For other uses, see Cardiac arrest (disambiguation).
Not to be confused with Heart attack.
| Cardiac arrest |
| Classification and external resources |
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CPR being administered during a simulation of cardiac arrest.
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| ICD-10 |
I46 |
| ICD-9 |
427.5 |
| DiseasesDB |
2095 |
| MeSH |
D006323 |
Cardiac arrest, also known as cardiopulmonary arrest or circulatory arrest, is the cessation of functional circulation of the blood due to failure of the heart to contract effectively.[1] Medical personnel may refer to an unexpected cardiac arrest as a sudden cardiac arrest (SCA).
A cardiac arrest is different from (but may be caused by) a heart attack, where blood flow to the muscle of the heart is impaired.[2] It is different from congestive heart failure, where circulation is substandard, but the heart is still pumping sufficient blood to sustain life.
Arrested blood circulation prevents delivery of oxygen and glucose to the body. Lack of oxygen and glucose to the brain causes loss of consciousness, which then results in abnormal or absent breathing. Brain injury is likely to happen if cardiac arrest goes untreated for more than five minutes.[3][4][5] For the best chance of survival and neurological recovery, immediate and decisive treatment is imperative.[6]
Cardiac arrest is a medical emergency that, in certain situations, is potentially reversible if treated early. Unexpected cardiac arrest can lead to death within minutes: this is called sudden cardiac death (SCD).[1] The treatment for cardiac arrest is immediate defibrillation if a "shockable" rhythm is present, while cardiopulmonary resuscitation (CPR) is used to provide circulatory support and/or to induce a "shockable" rhythm.
Contents
- 1 Classification
- 2 Signs and symptoms
- 3 Causes
- 3.1 Coronary heart disease
- 3.2 Non-ischemic heart disease
- 3.3 Non-cardiac
- 3.4 Risk factors
- 3.5 Hs and Ts
- 4 Diagnosis
- 5 Prevention
- 5.1 Code teams
- 5.2 Implantable cardioverter defibrillators
- 6 Management
- 6.1 Cardiopulmonary resuscitation
- 6.2 Defibrillation
- 6.3 Medications
- 6.4 Therapeutic hypothermia
- 6.5 Do not resuscitate
- 6.6 Chain of survival
- 6.7 Other
- 7 Prognosis
- 8 Epidemiology
- 9 References
- 10 External links
Classification
Clinicians classify cardiac arrest into "shockable" versus "non–shockable", as determined by the ECG rhythm. This refers to whether a particular class of cardiac dysrhythmia is treatable using defibrillation.[7] The two "shockable" rhythms are ventricular fibrillation and pulseless ventricular tachycardia while the two "non–shockable" rhythms are asystole and pulseless electrical activity.[8]
Signs and symptoms
Cardiac arrest is an abrupt cessation of pump function in the heart (as evidenced by the absence of a palpable pulse). Prompt intervention can usually reverse a cardiac arrest, but without such intervention it will almost always lead to death.[1] In certain cases, it is an expected outcome to a serious illness.[9]
However, due to inadequate cerebral perfusion, the patient will be unconscious and will have stopped breathing. The main diagnostic criterion to diagnose a cardiac arrest (as opposed to respiratory arrest which shares many of the same features) is lack of circulation; however, there are a number of ways of determining this. Near death experiences are reported by 10-20% of people who survived cardiac arrest.[10]
Causes
Coronary heart disease is the leading cause of sudden cardiac arrest. Many other cardiac and non-cardiac conditions also increase one's risk.
