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Cardiac Arrest

by Robert E O'Connor, MD, MPH

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 about 400,000 people/yr in the US, with a > 90% mortality.

Respiratory arrest and cardiac arrest are distinct, but without treatment, one inevitably leads to the other. (See also respiratory failure in Respiratory Failure and Mechanical Ventilation, dyspnea, and hypoxia in Oxygen Desaturation.)


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, GI hemorrhage, or trauma), ventilatory failure, and metabolic disturbance (including drug overdose).

In children, cardiac causes of sudden cardiac arrest are much less common (< 15 to 20%). Instead, predominant causes include trauma, poisoning, and various respiratory disorders (eg, airway obstruction, smoke inhalation, drowning, infection, SIDS).


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 ATP production leads to loss of membrane integrity with efflux of K and influx of Na and Ca. Excess Na causes cellular edema. Excess Ca 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 Ca channel, worsening intracellular Ca overload).

Inflammatory mediators (eg, IL-1B, TNF-α) 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.

Symptoms and Signs

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 sec) seizure.


  • Clinical evaluation

  • Cardiac monitor and ECG

  • Sometimes testing for cause (eg, echocardiography, chest x-ray, or chest ultrasonography)

Diagnosis 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 (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: H ypoxia, h ypovolemia, acidosis ( h ydrogen ion), h yperkalemia or h ypokalemia, h ypothermia, h ypoglycemia

  • T: T ablet or t oxin ingestion, cardiac t amponade, t ension pneumothorax, t hromboembolism (massive pulmonary embolus), t rauma

Unfortunately, many causes are not identified during 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 MI. Rapid bedside blood tests can detect abnormal levels of K 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

  • Early and effective bystander-initiated CPR

  • Witnessed arrest

  • In-hospital location (particularly a monitored unit)

  • Initial rhythm of VF or VT

  • Early defibrillation (of VT or VF after initial chest compression)

  • Postresuscitative care, including induced hypothermia (eg, deliberate cooling to 34° C), circulatory support, and access to cardiac catheterization

If many factors are favorable (eg, VF is witnessed in an ICU or emergency department), about 20% of patients survive to hospital discharge. 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 ranges between 1% and 70%; the wide range reflects reporting differences and inclusion criteria as well as differences in system effectiveness. About 8 to 30% of survivors have neurologic dysfunction, and one third return to prearrest status. In-hospital arrest survival is about 26%.


  • CPR

  • When possible, treatment of primary cause

  • Postresuscitative care

Rapid intervention is essential.

CPR (see Cardiopulmonary Resuscitation (CPR) in Adults) 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 yr.

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 O 2 delivery, antiplatelet therapy, and therapeutic hypothermia.

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