Cardiac Arrest

In adults, sudden cardiac arrest results primarily from cardiac disease (of all types, with most sudden cardiac arrest attributable to acute coronary syndromes, and a large majority associated with underlying cardiovascular disease). In a significant percentage of patients, sudden cardiac arrest is the first manifestation of heart disease (1). Other causes include circulatory shock due to noncardiac disorders (especially pulmonary embolism, gastrointestinal hemorrhage, or trauma), ventilatory failure, and metabolic disturbance (including drug overdose) (2).

In infants and children, cardiac causes of cardiac arrest are less common than in adults. The predominant cause of cardiac arrest in infants and children is respiratory failure due to various respiratory disorders (e.g., airway obstruction, drowning, infection, sudden infant death syndrome [SIDS], smoke inhalation). However, sudden cardiac arrest (the unexpected cessation of circulation without warning) in children and adolescents is most commonly due to arrhythmia resulting from a channelopathy or underlying structural cardiac abnormality (3, 4, 5, 6).

Cardiac arrest causes global ischemia with consequences at the cellular level that adversely affect organ function even after resuscitation and restoration of perfusion. The main consequences involve direct cellular damage and edema formation. Edema is particularly harmful in the brain, which has minimal room to expand, and often results in increased intracranial pressure and corresponding decreased cerebral perfusion postresuscitation.

Decreased adenosine triphosphate (ATP) production leads to loss of membrane integrity with efflux of potassium and influx of sodium and calcium. Excess intracellular sodium is one of the initial causes of cellular edema. Excess calcium damages mitochondria (depressing ATP production), increases nitric oxide production (leading to formation of damaging free radicals), and, in certain circumstances, activates proteases that further damage cells.

Abnormal ion flux also results in depolarization of neurons, releasing neurotransmitters, some of which are damaging (eg, glutamate activates a specific calcium channel, worsening intracellular calcium overload).

Inflammatory mediators (eg, interleukin-1B, tumor necrosis factor-alpha) are elaborated; some of them may cause microvascular thrombosis and loss of vascular integrity with further edema formation. Some mediators trigger apoptosis, resulting in accelerated cell death.

In critically or terminally ill patients, cardiac arrest is often preceded by a period of clinical deterioration with rapid, shallow breathing, arterial hypotension, and a progressive decrease in mental alertness.

In sudden cardiac arrest, collapse occurs without warning, occasionally accompanied by brief myoclonic jerks or other seizure-like activity.

• History and physical examination

• Cardiac monitoring and electrocardiography (ECG)

• Sometimes testing for cause (eg, echocardiography, chest imaging [radiography, ultrasound], electrolyte testing)

Diagnosis of cardiac arrest is by clinical findings of unconsciousness, apnea, and pulselessness. Arterial pressure is not measurable. Pupils dilate and become unreactive to light.

A cardiac monitor should be applied; it may indicate ventricular fibrillation (VF), ventricular tachycardia (VT), or asystole. Sometimes a perfusing rhythm (eg, bradycardia, extreme tachycardia) is present; this rhythm may represent true pulseless electrical activity (previously termed electromechanical dissociation) or extreme hypotension with failure to detect a pulse.

The patient is evaluated for potentially treatable causes; a useful memory aid is "Hs and Ts":

• H:Hypoxia, hypovolemia, acidosis (hydrogen ion), hyperkalemia or hypokalemia, hypothermia

• T:Tablet or toxin ingestion, cardiac tamponade, tension pneumothorax, thrombosis (pulmonary or coronary)

1, 2, 3). In pediatrics, however, blood glucose should be checked and hypoglycemia treated promptly as a potentially treatable cause of cardiac arrest (4).

Unfortunately, the cause of cardiac arrest often cannot be identified during cardiopulmonary resuscitation (CPR). Clinical examination, chest ultrasound during CPR, and chest radiographs taken after return of spontaneous circulation following needle thoracostomy can detect pneumothorax, which suggests tension pneumothorax as the cause of the arrest, particularly if the patient responds to relief of the pneumothorax.

