Epidemiology

In the United States, sudden cardiac death accounts for approximately 200,000 to 500,000 deaths per year, with nearly half of these events occurring outside the hospital. Regarding the primary inciting event, cardiac causes of sudden cardiac death are most common (Fig. 7.1). Even though individuals with established cardiac disease have a greater than 50% incidence of sudden death, only a minority of cardiac arrest incidents occur in this population. It is estimated that half of all deaths from cardiovascular disease are sudden and unexpected and occur soon after the onset of symptoms. Patient age at the time of cardiac arrest has two distinct peaks—infants younger than 6 months and adults 45 to 75 years of age. Most sudden deaths occur outside the hospital and are often unwitnessed.^1,²

Fig. 7.1 Primary inciting event in cardiopulmonary arrest.

Sudden death may occur for a range of reasons, including medical and traumatic. Of the medical events, cardiac causes are the most frequently encountered; in fact, 75% of sudden death events are related to cardiac causes. In this setting, acute dysrhythmias are common, whether they represent the primary event (e.g., sudden ventricular fibrillation) or a secondary process related to the primary event (e.g., acute pulmonary edema with progressive hypoxemia and resultant bradycardia).

Despite comprehensive resuscitation programs and extensive research initiatives, survival rates in most American communities after out-of-hospital cardiac arrest range from 2% to 5%, and survival rates after in-hospital arrest range from 25% to 30%. Despite improvements in prehospital- and hospital-based management strategies and increased awareness in the lay public, cardiac arrest is still associated with extremely high mortality and a dismal neurologic outcome. Immediate, high-quality cardiopulmonary resuscitation (CPR) and effective defibrillation are rarely accomplished quickly enough to increase the likelihood of an improved outcome.

When resuscitation is successful, cardiac dysrhythmias remain a primary concern in the early phase of management of cardiac arrest. The four basic dysrhythmias encountered in cardiac arrest victims include pulseless ventricular tachycardia (VT), ventricular fibrillation (VF), asystole, and pulseless electrical activity (PEA). Pulseless VT and VF result in death unless treated aggressively and rapidly. Asystole, or effective absence of cardiac electrical activity, is the true cardiac arrhythmia (i.e., absence of any rhythm). PEA constitutes a diverse range of rhythms and related clinical scenarios. PEA is an electrical rhythm (i.e., the cardiac rhythm) with absence of discernible mechanical contraction of the heart and no detectable perfusion. The frequency of the dysrhythmias differs depending on the clinical setting (Fig. 7.2).

Fig. 7.2 Cardiac arrhythmias encountered in cardiac arrest.

Note the preponderance of asystole in both groups, as well as increased rates of pulseless electrical activity (PEA) in the hospitalized patients and ventricular fibrillation and tachycardia (VT/VF) in the prehospital patients.

General Management Considerations

The core concepts of management of cardiorespiratory arrest include the following goals: reversing any immediately treatable cause and ensuring the basics of circulatory and respiratory support. In the early phases of cardiac arrest, circulation is the most important issue and is addressed by performing high-quality, uninterrupted chest compressions and defibrillation for shockable rhythms.

Resuscitation rates in patients with out-of-hospital and in-hospital cardiac arrest remain poor despite significant advances in the medical sciences. Contemporary research and recommendations have demonstrated that basic life support (BLS) interventions are very important therapies that have a positive impact on outcome.³ This same body of thought and investigation has suggested that advanced life support (ALS) treatments are of less value than originally thought.³ In addition, studies have demonstrated that early access to ALS treatment may be of less importance than previously believed.^3,⁴ In the final phase of the Ontario Prehospital Advanced Life Support trial it was reported that in a community in which early CPR and early defibrillation are achieved, there is no survival benefit with the addition of prehospital ALS interventions.³ ALS is of value, but it is limited and less valuable than BLS measures in the early phase of most cardiac arrest events.

The 2010 guidelines of the American Heart Association (AHA) further deemphasizes advanced interventions. The 2010 AHA Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care list five goals in the approach to cardiac arrest resuscitation: rapid activation of the emergency response team, effective and high-quality chest compressions, early access to defibrillation, effective ALS, and coordinated postresuscitation care.⁵ Only one of these five goals addresses ALS interventions.