Coronary heart disease
Approximately 60–70% of SCD is related to coronary heart disease.[11][12] Among adults, ischemic heart disease is the predominant cause of arrest[13] with 30% of people at autopsy showing signs of recent myocardial infarction.[citation needed]
Non-ischemic heart disease
A number of other cardiac abnormalities can increase the risk of SCD including: cardiomyopathy, cardiac rhythm disturbances, hypertensive heart disease,[11] congestive heart failure.[14]
In a group of military recruits aged 18–35, cardiac anomalies accounted for 51% of cases of SCD, while in 35% of cases the cause remained unknown. Underlying pathology included: coronary artery abnormalities (61%), myocarditis (20%), and hypertrophic cardiomyopathy (13%).[15] Congestive heart failure increases the risk of SCD by 5 fold.[14]
Many additional conduction abnormalities exist that place one at higher risk for cardiac arrest. For instance, long QT syndrome, a condition often mentioned in young people's deaths, occurs in 1/5000-1/7000 newborns and is estimated to be responsible 3000 deaths each year compared to the approximately 300000[16] cardiac arrests seen by emergency services . These conditions are a fraction of the overall deaths related to cardiac arrest, but represent conditions which may be detected prior to arrest, which may be treatable.
Non-cardiac
SCDs is unrelated to heart problems in 35% of cases. The most common non-cardiac causes: trauma, non-trauma related bleeding (such as gastrointestinal bleeding, aortic rupture, and intracranial hemorrhage), overdose, drowning and pulmonary embolism.[17] Environmental toxins from for example certain jellyfish may also cause cardiac arrest.
Risk factors
The risk factors for SCD are similar to those seen with coronary heart disease including: smoking, lack of physical exercise, obesity, diabetes, and family history.[18]
Hs and Ts
Main article: Hs and Ts
"Hs and Ts" is the name for a mnemonic used to aid in remembering the possible treatable or reversible causes of cardiac arrest.[7][19]
- Hs
- Hypovolemia - A lack of blood volume
- Hypoxia - A lack of oxygen
- Hydrogen ions (Acidosis) - An abnormal pH in the body
- Hyperkalemia or Hypokalemia - Both excess and inadequate potassium can be life-threatening.
- Hypothermia - A low core body temperature
- Hypoglycemia or Hyperglycemia - Low or high blood glucose
- Ts
- Tablets or Toxins
- Cardiac Tamponade - Fluid building around the heart
- Tension pneumothorax - A collapsed lung
- Thrombosis (Myocardial infarction) - Heart attack
- Thromboembolism (Pulmonary embolism) - A blood clot in the lung
- Traumatic cardiac arrest
Diagnosis
Cardiac arrest is synonymous with clinical death.
A cardiac arrest is usually diagnosed clinically by the absence of a pulse. In many cases lack of carotid pulse is the gold standard for diagnosing cardiac arrest, but lack of a pulse (particularly in the peripheral pulses) may result from other conditions (e.g. shock), or simply an error on the part of the rescuer. Studies have shown that rescuers often make a mistake when checking the carotid pulse in an emergency, whether they are healthcare professionals[20] or lay persons.[21]
Owing to the inaccuracy in this method of diagnosis, some bodies such as the European Resuscitation Council (ERC) have de-emphasised its importance. The Resuscitation Council (UK), in line with the ERC's recommendations and those of the American Heart Association,[19] have suggested that the technique should be used only by healthcare professionals with specific training and expertise, and even then that it should be viewed in conjunction with other indicators such as agonal respiration.[7]
Various other methods for detecting circulation have been proposed. Guidelines following the 2000 International Liaison Committee on Resuscitation (ILCOR) recommendations were for rescuers to look for "signs of circulation", but not specifically the pulse.[19] These signs included coughing, gasping, colour, twitching and movement.[22] However, in face of evidence that these guidelines were ineffective, the current recommendation of ILCOR is that cardiac arrest should be diagnosed in all casualties who are unconscious and not breathing normally.[19]
Prevention
With positive outcomes following cardiac arrest unlikely, an effort has been spent in finding effective strategies to prevent cardiac arrest. With the prime causes of cardiac arrest being ischemic heart disease, efforts to promote a healthy diet, exercise, and smoking cessation are important. For people at risk of heart disease, measures such as blood pressure control, cholesterol lowering, and other medico-therapeutic interventions are used.[1]
Code teams
In medical parlance, cardiac arrest is referred to as a "code" or a "crash". 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".
