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Cardiac arrest

Cardiac arrest, also known as sudden cardiac arrest (SCA), is a condition in which the heart suddenly and unexpectedly stops beating. When the heart stops, blood cannot circulate properly through the body and the blood flow to the brain and other organs is decreased. When the brain does not receive enough blood, this can cause a person to lose consciousness and brain cells begin to die within minutes due to a lack of oxygen. Coma and persistent vegetative state may result from cardiac arrest. Cardiac arrest is typically identified by the absence of a central pulse and abnormal or absent breathing.

Signs and symptoms
Cardiac arrest is not preceded by any warning symptoms in approximately 50 percent of people. For individuals who do experience symptoms, the symptoms are usually nonspecific to the cardiac arrest. For example, new or worsening chest pain, fatigue, blackouts, dizziness, shortness of breath, weakness, or vomiting. When cardiac arrest is suspected by a layperson (due to signs of unconsciousness, abnormal breathing or no pulse) it should be assumed that the victim is in cardiac arrest. Bystanders should call emergency medical services (such as 911, 999 or 112) and initiate CPR. == Risk factors ==
Risk factors
Major risk factors for cardiac arrest include age and underlying cardiovascular disease. A prior episode of sudden cardiac arrest increases the likelihood of future episodes. A 2021 meta-analysis assessing the recurrence of cardiac arrest in out-of-hospital cardiac arrest survivors identified that 15% of survivors experienced a second event, most often in the first year. Furthermore, of those who experienced recurrence, 35% had a third episode. Current cigarette smokers with coronary artery disease were found to have a two to threefold increase in the risk of sudden death between ages 30 and 59. Furthermore, it was found that former smokers' risk was closer to that of those who had never smoked. A statistical analysis of many of these risk factors determined that approximately 50% of all cardiac arrests occur in 10% of the population perceived to be at greatest risk, due to aggregate harm of multiple risk factors, demonstrating that cumulative risk of multiple comorbidities exceeds the sum of each risk individually. ==Causes and mechanisms==
Causes and mechanisms
. Changes in this pattern can result from injury to the cardiac muscle and lead to non-conducted beats and ultimately cardiac arrest. The underlying causes of sudden cardiac arrest can result from cardiac and non-cardiac causes. The most common underlying causes are different, depending on the patient's age. Common cardiac causes include coronary artery disease, non-atherosclerotic coronary artery abnormalities, structural heart damage, and inherited arrhythmias. Common non-cardiac causes include respiratory arrest, diabetes, medications, and trauma. The most common mechanism underlying sudden cardiac arrest is an arrhythmia (an irregular rhythm). This hemodynamic collapse results in poor blood flow to the brain and other organs, which if prolonged causes persistent damage. There are many different types of arrhythmias, but the ones most frequently recorded in sudden cardiac arrest are ventricular tachycardia and ventricular fibrillation. Both ventricular tachycardia and ventricular fibrillation can prevent the heart from generating coordinated ventricular contractions, thereby failing to sustain adequate blood circulation. Less common initial arrhythmias occurring in cardiac arrest include pulseless electrical activity and asystole. When an atherosclerotic plaque dislodges, it can block the flow of blood and oxygen through small arteries, such as the coronary arteries, resulting in ischemic injury. In the heart, this results in myocardial tissue damage which can lead to structural and functional changes that disrupt normal conduction patterns and alter heart rate and contraction. Indeed, postmortem examinations have shown that the most common finding in cases of sudden cardiac death is chronic, high-grade stenosis of at least one segment of a major coronary artery. While CAD is a leading contributing factor, this is an age-dependent factor, with CAD being a less common cause of sudden cardiac death in people under the age of 40. Non-atherosclerotic coronary artery abnormalities Abnormalities of the coronary arteries not related to atherosclerosis include inflammation (known as coronary arteritis), embolism, vasospasm, mechanical abnormalities related to connective tissue diseases or trauma, and congenital coronary artery anomalies (most commonly anomalous origin of the left coronary artery from the pulmonary artery). These