Management of Cardiac Arrest and Post–Cardiac Arrest Syndrome

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7 Management of Cardiac Arrest and Post–Cardiac Arrest Syndrome

William J. Brady, Peter P. Monteleone, Mark Sochor, Robert E. O’Connor

Key Points

• The ultimate outcome of patients with cardiac arrest is frequently poor but can be improved by immediate bystander cardiopulmonary resuscitation, early defibrillation, and postresuscitation treatment.

• The classic ABC (airway, breathing, circulation) prioritization has changed to CAB to reinforce and prioritize early initiation of high-quality chest compressions and deemphasize early invasive airway management.

• Early defibrillation in patients with ventricular fibrillation and pulseless ventricular tachycardia is aided by various strategies, including automatic external defibrillators and improved provider awareness.

• Interruptions in chest compressions during cardiopulmonary resuscitation should be limited to maximize resuscitation; such interruptions can contribute to an unfavorable outcome.

• Postresuscitation care should include consideration of both induced hypothermia and urgent coronary reperfusion therapy.

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.

Fig. 7.3 Ventricular fibrillation.

A, Coarse ventricular fibrillation. Note the large-amplitude deflections with no organized electrical activity. B, Ventricular fibrillation with low to intermediate deflections in amplitude; also, the absence of organized electrical activity is obvious. C, Very fine ventricular fibrillation. Note the apparent absence in this lead (lead II) of deflection. This rhythm may be incorrectly diagnosed as asystole if the patient is monitored solely with a single electrocardiographic lead. D, Sinus tachycardia with degeneration into ventricular fibrillation. Note the appearance of the R-on-T phenomenon, with the R wave of an early beat falling on the T wave of the preceding beat. The repolarization period of the electrocardiographic cycle is an electrically vulnerable period of the cardiac phase—insults, such as subsequent depolarizations, may cause the development of ventricular tachycardia or ventricular fibrillation. In this case, the patient has a short period of polymorphic ventricular tachycardia followed by coarse ventricular fibrillation. E, R-on-T phenomenon with the R wave (thin arrow) of an early beat falling on the T wave (thick arrow) of the preceding beat, followed by a short period of polymorphic ventricular tachycardia.

Fine VF may be confused with asystole. If the sensing electrode is oriented perpendicular to the primary depolarization vector, the amplitude of the deflections is minimal, thus mimicking asystole. Such mimicking can have a negative impact on patient care if electrical defibrillation is not considered. This potential pitfall can easily be avoided if the dysrhythmia is viewed in at least two or three simultaneous or consecutive electrocardiographic leads. Fine VF has a significantly greater incidence of post-countershock asystole than coarse VF does. In this instance, aggressive resuscitation will probably improve the hemodynamic state and increase the opportunity for ROSC.

Ventricular Tachycardia

VT is defined as three or more ventricular beats in succession with a QRS complex duration of greater than 0.12 second and a ventricular rate greater than 100 or 120 beats/min (Fig. 7.4). Most instances of VT are characterized by very rapid rates; however, patients may have slower versions of VT, particularly if using amiodarone.

Fig. 7.4 Morphologic description of ventricular tachycardia (VT).

Morphologically, VT can be divided into monomorphic and polymorphic based on the nature of the QRS complex. Polymorphic VT (PVT) can be further subdivided into torsades de pointes (TdP) PVT and non-TdP PVT—this distinction considers not only the morphology of the QRS complex but also other electrophysiologic issues (the repolarization state as manifested by the QT interval); with TdP PVT, prolongation of the QT interval is noted—this determination obviously can only be made when the patient has an electrocardiogram exhibiting a supraventricular rhythm.

From an electrocardiographic perspective (Fig. 7.5; also see Fig. 7.4), the morphology of the VT is of importance. MVT (Fig. 7.5, A and B) is identified when each consecutive waveform has a single morphology; that is, the beat-to-beat variation in QRS complex morphology is negligible. The rate is usually between 140 and 180 beats/min and very regular. MVT is the most common form of VT and is seen in 65% to 75% of patients with VT in the out-of-hospital setting (Fig. 7.6).^22,²³ In patients with MVT, the cause of the dysrhythmia is usually myocardial scarring from a previous infarct.

Fig. 7.5 Ventricular tachycardia.

A, Monomorphic ventricular tachycardia. Note the very wide QRS complex and rate of approximately 150 beats/min. B, Monomorphic ventricular tachycardia. Note the very rapid rate of approximately 240 beats/min. C, Polymorphic ventricular tachycardia (PVT). The QRS complex is continually changing (potentially both in amplitude and morphology) in any single lead. The QRS complex also tends to be greater than 0.12 second with beat-to-beat variations in morphology and width being encountered; significant variability in the R-R interval and QRS complex axis is noted as well. D, PVT, torsades de pointes (TdP) type. Note the marked, beat-to-beat variation in QRS complex morphology occurring in a gradual pattern. The QRS complex ranges from small to large with an undulating pattern, as though it is “twisting about a point”—the TdP version of PVT. TdP PVT has a characteristic appearance—the QRS complex varies in amplitude and appears to rotate about the isoelectric baseline in a semisinusoidal fashion. Also required for the electrocardiographic (and clinical) diagnosis of TdP is demonstration of abnormal repolarization manifested by prolongation of the QT interval on the electrocardiogram when the patient is in a supraventricular rhythm.