Extensive research has shown that patients in general wards often deteriorate for several hours or even days before a cardiac arrest occurs.[7][23] This has been attributed to a lack of knowledge and skill amongst ward based staff, in particular a failure to carry out measurement of the respiratory rate, which is often the major predictor of a deterioration[7] and can often change up to 48 hours prior to a cardiac arrest. In response to this, many hospitals now have increased training for ward based staff. A number of "early warning" systems also exist which aim to quantify the risk which patients are at of deterioration based on their vital signs and thus provide a guide to staff. In addition, specialist staff are being utilised more effectively in order to augment the work already being done at ward level. These include:
- Crash teams (or code teams) - These are designated staff members who have 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 defibrillator) and drugs called a "crash cart" or "crash trolley".
- Medical emergency teams - These teams respond to all emergencies, with the aim of treating the patient in the acute phase of their illness in order to prevent a cardiac arrest.
- Critical care outreach - As well as providing the services of the other two types of team, these teams are also 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.
In some medical facilities, the resuscitation team may purposely respond slowly to a patient in cardiac arrest, a practice known as slow code, or may fake the response altogether for the sake of the patient's family, a practice known as show code.[24] This is generally done for patients for whom performing CPR will have no medical benefit.[25] Such practices are ethically controversial,[26] and are banned in some jurisdictions.
Implantable cardioverter defibrillators
A technologically based intervention to prevent further cardiac arrest episodes is the use of an implantable cardioverter-defibrillator (ICD). This device is implanted in the patient and acts as an instant defibrillator in the event of arrhythmia. Note that standalone ICDs do not have any pacemaker functions, but they can be combined with a pacemaker, and modern versions also have advanced features such as anti-tachycardic pacing as well as synchronized cardioversion. A recent study by Birnie et al. at the University of Ottawa Heart Institute has demonstrated that ICDs are underused in both the United States and Canada.[27] An accompanying editorial by Simpson explores some of the economic, geographic, social and political reasons for this.[28] Patients who are most likely to benefit from the placement of an ICD are those with severe ischemic cardiomyopathy (with systolic ejection fractions less than 30%) as demonstrated by the MADIT-II trial.[29]
Management
Sudden cardiac arrest may be treated via attempts at resuscitation. This is usually carried out based upon basic life support (BLS) / advanced cardiac life support (ACLS),[19] pediatric advanced life support (PALS)[30] or neonatal resuscitation program (NRP) guidelines.
Cardiopulmonary resuscitation
CPR is a critical part of the management of cardiac arrest. It should be started as soon as possible and interrupted as little as possible. The component of CPR which seems to make the greatest difference is the chest compressions. Tracheal intubation has not been found to improve survival rates in cardiac arrest cases.[31] A 2009 study has found that assisted ventilation may worsen outcomes over placement of an oral airway with passive oxygen delivery.[32] Intubation in the prehospital environment has been associated with decreased survival.[33] Correctly performed bystander CPR has been shown to increase survival; it is performed in less than 30% of out of hospital arrests.[31] A 2013 review found some evidence that mechanical chest compressions (as performed by a machine) is better than manual chest compressions[34] while a 2011 and 2012 review considered the evidence insufficient.[35][36]
Defibrillation
Shockable and non–shockable causes of cardiac arrest is based on the presence or absence of ventricular fibrillation or pulseless ventricular tachycardia. The shockable rhythms are treated with CPR and defibrillation.
In addition, there is increasing use of public access defibrillation. This involves placing automated external defibrillators in public places, and training staff in these areas how to use them. This allows defibrillation to take place prior to the arrival of emergency services, and has been shown to lead to increased chances of survival. Some defibrillators even provide feedback on the quality of CPR compressions, encouraging the lay rescuer to press the patient's chest hard enough to circulate blood.[37] In addition, it has been shown that those who suffer arrests in remote locations have worse outcomes following cardiac arrest:[38] these areas often have first responders, whereby members of the community receive training in resuscitation and are given a defibrillator, and called by the emergency medical services in the case of a collapse in their local area.
