Cardiac Arrest

• Cardiac arrest involves cessation of cardiac mechanical activity as confirmed by absence of signs of circulation (eg, detectable pulse, unresponsiveness, and apnea).

PATHOPHYSIOLOGY

• Coronary artery disease is the most common finding in adults with cardiac arrest and causes ~80% of sudden cardiac deaths. In pediatric patients, cardiac arrest typically results from respiratory failure or progressive shock.

• Two different pathophysiologic conditions are associated with cardiac arrest:

✓ Primary: arterial blood is typically fully oxygenated at the time of arrest.

✓ Secondary: results from respiratory failure in which lack of ventilation leads to severe hypoxemia, hypotension, and cardiac arrest.

• Cardiac arrest in adults usually results from arrhythmias. Historically, ventricular fibrillation (VF) and pulseless ventricular tachycardia (PVT) were most common. The incidence of VF in out-of hospital arrests is declining, which is of concern because survival rates are higher after VF/PVT than with cardiac arrest resulting from nonshockable rhythms like asystole or pulseless electrical activity (PEA).

• Because in-hospital cardiac arrest is typically preceded by hypoxia or hypotension, asystole or PEA occurs more commonly than VF or PVT.

• Only 14% of pediatric patients with in-hospital arrest present with VF or PFT as the initial rhythm.

CLINICAL PRESENTATION

• Cardiac arrest may be preceded by anxiety, shortness of breath, chest pain, nausea, vomiting, and diaphoresis.

• After an arrest, individuals are unresponsive, apneic, and hypotensive without a detectable pulse. Extremities are cold and clammy, and cyanosis is common.

DIAGNOSIS

• Rapid diagnosis is vital to success of cardiopulmonary resuscitation (CPR). Patients must receive early intervention to prevent cardiac rhythms from degenerating into less treatable arrhythmias.

• Diagnosis is made by observation of clinical manifestations consistent with cardiac arrest. Diagnosis is confirmed by vital signs, especially heart rate and respirations.

• Electrocardiography (ECG) identifies the cardiac rhythm, which in turn determines drug therapy.

✓ VF is electrical anarchy of the ventricle resulting in no cardiac output and cardiovascular collapse.

✓ PEA is absence of a detectable pulse and presence of some type of electrical activity other than VF or PVT.

✓ Asystole is presence of a flat line on the ECG.

TREATMENT

• Goals of Treatment: 

Resuscitation goals are to preserve life, restore health, relieve suffering, limit disability, and respect the individual’s decisions, rights, and privacy. This can be accomplished via CPR by return of spontaneous circulation (ROSC) with effective ventilation and perfusion as quickly as possible to minimize hypoxic damage to vital organs. After successful resuscitation, primary goals include optimizing tissue oxygenation, identifying precipitating cause(s) of arrest, and preventing subsequent episodes.

GENERAL APPROACH

• The 2010 American Heart Association (AHA) guidelines for CPR and emergency cardiovascular care (ECC) state that the likelihood of successful outcome is enhanced if five critical elements in the “chain of survival” are implemented promptly: 

(1) immediate recognition of cardiac arrest and activation of the emergency response

system, 

(2) early CPR with an emphasis on chest compressions, 

(3) rapid defibrillation,

(4) effective advanced cardiac life support (ACLS), and 

(5) integrated postcardiac arrest care.

• Basic life support given by healthcare providers trained in CPR includes the following actions performed in this order:

✓ First, determine patient responsiveness. If unresponsive with no breathing or no normal breathing (ie, only gasping), activate the emergency medical response team and obtain an automated external defibrillator (AED) if available.

✓ Check for pulse, but if not definitely felt within 10 seconds, begin CPR and use the AED when available.

✓ Begin CPR with 30 chest compressions at a rate of at least 100/min and a compression depth of at least 2 in (5 cm) in adults and at least one third of the anteroposterior chest diameter in infants and children (~1.5 in [4 cm] in infants and 2 in [5cm] in children).

✓ Open the airway and deliver two rescue breaths, then repeat chest compressions.

Follow each cycle of 30 chest compressions by two rescue breaths.

✓ Continue cycles of 30 compressions/2 breaths until an AED arrives and is ready for

use or emergency medical service (EMS) providers take over care.

✓ If AED is available, check rhythm to determine if defibrillation is advised. If so, deliver one shock with immediate resumption of chest compressions/rescue breaths. After five cycles, reevaluate the rhythm to determine need for further defibrillation. Repeat this sequence until help arrives or the rhythm is no longer shockable.

