CHAPTER 63 APPROACHTOCARDIACARRESTANDLIFE-THREATENINGARRHYTHMIAS344

63APPROACH TO CARDIAC ARREST AND LIFE-THREATENING ARRHYTHMIAS ROBERT J. MYERBURG AND AGUSTIN CASTELLANOS

Cardiac arrest is characterized by an abrupt loss of consciousness because of absence of blood flow owing to loss of cardiac pumping action. If not treated promptly, it will lead to central nervous system injury or death within minutes. Cardiac arrest is often forewarned by a change in cardiovascular status, as indicated by the appearance or worsening of symptoms related to transient arrhythmias, such as palpitations, lightheadedness, or near-syncope or syncope (Chapter 62). Other forewarnings may include new or worsening chest pain, dyspnea, or weakness. These warning symptoms, however, are limited by their sensitivity and predictive power in individual patients. More-over, cardiac arrest may occur unexpectedly as a first cardiac event in an apparently healthy individual, in a patient with known previous cardiac disease, or as the final event in any fatal disease.The most common electrical mechanisms of cardiac arrest are the ventricu-

lar tachyarrhythmias (Chapter 65)ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT). In a substantial minority of cardiac arrests, severe bradyarrhythmia, asystole, or pulseless electrical activity is the first rhythm abnormality noted. The latter may be the primary mechanism of the cardiac arrest or a result of deterioration of VT/VF. Pulseless electrical activ-ity or asystole may also be seen after termination of VT/VF by electrical cardioversion. Pulseless electrical activity is defined as secondary when it occurs in the setting of predisposing factors, such as hypoxia or other meta-bolic disorders, and primary when it is the initial rhythm noted in patients with predisposing cardiac disorders. The probability of survival after interven-tion is far better for ventricular tachyarrhythmias than for bradyarrhythmic or asystolic mechanisms. The interval between cardiac arrest and the initiation of resuscitation and cardioversion is the major determinant of survival.

PREDISPOSING WIDEQRS COMPLEX TACHYCARDIAS

Sustained tachycardias with wide QRS complexes should be considered of ventricular origin and potentially high risk until determined otherwise. Most wide-QRS tachycardias are initially approached as a medical urgency or emergency, whereas most narrow-QRS tachycardias of supraventricular origin are approached with less urgency (Chapters 64 and 65).

Management of Sustained Ventricular TachycardiaSustained VT occurs most commonly in the presence of structural heart disease and must be interpreted as a forewarning of fatal arrhythmia in that setting. It is characterized by QRS complexes that are usually longer than 0.12

CHAPTER 63 APPROACHTOCARDIACARRESTANDLIFE-THREATENINGARRHYTHMIAS 345

second, with a mean vector that is markedly different from the QRS vector of normally conducted impulses. The rate of most VTs is between 140 and 200 impulses per minute, but rates may be slower or faster. VT may be electri-cally stable (such as monomorphic VT patterns at relatively slow rates; Fig. 63-1A) or unstable (such as polymorphic VTs or monomorphic VTs at rates exceeding 190 to 200 per minute; see Fig. 63-1B) (Chapter 65). Slower monomorphic VT may be better tolerated, whereas rapid VT is often associ-ated with hemodynamic instability. In the latter circumstance, VT must be managed as a life-threatening or imminently fatal event, analogous to a VT/VF cardiac arrest (see later) that is usually treated with electrical cardiover-sion as initial therapy. Long-term management strategies, often involving consideration of implantable cardioverter-defibrillator therapy, are based on consideration of the likelihood of recurrent tachycardias and the extent of underlying disease (Chapter 65). Some well-tolerated, slow monomorphic VTs, especially in the absence of structural heart disease, may be more benign and treated with less urgency, usually with antiarrhythmic drugs or -adrenergic blocking agents (see Table 64-5 in Chapter 64).