Fig. 7.6 Morphologic subtypes of ventricular tachycardia (VT) in prehospital cardiac arrest patients.

In patients with polymorphic VT (PVT), both non–torsades de pointes (Non-TdP) and TdP versions are seen in approximately equal frequency. MVT, Monophasic ventricular tachycardia.

PVT (see Fig. 7.4) is characterized by a frequently changing QRS complex (see Fig. 7-5, C and D). The QRS complex tends to be greater than 0.12 second with beat-to-beat variations in morphology and width. Significant variability in the R-R interval and QRS complex axis is present. Its rate is usually more rapid than that of MVT, with a range of 150 to 300 beats/min, and PVT accounts for 25% to 30% of cases of VT in patients with out-of-hospital cardiac arrest (see Fig. 7.6).^22,²³

The PVT subtype TdP (see Fig. 7.4) demonstrates polymorphous QRS complexes that vary from beat to beat (Fig. 7.7, A and B; also see Fig. 7.5, D). The variation is often quite pronounced and easily observed. TdP has a highly characteristic electrocardiographic pattern; the literal translation of the French term torsades de pointes—”twisting of the points”—elegantly describes the appearance of the QRS complex as it varies in amplitude and appears to rotate about the isoelectric baseline in a semisinusoidal fashion. Also required for electrocardiographic (and clinical) diagnosis of TdP is demonstration of abnormal repolarization as manifested by prolongation of the QT interval on the electrocardiogram when the patient is in a supraventricular rhythm (either before or after cardiac arrest) (Fig. 7.7, B).

Fig. 7.7 A, Torsades de pointes (TdP) polymorphic ventricular tachycardia. The appearance of the QRS complex is characteristic of this subtype of polymorphic ventricular tachycardia—in any single electrocardiographic lead it varies in both morphology and amplitude and appears to rotate about the isoelectric baseline in a semisinusoidal fashion. B, TdP polymorphic ventricular tachycardia. Note the polymorphous QRS complexes that vary from beat to beat. The variation is often quite pronounced, with marked variation easily observed in any single lead from one beat to the subsequent beat. TdP also demonstrates a highly characteristic electrocardiographic pattern; the literal translation of the French term torsades de pointes—”twisting of the points”—elegantly describes the appearance of the QRS complex as it varies in amplitude and appears to rotate about the isoelectric baseline in a semisinusoidal fashion. Also required for diagnosis is demonstration of abnormal repolarization as manifested by prolongation of the QT interval on the electrocardiogram when the patient is in a supraventricular rhythm (i.e., before arrest or after successful resuscitation and return of spontaneous circulation).

Management of Pulseless Ventricular Tachycardia and Ventricular Fibrillation

Resuscitative management of these two malignant dysrhythmias is similar. The basic approach (Table 7.1) includes CPR, with an emphasis on high-quality chest compressions, and electrical defibrillation. Once defibrillation has occurred, CPR is resumed for an additional 2 minutes. If the dysrhythmia persists on electrocardiographic analysis, a vasopressor is administered, either vasopressin or epinephrine. Epinephrine should be used in 1-mg doses, preferably administered via an intravenous or intraosseous line. If given by endotracheal tube (ETT), a larger dose of two to three times the intravenous dose is recommended. Dosing through the ETT is not currently considered to be the most effective means of delivering the medication. Epinephrine should be readministered every 3 to 5 minutes during the resuscitation. In certain situations such as ingestion of a cardiotoxic drug, higher doses of epinephrine may be required, but this issue has not been explored. Vasopressin is administered via the intravenous or intraosseous routes at a dose of 40 international units (IU). In multiple studies of vasopressin alone or vasopressin versus epinephrine in prehospital and hospital-based populations, no significant difference has been found in survival to hospital discharge.²⁴^–²⁶ A single dose of vasopressin may be used as either the first or second vasopressor administered, and epinephrine can be used in a primary or secondary role.