conditions account for 10-15% of cardiac arrest and sudden cardiac death. Left ventricular hypertrophy is a leading cause of sudden cardiac deaths in the adult population. This is because elevated blood pressure over the course of several years requires the heart to adapt to the requirement of pumping harder to adequately circulate blood throughout the body. If the heart does this for a prolonged period of time, the left ventricle can experience hypertrophy (grow larger) in a way that decreases the heart's effectiveness. Left ventricular hypertrophy can be demonstrated on an echocardiogram and electrocardiogram (EKG). These are frequently caused by genetic disorders. These conditions are a fraction of the overall deaths related to cardiac arrest but represent conditions that may be detected prior to arrest and may be treatable. The symptomatic expression of LQTS is quite broad and more often presents with syncope rather than cardiac arrest. The risk of cardiac arrest is still present, and people with family histories of sudden cardiac arrests should be screened for LQTS and other treatable causes of lethal arrhythmia. Higher levels of risk for cardiac arrest are associated with female sex, more significant QT prolongation, history of unexplained syncope (fainting spells), or premature sudden cardiac death. Although it is not recognized as an inherited condition, Wolff–Parkinson–White syndrome in which an accessory conduction pathway bypassing the atrioventricular node is present and can cause abnormal conduction patterns leading to supraventricular tachycardia, pre-excited atrial fibrillation, and cardiac arrest. Common non-cardiac causes include respiratory arrest, diabetes, certain medications, and blunt trauma (especially to the chest). • Respiratory arrest will be followed by cardiac arrest unless promptly treated. • Diabetes-related factors contributing to cardiac arrest include silent myocardial ischemia, nervous system dysfunction, and electrolyte disturbances leading to abnormal cardiac repolarization. • Certain medications can worsen an existing arrhythmia. Some examples include antibiotics like macrolides, diuretics, and heart medications such as anti-arrhythmic medications. Circadian patterns are also recognized as triggering factors in cardiac arrest. Per a 2021 systematic review, throughout the day there are two main peak times in which cardiac arrest occurs. The first is in the morning hours and the second is in the afternoon. Moreover, survival rates following cardiac arrest were lowest when occurring between midnight and 6am. Many of these non-cardiac causes of cardiac arrest are reversible. A common mnemonic used to recall the reversible causes of cardiac arrest is referred to as the Hs and Ts. The Hs are hypovolemia, hypoxia, hydrogen cation excess (acidosis), hyperkalemia, hypokalemia, hypothermia, and hypoglycemia. The Ts are toxins, (cardiac) tamponade, tension pneumothorax, thrombosis (myocardial infarction), thromboembolism, and trauma. Mechanism The definitive electrical mechanisms of cardiac arrest, which may arise from any of the functional, structural, or physiologic abnormalities mentioned above, are characterized by arrhythmias. Some of the electrophysiologic mechanisms underpinning ventricular fibrillations include ectopic automaticity, re-entry, and triggered activity. However, structural changes in the diseased heart as a result of inherited factors (mutations in ion-channel coding genes, for example) cannot explain the sudden onset of cardiac arrest. In ventricular tachycardia, the heart also beats faster than normal, which may prevent the heart chambers from properly filling with blood. Ventricular tachycardia is characterized by an altered QRS complex and a heart rate greater than 100 beats per minute. When V-tach is sustained (lasts for at least 30 seconds), inadequate blood flow to heart tissue can lead to cardiac arrest. Bradyarrhythmias occur following dissociation of spontaneous electrical conduction and the mechanical function of the heart resulting in pulseless electrical activity (PEA) or through complete absence of electrical activity of the heart resulting in asystole. Similar to the result of tachyarrhythmias, these conditions lead to an inability to sustain adequate cardiac output. ==Diagnosis==
Diagnosis
