Cardiac arrest is defined as the cessation of cardiac mechanical activity as confirmed by the absence of signs of circulation (e.g., a detectable pulse, unresponsiveness, and apnea). Cardiac arrest is the abrupt loss of heart function in a person who may or may not have diagnosed heart disease. The time and mode of death are unexpected. It occurs instantly or shortly after symptoms appear.
Cardiac arrest is caused when the heart’s electrical system malfunctions, causing arrhythmias. The most common arrhythmia in cardiac arrest is ventricular fibrillation. Cardiac arrest may be reversed if CPR (cardiopulmonary resuscitation) is performed and a defibrillator is used to shock the heart and restore a normal heart rhythm within a few minutes. Sudden cardiac arrest may be caused by almost any known heart condition.
Epidemiology of cardiac arrest
In adult patients, cardiac arrest usually results from the development of an arrhythmia. Historically, ventricular fibrillation (VF) and pulse less ventricular tachycardia (PVT) have been the most common initial rhythm; however, this has changed markedly over time. In one study of out-of-hospital arrests, VF was the first identified rhythm in 61% of patients in 1980 compared to 41% of patients in 2000, a reduction of greater than 30%.
More recently, a second study identified VF/PVT as the first recorded rhythm in only 13% of patients. The declining incidence of VF could potentially be due to its association with ischemia and other cardiac causes of arrest (vs non cardiac causes) and the improvements made in the treatment of coronary artery disease.
In contrast to out-of-hospital cardiac arrest, VF is the initial rhythm in roughly 20% to 35% of in-hospital cardiac arrests. As in-hospital cardiac arrest is typically preceded by hypoxia or hypotension, asystole, or pulseless electrical activity (PEA) occur more commonly. In fact, one study noticed an incidence of asystole and PEA of 35% and 32%, respectively, while the incidence of VF or PVT was only 23%.
This declining incidence of VF or PVT is somewhat concerning as survival rates are substantially higher compared to asystole or PEA. Hospital survival for in-hospital cardiac arrest related to VF or PVT is approximately 36% (vs 11% with asystole/PEA) with most patients having a good neurologic outcome. Survival for out-of hospital cardiac arrest due to VF or PVT is approximately 25% to 40%, with higher survival rates being observed in communities that have an organized rapid response system.
In contrast to adult patients, only 14% of pediatric patients with in-hospital arrest present with VF or PVT as the initial rhythm of which 29% survive to hospital discharge. This is probably because most pediatric arrests are respiratory-related as opposed to the primary cardiac etiology seen in adult patients. Unfortunately, survival following pediatric out-of-hospital cardiopulmonary arrest is roughly 7% with most survivors having a poor neurologic status.
The most common causes are
• Scarring from a prior heart attack or other causes: A heart that is scarred or enlarged from any cause is prone to develop life-threatening ventricular arrhythmias. The first six months after a heart attack is a particularly high-risk period for sudden cardiac arrest in patients with atherosclerotic heart disease.
• A thickened heart muscle (cardiomyopathy) from any cause (typically high blood pressure or valvular heart disease)—especially coupled with heart failure
• Heart medications: Under certain conditions, various heart medications can set the stage for arrhythmias that cause sudden cardiac arrest. Paradoxically, antiarrhythmic drugs used to treat arrhythmias can sometimes produce lethal ventricular arrhythmias even at normally prescribed doses (a “proarrhythmic” effect).
• Electrical abnormalities: Certain electrical abnormalities such as Wolff-Parkinson-White syndrome and long QT syndrome may cause sudden cardiac arrest in children and young people.
• Blood vessel abnormalities: Less often, inborn blood vessel abnormalities, particularly in the coronary arteries and aorta, may be present in young sudden death victims. Adrenaline released during intense physical or athletic activity often acts as a trigger for sudden cardiac arrest when these abnormalities are present.
• Recreational drug use: In people without organic heart disease, recreational drug use is an important cause of sudden cardiac arrest.
Management of sudden cardiac arrest
CPR is the procedure by which the basic life sustaining functions of blood flow and oxygenation can be briefly maintained to support the heart and central nervous system until more definitive treatment can restore normal function. Mouth-to-mouth breathing and chest compression can only partly compensate for normal cardiopulmonary function, but for a short time, tissue oxygenation can be sufficiently maintained to add a few minutes to the time available for definitive treatment—defibrillation. Though CPR expands the window of time for application of defibrillation, it does not replace defibrillation in saving the victim.
It is widely accepted that early defibrillation is the single most important factor in survival from SCA caused by ventricular fibrillation. The sooner the defibrillatory shock is administered, the more likely is the restoration of normal cardiac rhythm. Defibrillation administered less than three minutes after collapse in cardiac arrest is most likely to be successful. For each minute in duration of SCA, the likelihood of successful conversion decreases by approximately 10%.
The potential for success is clearly seen in arrests that have occurred in supervised cardiac rehabilitation programs. In these settings, where cardiac arrests actually occur during cardiac monitoring and are defibrillated in less than one minute, success rates are about 90%. Thus, much of the focus of attention in treatment of SCA is on providing rapid defibrillation.
Patients who survive cardiac arrest have an excellent prognosis: 83% are alive at one year and 57% at five years. This compares favorably with the survival rates for people of the same age who have not experienced a sudden cardiac arrest.
Early Institution of Advanced Life Support.
When sudden cardiac arrest is the result of ventricular fibrillation, electrical counter shock is the definitive treatment and may be the only emergency treatment necessary. In general, survival is unlikely if successful defibrillation is not accomplished at the site of the arrest.
The patient is then monitored carefully on the way to the hospital for more definitive diagnostic evaluation. On other occasions, more advanced treatment measures such as intubation or intravenous drugs may be indicated prior to arrival at the hospital emergency department, but defibrillation must be successfully accomplished first if transport, monitoring, and advanced treatment and diagnostic measures are to be worthwhile.
Adrenaline (epinephrine) has been used for many years although its place has never been subjected to trial against placebo in humans. Its use is supported by animal studies and its known effects in improving relative coronary and cerebral perfusion.
There has been a trend to the use of higher doses of adrenaline (epinephrine) in past years but evidence now links high dosage to poorer outcome, especially in asphyxial arrests. High dose (100microgm/kg) adrenaline (epinephrine) should be used therefore only in very specific circumstances e.g. if necessary after cardiac arrest associated with B blocker overdose.
Amiodarone is the treatment of choice in shock resistant ventricular fibrillation and pulseless ventricular tachycardia. This is based on evidence from adult cardiac arrest and experience with the use of amiodarone in children in the catheterisation laboratory setting. The dose of amiodarone for VF/pulseless VT is 5 mg/kg via rapid i.v. bolus.
There may be circumstances where the routine use of amiodarone should be omitted. This includes VF/pulseless VT caused by an overdose of an arrhythmogenic drug. Expert advice should be obtained from a Poisons Centre. Amiodarone is likely to be unhelpful in the setting of VF caused by hypothermia but may be used, nevertheless.
Lidocaine (lignocaine) is an alternative to amiodarone of the latter is unavailable. The dose is 1mg/kg IV or IO. It is DC shock that converts the heart back to a perfusing rhythm not the drug. The purpose of the anti-arrhythmic drug is to stabilise the converted rhythm and the purpose of adrenaline (epinephrine) is to improve myocardial oxygenation by increasing coronary perfusion pressure adrenaline (epinephrine) also increases the vigour and intensity of ventricular fibrillation which increases the success of defibrillation.