Distinguishing Supraventricular from Ventricular TachycardiasIt is important to distinguish between supraventricular tachycardia (SVT) (Chapter 64) and VT for both risk prediction and therapy. Although it is generally assumed that narrow-QRS tachycardias are supraventricular in origin, VT occasionally has a narrow QRS complex on a one- or two-lead rhythm strip, thereby mimicking SVT. Whenever possible, the diagnosis of tachycardia should be based on a 12-lead electrocardiogram (ECG). However, a standard ECG will not always suffice because patients with intraventricular conduction abnormalities (such as a left or right bundle branch block) will have wide-complex tachycardias during SVTs, usually with a QRS vector similar to that seen in normal sinus rhythm. In addition, when an SVT is very rapid, a functional bundle branch block may generate a widened QRS dura-tion and shift the axis transiently. In both these examples, the wide QRS may mimic VT, and it may be necessary to perform an electrophysiologic study to determine the diagnosis (Chapter 62).When wide-complex SVT is suspected clinically, transient vagal stimula-

tion by carotid sinus massage or an atrioventricular nodal blocking agent, such as intravenous adenosine (see Table 64-5 in Chapter 64), may be useful for slowing the rate or terminating an SVT. Intravenous calcium-blocking agents generally should not be used for the diagnosis or treatment of wide-QRS tachycardias, especially in the presence of structural heart disease, because of their myocardial depressant effects. The exception is when it is known with certainty that the tachycardia is an SVT in a patient with normal or near-normal left ventricular function.SVTs can result in a risk for generating life-threatening ventricular arrhyth-

mias in two circumstances. One is in patients with high-grade coronary artery stenoses, in whom rapid heart rates can cause myocardial ischemia because

of the dependence of coronary blood flow on the diastolic interval; the arrhythmia should be treated urgently, usually by electrical direct current (DC) cardioversion (Chapter 66), unless specific medical therapy is available and controls the rate promptly (Chapter 64). The second is in patients with Wolff-Parkinson-White syndrome, who may have ventricular rates greater than 300 beats per minute during atrial fibrillation when the accessory pathway has a short refractory period (see Fig. 64-19 in Chapter 64). This arrhythmia, which can cause hypotensive VT or VF, requires prompt therapy (Chapter 64).

GENERAL MANAGEMENT OF CARDIAC ARRESTBasic life-support (BLS) and advanced cardiac life support (ACLS) strategies for initial and definitive responses to cardiac arrest have improved survival in victims of cardiac arrest. The principles of BLS and ACLS apply to both in-hospital and out-of-hospital cardiac arrest, but their applications and out-comes depend on the setting. In the hospital, the probability of survival is determined by the specific patient category (acute syndromes better than end-stage diseases), the mechanism of cardiac arrest (better for tachyarrhyth-mias than for bradyarrhythmias, asystole, or pulseless electrical activity), and the hospital site (better in intensive care units or other monitored settings than on an unmonitored general care unit). In many acute care settings, including patients with acute coronary syndromes (Chapters 72 and 73), outcomes can be excellent. For other in-hospital settings and most out-of-hospital settings, the absolute number and proportion of survivors remain low, except in unique out-of-hospital settings that can provide an extraordi-narily rapid response time to victims in VF or VT. When immediate defibril-lation in highly protected environments is available, such as monitored intensive care units and electrophysiology laboratories, where response times of less than 60 seconds are the norm, the survival rate after VF is greater than 90% in the absence of pathophysiologic conditions that favor persistence of the potentially fatal arrhythmia.Once 2 to 3 minutes have elapsed from the onset of cardiac arrest to

attempted defibrillation, the survival probability falls below 50% in most in-hospital and out-of-hospital circumstances. Survival rates continue to fall rapidly thereafter, decreasing to 25% or less by 4 to 6 minutes and less than 10% by 10 minutes. Although immediate defibrillation is the preferred method within the first few minutes after the onset of cardiac arrest, a brief period of cardiopulmonary resuscitation (CPR) to provide oxygenation of the victim improves survivability when the time to defibrillation exceeds 4 to 5 minutes.

Basic Life SupportThe activities included within BLS encompass the initial responses for diag-nostic evaluation, followed by a seamless flow into establishing ventilation and perfusion through the techniques of CPR or the newly proposed concept of cardiocerebral resuscitation (see later). The first action is to confirm that the collapse is the result of a cardiac arrest. After an initial evaluation for response to voice or tactile stimulation, observation for respiratory move-ments and skin color, and simultaneous palpation of major arteries for the presence of a pulse, the determination that a life-threatening incident is in progress should immediately prompt a call to an emergency medical rescue system (911).The absence of respiratory efforts, or the presence of only gasping agonal

respirations in conjunction with an absent pulse, is diagnostic of cardiac arrest. Although the absence of a carotid or femoral pulse is a primary diag-nostic criterion for the health care professional, palpation for a pulse is no longer recommended for lay responders. The absence of respiratory efforts or severe stridor with persistence of a pulse suggests a primary respiratory arrest that may lead to cardiac arrest in a short time; skin color may be pale or intensely cyanotic. In the latter circumstance, initial efforts should include oropharyngeal exploration in search of a foreign body and the Heimlich maneuver, which entails wrapping the arms around the victim from the back and delivering a sharp thrust to the upper part of the abdomen with a closed fist, particularly in a setting in which aspiration is likely (e.g., collapse in a restaurant).Once a pulseless cardiac arrest is established, a blow to the chest (precor-