Critically, both BLS and ALS protocols and guidelines are important, but they are simply guides to management. Emergency physicians should use these protocols and guidelines as a framework to develop and implement the most appropriate management for their patients.

Cardiopulmonary Resuscitation

CPR can be performed in two basic fashions. The traditional, or conventional, method includes chest compressions with ventilations; the newer and probably superior method is termed compression-only CPR and involves chest compressions only with avoidance of early airway management. Each of the management priorities in CPR—circulation, airway, and breathing (CAB)—must be addressed either in sequential fashion (limited personnel available) or simultaneously (multiple personnel available).

With respect to resuscitation in general and CPR in particular, it is important to note that circulation now precedes airway and breathing. Adequate circulation, largely achieved by appropriate chest compressions with limited interruption and early defibrillation for shockable rhythms, is a necessity throughout the resuscitation event and is particularly important in its early phase. Achieving an adequate airway with appropriate oxygenation and ventilation is an important intervention, but it appears to be less important than early and continuous adequate, uninterrupted chest compressions. Rhythm analysis, pulse determinations, and other periods without chest compression must be minimized so that perfusion can be sustained.

Numerous investigations have demonstrated that chest compressions are delayed, frequently interrupted, and of poor quality. Wik et al found that CPR was performed only 48% of the time when indicated and that when it was performed, the mean rate was just 64 compressions per minute, with an appropriate depth (at least 5 cm) attained in only 28% of cases.⁶ Wang et al. and others reported that CPR was frequently interrupted for prolonged periods, anywhere from 1.8 to 7 minutes, to perform endotracheal intubation.^7,⁸

One of the key components of the 2010 AHA guidelines ⁵ is the change from performing the ABCs (airway, breathing, circulation) to the CABs,⁹ thus demonstrating how important compressions are relative to airway management and oxygenation—particularly early in cardiac arrest. Chest compression–only CPR has been proposed as an alternative method of basic resuscitation that is superior to traditional CPR with chest compressions and ventilations. The basic component of compression-only CPR is the performance of continuous, uninterrupted chest compressions of high quality. Compression-only CPR suggests that early management of the airway is not a priority.

Compression-only CPR has been shown to have similar efficacy to conventional CPR in terms of neurologically intact survival at 1 year in victims of witnessed cardiac arrest.¹⁰ In patients with an initially shockable rhythm, Kellum et al. demonstrated an increased survival rate with neurologically intact status after receiving compression-only CPR.¹¹ The SOS-KANTO (Survey of Survivors After out-of Hospital Cardiac Arrest in the Kanto Area of Japan) trial reviewed 4068 patients with witnessed out-of-hospital cardiac arrests, 1151 of whom received bystander CPR. The 439 subjects who received hands-only CPR showed similar neurologic outcome at 30 days as did those who received conventional CPR (6% versus 4% of survivors); no benefit was seen with the addition of mouth-to-mouth ventilation.¹² In 2008 using the concept of minimally interrupted cardiac resuscitation, Bobrow et al. demonstrated that cycles of 200 continuous compressions, followed by electrical defibrillation with immediate resumption of compressions before endotracheal intubation, resulted in an increased survival rate (1.8% versus 5.4%) in all patients. In the witnessed VF subgroup, the survival rate increased from 4.7% to 17.6%.¹³

When performing CPR, early emphasis on the airway and breathing components of CPR can hinder appropriate chest compressions and produce excessive ventilations. The concept of death by hyperventilation is based on overdistension of the thoracic cavity, which results in increased intrathoracic pressure. Increased intrathoracic pressure can impede venous return to the right side of the heart. Reduced venous return limits preload of the left ventricle, thereby resulting in diminished cardiac, cerebral, and vital organ perfusion. Excessive ventilation rates must be avoided; a ventilatory rate of 8 to 10 breaths/min is appropriate via either bag-mask ventilations or endotracheal tube.

Electrical Therapy

Electrical therapy—defibrillation and transcutaneous cardiac pacing—can be lifesaving when used in an appropriate and timely fashion. Early defibrillation improves survival rates, but only if accomplished within minutes. This therapy is appropriate only for pulseless VT and VF, and it has no indication in managing asystole or PEA rhythms.