Medications
Medications, while included in guidelines, have been shown not to improve survival to hospital discharge post out of hospital cardiac arrest. This includes the use of epinephrine, atropine, and amiodarone.[39][40] Vasopressin overall does not improve or worse outcomes but may be of benefit in those with asystole especially if used early.[41]
Epinephrine does appear to improve short term outcomes such as return of spontaneous circulation.[42] Some of the lack of long term benefit may be related to delays in epinephrine use.[43]
The 2010 guidelines, from the American Heart Association has removed its recommendation for using atropine in pulseless electrical activity and asystole due to the lack of evidence for its use.[44] Evidence is insufficient for lidocaine and amiodarone may be considered in those who continue in ventricular tachycardia or ventricular fibrillation despite defibrillation.[45] Thrombolytics when used generally may cause harm but may be of benefit in those with a pulmonary embolism as the cause of arrest.[46]
Therapeutic hypothermia
Main article: Therapeutic hypothermia
Cooling a person after cardiac arrest with return of spontaneous circulation (ROSC) but without return of consciousness may or may not improves outcomes.[47][48] This procedure is called therapeutic hypothermia. People are cooled over a 24 hour period, with a target temperature of 32–34 °C (90–93 °F). Death rates in the hypothermia group were initially believed to be 35% lower with generally mild complications.[47][49] A November 2013 trial, however, called this idea into question with findings that a temperature of 36 °C (97 °F) results in the same outcomes as 33 °C (91 °F).[48] And a second trial looking at earlier versus later cooling found no difference.[50]
Do not resuscitate
Some people choose to avoid aggressive measures at the end of life. A do not resuscitate order (DNR) in the form of an advance health care directive makes it clear that in the event of cardiac arrest, the person does not wish to receive cardiopulmonary resuscitation.[51] 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".[52]
Chain of survival
Several organisations promote the idea of a "chain of survival". The chain consists of the following "links":
- Early recognition - If possible, recognition of illness before the patient 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%.[7]
- Early CPR - improves the flow of blood and of oxygen to vital organs - an essential component of treating a cardiac arrest. In particular, by keeping the brain supplied with oxygenated blood, chances of neurological damage are decreased.
- Early defibrillation - is effective for the management of ventricular fibrillation and pulseless ventricular tachycardia[7] If defibrillation is delayed the rhythm is likely to degenerate into asystole for which outcomes are worse.
- Early advanced care - Early Advanced Cardiac Life Support is the final link in the chain of survival.
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, although in practice, Code Blue is often called in less life-threatening situations that require immediate attention from a physician.[citation needed]
Other
The precordial thump may be considered in those with witnessed, monitored, unstable ventricular tachycardia (including pulseless VT) if a defibrillator is not immediately ready for use, but it should not delay CPR and shock delivery or be used in those with unwitnessed out of hospital arrest.[53] Resuscitation with extracorporeal membrane oxygenation devices has been attempted with better results for in-hospital cardiac arrest (29% survival) than out of hospital cardiac arrest (4% survival) in populations selected to benefit most.[54]
Prognosis
The survival rate of people who receive initial emergency care by ambulance is only 2%, with 15% experiencing return of spontaneous circulation.[55] However, with defibrillation within 3–5 minutes, the survival rate increases to 30%.[56][57]
Since mortality in case of out-of-hospital cardiac arrest is high, programs were developed to improve survival rate. Although mortality in case of ventricular fibrillation is high, rapid intervention with a defibrillator increases survival rate.[13][58]
