Materiały źródłowe

• #1 Sudden Cardiac Death – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK507854/

  Sudden cardiac death (SCD) is death due to a cardiovascular or unidentifiable cause that occurs within an hour of the onset of symptoms. Death occurs when the heart stops beating or is not beating sufficiently to maintain perfusion and life. Those who have experienced sudden cardiac arrest (SCA) have a higher risk of SCD. Thus, addressing SCA risk factors reduces SCD risk. […] Cardiac arrest is defined as a sudden cessation of cardiac activity resulting in hemodynamic collapse. Sudden cardiac death (SCD) is defined as death presumed to be of a cardiac cause that occurs within 1 hour of the onset of cardiac symptoms or 24 hours of last being seen healthy and alive. Autopsies may reveal a cardiac etiology, though not all SCD cases have an identifiable cause. SCD may be the first presentation of cardiovascular diseases and accounts for half of cardiovascular deaths.

• #2 Pathophysiology and etiology of sudden cardiac arrest – UpToDate

  https://www.uptodate.com/contents/pathophysiology-and-etiology-of-sudden-cardiac-arrest/print

  Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) refer to the sudden cessation of cardiac activity with hemodynamic collapse, typically due to sustained ventricular tachycardia/ventricular fibrillation. […] The cardiac diseases that lead to the genesis of the arrhythmia resulting in cardiac collapse and sudden death are varied, and the association with sudden death in some cases is poorly understood. […] Identification of the patient at risk for sudden death and identification of the factors that precipitate the fatal arrhythmia continue to represent a major challenge. […] The exact mechanism of collapse in an individual patient is often impossible to establish since, for the vast majority of patients who die suddenly, cardiac activity is not being monitored at the time of their collapse. […] However, there have been many cases in which the initiating event has been witnessed or recorded. […] Ventricular tachycardia (VT) or ventricular fibrillation (VF) account for the majority of episodes.

• #3 Mechanisms of sudden cardiac death

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4237287/

  Worldwide, sudden cardiac death (SCD) is a major problem. It is most frequently caused by ventricular tachyarrhythmias: Monomorphic and polymorphic ventricular tachycardia (VT), torsade de pointes (TdP), and ventricular fibrillation (VF). […] Knowledge of the exact electrophysiologic mechanisms of ventricular tachyarrhythmias at the cellular level has been improved and mechanisms such as phase 2 reentry and reflection proposed to better understand why and how SCD occurs. […] If an ECG documentation is available at the time of sudden loss of consciousness, it shows ventricular fibrillation (VF) in 75%80%, only rarely (10%15%) bradyarrhythmia; in 5%10% the ECG does not show an arrhythmia. […] Bradyarrhythmias lead to sudden death only in rare cases because in most patients, endogenous release of catecholamines generates and sustains an escape rhythm that is sufficient to keep the patient alive.

• #4 Pathophysiology and etiology of sudden cardiac arrest – UpToDate

  https://www.uptodate.com/contents/pathophysiology-and-etiology-of-sudden-cardiac-arrest

  Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) refer to the sudden cessation of cardiac activity with hemodynamic collapse, typically due to sustained ventricular tachycardia/ventricular fibrillation. […] The cardiac diseases that lead to the genesis of the arrhythmia resulting in cardiac collapse and sudden death are varied, and the association with sudden death in some cases is poorly understood. […] The exact mechanism of collapse in an individual patient is often impossible to establish since, for the vast majority of patients who die suddenly, cardiac activity is not being monitored at the time of their collapse. […] Ventricular tachycardia (VT) or ventricular fibrillation (VF) account for the majority of episodes.

• #5 Sudden cardiac death: epidemiology, pathogenesis and management

  https://www.imrpress.com/journal/RCM/22/1/10.31083/j.rcm.2021.01.207/htm

  Sudden cardiac death (SCD) is an unexpected sudden death due to a heart condition, that occurs within one hour of symptoms onset. […] The predominant mechanism of SCD is a form of ventricular arrhythmia (VA). Ventricular arrhythmias are responsible for 84% of SCD. The most common type of ventricular arrhythmias that lead to SCD are VT and VF. […] At autopsy, coronary artery disease (CAD), hypertrophic cardiomyopathy (HCM) with or without obstruction, and valvular aortic stenosis are the most common causes of SCD. […] The most common cause of VF is acute coronary ischemia whereas increased risk of ventricular tachycardia (VT) commonly occurs in patients with structural heart disease as well as channelopathies. […] Metabolic derangement and oxidative stress particularly during myocardial ischemia may lead to SCD. […] SCD is triggered by a loss of function of one or more of the four vital systems: heart, brain, lungs, and vasculature system.

• #6 Mechanisms of sudden cardiac death

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4237287/

  In patients with an implantable cardioverter-defibrillator (ICD), up to 80% of all device-treated ventricular tachyarrhythmias are monomorphic ventricular tachycardia (VT). […] Monomorphic VT leads to SCD only if other special conditions contribute to an insufficient circulation or if it degenerates into polymorphic VT or ventricular fibrillation (VF). […] Polymorphic VT is estimated to be the cause of SCD in approximately 25% of the cases and is particularly frequent in acute myocardial ischemia. […] Torsade de pointes (TdP) tachycardia is a form of polymorphic VT characterized by a gradual change in the QRS amplitude and twisting of the QRS vector around the isoelectric line. […] Ventricular flutter and VF are responsible for 23% of out-of-hospital cardiac arrests treated by the emergency medical system. […] The exact pathophysiology of PEA is not clear. Likely, acute (severe) myocardial ischemia may play a role, and a third of patients with PEA have PCI performed during STEMI.

