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 categorization 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 nonmedical etiology (26%).[11]

Overall, the main underlying causes of cardiac arrest are ischemic heart disease (62.2%), unspecified cardiovascular disease (12.1%), and cardiomyopathy/dysrhythmias (9.3%).[12] Among patients with OHCA who were resuscitated and hospitalized 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 ages ≤18 years, 39% of sudden cardiac arrests are sports-related.[14]

VT and VF cardiac arrests are most often the result of ischemic heart disease and acute myocardial ischemia.[12] They may also present in the setting of nonischemic left ventricular dysfunction, premature ventricular beats (R-on-T phenomenon), prolonged QT interval secondary to medications, 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 ischemia/infarction, hypovolemia, hypoxia, and pulmonary embolism.[18]

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

In ventricular tachycardia (VT)/ventricular fibrillation (VF), acute myocardial ischemia 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 a re-entrant circuit generated by surviving myofibrils within areas of fibrosis.[21] Studies of nonischemic 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-depolarizations 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 subtypes of the disease, but the ultimate result is disordered repolarization and depolarization, 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 subtypes.[21] Drugs implicated in the acquired LQTS also cause alterations in ion channels leading to problems in depolarization/repolarization, 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 organized electrical depolarization 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 preload, increased afterload, or changes intrinsic to the myocardium (e.g., ischemia 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
Nonshockable rhythms (pulseless electrical activity and asystole).

Pathophysiology

Classification

Advanced cardiovascular life support pulseless arrest algorithm[1]