Survival is mostly related to the cause of the arrest (see above). In particular, patients who have suffered hypothermia have an increased survival rate, possibly because the cold protects the vital organs from the effects of tissue hypoxia. Survival rates following an arrest induced by toxins is very much dependent on identifying the toxin and administering an appropriate antidote. A patient who has suffered a myocardial infarction due to a blood clot in the left coronary artery has a lower chance of survival.[citation needed]
A study of survival rates from out of hospital cardiac arrest found that 14.6% of those who had received resuscitation by ambulance staff survived as far as admission to hospital. Of these, 59% died during admission, half of these within the first 24 hours, while 46% survived until discharge from hospital. This gives us an overall survival following cardiac arrest of 6.8%. Of these 89% had normal brain function or mild neurological disability, 8.5% had moderate impairment, and 2% suffered major neurological disability. Of those who were discharged from hospital, 70% were still alive 4 years later.[59]
A review into prognosis following in-hospital cardiac arrest found a survival to discharge of 14% although the range between different studies was 0-28%.[60]
Epidemiology
Based on death certificates sudden cardiac death accounts for about 15% of all death in Western countries[11] (330,000 per year in the United States).[31] The lifetime risk is three times greater in men (12.3%) than women (4.2%) based on analysis of the Framingham Heart Study.[61] However this gender difference disappeared beyond 85 years of age.[11]
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- ^ a b Nielsen, Niklas; Wetterslev, Jørn; Cronberg, Tobias; Erlinge, David; Gasche, Yvan; Hassager, Christian; Horn, Janneke; Hovdenes, Jan; Kjaergaard, Jesper; Kuiper, Michael; Pellis, Tommaso; Stammet, Pascal; Wanscher, Michael; Wise, Matt P.; Åneman, Anders; Al-Subaie, Nawaf; Boesgaard, Søren; Bro-Jeppesen, John; Brunetti, Iole; Bugge, Jan Frederik; Hingston, Christopher D.; Juffermans, Nicole P.; Koopmans, Matty; Køber, Lars; Langørgen, Jørund; Lilja, Gisela; Møller, Jacob Eifer; Rundgren, Malin; Rylander, Christian; Smid, Ondrej; Werer, Christophe; Winkel, Per; Friberg, Hans (17 November 2013). "Targeted Temperature Management at 33°C versus 36°C after Cardiac Arrest". New England Journal of Medicine 369 (23): 131117131833001. doi:10.1056/NEJMoa1310519. PMID 24237006.
- ^ Arrich, J; Holzer, M; Havel, C; Müllner, M; Herkner, H (Sep 12, 2012). "Hypothermia for neuroprotection in adults after cardiopulmonary resuscitation.". Cochrane database of systematic reviews (Online) 9: CD004128. doi:10.1002/14651858.CD004128.pub3. PMID 22972067.
- ^ Kim, F; Nichol, G; Maynard, C; Hallstrom, A; Kudenchuk, PJ; Rea, T; Copass, MK; Carlbom, D; Deem, S; Longstreth WT, Jr; Olsufka, M; Cobb, LA (Nov 17, 2013). "Effect of Prehospital Induction of Mild Hypothermia on Survival and Neurological Status Among Adults With Cardiac Arrest: A Randomized Clinical Trial.". JAMA: the Journal of the American Medical Association 311 (1): 45–52. doi:10.1001/jama.2013.282173. PMID 24240712.
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- ^ Cave, DM; Gazmuri, RJ, Otto, CW, Nadkarni, VM, Cheng, A, Brooks, SC, Daya, M, Sutton, RM, Branson, R, Hazinski, MF (2010-11-02). "Part 7: CPR techniques and devices: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care.". Circulation 122 (18 Suppl 3): S720–8. doi:10.1161/CIRCULATIONAHA.110.970970. PMC 3741663. PMID 20956223.
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- ^ "Resuscitation Council Comment on CPR study". Resuscitation Council UK. April 2007. Archived from the original on 2007-06-12. Retrieved 2007-06-14.
- ^ "CPR statistics". American Heart Association. Retrieved 2007-06-14.
- ^ Cardiopulmonary Resuscitation (CPR) Statistics
- ^ Bunch TJ, White RD, Gersh BJ, et al. (June 2003). "Long-term outcomes of out-of-hospital cardiac arrest after successful early defibrillation". N. Engl. J. Med. 348 (26): 2626–33. doi:10.1056/NEJMoa023053. PMID 12826637.
- ^ Cobbe SM, Dalziel K, Ford I, Marsden AK (June 1996). "Survival of 1476 patients initially resuscitated from out of hospital cardiac arrest". BMJ 312 (7047): 1633–7. doi:10.1136/bmj.312.7047.1633. PMC 2351362. PMID 8664715.