• #7 Sudden Cardiac Death – StatPearls – NCBI Bookshelf

  https://www.ncbi.nlm.nih.gov/books/NBK507854/

  SCD mostly results from an electrical accident in the form of ventricular arrhythmias or asystole. Some patients have an anatomic and functional substrate for developing life-threatening ventricular arrhythmias or asystole. However, many have transient events in the form of myocardial ischemia or infarction, metabolic abnormalities, and drug toxicities leading to ventricular tachyarrhythmias or asystole. This reflects an interplay between the arrhythmogenic substrates and transient events perturbing myocardial hemostasis and predisposing patients to life-threatening arrhythmias, SCA, and SCD. […] SCD risk is highest during the first few months after a myocardial infarction due to fatal tachyarrhythmias, reinfarction, or myocardial rupture. Ventricular fibrillation and tachycardia were initially identified as the most common causes of OHCA. However, recent studies show that asystole and pulseless electrical activity (PEA) are the most frequent initial rhythms in OHCAs. Approximately 50% of patients initially have asystole, and 19% to 23% have PEA as the first identifiable rhythm. Blood flow to the brain slows to essentially zero immediately following OHCA, leading to death.

• #8 A Clinical Perspective on Sudden Cardiac Death | AER Journal

  https://www.aerjournal.com/articles/clinical-perspective-sudden-cardiac-death?language_content_entity=en

  VT or VF was thought to be the most common cause of out-of-hospital cardiac arrest, accounting for approximately three-quarters of cases, the remaining 25 % being caused by bradyarrhythmias or asystole. […] More recent studies, however, suggest that the incidence of VF or pulseless VT as the first recorded rhythm in out-of-hospital cardiac arrest has declined to 30 % in the past few decades. […] Non-arrhythmic mechanisms, such as myocardial rupture or aortic aneurysm rupture, may also result in SCD.

• #9 Sudden Cardiac Death: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/151907-overview

  Sudden cardiac death (SCD) is an unexpected death due to cardiac causes that occurs in a short time period (generally within 1 hour of symptom onset) in a person with known or unknown cardiac disease. […] The most common electrophysiologic mechanisms leading to sudden cardiac death (SCD) are tachyarrhythmias such as ventricular fibrillation (VF) or ventricular tachycardia (VT). […] There are multiple factors at the organ (eg imbalance of autonomic tone), tissue (eg reentry, wave break, and action potential duration alternans), cellular (eg triggered activity, and automaticity) and subcellular (abnormal activation or deactivation of ion channels) level involved in generation of VT or VF in different conditions. […] Most cases of SCD occur in patients with structural abnormalities of the heart.

• #10 Mechanisms of sudden cardiac death

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4237287/

  In CPVT, ryanodine receptor mutations have been identified that lead to uncontrolled calcium release from the sarcoplasmic reticulum. […] Phase 2 reentry has been proposed as the mechanism responsible for the closely coupled extrasystole that precipitates VT/VF in Brugada and early repolarization syndromes.

• #11 Mechanisms of sudden cardiac death

  https://pmc.ncbi.nlm.nih.gov/articles/PMC4237287/

  Acute myocardial ischemia is considered to be the most important cause of SCD. […] The second mechanism by which coronary artery disease leads to SCD is scar-related VT. […] Hypertension predisposes independently to SCD via left ventricular hypertrophy (LVH). […] SCD in DCM is most frequently caused by ventricular tachyarrhythmia (approximately 50%), particularly VF, but can also be due to bradycardia and electromechanical dissociation. […] Brugada syndrome accounts for approximately 20% of SCD in patients with structural normal hearts. […] The typical arrhythmia leading to SCD in Brugada syndrome is therefore VF. […] The long QT syndrome (LQTS) consists of a number of familial diseases with genetic variations of different potassium and sodium channels. […] The characteristic ventricular arrhythmia in LQTS is TdP, typically triggered by a short-long-short cycle.

• #12 Sudden cardiac arrest – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/sudden-cardiac-arrest/symptoms-causes/syc-20350634

  The most common cause of sudden cardiac arrest is an irregular heart rhythm called ventricular fibrillation. Rapid, erratic heart signals cause the lower heart chambers to quiver uselessly instead of pumping blood. […] Heart conditions that can cause sudden cardiac arrest include: […] Sudden cardiac arrest may occur if the heart arteries become clogged with cholesterol and other deposits, reducing blood flow to the heart. […] If a heart attack occurs, often as a result of severe coronary artery disease, it can trigger ventricular fibrillation and sudden cardiac arrest. […] This condition usually happens when the walls in the heart muscle stretch. The heart muscle gets bigger or thicker. […] Leaking or narrowing of the heart valves can lead to stretching or thickening of the heart muscle.

• #13 Sudden Cardiac Death: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/151907-overview

  Myocardial infarction (MI) and post-MI remodeling of the heart is the most common structural abnormality in patients with SCD. […] Hypertrophic cardiomyopathy and dilated cardiomyopathy are associated with an increased risk of SCD. […] The strongest known predictor of SCD is significant left ventricular dysfunction of any cause. […] The interplay between the regional ischemia, LV dysfunction, and transient insulting events (eg, worsened ischemia, acidosis, hypoxemia, wall tension, drugs, metabolic disturbances) has been proposed as being the precipitator of sudden death. […] Cardiac arrest due to ventricular arrhythmias may be due to post-MI remodeling of the heart with scar formation and interstitial fibrosis (intramyocardial collagen deposition) or to acute MI/ischemia. […] A chronic infarct scar can serve as the focus for reentrant ventricular tachyarrhythmias.

• #14 A Clinical Perspective on Sudden Cardiac Death | AER Journal

  https://www.aerjournal.com/articles/clinical-perspective-sudden-cardiac-death?language_content_entity=en

  Sudden cardiac death (SCD) is usually defined as death due to cardiac causes occurring within 1 hour of the onset of symptoms. […] The main problem with SCD is that the majority of out-of-hospital sudden cardiac arrests occur among patients in whom cardiac arrest is the first clinical expression of the underlying disease or those in whom disease has previously been identified but classified as low risk. […] Following acute myocardial infarction there is increased risk of SCD during the first months due to tachyarrhythmias or other complications such as re-infarction or myocardial rupture, and myocardial scar predisposes to monomorphic ventricular tachycardia (VT). […] The most common causes of non-ischaemic SCD are currently cardiomyopathy related to obesity or alcoholism and fibrotic cardiomyopathy.

