Key Concepts

    • Cardiopulmonary resuscitation (CPR) quality is critical to successful resuscitation from cardiac arrest. Important benchmarks of quality CPR include compression rate 100–120 compressions/min, compression depth 5–6 cm, compression fraction at least 80%, full chest recoil between compressions, and a ventilation rate of 10 breaths/min.

    • Restoration of adequate cardiac function is the defining factor of return of spontaneous circulation (ROSC). Restoration of good neurologic function is the defining factor of a successful resuscitation.

    • Resuscitation of a cardiac arrest victim does not end with ROSC. Rapid diagnosis and proper management of the pathologic condition(s) that precipitated and resulted from the arrest, as well as goal-directed post–cardiac arrest care, can improve outcomes.

    • Immediate percutaneous coronary intervention is indicated in patients with ST segment elevation myocardial infarction following ROSC, independent of neurological status.

    • Hypothermic targeted temperature management (32°C–36°C [89.6°F–96.8°F] for 24 h) has been shown to improve survival and functional outcome of comatose cardiac arrest survivors.

Foundations

Background and Importance

Cardiopulmonary arrest is defined by the triad of unconsciousness, apnea, and pulselessness. It is estimated that more than 340,000 out-of-hospital cardiac arrests (OHCAs) occur annually in the United States, an estimated annual incidence of 140/100,000. Of these, approximately 180,000 are treated by emergency medical services (EMS). Most EMS-treated, OHCAs occur at home (70%) and are unwitnessed (50%). The proportion of EMS-treated cardiac arrest patients with an initial shockable rhythm of ventricular fibrillation (VF) or pulseless ventricular tachycardia (pVT) has declined over time to approximately 18%. Furthermore, the number of patients receiving bystander cardiopulmonary resuscitation (CPR) remains low, averaging 40%. Automated external defibrillators (AEDs) are applied prior to EMS arrival in a minority of cases.

Recent epidemiologic data from cardiac arrest registries indicate the survival rate to hospital discharge for EMS-treated, OHCA is about 10%. Comparatively, survival to hospital discharge following in-hospital cardiac arrest (IHCA) is about 26%. Of patients surviving to hospital discharge, independent of neurologic status on presentation, 79% have good neurologic function (cerebral performance category of 1 or 2). For comatose post-cardiac arrest patients who underwent hypothermic targeted temperature management (HTTM), the reported survival rate with good neurologic function has ranged from 20% to 50%. Regional and inter-institutional variability in survival exists after EMS-treated cardiac arrest. The entire system of care affects patient outcomes, and differences in outcomes across the country may reflect local practice variability and differences in delivery of the chain of survival.

Anatomy, Physiology, and Pathophysiology

Awareness of underlying causes of cardiac arrest helps direct therapy and diagnostic testing both during resuscitation and in the immediate post-cardiac arrest period ( Table 5.1 ).

TABLE 5.1
Common Causes of Non-traumatic Cardiac Arrest
General Specific Disease or Agent
Cardiac Coronary artery disease
Cardiomyopathies
Structural abnormalities
Valve dysfunction
Respiratory Hypoventilation CNS dysfunction
Neuromuscular disease
Toxic and metabolic encephalopathies
Upper airway obstruction CNS dysfunction
Foreign body
Infection
Trauma
Neoplasm
Pulmonary dysfunction Asthma, COPD
Pulmonary edema
Pulmonary embolus
Pneumonia
Circulatory Mechanical obstruction Tension pneumothorax
Pericardial tamponade
Pulmonary embolus
Hypovolemia Hemorrhage
Vascular tone Sepsis
Neurogenic
Metabolic Electrolyte abnormalities Hypokalemia or hyperkalemia
Hypermagnesemia
Hypomagnesemia
Hypocalcemia
Toxic Prescription medications Anti-dysrhythmics
Digoxin, beta blockers
Calcium channel blockers
Tricyclic antidepressants
Drugs of abuse Cocaine
Heroin
Toxins Carbon monoxide
Cyanide
Environmental Lightning
Electrocution
Hypothermia or hyperthermia
Drowning or near-drowning
CNS, Central nervous system; COPD, chronic obstructive pulmonary disease.

Cardiac arrest with presenting rhythm of VF or pVT often has a primary cardiac origin. Coronary artery disease is a common pathologic condition found in patients who experience OHCA, and multiple observational studies have demonstrated disease rates comparable to those of patients undergoing clinically indicated coronary angiography. , Other primary cardiac etiologies of cardiac arrest include syndromes associated with sudden cardiac death due to ventricular dysrhythmias, including hypertrophic cardiomyopathy, Brugada syndrome, long QT syndrome, short QT syndrome, catecholaminergic polymorphic ventricular tachycardia, and arrhythmogenic right ventricular cardiomyopathy.