dial thump) may be attempted by a properly trained rescuer as part of an initial response when monitoring and a defibrillator are not immediately available. A precordial thump should not be used in an unmonitored patient with a perceptible rapid tachycardia or without complete loss of conscious-ness because of concern about converting organized electrical activity into VF. The technique involves one or two blows delivered firmly to the junction

Monomorphic Nonsustained Ventricular Tachycardia

Polymorphic Nonsustained Ventricular TachycardiaA

BFIGURE 63-1. Nonsustained ventricular tachycardia.Monomorphic patterns (A) arecharacterizedbyaslowerandmorestableelectricalpatternthanpolymorphicpatterns(B).Both have long-term prognostic implications in patientswith advanced structural heartdisease,butmonomorphicpatternstendtobemorestableovertheshortterm.

CHAPTER 63 APPROACHTOCARDIACARRESTANDLIFE-THREATENINGARRHYTHMIAS346

of the middle and lower thirds of the sternum from a height of 8 to 10 inches, but the effort should be abandoned if a spontaneous pulse does not immedi-ately occur or if the patient begins to breathe.The precordial thump should be followed immediately by the initiation of

CPR so as to maintain viability of the central nervous system, heart, and other vital organs until a definitive intervention can be carried out. CPR can be performed by professional and paraprofessional personnel, by experienced emergency medical technicians, and by trained laypersons. Time is the key element for success, and there should be minimal delay between the diagno-sis and preparatory efforts in the initial response and institution of CPR. If only one witness is present, the only activity that should precede BLS is telephone contact (911) of emergency personnel.Clearing the airway, which is a critical step in preparing for successful

resuscitation, includes tilting the head backward and lifting the chin, in addi-tion to exploring the airway for foreign bodiesincluding denturesand removing them. The Heimlich maneuver should be performed if there is reason to suspect a foreign body lodged in the oropharynx, as suggested by severe respiratory stridor rather than by slow agonal respirations or apnea. When the person at the scene has insufficient physical strength to perform the maneuver, mechanical dislodgement of a foreign body can sometimes be achieved by abdominal thrusts with the unconscious patient in a supine posi-tion. If there is suspicion that respiratory arrest precipitated the cardiac arrest, particularly in the presence of a mechanical airway obstruction, a second precordial thump should be delivered after the airway has been cleared.With the head properly placed and the oropharynx clear, mouth-to-mouth

respiration can be initiated, but bystander compression-only CPR is as good as, if not better than, compression plus mouth-to-mouth respiration. 1 A variety of devices are available for establishing ventilation, including plastic oropharyngeal airways, esophageal obturators for establishing ventilation, a masked Ambu bag, and endotracheal tubes. Intubation is the preferred pro-cedure, but time should not be sacrificed, even in the in-hospital setting, while awaiting an endotracheal tube or a person trained to insert it quickly and properly. Temporary support with Ambu bag ventilation is the usual method in the hospital until endotracheal intubation can be accomplished; in the out-of-hospital setting, mouth-to-mouth resuscitation is performed while awaiting emergency rescue personnel. The lungs should be inflated twice in succession after every 30 chest compressions.The third element of BLS, circulation, is intended to maintain blood flow

until definitive steps can be taken. The rationale is based on the hypothesis that chest compression maintains an externally driven pump function by sequential emptying and filling of its chambers, with competent valves favor-ing the forward direction of flow. The palm of one hand is placed over the lower part of the sternum while the heel of the other rests on the dorsum of the lower hand. The sternum is then depressed with the resuscitators arms straight at the elbows to provide a less tiring and more forceful fulcrum at the junction of the shoulders and back. With this technique, sufficient force is applied to depress the sternum about 4 to 5 cm, with abrupt relaxation. The cycle is carried out at a rate of about 100 compressions per minute. In the 2005 modification of guidelines for emergency cardiac care, the integra-tion of respiratory and compression actions was changed to a compression-ventilation ratio of 30 : 2 for single responders to victims from infancy (excluding newborns) through adulthood, and two responders for adults.