✓ If rhythm is not shockable, continue chest compressions/rescue breath cycles until help arrives or spontaneous circulation returns. If rhythm is not shockable, it is likely to be either asystole or PEA.

• Central venous catheter access results in faster and higher peak drug concentrations than peripheral venous administration, but central line access is not needed in most resuscitation attempts. However, if a central line is already present, it is the access site of choice. If IV access (either central or peripheral) has not been established, insert a large peripheral venous catheter. If this is not successful, insert an intraosseous (IO) device.

• If neither IV nor IO access can be established, lidocaine, epinephrine, naloxone, and vasopressin may be administered endotracheally. The endotracheal dose should generally be 2 to 2.5 times larger than the IV/IO dose.

TREATMENT OF VENTRICULAR FIBRILLATION AND

PULSELESS VENTRICULAR TACHYCARDIA

Nonpharmacologic Therapy

• Administer electrical defibrillation with one shock using 360 J (monophasic defibrillator) or 120 to 200 J (biphasic defibrillator). After defibrillation is attempted, restart CPR immediately and continue for about five cycles (~2 min) before analyzing the rhythm or checking a pulse. If there is still evidence of VF/PVT after 2 minutes, then give pharmacologic therapy with repeat attempts at single-discharge defibrillation.

• Obtain endotracheal intubation and IV access when feasible, but not at the expense of stopping chest compressions. Once an airway is achieved, ventilate patients with 100% oxygen.

Pharmacologic Therapy

Epinephrine

• Epinephrine is a drug of first choice for treating VF, PVT, asystole, and PEA. It is an agonist of both α and β receptors, but effectiveness is primarily due to α effects. It increases systemic arteriolar vasoconstriction, thereby improving coronary and cerebral perfusion pressure during the low-flow state associated with CPR.

• The recommended adult dose of epinephrine is 1 mg administered by IV or IO injection every 3 to 5 minutes. Higher doses may be administered to treat specific disorders such as β-blocker and calcium channel blocker overdose.

Vasopressin

• Vasopressin is a potent nonadrenergic vasoconstrictor that increases blood pressure (BP) and systemic vascular resistance. Its vasoconstrictive properties are due primarily to effects on V1 receptors. The 2010 AHA guidelines indicate that vasopressin 40 units IV/IO can replace the first or second dose of epinephrine.

Antiarrhythmics

• The purpose of antiarrhythmic drug therapy after unsuccessful defibrillation and vasopressor administration is to prevent development or recurrence of VF and PVT by raising the fibrillation threshold. However, clinical evidence demonstrating improved survival to hospital discharge is lacking.

• Amiodarone is the recommended antiarrhythmic in patients with VF/VT unresponsive to CPR, defibrillation, and vasopressors. The dose is 300 mg IV/IO followed by a second dose of 150 mg.

• Lidocaine may be used if amiodarone is unavailable, but it has not been shown to improve rates of ROSC, admission to the hospital, or survival to discharge compared with amiodarone. The initial dose is 1 to 1.5 mg/kg IV. Additional doses of 0.5 to 0.75 mg/kg can be administered at 5- to 10-minute intervals to a maximum dose of 3 mg/kg if VF/PVT persists.

Magnesium

• Severe hypomagnesemia has been associated with VF/PVT, but routine administration of magnesium during cardiac has not improved clinical outcomes. Two trials showed improved ROSC in cardiac arrests associated with torsades de pointes. Therefore, limit magnesium administration to these patients. The dose is 1 to 2 g diluted in 10 mL of 5% dextrose in water administered IV/IO push over 15 minutes.

Thrombolytics

• Thrombolytic use during CPR has been investigated because most cardiac arrests are related to either myocardial infarction (MI) or pulmonary embolism (PE). Although several studies demonstrated successful use, few have shown improvements to hospital discharge, and an increase in intracranial hemorrhage was noted. Therefore, fibrinolytic therapy should not be used routinely in cardiac arrest but can be considered when PE is the presumed or known cause of the arrest.