Cardiac arrest is synonymous with clinical death. Moreover, in the post-resuscitation patient, a 12-lead EKG can help identify some causes of cardiac arrest, such as STEMI which may require specific treatments. Point-of-care ultrasound (POCUS) is a tool that can be used to examine the movement of the heart and its force of contraction at the patient's bedside. POCUS can accurately diagnose cardiac arrest in hospital settings, as well as visualize cardiac wall motion contractions. These images can help clinicians determine whether electrical activity within the heart is pulseless or pseudo-pulseless, as well as help them diagnose the potentially reversible causes of an arrest. Owing to the inaccuracy diagnosis solely based on central pulse detection, some bodies like the European Resuscitation Council have de-emphasized its importance. Instead, the current guidelines prompt individuals to begin CPR on any unconscious person with absent or abnormal breathing. Various other methods for detecting circulation and therefore diagnosing cardiac arrest have been proposed. Guidelines following the 2000 International Liaison Committee on Resuscitation recommendations were for rescuers to look for "signs of circulation" but not specifically the pulse. Per evidence that these guidelines were ineffective, the current International Liaison Committee on Resuscitation recommendation is that cardiac arrest should be diagnosed in all casualties who are unconscious and not breathing normally, a similar protocol to that which the European Resuscitation Council has adopted. This could help elucidate the cause of death in the patient. Other physical signs or symptoms can help determine the potential cause of the cardiac arrest. Below is a chart of the clinical findings and signs/symptoms a person may have and potential causes associated with them. == Prevention ==
Prevention
Primary prevention With the lack of positive outcomes following cardiac arrest, efforts have been spent finding effective strategies to prevent cardiac arrest events. The approach to primary prevention promotes a healthy diet, exercise, limited alcohol consumption, and smoking cessation. The risk of a transient catastrophic cardiac event increases in individuals with heart disease during and immediately after exercise. The study found that those who fell under the category of having "Southern [United States] diets" representing those of "added fats, fried food, eggs, organ and processed meats, and sugar-sweetened beverages" had a positive association with an increased risk of cardiac arrest, while those deemed following the "Mediterranean diets" had an inverse relationship regarding the risk of cardiac arrest. A Cochrane review published in 2016 found moderate-quality evidence to show that blood pressure-lowering drugs do not reduce the risk of sudden cardiac death. In certain high-risk patient populations, implantable cardioverter-defibrillators (ICD) are also used to prevent sudden cardiac death. Numerous studies have been conducted on the use of ICDs for the secondary prevention of SCD. These studies have shown improved survival with ICDs compared to the use of anti-arrhythmic drugs. Prevention of SCD with ICD therapy for high-risk patient populations has similarly shown improved survival rates in several large studies. The high-risk patient populations in these studies were defined as those with severe ischemic cardiomyopathy (determined by a reduced left ventricular ejection fraction (LVEF)). The LVEF criteria used in these trials ranged from less than or equal to 30% in MADIT-II to less than or equal to 40% in MUSTT. Alternatively, a wearable cardioverter defibrillator (eg, LifeVest) can be used instead of an implantable defibrillator, and the wearable option can be used as a temporary bridge to an implantable device. Such instances are endocarditis where an implantable device is at high risk of becoming infected if implanted too soon. Crash teams In hospital, a cardiac arrest is referred to as a "crash", or a "code". This typically refers to code blue on the hospital emergency codes. A dramatic drop in vital sign measurements is referred to as "coding" or "crashing", though coding is usually used when it results in cardiac arrest, while crashing might not. Treatment for cardiac arrest is sometimes referred to as "calling a code". Patients in general wards often deteriorate for several hours or even days before a cardiac arrest occurs. This has been attributed to a lack of knowledge and skill amongst ward-based staff, in particular, a failure to measure the respiratory rate, which is often the major predictor of a deterioration and can often change up to 48 hours prior to a cardiac arrest. In response, many hospitals now have increased training for ward-based staff. A number of "early warning" systems also exist that aim to quantify the person's risk of deterioration based on their vital signs and thus provide a guide to staff. In addition, specialist staff are being used more effectively to augment the work already being done at the ward level. These include: • Crash teams (or code teams) – These are