• #15 Sudden Cardiac Death: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/151907-overview

  Patients with nonischemic cardiomyopathies represent the second largest group of patients who experience SCD in the United States. […] The predominant mechanism of death appears to be ventricular tachyarrhythmia, although bradyarrhythmia and electromechanical dissociation also have been observed, especially in patients with advanced LV dysfunction. […] The mechanism of SCD in HCM is not entirely understood. […] The mechanism of arrhythmia in this setting is not clear, and hypertrophy may be a part of cardiac remodeling in these patients that provides the substrate for lethal arrhythmia with a disarray of cardiac myocytes and the presence of myocardial fibrosis. […] The mechanism of sudden death is unclear, and both malignant ventricular arrhythmia and bradyarrhythmia have been documented.

• #16 Sudden cardiac death after alcohol intake: classification and autopsy findings | Scientific Reports

  https://www.nature.com/articles/s41598-022-20250-3

  Alcohol is known to have an immediate effect on cardiac rhythm, and previous studies have found that a notable proportion of sudden cardiac deaths (SCD) occur after alcohol intake. […] The most common causes of death in alcohol-related SCDs were coronary artery disease (CAD) (63.7%), hypertensive myocardial disease (11.0%), alcoholic cardiomyopathy (9.5%), and obesity-related cardiomyopathy (8.4%), and the proportions of cardiac hypertrophy (70.1%) and myocardial fibrosis (91.9%) were high. […] Given that myocardial structural abnormalities are known to create an anatomic substrate that can maintain lethal ventricular arrhythmias leading to SCD, it is reasonable to hypothesize that alcohol intake may act as a trigger for lethal arrhythmias among those with pre-existing structural cardiac disease, either ischemic or non-ischemic.

• #17 Sudden cardiac arrest – Symptoms and causes – Mayo Clinic

  https://www.mayoclinic.org/diseases-conditions/sudden-cardiac-arrest/symptoms-causes/syc-20350634

  Sudden cardiac arrest in children or adolescents is often due to a heart condition that they’re born with. […] Conditions such as long QT syndrome and Brugada syndrome cause the heart to beat in an unorganized way. If the heart rhythm isn’t quickly restored, sudden death can occur. Young people with LQTS are especially at risk of sudden death.

• #18 Sudden Cardiac Arrest in Patient with Aortic Stenosis and Preexcitation

  https://clinmedjournals.org/articles/ijcc/international-journal-of-clinical-cardiology-ijcc-9-259.php?jid=ijcc

  Sudden cardiac death in WPW syndrome occurs in setting of atrial fibrillation conducting through the accessory bypass tract leading to ventricular fibrillation. The risk of sudden cardiac death in symptomatic patients with WPW syndrome is estimated to be around 0.25%/year or 3 to 4% over her lifetime.

• #18 Sudden Cardiac Arrest in Patient with Aortic Stenosis and Preexcitation

  https://clinmedjournals.org/articles/ijcc/international-journal-of-clinical-cardiology-ijcc-9-259.php?jid=ijcc

  58-year-old male sustained sudden cardiac arrest (SCA) due to ventricular fibrillation (VF) while at work and was resuscitated with shock therapy. […] Aortic stenosis as well as preexcitation can lead to sudden cardiac arrest. This is a unique case of a 58-year-old man who presented with sudden cardiac arrest in the presence of both severe aortic stenosis as well as preexcitation. […] The two major differentials of sudden cardiac death after the above investigations were severe aortic stenosis and WPW syndrome. […] The underlying mechanism of sudden cardiac death and aortic stenosis are following: 1) Abnormal Bezold-Jarisch reflex: Aortic stenosis leads to activation of left ventricular baroreceptors that cause hypotension and bradycardia leading to sudden cardiac death. In addition, these factors also contribute to decrease coronary blood supply resulting in myocardial ischemia and further leading to malignant tachycardia and sudden cardiac death. 2) Left ventricular hypertrophy: This leads to increased myocardial oxygen consumption and reduced coronary blood flow reserve. 3) Atrioventricular conduction disturbances: This results from contiguity between valvular-perivalvular calcification in his-Purkinje system.

• #19 Sudden Cardiac Death: Practice Essentials, Background, Pathophysiology

  https://emedicine.medscape.com/article/151907-overview

  The incidence of SCD has decreased significantly with advent of aortic valve replacement. […] The mechanism of sudden death is unclear, and both malignant ventricular arrhythmia and bradyarrhythmia have been documented. […] The predominant mechanism is ventricular arrhythmias. […] The clinical course of patients with long QT syndrome is quite variable, with some patients remaining asymptomatic while others develop torsade de pointes with syncope and sudden death. […] The risk of SCD is impacted by environmental factors such as hypokalemia, medications and the presence of sinus pauses. […] The probability that a specific patient has congenital long QT syndrome is divided to low, intermediate, and high probability based on the following criteria: (1) ECG criteria including long QT, torsade de pointes, notched T wave, T wave alternans, bradycardia for age; (2) clinical criteria including syncope with or without stress, deafness; and (3) family history of long QT syndrome or SCD.

• #20 Sudden Cardiac Arrest in Patient with Aortic Stenosis and Preexcitation

  https://clinmedjournals.org/articles/ijcc/international-journal-of-clinical-cardiology-ijcc-9-259.php?jid=ijcc

  Mechanical explanation of ventricular arrhythmias and aortic stenosis: Aortic stenosis leads to systolic pressure overload which causes myocardial hypertrophy in leads to structural remodeling with increased collagen, abnormal electrophysiological properties, decreased myocardial perfusion due to reduced coronary vasodilator reserve further leading to myocardial ischemia, myocardial death and scar formation. […] Electrophysiological mechanism of ventricular arrhythmia and aortic stenosis: This is resultant from reentry, stress-induced arrhythmia as well as triggered activity. […] Our patient had low output low gradient aortic stenosis which is defined as aortic stenosis with calculated valve area of less than 1 cm2 and presence of left ventricular dysfunction with left ventricular ejection fraction of less than 40% along with low cardiac output and low transaortic mean gradient of less than 30 mmHg. Modified dobutamine stress test can help differentiate true aortic stenosis from severe aortic stenosis and is also a predictor of worse outcome if there is no change in cardiac output.