Table 7.1 Ventricular Fibrillation and Pulseless Ventricular Tachycardia

TIME	TREATMENT PRIORITY	COMMENTS
Minute 0	Chest compressions	Compressions should be performed at a rate of 100/min. Initial compressions may improve shock efficacy by increasing the amplitude of ventricular fibrillation. Pulse checks and rhythm analysis should be performed no more often than every 2 min. Defibrillation should take place as soon as a device is available.
Minute 0-1	Defibrillation, followed by chest compressions IV access (if possible)	Because of the increased first shock conversion rate with biphasic energy and the importance of hands-off time, high-energy shock is recommended. IV access should not interfere with chest compressions.
Minute 3	Defibrillation, followed by immediate chest compressions Vasopressin, 40 IU Placement of an invasive airway (if possible)	Vasopressin or epinephrine may be given interchangeably initially. Placement of an invasive airway should not interfere with chest compressions. If an invasive airway is not possible at this time, noninvasive management of the airway is appropriate.
Minute 5	Defibrillation, followed by immediate chest compressions Amiodarone, 300 mg	CPR should take place over 2-min periods with intervening attempts at defibrillation. Lidocaine is an acceptable alternative antiarrhythmic agent.
Minute 6	Epinephrine, 1 mg	Medication is administered every 3-5 min for cardiac arrest; it should be realized that peak central levels may vary based on physiologic patient differences. If vasopressin is given first, epinephrine is administered in all subsequent doses.
Minute 7	Defibrillation, followed by immediate chest compressions	CPR should not be interrupted for periods longer than 15 seconds at a time.
Minute 9	Defibrillation, followed by immediate chest compressions Epinephrine, 1 mg	Other medications should be considered in patients with an identified underlying cause.
Minute 10	Amiodarone, 150 mg	Amiodarone can be repeated in 5 min at half the initial dose.

CPR, Cardiopulmonary resuscitation; IV, intravenous.

After the administration of a vasopressor, CPR should be continued for 2 minutes, followed by a second defibrillation. If the VT or VF persists, amiodarone or lidocaine should be administered. Amiodarone is the preferred agent and should be considered in patients with pulseless VT or VF that is unresponsive to CPR, a vasopressor, and defibrillation. It is administered to a pulseless patient in a bolus dose of 300 mg intravenously, and it can be repeated with a second dose of 150 mg intravenously. Amiodarone has demonstrated a benefit over both placebo and lidocaine in this patient group. Even though rates of ROSC and survival to hospital admission were greater in amiodarone-treated patients, ultimate survival to hospital discharge was no different.^27,²⁸

PVT should be managed in similar fashion to pulseless MVT or VF. CPR, defibrillation, a vasopressor, and antidysrhythmic agents are appropriate therapeutic interventions. In two comparisons of MVT and PVT in prehospital patients with cardiorespiratory arrest, MVT occurred (60%) more often than PVT (15%) and TdP (15%).^22,²³ Clinical outcomes were similar in both rhythm groups with similar therapies. Patients with the subset of TdP also fared as well as the non-TdP PVT and MVT groups.^22,²³ If sustained, PVT is always unstable and requires immediate attention. Initial therapy is unsynchronized electrical cardioversion. Antiarrhythmic therapy is warranted, including the use of magnesium and amiodarone intravenously. Caution is advised because the rhythm frequently recurs.

Pulseless Electrical Activity

Definition

PEA is indicative of a very serious underlying medical event, such as profound hypovolemia, massive myocardial infarction, large pulmonary embolism, significant electrolyte disorder, or cardiotoxic overdose. PEA features the unique combination of no discernible cardiac mechanical activity (i.e., a pulseless state) with persistent cardiac electrical activity (i.e., the cardiac rhythm). Essentially, any dysrhythmia other than VT or VF may be seen (Figs. 7.8 and 7.9).

Fig. 7.8 Electrical rhythm diagnoses in patients with pulseless electrical activity.

Fig. 7.9 Pulseless electrical activity (PEA).

This dysrhythmia requires the absence of detectable mechanical activity in the heart (i.e., absence of a pulse) with some form of organized electrical activity in the heart (i.e., a rhythm). Any dysrhythmia (other than ventricular fibrillation, ventricular tachycardia, or asystole) can be encountered in this cardiac arrest scenario. The most typical dysrhythmias seen in patients with PEA include both narrow– and wide–QRS complex bradycardias. A, Sinus bradycardia. B, Junctional bradycardia. C, Atrial fibrillation with slow ventricular response. D, Third-degree atrioventricular block. E, Idioventricular bradycardia. F, Idioventricular bradycardia. G, Idioventricular rhythm. H, Idioventricular rhythm. I, Sinus tachycardia. J, Sinus tachycardia with bundle branch block morphology.

Pathophysiology

PEA must be separated into pseudo and true subtypes. Pseudo-PEA occurs when cardiac electrical activity (i.e., a cardiac rhythm) is present but a palpable pulse is absent and myocardial contractions are demonstrated by echocardiography or some other imaging modality. In true PEA, cardiac electrical activity in the form of a rhythm is noted, but absolutely no mechanical contraction of the heart is occurring.

It is important to distinguish the two subtypes of PEA. With pseudo-PEA, a significant pathophysiologic event has impaired the cardiovascular system’s ability to perfuse. These cases usually involve profound hypovolemia as a result of hemorrhage, obstruction to forward flow secondary to massive pulmonary embolism, tension pneumothorax, or cardiac tamponade; hypocontractile states with poor vascular tone such as advanced anaphylactic or septic shock; or very rapid tachydysrhythmia. Rhythms in these situations usually include tachycardias, predominantly sinus tachycardia or atrial fibrillation with rapid ventricular response. A directed therapeutic approach coupled with aggressive resuscitation will provide patients with pseudo-PEA with the best chance for survival.