For two-rescuer CPR for infants and children, the former compression- ventilation ratio of 15 : 2 was retained. Another recently suggested modifica-tion, which is intended to encourage more bystander CPR by untrained or remotely trained bystanders who lack confidence, is the hands-only (car-diac-only, compression-only) technique, which uses 200 successive com-pressions without interruption. This variation, which may be more effective than compression-ventilation sequences, also allays concerns about bystander mouth-to-mouth ventilation of unknown victims in the absence of mechani-cal airway devices.

Automated External DefibrillatorsIntermediate Life SupportBecause time to defibrillation is the major determinant of survival, despite any temporizing benefit of BLS, and because ACLS strategies are generally implemented by in-hospital personnel or out-of-hospital emergency medical rescue system responders, an intermediate strategy has emerged that is based on the availability of automated external defibrillators (AEDs) for use by nonconventional first responders. Referred to as public access defibrillation or lay first-responder systems, the strategy relies on devices that prompt the user to deliver a defibrillation shock when deemed appropriate by a comput-erized rhythm detection system in the device. The operators can be trained police officers, security guards, airline personnel, or trained (or even untrained) lay responders (Table 63-1). A number of studies have suggested improved survival rates when such strategies are deployed in public sites, but an initial study of a home deployment strategy was disappointing. 2 Further study is warranted because most out-of-hospital cardiac arrests occur at home. AED programs are not a replacement for ACLS (see later), but rather an intermediate supplement to the BLS-ACLS sequence that is intended to attempt earlier defibrillation while awaiting the arrival of ACLS-trained emergency rescue personnel.

Advanced Cardiac Life SupportACLS methods, other than those directly related to control of tachyarrhyth-mias, have led to the generation of comprehensive protocols to guide respond-ers over a broad expanse of clinical circumstances and mechanisms of cardiac arrest ranging from transient clinical events to end-stage multisystem disease. The general goals of ACLS are to restore a hemodynamically effective cardiac rhythm, optimize ventilation, and maintain and support the restored circula-tion. During ACLS, the patients cardiac rhythm is promptly cardioverted or defibrillated as the first priority, if appropriate equipment is immediately avail-able. If cardiac arrest has lasted for 4 to 5 minutes before the availability of a defibrillator, a short period of closed-chest cardiac compression immediately before defibrillation increases the probability of survival. 3 Additional survival benefit has not been observed for delays greater than 10 minutes.After the initial attempt to restore a hemodynamically effective rhythm,

the patient is intubated and oxygenated, if needed, and the heart is paced if a bradyarrhythmia or asystole occurs. An intravenous line is established to deliver medications. After intubation, the goal of ventilation is to reverse hypoxemia and not merely to achieve a high alveolar Po2. When available, oxygen rather than room air should be used to ventilate the patient, and arte-rial O2 saturation should be monitored, when possible. In the out-of-hospital setting, a face mask or an Ambu bag by means of an endotracheal tube is generally used.

TABLE 63-1 AUTOMATEDEXTERNALDEFIBRILLATORSTRATEGIESFORRAPIDRESPONSETOCARDIACARRESTSCAUSEDBYVENTRICULARFIBRILLATION

DEPLOYMENT EXAMPLES RESCUERS ADVANTAGES LIMITATIONSEmergency vehicles Police cars

Fire enginesAmbulances

Trained emergency personnel Experienced usersBroad deploymentObjectivity

Deployment timeArrival delaysCommunity variations

Public access sites Public buildingsStadiums, mallsAirportsAirliners

Security personnelDesignated rescuersRandom laypersons

Population densityShorter delaysLay and emergency personnel access

Low event ratesInexperienced usersPanic and confusion

Multifamily dwellings ApartmentsCondominiumsHotels

Security personnelDesignated rescuersFamily members

Familiar locationsDefined personnelShorter delays

Infrequent useLow event ratesGeographic factors

Single-family dwellings Private homesApartmentsNeighborhood Heart Watch

Family members Immediate accessFamiliar setting

AcceptanceVictim may be aloneOne-time user; panic

CHAPTER 63 APPROACHTOCARDIACARRESTANDLIFE-THREATENINGARRHYTHMIAS 347

MANAGEMENT OF TACHYARRHYTHMIC CARDIAC ARRESTS

Direct Current CardioversionWhen VF or a rapid VT is identified on a monitor or by telemetry, defibril-lation should be performed immediately (Fig. 63-2). When a reversible cause, such as an acute ischemic syndrome or electrolyte disturbance, is the mechanism, normal rhythm can be successfully restored in up to 90% of VF victims weighing up to 90 kg with a DC monophasic shock of up to 360 J, or a with a biphasic shock of up to 200 J, delivered within 2 to 3 minutes. Failure of the initial shock to restore an effective rhythm is a poor prognostic sign. Although some algorithms suggest a succession of monophasic shock ener-gies from 200 to 360 J, or biphasic waveforms from 100 to 200 Joules, during a sequence of attempts to defibrillate, there is little to be gained from begin-ning with energies less than 300 J monophasic or less than 150 J biphasic during a cardiac arrest response.After a single shock at 300 or 360 J of monophasic energy, or 150 or 200