• #21 Sudden Cardiac Arrest | Sudden Cardiac Death | MedlinePlus

  https://medlineplus.gov/suddencardiacarrest.html

  Coronary artery disease (CAD), also called ischemic heart disease. CAD happens when the arteries of the heart cannot deliver enough oxygen-rich blood to the heart. It is often caused by the buildup of plaque, a waxy substance, inside the lining of larger coronary arteries. The plaque blocks some or all of the blood flow to the heart. […] Some types of physical stress can cause your heart’s electrical system to fail, such as intense physical activity in which your body releases the hormone adrenaline. This hormone can trigger SCA in people who have heart problems. […] Very low blood levels of potassium or magnesium. These minerals play an important role in your heart’s electrical system. […] Major blood loss […] Severe lack of oxygen […] Certain inherited disorders which can cause arrhythmias or problems with the structure of your heart […] Structural changes in the heart, such as an enlarged heart due to high blood pressure or advanced heart disease. Heart infections can also cause changes to the structure of the heart.

• #22 Causes of Cardiac Arrest | American Heart Association

  https://www.heart.org/en/health-topics/cardiac-arrest/causes-of-cardiac-arrest

  Cardiac arrest may be caused by almost any known heart condition. […] Most cardiac arrests occur when a diseased heart’s electrical system malfunctions. This malfunction causes an abnormal heart rhythm such as ventricular tachycardia or ventricular fibrillation. Some cardiac arrests are also caused by extreme slowing of the heart’s rate (bradycardia). […] Irregular heartbeats such as these are life-threatening. […] A heart that’s scarred or enlarged from any cause is prone to develop life-threatening ventricular arrhythmias. The first six months after a heart attack is a high-risk period for sudden cardiac arrest in patients with atherosclerotic heart disease (the buildup of fatty deposits, or plaque, in the arteries). […] A diseased heart muscle can make you more prone to sudden cardiac arrest, especially if you also have heart failure.

• #23 Sudden Cardiac Arrest and the Hs and Ts – ACLS.com

  https://acls.com/articles/reversible-causes-of-cardiac-arrest-hs-and-ts/

  Sudden cardiac arrest is a major healthcare problem in the United States that accounts for up to 350,000 deaths per year. […] Many different traumatic and medical conditions can lead to cardiac arrest in both adults and children. This includes electrical abnormalities, inherited disorders and structural changes in the heart. […] Treating the cause of hypoxia/hypoxemia must be done quickly because this is one of the potentially reversible causes of cardiac arrest. […] One common cause of cardiac arrest is hypovolemia, which can develop due to a reduced intravascular volume (i.e. hemorrhage). […] Hypothermia can be estimated and further subdivided by using the Swiss staging system. […] Electrolyte abnormalities can cause cardiac arrhythmias or cardiac arrest, and life-threatening arrhythmias are associated most commonly with potassium disorders, particularly hyperkalemia.

• #24 Sudden Cardiac Arrest and the Hs and Ts – ACLS.com

  https://acls.com/articles/reversible-causes-of-cardiac-arrest-hs-and-ts/

  Hyperkalemia is the most common electrolyte disorder associated with cardiac arrest. […] Hypokalemia increases the incidence of arrhythmias and sudden cardiac death. […] Acidosis can be either metabolic or respiratory. Either cause can lead to cardiac arrest. […] Tension pneumothorax is defined as hemodynamic compromise in a patient with an expanding intrapleural air mass. It is a treatable cause of cardiac arrest and should be excluded during CPR. […] Cardiac tamponade occurs when the pericardial sac is filled with fluid under pressure, which leads to compromise of cardiac function and ultimately cardiac arrest. […] Cardiac arrest from acute pulmonary embolism is the most serious clinical presentation of venous thromboembolism, in most cases originating from a deep venous thrombosis (DVT). […] Coronary heart disease is the most frequent cause of out-of-hospital cardiac arrest.

• #25 Pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest | Intensive Care Medicine Experimental | Full Text

  https://icm-experimental.springeropen.com/articles/10.1186/s40635-020-00307-1

  The developing hypocapnia can nullify the beneficial effects of the hypothermia. […] The aim of this review was to describe the pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest. […] The aim of this review is to discuss the pathophysiology of arterial blood gases and pH in mechanically ventilated patients after cardiac arrest and their clinical consequences. […] The pathophysiological effects of acidosis on cardiomyocytes are well described; extracellular and intracellular acidosis reduces the number of adrenoreceptors expressed on the cell membrane, in particular beta receptors, and contributes to reduced contractile responsiveness to catecholamines. […] The pathophysiological effects of carbon dioxide have a strong impact on the context of catecholamine administration and pH variations, but these effects are still poorly understood.

• #26 Pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest | Intensive Care Medicine Experimental | Full Text

  https://icm-experimental.springeropen.com/articles/10.1186/s40635-020-00307-1

  Post cardiac arrest syndrome is associated with high morbidity and mortality, which is related not only to a poor neurological outcome but also to respiratory and cardiovascular dysfunctions. […] The control of gas exchange, and in particular oxygenation and carbon dioxide levels, is fundamental in mechanically ventilated patients after resuscitation, as arterial blood gases derangement might have important effects on the cerebral blood flow and systemic physiology. […] In particular, the pathophysiological role of carbon dioxide (CO2) levels is strongly underestimated, as its alterations quickly affect also the changes of intracellular pH, and consequently influence metabolic energy and oxygen demand. […] Hypo/hypercapnia, as well as mechanical ventilation during and after resuscitation, can affect CO2 levels and trigger a dangerous pathophysiological vicious circle related to the relationship between pH, cellular demand, and catecholamine levels.