Cardiac arrest can result from non-cardiac origins, and common etiologies include circulatory causes, metabolic disturbances, and drug toxicities. Circulatory etiologies of cardiac arrest include tension pneumothorax, pericardial tamponade, pulmonary embolus, and hypovolemia/hemorrhage. These conditions must be recognized early to manage the underlying problem and maximize the chance of a successful resuscitation. The most common electrolyte disturbance leading to cardiac arrest is hyperkalemia, which results in progressive widening of the QRS complex that can deteriorate to pVT, VF, asystole, or pulseless electrical activity (PEA). Cardiac arrest from drug toxicity has specific characteristics, depending on the offending agent and presenting toxidrome. Specific therapy directed at drug toxicity (e.g., naloxone for opiate overdose) is essential, but may not be immediately effective depending on the agent involved. Prolonged resuscitation efforts that provide adequate perfusion may be needed (e.g., veno-arterial extracorporeal membrane oxygenation [VA-ECMO] for refractory cardiac arrest due to local anesthetic systemic toxicity).

Environmental etiologies including electrocution, hypothermia, and drowning can also result in cardiac arrest. Electrocution causes cardiac arrest through primary dysrhythmias or apnea. Alternating current in the range of 100 mA to 1 A (household and light industry) generally causes VF, whereas currents greater than 10 A (heavy industry or electrical transmission infrastructure) can cause ventricular asystole. Lightning produces a massive direct current electrocution that can result in asystole and prolonged apnea (see Chapter 130). Hypothermia-induced cardiac arrest can manifest with any electrocardiographic rhythm, and successful resuscitation depends on rapid rewarming, which often requires invasive measures (e.g., intravascular rewarming, peritoneal or thoracic lavage, or VA-ECMO; see Chapter 128). Once circulation is restored, patients should be warmed to a target of 32°C to 36°C (89.6° to 96.8°F) for 24 hours. Drowning is a form of asphyxia usually resulting in bradyasystolic arrest. Patients experiencing cardiac arrest secondary to hypothermia or drowning may benefit from prolonged resuscitation efforts.

Management

Decision Making

Prehospital

Most cardiac arrest cases managed in the emergency department (ED) initially occur outside the hospital. An increasing number of first responders, nontraditional providers (e.g., teachers, flight attendants), and public venues (e.g., airports, casinos, sports arenas, schools) are being equipped with AEDs. When coupled with regional and statewide campaigns to improve bystander CPR rates, including hands-only and dispatcher-assisted CPR, dramatic resuscitation rates have been achieved in communities where lay public providers feel empowered to respond within the first few minutes of arrest. Programs that fail to improve rates of bystander CPR or AED use within this critical time window are less likely to achieve increased survival rates.

Advanced life support units staffed by paramedics often have standing orders to follow advanced cardiac resuscitation protocols. In cases of cardiac arrest refractory to properly performed advanced prehospital measures, the patient may be pronounced dead at the scene per protocols. However, if advanced hospital-based resuscitation strategies such as extracorporeal cardiopulmonary resuscitation (ECPR) or percutaneous coronary intervention (PCI) are available, then transport to a comprehensive resuscitation center may still be warranted. In systems where patients are transported in cardiac arrest, mechanical CPR results in better quality chest compressions during transport and is likely to be safer for EMS providers. Mechanical CPR can minimize interruptions in chest compressions, eliminate the need to switch rescuers due to provider fatigue, and can deliver consistent depth and rate of compressions.

History and Physical Examination

It is often difficult to determine the cause of cardiac arrest at presentation. Although a differential diagnosis can be formulated based on history, physical examination, and electrocardiographic rhythm on arrival, key information is often unreliable or not available. The differential diagnosis can potentially be narrowed by the patient’s age, underlying diseases, and medications, when known.

Historical information from family, bystanders, and EMS personnel provides key information regarding cause and prognosis. Information surrounding the event includes whether the arrest was witnessed, time of arrest, what the patient was doing (e.g., eating, exercising, trauma), possibility of drug ingestion, whether bystander CPR was performed, time of initial CPR, initial electrocardiographic rhythm, and interventions by EMS providers. Important past medical history includes baseline health, previous heart, lung, or renal disease, malignancy, hemorrhage, infection, and risk factors for coronary artery disease and pulmonary embolism. The patient’s current medications and allergies should be obtained if possible.

Physical examination of a cardiac arrest patient is necessarily focused on a few key goals: (1) ensuring the adequacy of airway patency and ventilation; (2) confirming the diagnosis of cardiac arrest; (3) finding evidence of the cause; and (4) monitoring for complications of therapeutic interventions. This examination occurs in descending order of importance, simultaneously with therapeutic interventions, and is repeated frequently to assess for response to therapy and occurrence of complications ( Table 5.2 ). After the initial minutes of cardiac arrest, the physical examination may provide little evidence of the duration of arrest. Pupils dilate within 1 minute but may constrict if CPR is initiated immediately and performed effectively. Dependent lividity and rigor mortis develop after hours of cardiac arrest. Temperature is an unreliable predictor of duration of cardiac arrest because it does not decrease significantly during the first hours of arrest, and hypothermia may cause cardiac arrest or be caused by prolonged arrest.