True PEA occurs with primary electromechanical uncoupling of myocytes. From a cardiac electrical perspective, this uncoupling event is usually characterized by abnormal automaticity and disrupted cardiac conduction that results in the continued presence of a cardiac rhythm. Mechanically, this uncoupling is probably due to global myocardial energy depletion. Local myocardial tissue issues (hypoxia, acidosis, hyperkalemia, and ischemia) also contribute to this electromechanical dissociation. True electromechanical dissociation is seen in patients with prolonged cardiac arrest states, including metabolic, hypothermic, and poisoning sudden death scenarios. Another important subgroup of true PEA is characterized by patients with prolonged VF who are defibrillated to an electromechanical dissociation state with a broad QRS complex, bradycardic rhythm. In this instance, nearly complete exhaustion of energy substrate associated with profound hypoxia and acidosis accounts for this dismal scenario.

The PEA event usually starts with impaired perfusion and progresses to pseudo-PEA with continued cardiac contractions. Absence of a discernible pulse followed by loss of cardiac mechanical activity yields the development of true PEA.

Clinical Presentation

Causes of PEA are numerous (see Table 7.1), spanning all of acute care medicine, and include profound hypovolemia, cardiac tamponade, large anterior wall myocardial infarction, tension pneumothorax, massive pulmonary embolism, severe sepsis, anaphylactic reaction with shock, significant electrolyte abnormality (e.g., disorders of potassium), pronounced metabolic acidosis, substantial cardiotoxin ingestion, and hypothermia. These conditions have a final common pathophysiologic denominator of severe hypovolemia (absolute or relative), marked obstruction to flow, profound hypocontractility, or any combination of the three. The PEA rhythm manifestations are numerous. The most frequent dysrhythmias seen in PEA include idioventricular, junctional, and sinus bradycardia (see Figs. 7.8 and 7.9). Some causes of PEA are reversible if recognized early and treated correctly in the initial phases of resuscitation. Hemorrhagic shock, pulmonary embolism, pericardial effusion, and tension pneumothorax can all lead to PEA and are potentially reversible.

The electrocardiographic rhythm may be a useful guide to the etiology and a key to successful resuscitation.²⁹ Rapid, narrow–QRS complex tachycardic manifestations are associated with a somewhat better opportunity for survival. Profound hypovolemia is the most frequently encountered event in patients with PEA. In an attempt to maintain cardiac output, the heart will increase its rate. This increased rate will usually be in the form of sinus tachycardia. In patients with atrial fibrillation, a rapid ventricular response will be present and create a manifestation that is probably a pseudo-PEA cardiac arrest.

Only 2% to 3% of patients with PEA as the initial or primary dysrhythmia in cardiac arrest survive to hospital discharge neurologically intact. Electrocardiographic variables may be predictive of successful resuscitation.^29,³⁰ Rapid rhythm rates are much more frequently associated with ROSC than sinus bradycardia is. The width of the QRS complex is also potentially predictive of resuscitative outcome. Progressively wider QRS complexes are found in patients with a lower likelihood of restoration of spontaneous perfusion. In this risk prognostication application, an idioventricular rhythm is associated with a lower chance of resuscitation than is sinus bradycardia with a normal QRS complex duration. Other electrocardiographic findings encountered in PEA patients successfully resuscitated include the development of P waves and shortened QT intervals.

Management

Management of a patient in PEA arrest should focus on standard resuscitation treatments and rapid identification and correction of reversible causes, but it is otherwise similar to the treatment of pulseless VT and VF (Table 7.2).

Table 7.2 Etiologies, Pathophysiologic Events, and Specific Therapies for Cardiac Arrest with Pulseless Electrical Activity

In the 2010 AHA guidelines, atropine was removed from the PEA and asystole algorithm. Atropine was removed not because of any harm induced but because of lack of efficacy.^5,⁹ The clinician at the bedside should use clinical judgment to determine whether atropine should be administered in this rhythm scenario. Epinephrine is recommended at a dose of 1 mg intravenously, repeated every 3 to 5 minutes during resuscitation. Vasopressin, 40 IU intravenously, can also be used once in the resuscitation event. Aggressive volume replacement with either crystalloid or colloid is recommended. Attention to the various causes and focused treatment of PEA is encouraged early in the resuscitation (see Table 7.1).

Asystole

In asystole, the electrocardiogram demonstrates a flat line or nearly flat line (Fig. 7.10). Minimal undulations of the waveform resulting from electrocardiographic baseline drift can be seen. Several pitfalls must be avoided in the apparent asystolic manifestation, including monitor malfunction, disconnection of electrocardiographic leads, and fine VF with minimal amplitude in the imaging lead. The last potential error can be detected by confirming asystole with at least two leads oriented in perpendicular fashion (see Fig. 7.10).

Fig. 7.10 Asystole.

Note the proper determination of asystole in three simultaneous electrocardiographic leads. It is important to view any rhythm with at least two different electrocardiographic leads.