• #27 Pathophysiology and clinical consequences of arterial blood gases and pH after cardiac arrest | Intensive Care Medicine Experimental | Full Text

  https://icm-experimental.springeropen.com/articles/10.1186/s40635-020-00307-1

  CO2 alterations during resuscitation can quickly cause abrupt intracellular and extracellular pH changes; hypocapnia, as consequence of hyperventilation, increases the demand of metabolic energy and O2, while ATP production is often reduced, thus determining a sympathetic-like activation which further increases the energy demand. […] The increased production of catecholamines is a compensatory phenomenon in acidosis, and there is a positive feedback between catecholamine production and H+ concentration: the catecholamine-sensitivity is very low in acidosis, though their production is high. […] Thus, the beneficial or harmful effect of catecholamines depends on different factors including pH, levels of PaCO2, and lactate. […] Although from these pathophysiological concepts, it is clear that the best way to terminate this vicious circle is to elevate PaCO2 levels, as acidosis can slow down the enzymatic intracellular and membrane processes by reducing energy demand.

• #28 Causes of Cardiac Arrest | American Heart Association

  https://www.heart.org/en/health-topics/cardiac-arrest/causes-of-cardiac-arrest

  Under certain conditions, some heart medications can set the stage for arrhythmias that cause sudden cardiac arrest. […] Significant changes in blood levels of potassium and magnesium (from using diuretics, for example) can also cause life-threatening arrhythmias and cardiac arrest. […] These, including Wolff-Parkinson-White syndrome and long QT syndrome, may cause sudden cardiac arrest in children and young people. […] Adrenaline released during intense physical activity can trigger sudden cardiac arrest when these abnormalities are present. […] Recreational drug use – This can be associated with cardiac arrest in otherwise healthy people. […] Commotio cordis occurs as a result of a blow to the left side of the chest during a narrow window in the heart rhythm.

• #29 The role of toxic substances in sudden cardiac death | Spanish Journal of Legal Medicine

  https://www.elsevier.es/en-revista-spanish-journal-legal-medicine-446-articulo-the-role-toxic-substances-in-S2445424918300037

  The use of toxic substances is a main risk factor for sudden cardiac death. […] The harmful effects are particularly important for the cardiovascular system, and are a significant risk factor for sudden cardiac death (SCD). Toxic substances, through transient functional disturbances, interact with the anatomical substrate responsible for SCD, triggering a fatal arrhythmia. […] This article reviews the association between the use of toxic substances and SCD, providing data on the mechanism of action and the condition induced by the main substances. […] The prevalence of SCD associated with toxic substances is not well defined and the pathophysiological mechanisms are not clearly established. […] The macroscopic and histopathological study will also make it possible to determine the existence of organic disease in relation to the acute or chronic use of toxic substances.

• #30 Sudden cardiac death after alcohol intake: classification and autopsy findings | Scientific Reports

  https://www.nature.com/articles/s41598-022-20250-3

  Although a common paradigm indicates that great majority of the SCDs after middle age is due to CAD, less than two-thirds of alcohol related SCDs had evidence of CAD in the autopsy, and less than 10% had alcoholic cardiomyopathy, but, intriguingly, still more than 90% had myocardial fibrosis and 70% had cardiac hypertrophy. […] Interestingly, most of our alcohol related SCDs occurred during the late stage of alcohol inebriation. […] The association between alcohol intake and SCD seems to be somewhat analogous to alcohol intake and atrial fibrillation, which also occurs mostly several hours after alcohol intake or during the late stage of inebriation, reinforcing the hypothesis that alcohol has the greatest arrhythmogenic potential during the late stage of inebriation. […] In conclusion, a significant proportion of SCDs occur immediately after alcohol intake and most of these events occur at the late stage of inebriation.

• #31 The role of toxic substances in sudden cardiac death | Spanish Journal of Legal Medicine

  https://www.elsevier.es/en-revista-spanish-journal-legal-medicine-446-articulo-the-role-toxic-substances-in-S2445424918300037

  The possibility of using recreational drugs should be taken into account in all sudden deaths of adolescents, young people or even middle-aged adults, particularly males. […] In the prevention of SCD, it is important to identify the modifiable risk factors which trigger fatal arrhythmia, as this offers a good approximation for the development of effective strategies.

• #32 Mechanism behind sudden cardiac deaths in sports uncovered | University of Oxford

  https://www.ox.ac.uk/news/2017-08-10-mechanism-behind-sudden-cardiac-deaths-sports-uncovered

  Researchers have worked out the mechanism behind sudden cardiac deaths that follow a hard blow to the chest. […] Cardiac arrhythmias caused by a short, hard impact without visible lesions of heart muscle are called Commotio cordis, which can be responsible for sudden cardiac death after chest impact of baseballs and ice hockey pucks in professional sports. […] Commotio cordis is believed to be rare, but is one of the most frequent causes of sudden cardiac death among young, otherwise healthy athletes. […] Previous studies on animals have shown that the window of time during the normal cycle of a beating heart in which Commotio cordis can lead to sudden death is very short indeed: only about 20 milliseconds, or 2% of the normal cardiac cycle. […] In a collaborative BHF-funded study, the cellular mechanism of Commotio cordis has now been elucidated. This involves activation of so-called ion channels – membrane proteins in heart muscle cells that trigger a new stray wave when physically stimulated.

• #33 Sudden Cardiac Arrest Caused by a Ball Impact to the Chest Wall: Commotio Cordis | Mandourah | Journal of Medical Cases

  https://www.journalmc.org/index.php/JMC/article/view/2941

  A sudden cardiac death caused by a blunt forceful trauma in the chest wall region is called commotio cordis. […] Commotio cordis by definition is blunt trauma to the chest wall in the area of the cardiac silhouette causing a ventricular fibrillation. […] The actual mechanism of the induction of the ventricular fibrillation is complicated but can be simplified as a forced depolarization in the impact area caused by a disturbance of the KATP channel, which, if happened in a specific time in the cardiac cycle specifically within 20 – 10 ms before the T wave peak, will lead to a ventricular fibrillation.

