of the cardiac arrest victim is delayed due to interventions, the relevant physiopathological element remains sudden and unexpected cardiac arrest, which ultimately leads to existus, even if it is delayed by artificial methods. Thus, the terminology used must reflect the fact that the key event was cardiac arrest and that death was due to its delayed consequences.
Intensive epidemiological studies have identified populations at high risk for MSCs. In addition, a number of pathological data provide information about pre-existing structural abnormalities in MSC victims and clinical/physiological studies have begun to identify a group of transient factors that can turn a long-lasting, clinically stable structural abnormality into a clinically unstable one.
These are represented by: 1. coronary heart disease (a. coronary abnormalities represented by: i. chronic atherosclerotic lesions, ii. acute active lesions such as plaque cracking, platelet aggregation or acute thrombosis and iii. anatomical abnormalities of the coronary arteries and b. myocardial infarction either cured or acutely), 2. myocardial hypertrophy (which may be secondary a. or b. obstructive or non-obstructive hypertrophic cardiomyopathy), 3. dilatative cardiomyopath (primary muscle disease), 4. inflammatory and infiltrating diseases (a. myocarditis, b. non-infectious inflammatory diseases or c. infiltrating diseases), 5. heart valve disease, 6. structural electrophysiological abnormalities (such as a. abnormal beams in Wolff-Parkinson-White syndrome, b. driving system disease or c. membrane channel structure such as the case of prolonged, congenital QT syndrome).
Of course there are also associated functional factors such as: 1. alterations in coronary blood flow (a. transient ischemia or b. reperfusion after ischemia), 2. low heart rate (such as a. chronic or acute decompensated heart failure or b. shock), 3. systemic metabolic abnormalities (a. electrolyte imbalances such as hypopotasemia and b. hypoxemia or acidosis), 4. neurophysiological disturbances (such as a. central, nerve and/ or humoral autonomic fluctuations or b. receptor functions), 5. toxic responses (such as a. proarrhythmic effects of medication, b. cardiac toxins such as cocaine or digital intoxication and c. drug interactions). This information leads to an understanding of the causes and mechanisms of the MSC.
Heart disorders are the most common cause of sudden natural death. The incidence of sudden death peaks initially between birth and the age of 6 months (sudden infant death syndrome), and then drops sharply/ steeply, remaining at a low level throughout childhood and adolescence. The incidence begins to increase in young adults, reaching a second peak between 45 and 75 years of age. Moreover, aging is an important risk factor for sudden cardiac death and the proportion of heart disease, of all types of natural sudden deaths, increases dramatically with age.
From 1 to 13 years, only one in five sudden natural deaths are due to cardiac causes. Between the ages of 14 and 21 the proportion increases to 30% and then to 88% in middle-aged and elderly people. Young and middle-aged men and women have different susceptibility to MSCs, but gender differentiation disappears with advancing age. The total ratio of men to women is approximately 4:1, but in the 45-64 age group, MSC in men increases and the proportion is almost 7:1. This percentage drops to about 2:1 between 65 and 74 years of age. The difference in the risk of MSC goes parallel to the risk for other manifestations of coronary heart disease in men and women.
As the range of other manifestations of coronary heart disease closes in the seven and eight months of life, the risk of MSC decreases. Despite the lower incidence in women, coronary risk factors are still present in this category (smoking, diabetes, hyperlipidemia, hypertension) and MSC remains an important clinical and epidemiological problem. hereditary factors contribute to the risk to MSCs, but in a non-specific manner. They represent the expression of hereditary predisposition to coronary heart disease.
With the exception of a few specific syndromes, such as genetic hyperlipoproteinemia, congenital prolonged QT interval syndrome and a number of myopathic and dysplastic syndromes, there are no specific hereditary risk factors for MSC. As for the major categories of structural causes and functional factors contributing to MSC syndrome (previously presented), in the world and especially in the West, coronary atherosclerotic disease is the most common structural abnormality associated with MSC, up to 80% of all MSIs due to its consequences.
Cardiomyopathy is involved in 10-15% of cases of MSC, and all other etiological factors cause only 5-10% of these incidents. Transient ischemia of the heart with scarring or hypertrophy, hemodynamic and hydroelectrolytic disorders, fluctuations in the autonomic nervous system and transient electrophysiological changes (e.g. proarrhythmia) caused by drugs and other chemicals, were involved as mechanisms responsible for the transition from stability to electrophysiological instability. In addition, spontaneous reperfusion of ischemic myocardium, caused by vasomotor changes in the coronary vessels and/ or spontaneous thrombolysis, may cause transient electrophysiological instability and arrhythmia.
Let's move on to anatomology! Data obtained through necropsy of MSC victims are added to clinical observations on the prevalence of coronary heart disease as a major structural factor. More than 80% of MSC victims have anatomological sequelae of coronary heart disease. These sequelae usually associate extensive, chronic atherosclerotic lesions of epicardial coronarys and acute coronary lesions, the latter being a combination of cracked or broken plaques, platelet aggregates, hemorrhages and thrombosis.
In one of the studies, chronic coronary atherosclerosis, present in two or more vessels with a minimum of 75% stenosis, was found in 75% of the victims. In another study, cracked atherosclerotic plaques, platelet aggregates and/ or acute thrombosis were observed in 95% of cases of necropsy individuals after MSC. Many of these acute changes overlapped with pre-existing chronic lesions. Then, 70-75% of men with sudden death had a history of myocardial infarction (MI), but only 20-30% had recently suffered an acute infarction. An increased incidence of left ventricular hypertrophy (VS) coexists with a history of IM.
I will complete this post with some elements about the clinical definition of forms of cardiovascular collapse. Cardiovascular collapse is a general term that denotes decreased actual blood flow due to cardiac dysfunction and/ or peripheral vascularity. Cardiovascular collapse can be caused by vasopressor syncope (vasovagal syncope, postural hypotension with syncope or neurocardiogenic syncope), a severe transient bradycardia or cardiac arrest.
The latter is different from transient forms of cardiovascular collapse in that it requires an intervention for resuscitation. In contrast, vasodepressor syncope and several of the primary bradyarrhythmic syncopes are transient and the patient regains consciousness spontaneously. The most common electrical mechanism of cardiac arrest is ventricular fibrillation (VF), responsible for 65-80% of cardiac arrests. Persistent severe bradyarithmias, asystolia, electromechanical dissociation (organized electrical activity is present, but there is no mechanical response) are trigger inghering causes in another 20-30% of cases.
Ventricular tachycardia (TV) supported with hypotension is uncommon. Acute cardiac rate-lowering states, suddenly installed, may also be clinically present as cardiac arrest. Causes include massive acute pulmonary embolism, internal bleeding by rupture of an aortic aneurysm, intense anaphylaxis, heart tear after myocardial infarction and sudden, fatal arrhythmia due to electrolyte disturbances.
I'm done! I'm going to continue on the 6th with the presentation of the clinical characteristics of cardiac arrest...
Let's hear it all right
and have to deal only with understanding, love and gratitude!
Dorin, Merticaru