Management

Resuscitation should follow a similar algorithm as that for PEA (Table 7.3), with the notable exception of consideration of cardiac pacing. Even though several trials have not demonstrated a benefit of transcutaneous pacing in patients with asystolic arrest,^15,¹⁶ it is not unreasonable to consider a short course of cardiac pacing if performed very early in the resuscitation. A comment should be made on the choice of vasopressor. One large study demonstrated a short-term survival benefit of vasopressin with respect to epinephrine in these patients, and this benefit remained apparent at hospital discharge.²⁶

Table 7.3 Pulseless Electrical Activity and Asystole

TIME	TREATMENT PRIORITY	COMMENTS
Minute 0	Chest compressions	Compressions should be performed at a rate of 100/min. Pulse checks and rhythm analysis should be performed no more frequently than every 2 min. With a narrow-complex rhythm, assess for occult blood flow (i.e., pseudo-PEA).
Minute 1	Chest compressions IV or IO access Vasopressor	Perform interventions but do not interrupt chest compressions for more than 15 sec after each 2-min cycle. Early IV or IO access for drug administration is now preferred. Vasopressin or epinephrine may be given interchangeably initially.
Minute 2	Chest compressions Placement of an invasive airway	Placement of an invasive airway is not a priority unless bag-mask ventilation is inadequate. An invasive airway can be placed, but its placement should not interrupt chest compressions. Atropine, 1 mg intravenously, can be given at this time if so desired, though its impact is minimal.
Minute 4	Chest compressions Vasopressor	Chest compressions should be interrupted only to change compressors (no longer than 15 sec). If epinephrine was given initially, vasopressin can now be administered; epinephrine is then administered in all subsequent doses.
Minute 5	Chest compressions Supplemental medications	Underlying causes may necessitate the administration of adjunctive medications.
Minute 7	Chest compressions Vasopressor	Medication should be administered every 3-5 min for cardiac arrest; it should be realized that peak central levels may vary based on physiologic patient differences. Atropine, 1 mg intravenously, can be given at this time if so desired.
Minute 10	Chest compressions Vasopressor	At 10 min the outcome-related implications should be weighed because survival to discharge decreases after this point without ROSC.

IO, Intraosseous; IV, intravenous; PEA, pulseless electrical activity; ROSC, return of spontaneous circulation.

Special Arrest Populations and Scenarios

Traumatic Injury

Multiple traumatic causes can lead to cardiac arrest. The prognosis of patients with out-of-hospital cardiac arrest as a result of trauma is poor, particularly in the setting of blunt injury.³¹

In cases of traumatic arrest in which a clear etiology is not readily apparent, aggressive resuscitation is indicated, although the prognosis is bleak. General trauma management should be performed while specific therapy is aimed at the medical portion of the cardiorespiratory arrest. Standard ALS interventions aimed at management of the dysrhythmia should be pursued with the realization that the likelihood of successful resuscitation is minimal. Pulseless VT and VF should be defibrillated immediately on recognition. In most traumatic situations, the underlying etiology must be corrected for return of circulation to occur.^5,⁹ Medical therapies are unlikely to correct traumatized tissue and restore spontaneous circulation.

If definitive surgical intervention is available, resuscitative thoracotomy may be a reasonable intervention for a subset of trauma patients. This subset includes any traumatic arrest patient with the following features: witnessed arrest in the emergency department, arrest time less than 5 minutes with penetrating cardiac injury, arrest time less than 15 minutes with penetrating thoracic injury, or any exsanguinating abdominal vascular injury in which secondary signs of life are present (e.g., pupillary reflexes, spontaneous movement, organized electrocardiographic activity).^5,^9,³² Thoracotomy allows internal cardiac massage and defibrillation, relief of pericardial tamponade, direct control of cardiac or thoracic hemorrhage, and cross-clamping of the aorta. Many of these interventions require a high degree of technical skill and should be attempted only by experienced providers; however, outcomes are predictably poor.

Status Asthmaticus

More than 4000 deaths occur annually as a result of asthma. Two general scenarios in decompensated asthma patients most often account for the cardiac arrest. The first is the sudden onset of a severe exacerbation that rapidly worsens and progresses to full cardiorespiratory arrest. The second scenario involves patients with progressive bronchospasm that is unresponsive to maximal therapy. Progressive hypoxia and hypercapnia with metabolic and respiratory acidosis are responsible for the ultimate decline. At times in this setting, complications of therapy such as barotrauma account for the hemodynamic decline.

The mainstay of therapy in treating asthma-induced arrest is overcoming hypoxia and bronchoconstriction. In these cases, endotracheal intubation should be performed rapidly, and barotrauma (primarily pneumothorax) must be avoided. Decreasing tidal volumes to 5 to 6 mL/kg and reducing the ventilatory rate to 8 to 10 breaths/min can avoid excessive increases in lung volumes caused by breath stacking with prolonged expiratory phases. This technique is an extension of controlled hypoventilation, or permissive hypercapnia. If resuscitation is successful with return of spontaneous perfusion, sodium bicarbonate is administered intravenously to maintain the serum pH level greater than 7.15 to 7.20.

External compression of the thorax during the expiratory phase to maximize exhalation has been proposed,³³ but its use remains controversial and it will probably be difficult to coordinate during compressions. Needle or tube thoracostomy decompression should be performed if pneumothorax is detected or suspected. Bilateral decompression for refractory arrest is warranted given the potential for masking the lateralizing signs of pneumothorax.