• #34 Mechanism behind sudden cardiac deaths in sports uncovered | University of Oxford

  https://www.ox.ac.uk/news/2017-08-10-mechanism-behind-sudden-cardiac-deaths-sports-uncovered

  If, and only if, this occurs exactly at the boundary with a preceding wave edge, circular currents form, which prevent coordinated heart beats. […] Our work shows that there is a critical window in which Commotio cordis can interfere with the hearts rhythm, which is limited by time as well as a defined space. […] The researchers also identified two types of excitation patterns, only one of which is susceptible to Commotio cordis. […] Only in the first case, i.e. only if there is a clearly defined boundary of the receding excitation wave, can sudden cardiac death be triggered, if the most unfavourable factors are combined. […] This combination of constraints involving time, location and critical wave pattern explains why the nature of Commotio cordis has remained obscure for such a long time.

• #35 Cardiac Arrest – Critical Care Medicine – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/critical-care-medicine/cardiac-arrest-and-cardiopulmonary-resuscitation-cpr/cardiac-arrest

  Cardiac arrest causes global ischemia with consequences at the cellular level that adversely affect organ function even after resuscitation and restoration of perfusion. The main consequences involve direct cellular damage and edema formation. Edema is particularly harmful in the brain, which has minimal room to expand, and often results in increased intracranial pressure and corresponding decreased cerebral perfusion postresuscitation. […] Decreased adenosine triphosphate (ATP) production leads to loss of membrane integrity with efflux of potassium and influx of sodium and calcium. Excess intracellular sodium is one of the initial causes of cellular edema. Excess calcium damages mitochondria (depressing ATP production), increases nitric oxide production (leading to formation of damaging free radicals), and, in certain circumstances, activates proteases that further damage cells.

• #36 Postcardiac arrest syndrome: from immediate resuscitation to long-term outcome | Annals of Intensive Care | Full Text

  https://annalsofintensivecare.springeropen.com/articles/10.1186/2110-5820-1-45

  The prognosis for postcardiac arrest patients remains very bleak, not only because of anoxic-ischemic neurological damage, but also because of the „postcardiac arrest syndrome,” a phenomenon often severe enough to cause death before any neurological evaluation. […] The main component of the postcardiac arrest syndrome is an early but severe cardiocirculatory dysfunction that may lead to multiple organ failure and death. […] The pathophysiology of postcardiac arrest syndrome is complex and remains partially understood. […] It seems, however, dominated by a global ischemia-reperfusion phenomenon (affecting all organs) and a nonspecific activation of the systemic inflammatory response. […] The pathophysiology of this syndrome explains the observed features and justifies the therapeutic interventions that must be performed to achieve a favorable neurological evolution.

• #37 Postcardiac arrest syndrome: from immediate resuscitation to long-term outcome | Annals of Intensive Care | Full Text

  https://annalsofintensivecare.springeropen.com/articles/10.1186/2110-5820-1-45

  The postcardiac arrest syndrome presents a set of relatively stereotyped events. […] Its intensity varies but is roughly proportional to the duration of „no flow” and „low flow,” as well as difficulty encountered during initial resuscitation. […] The postcardiac arrest shock, initially described by Negovsky in 1975, is a mixed shock, with cardiogenic and vasodilatory components and is characterized by a severe but reversible systolic dysfunction. […] The anoxic-ischemic neurological damages remain the leading cause of deaths occurring in patients initially resuscitated from CA. […] Without specific and prompt treatment, postcardiac arrest shock usually leads to a multiple organ failure and early death. […] Many mechanisms that occur after CA make cardiopulmonary resuscitation survivors prone to infectious complications.

• #38 Cardiac Arrest – Critical Care Medicine – Merck Manual Professional Edition

  https://www.merckmanuals.com/professional/critical-care-medicine/cardiac-arrest-and-cardiopulmonary-resuscitation-cpr/cardiac-arrest

  Abnormal ion flux also results in depolarization of neurons, releasing neurotransmitters, some of which are damaging (eg, glutamate activates a specific calcium channel, worsening intracellular calcium overload). […] Inflammatory mediators (eg, interleukin-1B, tumor necrosis factor-alpha) are elaborated; some of them may cause microvascular thrombosis and loss of vascular integrity with further edema formation. Some mediators trigger apoptosis, resulting in accelerated cell death.

• #39 Cardiac Arrest & Death | NYU Langone Health

  https://med.nyu.edu/research/parnia-lab/cardiac-arrest-death

  From a biological perspective, cardiac arrest is synonymous with death by cardiorespiratory criteria, which is declared based on the absence of heartbeat and respiration and the loss of brain function. Deprived of blood flow and oxygen, the cells of the body begin their own process of death. Different cell types die at different rates. Contrary to previous notions that brain cells die within 5 to 10 minutes, evidence now suggests that if left alone, the cells of the brain die slowly over a period of many hours, even days after the heart stops and a person dies. […] Paradoxically, it is the reintroduction of oxygen to deprived cells after the heart is restarted that causes the cells to suddenly die much more rapidly. The longer someone has been left without a heartbeat, the greater this cell injury processas a result, someone with less than 5 minutes without blood flow to the brain has a much higher likelihood of recovery compared to someone who experiences 30 minutes without blood flow. Minimizing the amount of time that cells are deprived of oxygen is critical to halting the process of cell damage and death.

• #40 RETRACTED ARTICLE: Cardiac arrest triggers hippocampal neuronal death through autophagic and apoptotic pathways | Scientific Reports

  https://www.nature.com/articles/srep27642

  The mechanism of neuronal death induced by ischemic injury remains unknown. We investigated whether autophagy and p53 signaling played a role in the apoptosis of hippocampal neurons following global cerebral ischemia-reperfusion (I/R) injury, in a rat model of 8-min asphyxial cardiac arrest (CA) and resuscitation. Increased autophagosome numbers, expression of lysosomal cathepsin B, cathepsin D, Beclin-1 and microtubule-associated protein light chain 3 (LC3) suggested autophagy in hippocampal cells. The expression of tumor suppressor protein 53 (p53) and its target genes: Bax, p53-upregulated modulator of apoptosis (PUMA) and damage-regulated autophagy modulator (DRAM) were upregulated following CA. These results indicate that CA affects both autophagy and apoptosis, partially mediated by p53. Autophagy plays a significant role in hippocampal neuronal death induced by cerebral I/R following asphyxial-CA.