Defibrillators exist in two basic styles—monophasic and biphasic. Most commercially available defibrillators (automatic and manual) are biphasic, although many monophasic models remain in use today. No defibrillator style, monophasic or biphasic, is associated with unequivocally higher rates of successful resuscitation or survival to hospital discharge. The biphasic defibrillator has achieved a higher rate of termination of pulseless VT and VF, but this early benefit has not translated into survival to hospital discharge with meaningful quality of life. When using a monophasic defibrillator, a 360-J shock should be applied; if a biphasic unit is in operation, the equivalent, device-specific maximal emergency should be applied. In either type of device, a single shock is delivered initially and in subsequent defibrillations.

Use of an automated external defibrillator (AED) is a lifesaving intervention when applied appropriately. Use of an AED by trained lay rescuers (the Public Access Defibrillation [PAD] program) has resulted in a markedly shorter time to defibrillation and an improved rate of resuscitation. AED use by nontrained rescuers in a PAD application has anecdotally demonstrated positive outcomes, but its use by untrained personnel requires additional investigation. The Targeted First Responder (TFR) application has also demonstrated significant success.

No conclusive data are available on the ideal timing of the initial defibrillation, regardless of the downtime. The AHA recommendation states that a patient in cardiac arrest with a shockable rhythm should undergo electrical defibrillation as soon as possible. Chest compressions should be initiated as soon as the defibrillator is located, applied, and activated.

The most recent analysis of the timing of initial defibrillation suggests that there is no benefit with delayed defibrillation, even in patients with prolonged downtimes. Simpson et al. performed a meta-analysis of the existing literature and noted that no benefit was found in delaying the first shock in patients with prolonged downtimes or unwitnessed arrest (or both).¹⁴ The cumulative data demonstrated no benefit in providing chest compression before defibrillation versus immediate defibrillation and also no harm in performing CPR before the initial defibrillation. The 2010 AHA guidelines^5,⁹ also acknowledged that the literature does not support a chest compression–first approach, thus suggesting that clinicians should provide both therapies (chest compression and defibrillation) and base the time of the first defibrillation on analysis of the setting, personnel, and equipment parameters for individual cases.

The other primary form of electrical therapy used in managing cardiac arrest is transcutaneous cardiac pacing. Very early use of transcutaneous ventricular pacing can be considered, although conclusive supporting evidence is lacking. Transcutaneous pacing is much less effective after the loss of spontaneous circulation or prolonged cardiac arrest.^15,¹⁶ Transcutaneous pacing is a rapid, minimally invasive means of treating asystole and PEA bradyarrhythmias. Transcutaneous pacing electrodes are applied to the skin of the anterior and posterior chest walls, and pacing is initiated with a portable pulse generator. In an emergency situation, this type of pacing technique is easily and rapidly accomplished when compared with other methods of cardiac pacing.

Pharmacologic Therapy

Although numerous medications may be used in a resuscitation event, several “code drugs” are of potential importance, including epinephrine, vasopressin, atropine, amiodarone, lidocaine, magnesium, calcium, and sodium bicarbonate. Research into resuscitation after cardiac arrest has demonstrated that BLS interventions significantly contribute to favorable outcomes and that ALS treatments are less valuable than originally thought.^3,¹⁷ A review of the issue has suggested that the use of cardioactive medications can increase the rate of successful resuscitation but does not alter the ultimate survival rate or have an impact on neurologic status at discharge among survivors.¹⁸

Because these code drugs are still used with significant frequency by clinicians during resuscitation of patients in cardiac arrest, an understanding of these medications and their potential impact is essential. The code drugs are separated into several subcategories, including vasopressors (epinephrine and vasopressin), parasympatholytic drugs (atropine), antiarrhythmic agents (lidocaine and amiodarone), electrolytes (calcium and magnesium), buffer (sodium bicarbonate), and fibrinolytic medications.

The two primary vasopressor agents used in resuscitation are epinephrine and vasopressin. Epinephrine and vasopressin have demonstrated increased rates of return of spontaneous circulation (ROSC) but have not produced meaningful increases in survival to hospital discharge with intact neurologic status. Both vasopressors are indicated in all three cardiac arrest treatment scenarios, including pulseless VT and VF, PEA, and asystole. These medications can be used interchangeably in the cardiac arrest scenario; that is, use of one type of vasopressor does not preclude future use of the other agent in that same resuscitation. The vasopressor class of resuscitative agents can increase the rate of ROSC. To date, however, no single report has demonstrated an improvement in overall ultimate survival, with or without a measure of neurologic status, as a function of vasopressor application.