TREATMENT OF PULSELESS ELECTRICAL ACTIVITY AND ASYSTOLE

Nonpharmacologic Therapy

• Successful treatment of PEA and asystole depends on diagnosis of the underlying

cause. Potentially reversible causes include: 

(1) hypovolemia, 

(2) hypoxia, 

(3) acidosis,

(4) hyper- or hypokalemia, 

(5) hypothermia, 

(6) hypoglycemia, 

(7) drug overdose,

(8) cardiac tamponade, 

(9) tension pneumothorax, 

(10) coronary thrombosis,

(11) pulmonary thrombosis, and 

(12) trauma.

• PEA and asystole are treated the same way. Both conditions require CPR, airway control, and IV access. Avoid defibrillation in asystole because the resulting parasympathetic discharge can reduce the chance of ROSC and decrease the likelihood of survival. If available, transcutaneous pacing can be attempted.

• Epinephrine 1 mg administered by IV or IO injection every 3 to 5 minutes.

• Vasopressin 40 units IV/IO can replace the first or second dose of epinephrine.

• Atropine should not be routinely administered for treatment of asystole or PEA

because there are no prospective controlled trials showing benefit and there is conflicting evidence from retrospective and observational reports. The 2010 AHA guidelines removed atropine from the ACLS cardiac arrest algorithm.

ACID–BASE MANAGEMENT

• Acidosis occurs during cardiac arrest because of decreased blood flow or inadequate ventilation. Chest compressions generate only ~20% to 30% of normal cardiac output, leading to inadequate organ perfusion, tissue hypoxia, and metabolic acidosis. Lack of ventilation causes CO2 retention, leading to respiratory acidosis. The combined acidosis reduces myocardial contractility and may cause arrhythmias.

• Routine use of sodium bicarbonate in cardiac arrest is not recommended because there are few clinical data supporting its use, and it may have detrimental effects. It can be used in special circumstances (eg, preexisting metabolic acidosis, hyperkalemia, and tricyclic antidepressant overdose). The dosage should be guided by laboratory analysis if possible.

POSTRESUSCITATIVE CARE

• ROSC from a cardiac arrest may be followed by a post-cardiac arrest syndrome characterized by brain injury, myocardial dysfunction, systemic ischemia/reperfusion response, and persistent precipitating pathology.

• It is imperative to ensure adequate airway and oxygenation. Raise the head of the bed to 30 degrees to reduce risk for aspiration, ventilator-associated pneumonia, and cerebral edema. After use of 100% oxygen during the resuscitation effort, titrate the oxygen fraction down as tolerated to avoid oxygen toxicity. Overventilation can be avoided by using end-tidal (ET) CO2 measurements targeting an ETCO2 of 40–45 mmHg [5.3–6.0 kPa]).

• Evaluate for ECG changes consistent with acute myocardial infarction as soon as possible and perform revascularization as appropriate.

• Hypothermia can protect from cerebral injury by suppressing chemical reactions that occur after restoration of blood flow. The 2010 AHA guidelines recommend that unconscious adult patients with ROSC after out-of-hospital VF cardiac arrest be cooled to 32–34°C (89.6–93.2°F) for 12 to 24 hours. Cooling may also be considered for comatose adults patients with ROSC after out-of-hospital arrests with an initial rhythm of asystole or PEA or after in-hospital cardiac arrest of any initial rhythm.

There is insufficient evidence to recommend therapeutic hypothermia in children. Potential complications of hypothermia include coagulopathy, dysrhythmias, hyperglycemia, increased incidence of pneumonia and sepsis, and profound effects on drug distribution and elimination.

EVALUATION OF THERAPEUTIC OUTCOMES

• Monitoring should occur both during the resuscitation attempt and in the postresuscitation phase. The optimal outcome following CPR is an awake, responsive, spontaneously breathing patient. Ideally, patients must remain neurologically intact with minimal morbidity after the resuscitation.

• Assess and document heart rate, cardiac rhythm, and BP throughout the resuscitation attempt and after each intervention. Determination of the presence or absence of a pulse is paramount to deciding which interventions are appropriate.

• Coronary perfusion pressure (CPP) and central venous oxygen saturation (ScvO2) can provide useful information on the patient’s response to therapy.

• ETCO2 monitoring is a safe and effective method to assess cardiac output during CPR and has been associated with ROSC.

• Consider the precipitating cause of the cardiac arrest (eg, MI, electrolyte imbalance, primary arrhythmia). Review prearrest status carefully, particularly if the patient was receiving drug therapy.

• Address any altered cardiac, hepatic, and renal function resulting from ischemic damage during the arrest.

• Assess neurologic function by the Cerebral Performance Category and the Glasgow Coma Scale.