• #41 RETRACTED ARTICLE: Cardiac arrest triggers hippocampal neuronal death through autophagic and apoptotic pathways | Scientific Reports

  https://www.nature.com/articles/srep27642

  Ischemia-reperfusion (I/R) injury following CA results in neuronal death by apoptosis and necrosis, however, the molecular mechanisms are still unclear. Emerging evidence suggests excessive autophagy in several cerebral ischemic and neurodegenerative diseases. However, its role in neuronal apoptosis remains to be elucidated. Autophagy may contribute to cell survival in some degenerative diseases via degradation of damaged and misfolded proteins. Conversely, excessive autophagy negatively impacts cell survival, thereby, causing cell death. However, the mechanism underlying cell death remains unknown. Increasing evidence, including the fact that several regulators are involved in both apoptosis and autophagy activation, suggests that autophagy and apoptosis are mutually influenced by each other in a complex interaction.

• #42 RETRACTED ARTICLE: Cardiac arrest triggers hippocampal neuronal death through autophagic and apoptotic pathways | Scientific Reports

  https://www.nature.com/articles/srep27642

  The current study demonstrates that ischemic CA injury leads to cell death and increased autophagic activity, marked by accumulation of autophagosomes, autolysosomes and other biomarkers. The increase in autophagosomes and LC3-II following CA is not likely due to decreased autophagic activity since an increase in active lysosomal cathepsins was also observed. Additionally, lysosomal inhibitor, E64, increased LC3-II expression, while class III PI3k inhibitor, 3-MA, decreased the levels of LC3-II. […] Our findings further indicate autophagic mechanisms in hippocampal neuronal injury during cerebral ischemia following CA. An early decrease in the number of hippocampus CA1 pyramidal neurons has been reported after severe ischemic insults. Our rescue studies demonstrated that 3-MA pretreatment within a critical time window of 1.5h after ROSC inhibited apoptosis in hippocampal pyramidal neurons in both CA1 and CA3. Thus, autophagy may mediate early signaling of cell death in hippocampal neurons. The interaction of autophagy with apoptosis and necrosis drives the cell to apoptotic or necrotic death, indicating that autophagy inhibition was ineffective.

• #43 RETRACTED ARTICLE: Cardiac arrest triggers hippocampal neuronal death through autophagic and apoptotic pathways | Scientific Reports

  https://www.nature.com/articles/srep27642

  Our findings suggest that 3-MA, the BFA and PFT- significantly inhibit the hippocampal cell death induced by CA. PFT- is a known inhibitor of p53 while 3-MA is known as an autophagy marker. In addition, the inhibition of p53 attenuated autophagy and hippocampal neuronal apoptosis. These results suggest that inhibition of p53 may inhibit both apoptosis and autophagic cell death, simultaneously. Therefore, p53 targeting might represent a neuroprotective intervention for various neuronal ischemic diseases. Further studies are needed to elucidate the detailed mechanism and to develop autophagic or p53-pathway targeted interventions to treat CA and to move this towards translational studies. […] In conclusion, this study suggests that both autophagy and apoptosis mediate cell death following CA. Autophagy activation was partially mediated by p53, contributed to CA-induced hippocampal neuronal death and preceded the apoptotic process. Further studies to identify the role of autophagy following CA are needed to elucidate the pathogenesis of cerebral ischemic diseases involving protein misfolding.

• #44 Sudden cardiac death: epidemiology, pathogenesis and management

  https://www.imrpress.com/journal/RCM/22/1/10.31083/j.rcm.2021.01.207

  Sudden cardiac death (SCD) is an unexpected sudden death due to a heart condition, that occurs within one hour of symptoms onset. SCD is a leading cause of death in western countries, and is responsible for the majority of deaths from cardiovascular disease. Moreover, SCD accounts for mortality in approximately half of all coronary heart disease patients. […] In this article, we sought to review established and new modes of screening patients at risk for SCD, treatment and prevention of SCD, and the role of new technologies in the field. Further, we delineate the current epidemiologic trends and pathogenesis. In particular, we describe the advancement in molecular autopsy and genetic testing, the role of target temperature management, extracorporeal membrane oxygenation (ECMO), cardiopulmonary resuscitation (CPR), and transvenous and subcutaneous implantable cardioverter devices (ICDs).

• #45 Cardiac arrest – BHF

  https://www.bhf.org.uk/informationsupport/conditions/cardiac-arrest

  A heart attack can lead to a cardiac arrest as youre at higher risk of having ventricular fibrillation. […] A cardiac arrest is an emergency. […] Starting immediate CPR is vital as it keeps blood and oxygen moving to the brain and around the body. A defibrillator will then deliver a controlled electric shock to try and get the heart beating normally again. […] Doctors will want to work out what caused the cardiac arrest. They can then recommend medication and treatment, such as a pacemaker or implantable cardioverter defibrillator (ICD), to reduce the risk of it happening again. […] A lack of oxygen to the brain during a cardiac arrest can sometimes have long-term effects on your brain. Effects can include personality changes, problems with memory, feeling tired, dizziness or balance issues, aphasia/dysphasia (problems with speech and language), myoclonus (involuntary movements), permanent brain injury. […] Your doctor may suggest making lifestyle changes to reduce your risk of another cardiac arrest.

• #46 Sudden Cardiac Death, Cardiac Arrest, and Heart Disease

  https://www.webmd.com/heart-disease/sudden-cardiac-death

  Emergency treatment includes cardiopulmonary resuscitation (CPR) and defibrillation. CPR is a manual technique using repetitive pressing to the chest and breathing into the person’s airways that keeps enough oxygen and blood flowing to the brain until the normal heart rhythm is restored with an electric shock to the chest, a procedure called defibrillation. […] For patients with coronary artery disease, an interventional procedure such as angioplasty (blood vessel repair) or bypass surgery may be needed to improve blood flow to the heart muscle and reduce the risk of SCD.