Standard ALS strategies also apply to dysrhythmias. Epinephrine is likely to be the most useful of the standard drug therapies. Correction of profound acidosis via the empiric use of sodium bicarbonate may be necessary to achieve responsiveness to sympathomimetic agents. The addition of isoproterenol, aminophylline, terbutaline, and magnesium may be considered for improved bronchodilation, but their benefit in patients with asthma-induced cardiac arrest has not been reported, and they are unlikely to achieve success.

Pregnancy

Causes of cardiac arrest specific to pregnant patients are maternal hemorrhage, toxemia, HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count), amniotic fluid emboli, and adverse effects of maternal care, including tocolytic and anesthetic therapies. Pregnancy also increases the likelihood of certain nonobstetric causes, including pulmonary embolism, septic shock, cardiovascular diseases such as cardiomyopathy and myocardial infarction, endocrine disorders, and collagen vascular disease. Traumatic causes of arrest should also be considered because of documented increased rates of abuse and homicide in pregnant women.

Cesarean delivery should be accomplished as soon as cardiac arrest is identified in a pregnant patient. The highest survival rates for infants older than 24 to 25 weeks’ gestational age occurs in deliveries performed within 5 minutes of arrest of the mother. This intervention is most appropriately performed by a multidisciplinary team skilled in emergency obstetric surgery.³⁴

Pregnant patients should be placed in the left lateral decubitus position. Displacement of the gravid uterus should be performed by elevating the right hip and lumbar region 15 to 30 degrees from the supine position. Manual displacement of the uterus by lifting it with two hands and directing it toward the upper left part of the patient’s abdomen can be performed before blanket roll placement and afterward to optimize venous return.³⁴

Poisoning

Toxidromes may be masked in the setting of cardiac arrest because of prolonged hypoxia and hypoperfusion and thus complicate the selection of specific antidotes or therapies. Once poisoning is suspected, consultation with a medical toxicologist or poison control center should be sought if feasible.

In the setting of an unknown toxin or mixed ingestion, standard ALS algorithms are unlikely to be harmful and probably represent the most appropriate course of action. When specific antidotes are required, ACLS is insufficient. If a specific toxin is suspected based on the history or clinical signs, one should consider adding targeted therapies. It is also extremely important to remember that a single reported toxic ingestion is often accompanied by unreported accessory ingestions. Differential diagnoses and treatments must thus be kept broad when targeting treatment. When poisoning is suspected, prolonged resuscitation attempts might be warranted.

Electrical Injury

The heart is particularly sensitive to electrical injury. Alternating current is likely to produce VT through a mechanism similar to the R-on-T phenomenon, whereas a lightning strike can produce asystole or VT through depolarization of the myocardium by a direct current shock.

ALS algorithms do not require modification for electrically induced cardiac arrest. The potential for successful resuscitation is higher than that for other causes of cardiac arrest given that these patients are typically younger and lack coexisting cardiopulmonary disease. Trauma and burn care is often required because they are common sequelae of electrical shock and lightning injury.

Hypothermia

Severe hypothermia causes marked functional depression of all critical organ systems. Such dysfunction can lead to cardiovascular collapse but may also have a protective effect that allows successful resuscitation. Clinical judgment should prevail in the decision whether to attempt resuscitation. The often-quoted maxim—”one is not dead until he/she is warm and dead”—applies only in select situations and is not a blanket statement pertaining to all patients in cardiopulmonary arrest. The two basic types of patients who may actually benefit from rewarming therapy while in cardiorespiratory arrest include a full arrest patient who has very rapidly had a precipitous decline in body temperature (e.g., fall into a frigid lake in a very cold climate) and a profoundly hypothermic individual with signs of life in whom cardiorespiratory arrest has developed while in the emergency department. In other instances, resuscitation is futile and is therefore not recommended. If drowning occurs before hypothermia, the chances of resuscitation are markedly reduced. If the decision is made to attempt resuscitation in a patient with complete cardiopulmonary arrest and absence of signs of life, the patient should be orotracheally intubated and undergo CPR with chest compressions. Further efforts will then be guided by the core temperature, which should be measured as soon as possible. Needle-type electrodes, if available, are preferred for cardiac monitoring. For severe hypothermia with a core temperature lower than 30° C, aggressive active internal rewarming should be undertaken, including warmed, humidified oxygen and intravenous fluids, pleural or peritoneal lavage, and partial or complete cardiopulmonary bypass. A single attempt at defibrillation should be made for pulseless VT or VF. All ALS medications should be withheld. Both of these modifications are due to the likelihood that a hypothermic heart will remain unresponsive to subsequent shocks and medications are likely to accumulate and reach toxic levels.

For moderate hypothermia—body temperature of 30° C to 34° C—or once rewarming has raised the core temperature to 30° C, defibrillation should resume per ALS guidelines. Medications may be administered at standard doses, but the interval of administration should be increased. Active internal rewarming should be undertaken or continued. If the hypothermia is mild—temperature higher than 34° C—or when rewarming raises the core temperature to 34° C, standard ALS guidelines may be applied, including decisions regarding termination of resuscitation efforts. If rewarming efforts occur for longer than 45 minutes, volume expansion will probably be necessary because of vasodilation.

