Cardiac arrest

Sudden cardiac arrest is the term used to describe the ultimate result of four different cardiac arrhythmias: ventricular tachycardia (VT), ventricular fibrillation (VF), pulseless electrical activity (PEA), and asystole. Each of these rhythms may present in different clinical scenarios, though VT and VF are the most common causes of sudden cardiac arrest.[9]

Cardiac arrest results from many disease processes; a consensus statement by the International Liaison Committee on Resuscitation recommends categorisation into events with medical causes or external causes (drowning, trauma, asphyxia, electrocution, and drug overdose).[10] In a Swedish registry of 70,846 out-of-hospital cardiac arrests (OHCAs) from 1992 to 2014, 92% of cases had medical causes. Trauma was the most common cause of non-medical aetiology (26%).[11]

Overall, the main underlying causes of cardiac arrest are ischaemic heart disease (62.2%), unspecified cardiovascular disease (12.1%), and cardiomyopathy/dysrhythmias (9.3%).[12] Among patients with OHCA who were resuscitated and hospitalised from 2012 to 2016, acute coronary syndrome and other cardiac causes accounted for the largest proportion of cases. Among patients with in-hospital cardiac arrests, respiratory failure was the most common cause.[13] Causes of sudden cardiac death vary by age, with a higher incidence of cardiomyopathies, dysrhythmias, myocarditis and coronary abnormalities in younger people, and more chronic structural heart disease in older people.[7] Among people aged ≤18 years, 39% of sudden cardiac arrests are sports-related.[14]

VT and VF cardiac arrests are most often the result of ischaemic heart disease and acute myocardial ischaemia.[12] They may also present in the setting of non-ischaemic left ventricular dysfunction, premature ventricular beats (R-on-T phenomenon), prolonged QT interval secondary to medicines, electrolyte abnormalities, familial syndromes of conduction abnormality (disorders in cardiac ion channels), other cardiomyopathies, and drug intoxications (e.g., cocaine).[15][16][17]

The most common causes of PEA are myocardial ischaemia/infarction, hypovolaemia, hypoxia, and pulmonary embolism.[18]

Other potential causes of cardiac arrest, all of which require emergency treatment, include hypoxia, hypovolaemia, hyperkalaemia, hydrogen ion excess (acidosis), hypothermia, hypo- or hyperglycaemia, trauma, tension pneumothorax, obstructive shock (pulmonary embolism, myocardial infarction), toxins, and cardiac tamponade.[19]

In ventricular tachycardia (VT)/ventricular fibrillation (VF), acute myocardial ischaemia results in changes in the concentration of many components of the intracellular and extracellular milieu (e.g., pH, electrolytes, and adenosine triphosphate). In turn, these changes form the basis for pathogenic impulse formation and propagation of arrhythmia.[20] In patients with areas of myocardial scarring, the mechanism for arrhythmia is likely to be a re-entrant circuit generated by surviving myofibrils within areas of fibrosis.[21] Studies of non-ischaemic dilated cardiomyopathy have shown that the mechanism of arrhythmia is not re-entry, but more likely the initiation of VT/VF from early or late after-depolarisations in the setting of a prolonged action potential duration, which in turn is due to the altered function of various ion channels.[22]

Another cause of VT/VF is the congenital long QT syndrome (LQTS), an inherited disorder of conduction. Various mutations in ion channels are seen in the different sub-types of the disease, but the ultimate result is disordered repolarisation and depolarisation, which prolongs the action potential duration and therefore the QT interval.[23] Events in these patients often occur at times of increased sympathetic surge, though the specific triggers vary among each of the mutational sub-types.[21] Drugs implicated in the acquired LQTS also cause alterations in ion channels leading to problems in depolarisation/repolarisation, and may uncover otherwise silent mutations involved in LQTS.[24] Culprit drugs include class IA anti-arrhythmics (e.g., procainamide), class III anti-arrhythmics (e.g., amiodarone), macrolide antibiotics, pentamidine, antimalarials, antipsychotics, arsenic trioxide, and methadone.[25]

Pulseless electrical activity is defined by the presence of organised electrical depolarisation of the myocardium without appropriate myocardial contraction, and hence inadequate circulation. The mechanism for this disorder is a loss of contractile force despite normal electrical stimulation, which may be due to decreased pre-load, increased after-load, or changes intrinsic to the myocardium (e.g., ischaemia and changes in ion concentrations) that impair inotropy.[26]

Advanced cardiovascular life support pulseless arrest algorithm[1]

Cardiac arrest is approached as a dichotomy of:

Shockable rhythms (pulseless ventricular tachycardia and ventricular fibrillation), and
Non-shockable rhythms (pulseless electrical activity and asystole).

Pathophysiology

Classification

Advanced cardiovascular life support pulseless arrest algorithm[1]