• #47 Postcardiac arrest syndrome: from immediate resuscitation to long-term outcome | Annals of Intensive Care | Full Text

  https://annalsofintensivecare.springeropen.com/articles/10.1186/2110-5820-1-45

  The therapeutic management of the postcardiac arrest syndrome has two main goals: the initial treatment of shock and organ failures, and the optimization of cerebral protection. […] The existence of further cerebral damage during the reperfusion phase encouraged intense research on the benefit of treatments designed to limit the neurological consequences of the postcardiac arrest syndrome. […] Achieving and maintaining a perfect homeostasis, particularly in terms of metabolism, are the major goals of post cardiac arrest management. […] Immediately after CA, no clinical signs or investigations accurately predict the patient’s outcome. […] After ROSC, accurate prognostication can only occur after 72 hours have elapsed from all factors that may alter neurological evaluation. […] Accurate assessment of prognosis is necessary to identify patients who will really benefit from intensive care and to avoid extending unnecessary treatments to those who have no reasonable chance of recovery.

• #48 Study IDs Nonclinical, Modifiable Risk Factors Tied to Sudden Cardiac Arrest – Renal and Urology News

  https://www.renalandurologynews.com/news/study-ids-nonclinical-modifiable-risk-factors-tied-to-sudden-cardiac-arrest/

  An estimated 40 to 63 percent of sudden cardiac arrest cases could be prevented by improving unfavorable profiles. […] Modifiable, nonclinical risk factors such as lifestyle modifications and physical measures may reduce the risk for sudden cardiac arrest (SCA), according to a study published online April 28 in the Canadian Journal of Cardiology. […] The researchers found that during a median follow-up duration of 13.8 years, SCA was associated with 56 risk factors spanning lifestyles, physical measures, psychosocial factors, socioeconomic status, and the local environment. […] An estimated 40 to 63 percent of SCA cases could be prevented by improving unfavorable profiles. Lifestyle modifications accounted for the largest proportion of preventable cases, followed by improvements in physical measures, psychosocial factors, socioeconomic status, and the local environment. […] Theoretically, disease prevention through lifestyle modification represents a low-cost, easily implemented, highly feasible and high-yield approach, although poor compliance of individuals has made this difficult to achieve, the authors write.

• #49 Study IDs Nonclinical, Modifiable Risk Factors Tied to Sudden Cardiac Arrest – Endocrinology Advisor

  https://www.endocrinologyadvisor.com/news/study-ids-nonclinical-modifiable-risk-factors-tied-to-sudden-cardiac-arrest/

  An estimated 40 to 63% of sudden cardiac arrest cases could be prevented by improving unfavorable profiles. […] Modifiable, nonclinical risk factors such as lifestyle modifications and physical measures may reduce the risk for sudden cardiac arrest (SCA), according to a study published online April 28 in the Canadian Journal of Cardiology. […] The researchers found that during a median follow-up duration of 13.8 years, SCA was associated with 56 risk factors spanning lifestyles, physical measures, psychosocial factors, socioeconomic status, and the local environment. […] An estimated 40 to 63 percent of SCA cases could be prevented by improving unfavorable profiles. Lifestyle modifications accounted for the largest proportion of preventable cases, followed by improvements in physical measures, psychosocial factors, socioeconomic status, and the local environment. […] Theoretically, disease prevention through lifestyle modification represents a low-cost, easily implemented, highly feasible and high-yield approach, although poor compliance of individuals has made this difficult to achieve, the authors write.

• #50 Sports Participation and Sudden Cardiac Arrest

  https://www.acc.org/latest-in-cardiology/articles/2016/06/28/07/06/sports-participation-and-sudden-cardiac-arrest

  The main goal of screening competitive athletes for sports participation is to identify or raise suspicion of cardiovascular abnormalities that are potentially responsible for SCD on the athletic field. […] The use of screening ECGs in preparticipation screening for young competitive athletes remains controversial. […] Current guidelines emphasize screening competitive athletes with a comprehensive history and physical examination.

• #51 Sudden cardiac death in heart failure with preserved ejection fraction: an updated review | International Journal of Arrhythmia | Full Text

  https://arrhythmia.biomedcentral.com/articles/10.1186/s42444-021-00059-3

  Despite the advances in medical and device therapies for heart failure (HF), sudden cardiac death (SCD) remains a tremendous global burden in patients with HF. […] Although patients with HF with preserved ejection fraction (HFpEF) were less prone to SCD compared to patients with HF with reduced ejection fraction (HFrEF), patients with HFpEF did account for a significant proportion of all HF patients who encountered SCD. […] There is a great unmet need in the field of SCD in HFpEF regarding risk stratification and appropriate device therapy with ICD implantation. […] We also aim at clarifying the mechanisms, risk factors, and prevention of SCD in HFpEF. […] Previous studies in HFpEF population showed that the causes of death were cardiovascular origin in 60-70% patients, with the majority being SCD (20-40%).

• #52 FDA Clears Novel Wearable Defibrillator to Prevent Sudden Cardiac Arrest

  https://www.thecardiologyadvisor.com/news/fda-clears-novel-wearable-defibrillator-to-prevent-sudden-cardiac-arrest/

  The FDA has cleared the Jewel Patch Wearable Cardioverter Defibrillator (Patch-WCD) for adult patients aged 18 years and older who are at risk for sudden cardiac arrest, and either are not candidates for or refuse an implantable defibrillator. […] The system uses a proprietary algorithm to detect and classify shockable arrhythmias (ie, rapid ventricular tachycardia, coarse ventricular fibrillation). […] The FDA clearance of the Jewel Patch-WCD was supported by data from a prospective, single arm study (ClinicalTrials.gov Identifier: NCT05201495) that included patients at risk of sudden cardiac arrest due to ventricular tachycardia/ventricular fibrillation and who were not candidates or who refused an implantable defibrillator. […] Findings showed the Jewel Patch-WCD was safe and effective. […] During the study 11 shocks were administered in 9 patients, with 9 shocks considered appropriate. […] No patient deaths or missed episodes were reported during the trial.

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