Submersion Injury and Near-Drowning

Cardiac arrest after submersion is usually due to hypoxia as a result of suffocation, but it may also be secondary to head or spinal cord injury. For this reason, early intubation is suggested if feasible and should be performed with manual stabilization of the cervical spine. Aspiration of large volumes of fluid with submersion is rare, but increased inspiratory and positive end-expiratory pressure may be required to achieve adequate oxygenation because of pulmonary edema.

Routine ALS algorithms should be used for cardiac arrhythmias without modification. Electrolyte and acid-base disturbances are unlikely causes of cardiac arrest in the early manifestations of submersion injury and do not warrant empiric therapy. Correction of acidosis should be considered in patients who later deteriorate during observation. The prognosis depends on the duration of submersion and the severity and duration of hypoxia. Hypothermia and trauma are common confounders of submersion injury, and appropriate therapy should be applied.

Postresuscitation Phase

Post–Cardiac Arrest Syndrome

Management of resuscitated cardiac arrest patients has undergone significant change in the past decade. The concept of post–cardiac arrest syndrome has been developed.^35,³⁶ This syndrome, thought to occur in the initial 72 hours after ROSC, is a unique pathophysiologic entity found in patients who have been resuscitated from cardiorespiratory arrest. The primary considerations include CNS injury, myocardial dysfunction, systemic hypoperfusion with reperfusion-related damage, and the precipitating event. Brain injury from ischemia is responsible for many patient deaths, including approximately 70% of patients resuscitated after out-of-hospital arrest and 25% of individuals resuscitated after in-hospital arrest. The basic reasons for CNS injury include a limited tolerance for brain ischemia coupled with a unique response to reperfusion. Brain injury is an ongoing phenomenon, even after successful resuscitation, that usually results from a number of different pathophysiologic events. Injury can continue for 6 to 72 hours after the return of spontaneous perfusion despite adequate systemic blood pressure.

Mechanisms responsible for the CNS injury include the development of cerebral edema, dysfunctional circulation, disruption of the blood-brain barrier, and multiple small infarctions. Cerebral edema alters perfusion, hastens the production of inflammatory mediators, and produces cellular dysfunction. Dysfunctional circulation can occur at the microcirculatory level despite an intact macrocirculation. The cerebral edema and altered microcirculation disrupt the blood-brain barrier, whereas the altered perfusion produces ischemia and multiple small CNS infarctions. Three additional issues contribute to CNS injury: pyrexia, hyperglycemia, and seizure. The final common pathway of CNS injury is neuronal cell death with brain malfunction, poor neurologic recovery, and patient demise.

Myocardial dysfunction has a significant negative impact on survival, and it is both reversible and responsive to therapy. The myocardial dysfunction is not always due to infarction. Most often, myocardial stunning is responsible for the cardiac dysfunction and produces significant and profound reductions in cardiac output. Continued myocardial dysfunction results in respiratory compromise, impaired systemic perfusion, and worsening of multiorgan malfunction. Myocardial dysfunction is usually rapidly apparent after return of perfusion, thus requiring very close hemodynamic monitoring. As the exogenous catecholamines are metabolized once perfusion is restored, hypoperfusion becomes obvious. Hypoperfusion can be worsened by the use of sedative-hypnotic agents for the control of agitation and maintenance of unresponsiveness in a chemically paralyzed patient.

Increasing tachycardia and left ventricular end-diastolic pressure are seen within minutes of ROSC, whereas decreasing mean arterial pressure is not usually apparent for many hours after resuscitation. Hypotension is generally obvious at 4 to 6 hours, reaches a nadir at 8 hours, and classically recovers by 24 to 72 hours. This myocardial dysfunction creates additional tissue hypoxia and acidosis, intensifies the multiorgan injury, and contributes to a significantly increased risk for death.

Finally, the precipitating event must be considered for effective management of a postresuscitation patient. It is a major determinant of survival with a very broad range of potential events, involves both cardiac and noncardiac causes, and occurs over acute, acute-on-chronic, and chronic periods.

Postresuscitation Management

Management considerations (Figs. 7.11 and 7.12) must address the following issues: CNS injury, myocardial dysfunction, systemic hypoperfusion, multiorgan failure, and the precipitating cause of the cardiac arrest. Multidisciplinary critical care support along with appropriate respiratory and hemodynamic support is vital. Two specific treatment considerations, therapeutic (induced) hypothermia and emergency coronary reperfusion, must be emphasized in these resuscitated patients.

Fig. 7.11 Phases of post–cardiac arrest syndrome with the primary management goals.

Fig. 7.12 Resuscitative management of patients with post–cardiac arrest syndrome.

(Modified from Nolan JP, Neumar RW, Adrie C, et al. ILCOR consensus statement: post-cardiac arrest syndrome: epidemiology, pathophysiology, treatment, and prognostication. Resuscitation 2008;79:350-79; and Peberdy MA, Callaway CW, Neumar RW, et al. Part 9: post–cardiac arrest care: 2010 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science. Circulation 2010;122:S768-86.)