J biphasic, the patient should be checked for restoration of a spontaneous pulse; CPR should be continued for five cycles if a pulse remains absent. Subsequently, a second shock should be delivered, followed by epinephrine, 1 mg intravenously (IV). If a pulse is still absent, CPR is repeated for five cycles before the next shock. Epinephrine may be repeated at 3- to 5-minute

intervals with defibrillator shocks in between, but high-dose epinephrine does not appear to provide added benefit. Vasopressin, 40 U given IV once, is an equally good alternative to epinephrine, 4 but the combination does not appear to be better than either one alone. 5 This algorithm is based on the 2005 update. In a 2008 advisory, use of 200

compression-only sequences was suggested as an alternative to standard CPR cycles between shocks.

Pharmacotherapy for Resistant ArrhythmiasFor a patient who continues in VF or pulseless VT despite multiple attempts at DC cardioversion after epinephrine, or who has recurrent episodes of VF or VT after cardioversion, electrical stability may be achieved by administer-ing intravenous antiarrhythmic agents while continuing resuscitative efforts (see Fig. 63-2). Amiodarone (150 mg IV over a 10-minute period, followed by 1 mg/minute for up to 6 hours and 0.5 mg/minute thereafter) is the initial treatment of choice. 6 Additional bolus dosing, to a maximum of 500 mg, can be tried if the initial bolus is unsuccessful. Amiodarone need not be given as a routine to individuals who respond to initial defibrillation with a persis-tently stable rhythm, but it is preferred for those who have recurrent episodes of VT or VF after initial defibrillation and oxygenation.If there is sufficient clinical evidence that the cardiac arrest was heralded

by the onset of an acute coronary syndrome, lidocaine (1.0- to 1.5-mg/kg bolus given IV, with the dose repeated in 2 minutes) may be used instead of amiodarone, or if amiodarone has failed. When acute or intermittent ischemia is not thought to be the mechanism, intravenous amiodarone is the preferred initial drug, but lidocaine may be tried if amiodarone fails. Intrave-nous procainamide (loading infusion of 100 mg/5 minutes to a total dose of 500 to 800 mg, followed by a continuous infusion at 2 to 5 mg/minute) is now rarely used but may be tried in those with persisting, hemodynamically unstable arrhythmias.In patients with acute hyperkalemia as the triggering event for resistant

VF, hypocalcemia, or arrest potentially caused by excess doses of calcium-blocking drugs, 10% calcium gluconate (5 to 20 mL infused at a rate of 2 to 4 mL/minute) may be helpful. Otherwise, calcium should not be used rou-tinely during resuscitation, even though ionized Ca2+ levels may be low during resuscitation from cardiac arrest.Some resistant forms of polymorphic VT (torsades de pointes), rapid mono-

morphic VT, ventricular flutter (rate > 260/minute), or resistant VF respond to MgSO4 (1 to 2 g IV given over a 1- to 2-minute period) or to -blocker therapy (propranolol, 1-mg boluses IV to a total dose of up to 15 to 20 mg; or metoprolol, 5 mg IV, up to 20 mg). MgSO4 is specifically indicated for polymorphic VTs due to inherited or acquired (drug-induced) long QT pat-terns (Chapter 65). This VT pattern also occurs with marked hypokalemia, so 20 mEq/hour of intravenous potassium chloride should be included in the treatment of patients who have a serum K+ of less than 3 mEq/L and whose polymorphic VT is resistant to other therapies. However, hypokalemia also may follow the acid-base and electrolyte shifts associated with prolonged arrests and should not be considered a primary cause of the cardiac arrest in that circumstance.