Atropine is a parasympatholytic drug that enhances both sinoatrial node automaticity and atrioventricular conduction via direct vagolytic action. In cardiac arrest, atropine can be considered in patients with both asystole and PEA, particularly those with bradydysrhythmic electrical activity. It is important to note that the AHA has removed atropine from all cardiac arrest algorithms.^5,⁹ Removal of atropine is based not on any negative impact on patient outcome but on a significant lack of benefit.^5,⁹ Atropine is still recommended in patients with compromising bradydysrhythmia with intact perfusion.^5,^9,^19,²⁰

Amiodarone and lidocaine are the primary antidysrhythmic agents used in cardiac arrest resuscitation scenarios. Amiodarone has a very broad range of mechanisms, including sodium and calcium blockade, antagonism of potassium efflux, and adrenergic blocking effects. In cardiac arrest, indications for its use include pulseless VT and VF unresponsive to CPR, defibrillation, and an initial vasopressor. Although amiodarone has demonstrated impressive results in terms of ROSC after cardiac arrest, it has not altered the ultimate outcome—meaningful survival to hospital discharge. Lidocaine is a well-known and widely used antidysrhythmic agent with limited efficacy in cardiac arrest. Unfortunately, lidocaine has demonstrated no alteration in outcomes of patients with out-of-hospital cardiac arrest secondary to pulseless VT and VF. Furthermore, when compared with amiodarone, lidocaine has been shown to have a less favorable rate of ROSC and an increased rate of asystole in general and following defibrillation. Like amiodarone, it may be used in patients with pulseless VT and VF unresponsive to initial therapies. At the present time, lidocaine is best considered an alternative to amiodarone for refractory pulseless VT and VF.

The electrolytes magnesium and calcium play a limited role in resuscitation. Magnesium should be used in patients with polymorphic VT (PVT) thought to be torsades de pointes (TdP). Possible secondary indications for magnesium include PEA cardiac arrest potentially resulting from hyperkalemia and cardiorespiratory arrest related to toxemia of pregnancy. Use of calcium should be limited to cardiac arrest involving excessive parenteral magnesium administration, hyperkalemia, and cardiotoxin ingestion.

Sodium bicarbonate is a potent buffer, but no evidence supports its widespread use for cardiac arrest. Sodium bicarbonate can adversely affect perfusion in certain vascular beds, unfavorably alter acid-base status at the tissue and cellular levels, and promote hyperosmolarity and hypernatremia. Sodium bicarbonate has several specific clinical scenarios in which it is potentially indicated: tricyclic antidepressant overdose (and other sodium channel blocking agents), severe acidosis (metabolic and respiratory), hyperkalemia, and prolonged cardiac arrest.

Acute thrombosis with or without embolization, either coronary or pulmonary, can cause cardiac arrest. Many investigators have considered the early use of fibrinolytic agents in the management of cardiac arrest with known or presumed acute thrombosis. Anecdotal reports describe the cases of adult patients who have been successfully resuscitated following the administration of a fibrinolytic agent when the condition leading to the arrest was acute myocardial infarction (AMI) or acute pulmonary embolism.²¹ The 2010 AHA guidelines state that the evidence is insufficient to advocate the routine use of fibrinolytic agents during cardiac arrest but that its use should be considered on a case-by-case basis. Fibrinolytic agents are a level IIb recommendation in cardiac arrest secondary to pulmonary embolism.^5,⁹

The Airway

The AHA has moved away from the airway-first strategy with a reordering of the resuscitation alphabet from the ABCs to the CABs, thus highlighting the relative importance of circulation over airway management.^5,⁹ This change in strategy is based on the relative importance of circulation but also on the fact that airway interventions, particularly placement of an invasive airway, can interrupt continuous chest compressions and lessen the central nervous system (CNS), cardiac, and systemic perfusion produced by CPR. The airway should be managed invasively once appropriate chest compressions have been initiated and sustained and defibrillation has taken place. Management of the airway must not hinder appropriate chest compressions and other basic interventions. In cardiac arrest scenarios caused by a compromised airway or inadequate oxygenation and ventilation, or both, attention to invasive management of the airway is important.