- ^ Ballew KA (May 1997). "Cardiopulmonary resuscitation". BMJ 314 (7092): 1462–5. doi:10.1136/bmj.314.7092.1462. PMC 2126720. PMID 9167565.
- ^ "Abstract 969: Lifetime Risk for Sudden Cardiac Death at Selected Index Ages and by Risk Factor Strata and Race: Cardiovascular Lifetime Risk Pooling Project -- Lloyd-Jones et al. 120 (10018): S416 -- Circulation".
External links
- The Center for Resuscitation Science at the Hospital of the University of Pennsylvania
- Cardiovascular disease: heart disease
- Circulatory system pathology
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| Ischaemic |
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Coronary disease
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- Coronary artery disease (CAD)
- Coronary artery aneurysm
- Coronary artery dissection
- Coronary thrombosis
- Coronary vasospasm
- Myocardial bridge
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Active ischemia
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- Angina pectoris
- Prinzmetal's angina
- Stable angina
- Acute coronary syndrome
- Myocardial infarction
- Unstable angina
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Sequelae
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- hours
- Hibernating myocardium
- Myocardial stunning
- days
- weeks
- Aneurysm of heart / Ventricular aneurysm
- Dressler's syndrome
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| Layers |
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Pericardium
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- Pericarditis
- Acute
- Chronic / Constrictive
- Pericardial effusion
- Cardiac tamponade
- Hemopericardium
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Myocardium
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- Myocarditis
- Cardiomyopathy: Dilated (Alcoholic), Hypertrophic, and Restrictive
- Loeffler endocarditis
- Cardiac amyloidosis
- Endocardial fibroelastosis
- Arrhythmogenic right ventricular dysplasia
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Endocardium /
valves
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Endocarditis
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- infective endocarditis
- Subacute bacterial endocarditis
- non-infective endocarditis
- Libman–Sacks endocarditis
- Nonbacterial thrombotic endocarditis
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Valves
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- mitral
- regurgitation
- prolapse
- stenosis
- aortic
- tricuspid
- pulmonary
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Conduction /
arrhythmia |
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Bradycardia
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- Sinus bradycardia
- Sick sinus syndrome
- Heart block: Sinoatrial
- AV
- Intraventricular
- Bundle branch block
- Right
- Left
- Left anterior fascicle
- Left posterior fascicle
- Bifascicular
- Trifascicular
- Adams–Stokes syndrome
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Tachycardia
(paroxysmal and sinus)
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Supraventricular
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- Atrial
- Junctional
- AV nodal reentrant
- Junctional ectopic
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Ventricular
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- Accelerated idioventricular rhythm
- Catecholaminergic polymorphic
- Torsades de pointes
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Premature contraction
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Pre-excitation syndrome
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- Lown–Ganong–Levine
- Wolff–Parkinson–White
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Flutter / fibrillation
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- Atrial flutter
- Ventricular flutter
- Atrial fibrillation
- Ventricular fibrillation
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Pacemaker
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- Ectopic pacemaker / Ectopic beat
- Multifocal atrial tachycardia
- Pacemaker syndrome
- Parasystole
- Wandering pacemaker
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Long QT syndrome
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- Andersen–Tawil
- Jervell and Lange-Nielsen
- Romano–Ward
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Cardiac arrest
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- Sudden cardiac death
- Asystole
- Pulseless electrical activity
- Sinoatrial arrest
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Other / ungrouped
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- hexaxial reference system
- Right axis deviation
- Left axis deviation
- QT
- T
- ST
- Osborn wave
- ST elevation
- ST depression
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| Cardiomegaly |
- Ventricular hypertrophy
- Left
- Right / Cor pulmonale
- Atrial enlargement
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| Other |
- Cardiac fibrosis
- Heart failure
- Diastolic heart failure
- Cardiac asthma
- Rheumatic fever
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noco/cong/tumr, sysi/epon, injr
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proc, drug (C1A/1B/1C/1D), blte
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