designated staff members with particular expertise in resuscitation who are called to the scene of all arrests within the hospital. This usually involves a specialized cart of equipment (including a defibrillator) and drugs called a "crash cart" or "crash trolley". • Medical emergency teams – These teams respond to all emergencies with the aim of treating people in the acute phase of their illness in order to prevent a cardiac arrest. These teams have been found to decrease the rates of in-hospital cardiac arrest (IHCA) and improve survival. • Critical care outreach – In addition to providing the services of the other two types of teams, these teams are responsible for educating non-specialist staff. In addition, they help to facilitate transfers between intensive care/high dependency units and the general hospital wards. This is particularly important as many studies have shown that a significant percentage of patients discharged from critical care environments quickly deteriorate and are re-admitted; the outreach team offers support to ward staff to prevent this from happening. ==Management==
Management
Sudden cardiac arrest may be treated via attempts at resuscitation. This is usually carried out based on basic life support, advanced cardiac life support (ACLS), pediatric advanced life support (PALS), or neonatal resuscitation program (NRP) guidelines. Cardiopulmonary resuscitation Early cardiopulmonary resuscitation (CPR) is essential to surviving cardiac arrest with good neurological function. It is recommended that it be started as soon as possible with minimal interruptions once begun. The components of CPR that make the greatest difference in survival are chest compressions and defibrillating shockable rhythms. After defibrillation, chest compressions should be continued for two minutes before another rhythm check. It is unclear if a few minutes of CPR before defibrillation results in different outcomes than immediate defibrillation. Correctly performed bystander CPR has been shown to increase survival, however it is performed in fewer than 30% of out-of-hospital cardiac arrests (OHCAs) . Likewise, a 2022 systematic review on exercise-related cardiac arrests supported early intervention of bystander CPR and AED use (for shockable rhythms) as they improve survival outcomes. If high-quality CPR has not resulted in return of spontaneous circulation and the person's heart rhythm is in asystole, stopping CPR and pronouncing the person's death is generally reasonable after 20 minutes. Some of these cases should have longer and more sustained CPR until they are nearly normothermic. If this occurs, then modification to existing oropharyngeal suction may be required, such as using suction-assisted airway management. Tracheal intubation has not been found to improve survival rates or neurological outcomes in cardiac arrest, and in the prehospital environment, may worsen it. Endotracheal tubes and supraglottic airways appear equally useful. When done by emergency medical personnel, 30 compressions followed by two breaths appear to be better than continuous chest compressions and breaths being given while compressions are ongoing. Defibrillation Defibrillation is indicated if a shockable rhythm is present; the two shockable rhythms are ventricular fibrillation and ventricular tachycardia. These shockable rhythms have a 25-40% likelihood of survival, compared with a significantly lower rate (less than 5%) in non-shockable rhythms. The non-shockable rhythms include asystole and pulseless electrical activity. Ventricular fibrillation involves the ventricles of the heart rapidly contracting in an disorganized pattern, and thereby limiting blood flow from the heart. This is due to an uncoordinated electrical activity. The electrocardiogram (ECG) shows irregular QRS complexes at a very high rate (>300 beats per minute). In ventricular tachycardia, the ECG will show a wide complex rhythm at a rate higher than 100 beats per minute. These two rhythm lead to hemodynamic instability and compromise, resulting in poor perfusion to vital organs (including the heart itself). A defibrillator — either implanted or external — delivers an electrical current that results in the entire myocardium simultaneously depolarized thereby stopping the arrhythmia. Defibrillators can deliver energy as monophasic or biphasic waveforms, although biphasic defibrillators are now the most common. Prior studies suggest that biphasic shock is more likely to produce successful defibrillation after a single shock, however rate of survival is comparable between the methods. There is increasing use of public access to defibrillators. This typically involves placing AEDs in publicly-accessible places and