Management of Specific Dysrhythmias

Ventricular Fibrillation and Pulseless Ventricular Tachycardia

VF and pulseless VT are discussed together because they occur in the same clinical settings and have similar mechanisms, causes, and modes of therapy. The only clinically significant classification system of VF concerns the amplitude of the chaotic waveform deflections. Regardless of the mor-phology of VF, without prompt therapy, VF invariably results in death.

VF is divided into two clinical types. It is considered primary in the absence of acute left ventricular dysfunction and cardiogenic shock, and it is noted in approximately 5% of patients with AMI. The majority of primary VF episodes occur within the first 4 hours of AMI, and 80% are seen within the initial 12-hour period of infarction. VF may represent abrupt reperfusion, but recurrent or ongoing ischemia is more likely. The overall prognosis for patients with primary VF does not differ from that in AMI patients without VF after a brief period of increased inpatient mortality. Secondary VF can occur at any time in the course of AMI; may be complicated by acute heart failure, cardiogenic shock, or both; and occurs in up to 7% of patients with AMI. Unlike primary VF, the prognosis for patients with secondary VF is poor, with in-hospital mortality approaching 60%, and long-term mortality beyond 5 years remains poor.

In contrast to VF, VT usually originates from a specific focus in the ventricular myocardium or in the infranodal conduction pathway. VT is defined as a rapid, wide regular QRS complex tachycardia originating from infranodal cardiac tissue. VT can be classified from several different perspectives, including the overall clinical findings (stable versus unstable), the hemodynamic state (presence or absence of a pulse), its temporal course (sustained versus nonsustained), and its morphology (monomorphic versus polymorphic). In sudden cardiac death, it is most appropriate to consider VT from the perspective of the overall clinical findings, with an emphasis on the temporal and hemodynamic factors. In this instance, VT is considered pulseless and sustained and thus unstable. Pulseless VT accounts for a minority of the rhythms seen in cardiac arrest and has the most favorable prognosis. This relatively infrequent occurrence results from an early appearance with rapid degeneration. If therapy is not initiated in arrest events, this rhythm rapidly decompensates into more malignant rhythms such as VF or asystole.

Pathophysiology

These malignant dysrhythmias most often arise as a result of direct myocardial damage (i.e., AMI, myocarditis, cardiomyopathy), medication toxicity, or electrolyte abnormality. The pathophysiology usually involves either a reentry phenomenon or triggered automaticity. A reentry circuit within the ventricular myocardium is the most common source. The properties of a reentry circuit involve two pathways of conduction with differing electrical characteristics. The reentry circuits that provide the substrate for VT and VF generally occur in a zone of acute ischemia or chronic scarring. This dysrhythmia is usually initiated by an ectopic beat, although a number of other factors can be the primary initiating event, including acute coronary ischemia, electrolyte disorders, and dysautonomia. Triggered automaticity of a group of cells can result from various cardiac anomalies, including congenital heart disease, acquired heart ailments, electrolyte disorders, and medication toxicity.

One electrophysiologic model describes these ventricular dysrhythmias with respect to morphology and suggests that the three entities (VF, PVT, and monophasic VT [MVT]) are manifested across an electrophysiologic spectrum. This model notes that PVT differs from VF and MVT in frequency, amplitude, and variability, thus suggesting that MVT, PVT, and VF are states of electrical activity occurring across a spectrum of ventricular dysrhythmia. In this model, MVT is the most highly organized rhythm, whereas VF is the least; PVT represents an intermediate entity between the two end points of the spectrum.

Clinical Presentation

Ventricular Fibrillation

VF results in a lack of spontaneous perfusion except in the rare case of a witnessed, recent onset in which the patient is able to cough, thereby enabling perfusion to continue for a short period. VF is diagnosed electrocardiographically (Fig. 7.3) in pulseless and apneic patients by the presence of lower amplitude and chaotic activity. The rate of the deflections is usually between 200 and 500 depolarizations per minute. Morphologically, VF is divided into coarse (Fig. 7.3, A) and fine (Fig. 7.3, B and C). Coarse VF tends to occur early after cardiac arrest; is characterized by high-amplitude, or coarse, waveforms; and has a better prognosis than fine VF does. With continued cardiac arrest the amplitude dampens, with a less dramatic appearance of the dysrhythmia and fine VF (Fig. 7.3, B and C) ultimately being produced. The R-on-T phenomenon can result in VF as noted in Figure 7.3, D and E.