TABLE 5.2
Physical Examination Findings Indicating Potential Cause of Cardiac Arrest and Complications of Therapy
Physical Examination Abnormalities Potential Causes
General Pallor Hemorrhage
Cold Hypothermia
Airway Secretions, vomitus, or blood Aspiration
Airway obstruction
Resistance to positive-pressure ventilation Tension pneumothorax
Airway obstruction
Bronchospasm
Neck Jugular venous distention Tension pneumothorax
Cardiac tamponade
Pulmonary embolus
Tracheal deviation Tension pneumothorax
Chest Median sternotomy scar Underlying cardiac disease
Lungs Unilateral breath sounds Tension pneumothorax
Right mainstem intubation
Aspiration
Distant or no breath sounds or no chest expansion Esophageal intubation
Airway obstruction
Severe bronchospasm
Wheezing Aspiration
Bronchospasm
Pulmonary edema
Rales Aspiration
Pulmonary edema
Pneumonia
Heart Diminished heart tones Hypovolemia
Cardiac tamponade
Tension pneumothorax
Pulmonary embolus
Abdomen Distended and dull Ruptured abdominal aortic aneurysm or ruptured ectopic pregnancy
Distended, tympanitic Esophageal intubation
Gastric insufflation
Rectal Blood, melena Gastrointestinal hemorrhage
Extremities Asymmetrical pulses Aortic dissection
Arteriovenous shunt or fistula Hyperkalemia
Skin Needle tracks or abscesses Intravenous drug abuse
Burns Smoke inhalation
Electrocution

Resuscitation

Management of cardiac arrest occurs in an orchestrated effort by a health care team led by a clinician who can monitor the efficacy and response to therapeutic interventions. Interventions should be performed rapidly and efficiently to maximize the chances of a good neurologic outcome. Restoration of adequate cardiac function is the defining factor of return of spontaneous circulation (ROSC), but restoration of good neurologic function is the defining metric of a successful resuscitation. The likelihood of achieving both of these goals decreases with every minute that the patient remains in cardiac arrest. Fig. 5.1 depicts an algorithm for the management of cardiac arrest.

Fig. 5.1, Emergency Treatment Algorithm for Treatment of Cardiac Arrest.

The goal of CPR is to maintain vital organ perfusion until ROSC is achieved. The quality of CPR is perhaps the most underappreciated component of the resuscitation effort. Important quality performance measures include compression rate (100 to 120 compressions/min), compression depth (5 to 6 cm), chest compression fraction at least 80% (i.e., CPR performed 80 out of every 100 seconds of the pulseless interval), full chest recoil between compressions (no residual leaning between compressions), and ventilation rate (10 ventilations/min).

While chest compression–only CPR (hands-only-CPR) is recommended for lay-providers in the out-of-hospital setting, trained providers who are willing and able to provide ventilations should do so. A 30:2 compression-to-ventilation ratio is currently recommended for health care professionals in all adult resuscitation scenarios until an advanced airway has been established. While either bag-mask ventilation or an advanced airway strategy may be considered in any setting for adult cardiac arrest, the strategy employed should minimize CPR interruptions. If an advanced airway strategy is pursued, a supraglottic airway may be used and can be placed without interruptions to CPR. Endotracheal intubation may also be pursued in settings with high intubation success rates. Once an advanced airway is secured, CPR should be performed continuously, without pausing for ventilation, while providing one ventilation every 6 seconds (10 ventilations/min). Hyperventilation during CPR should be avoided, as it is associated with reduced cardiac output during CPR.

Ventricular Fibrillation and Pulseless Ventricular Tachycardia

Cardiac arrest with presenting rhythm of VF or pVT often has a primary cardiac origin. VF and pVT are treated identically as they are generally caused by the same mechanisms and respond to the same interventions. Therapy for VF and pVT includes defibrillation, high-quality CPR, and administration of vasopressors and anti-dysrhythmic agents.

For a pulseless unresponsive patient in VF or pVT, chest compressions should be initiated immediately and continued until a defibrillator is available. Current consensus favors delivering a single countershock with minimal pause in chest compressions. Defibrillation is followed immediately by the resumption of chest compressions for 2 minutes before a rhythm check and additional defibrillation, as appropriate. If a patient is defibrillated into a different pulseless rhythm (PEA or asystole), subsequent treatment should be modified to address those specific rhythms.

Traditional monophasic defibrillators have almost completely been replaced by defibrillators using biphasic waveforms. With biphasic defibrillation, the energy required for successful defibrillation (the defibrillation threshold) is lower than with monophasic defibrillation. The biphasic waveform increases the likelihood of initial defibrillation success and decreases the likelihood of post–countershock myocardial dysfunction. However, data are currently inadequate to conclude that a biphasic or monophasic waveform is superior in achieving ROSC or survival to hospital discharge. Health professionals should use device-specific manufacturer-recommended countershock energies for biphasic defibrillators, while the recommended energy for a single monophasic defibrillation is 360 J. Assurance of maximal compression fraction can be accomplished by placing defibrillation pads early in the resuscitation sequence, thus not requiring a pause while defibrillation paddles and conducting gel are placed for each shock, and continuing chest compressions while the defibrillator charges.

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