training staff in these areas on how to use them. This allows defibrillation to occur prior to the arrival of emergency services, which has been shown to increase the chances of survival. People who have cardiac arrests in remote locations have worse outcomes. Defibrillation cannot reverse asystole or pulseless electrical activity, and CPR must be initiated first in these cases. A similar concept, cardioversion, utilizes the same defibrillation machine but is used for other rhythms such as atrial fibrillation and supraventricular tachycardia. In these rhythms, the machine is "synchronized" to the QRS complex to avoid shocking on the T wave (and inducing VT or VF). Cardioversion can be done electively for rhythm control, or urgently if the rhythm is unstable. Medications Medications recommended in the ACLS protocol include epinephrine, amiodarone, and lidocaine. Epinephrine in adults improves survival but does not appear to improve neurologically normal survival. In ventricular fibrillation and pulseless ventricular tachycardia, 1 mg of epinephrine is given every 3–5 minutes, following an initial round of CPR and defibrillation. Amiodarone and lidocaine are anti-arrhythmic medications. Amiodarone is a class III antiarrhythmic. Amiodarone may be used in cases of ventricular fibrillation, ventricular tachycardia, and wide complex tachycardia. Lidocaine is a Class IB anti-arrhythmic, also used to manage acute arrhythmias. Anti-arrhythmic medications may be used after an unsuccessful defibrillation attempt. However, neither lidocaine nor amiodarone improves survival to hospital discharge, despite both equally improving survival to hospital admission. The first dose is given as a 300 mg bolus. The second dose is given as a 600 mg bolus. Calcium, given as calcium chloride, works as an inotrope and vasopressor. Calcium is used in specific circumstances such as electrolyte disturbances (hyperkalemia) and calcium-channel blocker toxicity. Overall, calcium is not routinely used during cardiac arrest as it does not provide additional benefit (compared to non-use) and may even cause harm (poor neurologic outcomes). Vasopressin overall does not improve or worsen outcomes compared to epinephrine. The use of atropine, lidocaine, and amiodarone have not been shown to improve survival from cardiac arrest. Calcium levels are considered a key factor contributing to cardiac arrests in this population. Tricyclic antidepressant (TCA) overdose can lead to cardiac arrest with typical ECG findings including wide QRS and prolonged QTc. Treatment for this condition includes activated charcoal and sodium bicarbonate. Magnesium can be given at a dose of 2 g (iv or oral bolus) to manage torsades de points. However, without specific indication, magnesium is not generally given in cardiac arrest. In people with a confirmed pulmonary embolism as the cause of arrest, thrombolytics may be of benefit. The process involves cooling for a 24-hour period, with a target temperature of , followed by gradual rewarming over the next 12 to 24 hrs. There are several methods used to lower the body temperature, such as applying ice packs or cold-water circulating pads directly to the body or infusing cold saline. The effectiveness of TTM after OHCA is an area of ongoing study. Several recent reviews have found that patients treated with TTM have more favorable neurological outcomes. Osborn waves on ECG are frequent during TTM, particularly in patients treated with 33 °C. Osborn waves are not associated with increased risk of ventricular arrhythmia, and may be considered a benign physiological phenomenon, associated with lower mortality in univariable analyses. Other directives may be made to stipulate the desire for intubation in the event of respiratory failure or, if comfort measures are all that are desired, by stipulating that healthcare providers should "allow natural death". Chain of survival Several organizations promote the idea of a chain of survival. 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. Early recognition that a cardiac arrest has occurred is key to survival, for every minute a patient stays in cardiac arrest, their chances of survival drop by roughly 10%. 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 blue, which usually denotes impending or acute onset of cardiac arrest or respiratory failure. Other Resuscitation with extracorporeal membrane oxygenation devices has been attempted with better results for in-hospital cardiac arrest (29% survival) than OHCA (4% survival) in populations selected to benefit most. Cardiac catheterization in those who have survived an OHCA appears to improve outcomes, although high-quality evidence is lacking. It is recommended to be done as soon as possible in those who have had a cardiac arrest with ST elevation due to underlying heart problems. ==Prognosis==
