Cardiac arrest is the cessation of cardiac mechanical activity resulting in the absence of circulating blood flow. Cardiac arrest stops blood from flowing to vital organs, depriving them of oxygen, and, if left untreated, results in death. Sudden cardiac arrest is the unexpected cessation of circulation within a short period of symptom onset (sometimes without warning). Sudden cardiac arrest occurs outside the hospital in more than 350,000 people/year in the US, with a 90% mortality.
(See also the American Heart Association's 2018 update of heart disease and stroke statistics for out-of-hospital and in-hospital cardiac arrest.)
In adults, sudden cardiac arrest results primarily from cardiac disease (of all types, but especially coronary artery disease). In a significant percentage of patients, sudden cardiac arrest is the first manifestation of heart disease. Other causes include circulatory shock due to noncardiac disorders (especially pulmonary embolism, gastrointestinal hemorrhage, or trauma), ventilatory failure, and metabolic disturbance (including drug overdose).
In infants and children, cardiac causes of sudden cardiac arrest are less common than in adults. The predominant cause of sudden cardiac arrest in infants and children is respiratory failure due to various respiratory disorders (eg, airway obstruction, smoke inhalation, drowning, infection, sudden infant death syndrome [SIDS]). Other causes of sudden cardiac arrest include trauma and poisoning.
Cardiac arrest causes global ischemia with consequences at the cellular level that adversely affect organ function after resuscitation. 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. 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.
Decreased adenosine triphosphate (ATP) production leads to loss of membrane integrity with efflux of potassium and influx of sodium and calcium. Excess sodium causes 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 a brief (< 5 seconds) seizure.
Diagnosis of cardiac arrest is by clinical findings of apnea, pulselessness, and unconsciousness. Arterial pressure is not measurable. Pupils dilate and become unreactive to light after several minutes.
A cardiac monitor should be applied; it may indicate ventricular fibrillation (VF), ventricular tachycardia (VT), or asystole. Sometimes a perfusing rhythm (eg, extreme bradycardia) is present; this rhythm may represent true pulseless electrical activity (PEA, or 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":
Unfortunately, many causes are not identified during cardiopulmonary resuscitation (CPR). Clinical examination, chest ultrasonography, and chest x-ray can detect tension pneumothorax. Cardiac ultrasonography 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 (MI). Rapid bedside blood tests can detect abnormal levels of potassium or glucose. History given by family or rescue personnel may suggest overdose.
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 include
If many factors are favorable (eg, VF is witnessed in an ICU or emergency department), about 50% of adults survive to hospital discharge. Overall, in-hospital arrest (VT/VF and asystole/PEA) survival is about 25%.
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 about 10%.
Only about 10% of all cardiac arrest survivors have good central nervous system function at hospital discharge.
1. Bernard SA, Gray TW, Buist MD, et al: Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med 346:557–563, 2002. doi 10.1056/NEJMoa003289.
2. Nielsen N, Wetterslev J, Cronberg T, et al: Targeted temperature management at 33°C versus 36°C after cardiac arrest. N Engl J Med 369:2197–2206, 2013. doi: 10.1056/NEJMoa1310519.
Rapid intervention is essential.
(See also the American Heart Association's guidelines for CPR and emergency cardiovascular care.)
Cardiopulmonary resuscitation (CPR) is an organized, sequential response to cardiac arrest; rapid initiation of uninterrupted chest compressions ("push hard and push fast") and early defibrillation of patients who are in VF or VT (more commonly adults) are the keys to success.
In children, who most often have asphyxial causes of cardiac arrest, the presenting rhythm is typically a bradyarrhythmia followed by asystole. However, about 15 to 20% of children (particularly when sudden cardiac arrest has not been preceded by respiratory symptoms) present with VT or VF and thus also require prompt defibrillation. The incidence of VF as the initial recorded rhythm increases in children > 12 years.
Primary causes must be promptly treated. If no treatable conditions are present but cardiac motion is detected or pulses are detected by Doppler, severe circulatory shock is identified, and IV fluid (eg, 1 L 0.9% saline, whole blood, or a combination for blood loss) is given. If response to IV fluid is inadequate, most clinicians give one or more vasopressor drugs (eg, norepinephrine, epinephrine, dopamine, vasopressin); however, there is no firm proof that they improve survival.
In addition to treatment of cause, postresuscitative care typically includes methods to optimize oxygen delivery, rapid coronary angiography in patients with suspected cardiac etiology, and targeted temperature management (32 to 36° C in adults) and therapeutic normothermia (36 to 37.5° C in children and infants––1, 2).
1. Moler FW, Silverstein FS, Holubkov R, et al: Therapeutic hypothermia after in-hospital cardiac arrest in children. N Engl J Med 376:318–332, 2017. doi: 10.1056/NEJMoa1610493
2. Moler FW, Silverstein FS, Holubkov R, et al: Therapeutic hypothermia after out-of-hospital cardiac arrest in children. N Engl J Med 372:1898–1908, 2015. doi: 10.1056/NEJMoa1411480
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