Therapeutic hypothermia (TH), or induction of lower body temperatures in unresponsive patients resuscitated from cardiac arrest, is strongly encouraged in certain individuals. The AHA notes that “…therapeutic hypothermia in the resuscitated cardiac arrest patient can markedly improve outcome…both in terms of rates of survival and neurologic status.”^35,³⁶ TH is currently recommended for victims resuscitated after out-of-hospital cardiac arrest with initial rhythms of either pulseless VT or VF who remain unconscious. TH should also be considered in patients resuscitated from cardiac arrest associated with other initial rhythms (i.e., PEA and asystole) and in survivors of in-hospital cardiac arrest.^35,³⁶ The actual beneficial mechanisms for TH are not fully known, but the basic accepted mechanism involves suppression of the chemical cascade associated with the total-body ischemia and reperfusion injury. These mechanisms probably involve a number of different protective processes, including a reduction in the metabolic rate, oxygen use, and CNS electrical activity. TH probably interrupts the injury process at many points in the pathophysiologic response to cardiac arrest and subsequent reperfusion. Regardless of the modes of action of this intervention, TH has been demonstrated to provide CNS protection, reduce the incidence of multiorgan failure syndrome, increase survival, and improve functional abilities. The outcome after cardiac arrest with our present abilities remains suboptimal. Use of TH can increase the rate of functional survival, but it is not a miracle cure.

Indications for TH include the following qualifiers: nontraumatic cardiac arrest, resuscitation with spontaneous perfusion, unresponsive status, and age between 18 and 75 years. Any set of indications for a clinical therapy is open to discussion and further consideration. Several qualifications are needed. First, primary cardiac arrest is the most appropriate indication for TH. Noncardiac causes of arrest such as sepsis, a CNS event, ingestion, trauma, and others are unlikely to benefit. Primary cardiac arrest, or an event related to cardiac arrhythmia that is due to a cardiac cause, is the most appropriate for TH. Certain other victims of noncardiac causes of arrest can be considered for TH. These potential additional indications include victims of a sudden event that when corrected does not leave a significant, lasting injury or process other than post–cardiac arrest syndrome. Consideration should be made for patients with sudden choking or hanging that leads to respiratory failure and subsequent cardiac arrest.

Second, resuscitated patients should be relatively stable in terms of the ABCs, which means that they are endotracheally intubated and undergoing mechanical ventilatory support with intact perfusion. Significant difficulties with oxygen and ventilation must be addressed before the use of TH. Perfusion must be intact, whether spontaneously or supported by intravenous fluids, vasopressors, or inotropes, and it should be understood that significant difficulties in maintaining perfusion should delay the use of TH. Third, the patient must be unresponsive. Multiple different descriptors have been used to describe the patient’s mental status, including unresponsive, comatose, or possessing a Glasgow Coma Scale score of 8 or less.

The last basic indication is age. The most appropriate patient is an adult. The most frequently listed age range is 18 to 75 years, thus removing all children and the extreme elderly from consideration. This age indication is at best a guide, and certain younger and older patients represent appropriate candidates for TH. A major consideration in these two excluded groups is that a primary cardiac etiology is less often the primary causative event in the development of cardiac arrest. Sepsis, trauma, ingestion, and other conditions are frequent causes of cardiac arrest in these two age groups and may exclude these candidates from consideration of TH. Clinician judgment with consideration of individual patient issues will be the most appropriate determinant of therapy with respect to the age extremes.

A thorough discussion of the process and technique of cooling is beyond the scope of this chapter. Highlights of TH include the following issues:

• Patients should be cooled as soon as possible after ROSC, ideally within 4 to 6 hours. Cooling should last for approximately 18 hours once the target temperature has been reached.

• The goal temperature is 32° C to 34° C.

• The patient is probably mechanically ventilated via an ETT.

• Pain medication and sedative agents are probably required for patient comfort and safety. Chemical paralytic agents are used with caution because seizures cannot be detected as easily.

• Shivering should be avoided if at all possible because of the related heat production, and appropriate treatment should be provided if it develops.

• Biometric surveillance should include an electrocar-diogram, blood pressure, core temperature, oxygen saturation, and end-tidal CO₂ monitoring. Continuous electrocardiographic monitoring can also be considered. Laboratory studies should include electrolytes and serum glucose.

• The most appropriate cooling method is debatable. Two basic approaches have been advocated, but thus far neither therapy has proved to be superior. Rapid infusion of 2 L of chilled normal saline (4° C) represents the least challenging approach. The chilled saline is used in conjunction with cooling blankets and ice packs applied to the neck, armpits, groin, and other areas. The other technique, which is both more invasive and more expensive, involves the use of an intravascular cooling machine. This technique, once the intravascular catheter has been placed, is easier to use in terms of reaching the target temperature and maintaining this temperature.

• If instability develops, all cooling must be halted immediately and appropriate therapy initiated to address the current clinical situation.