Prognosis
The overall rate of survival among those who have OHCA is 10%. Among those who have an OHCA, 70% occur at home, and their survival rate is 6%. For those who have an in-hospital cardiac arrest (IHCA), the survival rate one year from at least the occurrence of cardiac arrest is estimated to be 13%. For IHCA, survival to discharge is around 22%. In those over the age of 70 who have a cardiac arrest while in hospital, survival to hospital discharge is less than 20%. How well these individuals manage after leaving the hospital is not clear. Survival to discharge from the hospital is more likely among people whose cardiac arrest was witnessed by a bystander or emergency medical services, who received bystander CPR, and who live in Europe and North America. Rates of survival are better in those who had someone witness their collapse, received bystander CPR or had either V-fib or V-tach when assessed. Survival among those with V-fib or V-tach is 15 to 23%. Hypoxic ischemic brain injury is a concerning outcome for people suffering a cardiac arrest. Most improvements in cognition occur during the first three months following cardiac arrest, with some individuals reporting improvement up to one year post-cardiac arrest. 50 – 70% of cardiac arrest survivors report fatigue as a symptom. ==Epidemiology==
Epidemiology
United States The risk of cardiac arrest varies with geographical region, age, and gender. The lifetime risk is three times greater in men (12.3%) than women (4.2%) based on analysis of the Framingham Heart Study. This gender difference disappeared beyond 85 years of age. Around half of these individuals are younger than 65 years of age. Based on death certificates, sudden cardiac death accounts for about 20% of all deaths in the United States. In the United States, approximately 326,000 cases of out-of-hospital and 209,000 cases of IHCA occur among adults annually, which works out to be an incidence of approximately 110.8 per 100,000 adults per year. Rates are lower in Canada. Other regions Non-Western regions of the world have differing incidences. The incidence of sudden cardiac death in China is 41.8 per 100,000 and in South India is 39.7 per 100,000. ==Society and culture==
Society and culture
Names In many publications, the stated or implicit meaning of "sudden cardiac death" is sudden death from cardiac causes. Some physicians call cardiac arrest "sudden cardiac death" even if the person survives. Thus one can hear mentions of "prior episodes of sudden cardiac death" in a living person. In 2021, the American Heart Association clarified that "heart attack" is often mistakenly used to describe cardiac arrest. While a heart attack refers to death of heart muscle tissue as a result of blood supply loss, cardiac arrest is caused when the heart's electrical system malfunctions. Furthermore, the American Heart Association explains that "if corrective measures are not taken rapidly, this condition progresses to sudden death. Cardiac arrest should be used to signify an event as described above, that is reversed, usually by CPR and/or defibrillation or cardioversion, or cardiac pacing. Sudden cardiac death should not be used to describe events that are not fatal". Slow code A "slow code" is a slang term for the practice of deceptively delivering sub-optimal CPR to a person in cardiac arrest, when CPR is considered to have no medical benefit. A "show code" is the practice of faking the response altogether for the sake of the person's family. Such practices are ethically controversial and are banned in some jurisdictions. The European Resuscitation Council Guidelines released a statement in 2021 that clinicians are not suggested to participate/take part in "slow codes". ==Children==
Children
In children, the most common cause of cardiac arrest is shock or respiratory failure that has not been treated. In childhood hypertrophic cardiomyopathy, previous adverse cardiac events, non-sustained ventricular tachycardia, syncope, and left ventricular hypertrophy have been shown to predict sudden cardiac death. Other causes can include drugs, such as cocaine and methamphetamine, or overdose of medications, such as antidepressants. The use of calcium in children has been associated with poor neurological function as well as decreased survival. Correct dosing of medications in children is dependent on weight, and to minimize time spent calculating medication doses, the use of a Broselow tape is recommended. Rates of survival in children with cardiac arrest are 3 to 16% in North America. == See also ==
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