Cardiac Arrest

Introduction

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

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.

• Once ACLS providers arrive, further definitive therapy is given following the ACLS algorithm
• 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.

Pharmacologic Therapy

• 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.

Epinephrine

• Vasopressin is a potent noradrenergic 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

Vasopressin

• 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.

Antiarrhythmics

• 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.