Echocardiography can detect cardiac contractions and recognize cardiac tamponade, extreme hypovolemia (empty heart), right ventricular overload suggesting pulmonary embolism, and focal wall motion abnormalities suggesting myocardial infarction, and it helps quickly identify treatable causes of cardiac arrest (5). However, further studies are needed to determine whether there are long-term survival benefits from the use of ultrasound during resuscitation. Transthoracic cardiac ultrasound should not be done if it requires significant interruption in CPR.

Rapid bedside blood tests can detect abnormal levels of potassium, profound anemia, and severely low levels of glucose, all of which may be causes of cardiac arrest.

History given by family or rescue personnel may suggest overdose.

• High-quality CPR, including rapid defibrillation for shockable rhythms (ventricular fibrillation [VF] or ventricular tachycardia [VT])

• When possible, treatment of primary cause

• Postresuscitative care

Rapid intervention is essential.

Cardiopulmonary resuscitation (CPR1, 2, 3).

In children, who most often have asphyxial causes of cardiac arrest, the presenting rhythm is typically a bradyarrhythmia followed by asystole. However, when cardiac arrest has not been preceded by respiratory symptoms, children present with VT or VF and thus also require prompt defibrillation (3). The incidence of VF as the initial recorded rhythm increases in children > 12 years (3, 4).

epinephrineepinephrine. For non-shockable rhythms, early administration of epinephrine has been associated with improved neurologically intact survival (5, 6).

After return of pulses, postresuscitative care focuses on determination and treatment of cause, stabilization and prevention of rearrest, and optimization of neurologic outcome. In addition to treatment of cause, postresuscitative care may include methods to optimize oxygenation and ventilation and rapid coronary angiography in patients who have a ST-segment elevation myocardial infarction (STEMI). The 2020 AHA guidelines suggest that delayed coronary angiography should also be considered for patients without STEMI. Recommendations are for targeted temperature management to therapeutic normothermia < 37.5° C, although with a lower temperature boundary of 32° C (7, 8). Research is ongoing to determine whether targeted temperature management with controlled hypothermia (32° C to 34° C) benefit select cardiac arrest survivors (9).

Survival to hospital discharge, particularly neurologically intact survival, is a more meaningful outcome than simply return of spontaneous circulation.

Survival rates vary significantly; favorable factors for neurologically intact survival include

• Early and effective bystander-initiated CPR

• Witnessed arrest

• In-hospital location (particularly a monitored unit)

• Initial rhythm of ventricular fibrillation (VF) or ventricular tachycardia (VT)

• Early defibrillation of VF or VT

• Postresuscitative care, including circulatory support and access to cardiac catheterization

• In adults, targeted temperature management (body temperature of 32 to 36° C for ≥ 24 hours) and avoidance of hyperthermia

While the American Heart Association 2020 Advanced Cardiac Life Support (ACLS) guidelines recommend cooling to a temperature range between 32° C and 36° C, more recent recommendations from the International Liaison Committee on Resuscitation Advanced Life Support (ALS) suggest actively preventing fever with a target temperature of ≤ 37.5° C rather than active cooling. It is still unclear whether certain groups of patients with cardiac arrest will have improved neurologically intact survival with targeted hypothermia management rather than with maintaining normothermia (1, 2, 3, 4, 5).

If many factors are favorable (eg, VF is witnessed in an intensive care unit or emergency department), up to around 40%of adults with inpatient cardiac arrest may survive to hospital discharge (6). Overall in the United States, survival to hospital discharge in patients experiencing in-hospital arrest exceeds 30% (7).

A significant proportion of successfully resuscitated patients have short-term or long-term cerebral dysfunction manifested by altered alertness (from mild confusion to coma), seizures, or both (8, 9).

When factors are uniformly unfavorable (eg, patient in asystole after unwitnessed, out-of-hospital arrest), survival is unlikely. Overall, reported survival after out-of-hospital arrest is approximately 10%.

Less than 10% of all patients with cardiac arrest, either in-hospital or out-of-hospital, are discharged with good neurologic function, defined as minimal to moderate cerebral disability with ability to perform the majority of activities of daily living independently, at hospital discharge (10, 11).