MANAGEMENT OF CARDIAC ARREST CAUSED BY ASYSTOLE, BRADYARRHYTHMIAS, OR PULSELESS ELECTRICAL ACTIVITY

The approach to a patient with bradyarrhythmic or asystolic arrest or with pulseless electrical activity differs from the approach to patients with tachyar-rhythmic events (VT/VF). Once this form of cardiac arrest is recognized, efforts should focus on first establishing control of the patients cardiorespira-tory status (i.e., continue CPR, intubate, and establish intravenous access), then reconfirming the rhythm (in two leads if possible), and finally taking actions that favor the emergence of a stable spontaneous rhythm or attempt to pace the heart. Possible reversible causes, particularly for bradyarrhythmia and asystole, should be considered and excluded (or treated) promptly (Fig. 63-3), including hypovolemia, hypoxia, cardiac tamponade, tension pneu-mothorax, preexisting acidosis, drug overdose, hypothermia, and hyperkale-mia. Epinephrine (1.0 mg IV every 3 to 5 minutes) and atropine (1.0 to 2.0 mg IV) or isoproterenol (up to 15 to 20 g/minute IV), which are com-monly used in an attempt to elicit spontaneous electrical activity or increase the rate of a bradycardia, have only limited success. In the absence of an intravenous line, epinephrine (1 mg, i.e., 10 mL of a 1 : 10,000 solution) may be given by the intracardiac route, but there is danger of coronary or myocar-dial laceration. Sodium bicarbonate, 1 mEq/kg, may be tried for known or

ECGDocumented ventricular fibrillation or pulseless ventricular tachycardia

Defibrillate once for persistent VF/VT300-360 J (monophasic); 120-150 J (biphasic)

Resume CPR; check rhythm

Epinephrine, 1 mg IVRepeat q 3-5 min

Vasopressin, 40 units IV once

If not successful, continue CPR for 5 cycles

If not successful, continue CPR,IV access, intubate

If not successful or VF/VT recurs,continue CPR, start antiarrhythmic

drug protocol

Epinephrine, increase dose

NaHCO3, 1 mEq/kg (for K+)

Antiarrhythmic drugs

Check rhythm; if VF/VT, deliver second shock

Check rhythm; continue CPR

Defibrillate, 360 J within 30 to 60 sec

Defibrillate, 360 J: Drugshockdrugshock

Magnesium sulfate: 12 g IV (polymorphic VT)Procainamide: 30 mg/min, to 17 mg/kg (monomorphic VT)

or

Amiodarone: 150 mg over 10 min, then 1 mg/minLidocaine: 1.5 mg/kg; repeat in 3-5 min

FIGURE 63-2. Generalalgorithmforadvancedcardiaclifesupport(ACLS)responsetoventricularfibrillation(VF)orpulselessventriculartachycardia(VT).Formoredetail,seetheACLSguidelinesinSuggestedReadings.Note:Ina2008advisory,200compression-onlysequencesweresuggestedasanalternativetostandardCPRcyclesbetweenshocks,andthisapproachisunderconsiderationforfutureguidelines.CPR=cardiopulmonaryresusci-tation;ECG=electrocardiogram.

strongly suspected preexisting hyperkalemia or bicarbonate-responsive acidosis.External pacing systems (Chapter 66) should be used for out-of-hospital

bradycardic or asystolic arrest, although its influence on outcome is not well documented. In the hospital setting, external pacing is generally used during the initial response to a bradycardic or asystolic arrest, but it should be super-seded by transvenous pacing if the arrest is prolonged, if continuous pacing is needed, or if the external device fails to pace. Unfortunately, an asystolic patient continues to have a very poor prognosis despite available techniques.

ADJUNCTIVE THERAPEUTIC ACTIONSDuring or after therapy targeted to restoration of an electrically stable cardiac rhythm, the patients general metabolic state should be addressed by improv-ing oxygenation and reversing acidosis. Intravenous sodium bicarbonate (1 mEq/kg), with up to 50% of this dose repeated every 10 to 15 minutes during the course of CPR, is recommended for patients with known or sus-pected preexisting bicarbonate-responsive causes of acidosis, for certain drug overdoses (Chapter 110), and after prolonged and unsuccessful attempts at resuscitation. Caution must be exercised, however, because excessive quanti-ties of sodium bicarbonate can be deleterious by causing alkalosis, hyperna-tremia, and hyperosmolality. When possible, arterial pH, Po2, and Pco2 should be monitored during the resuscitation. In addition, moderate thera-peutic hypothermia (32 to 34 C) is now recommended for postcardiac arrest improvement of cerebral function and of survival 7 as part of the concept of cardiocerebral resuscitation.

LONG-TERM MANAGEMENTSurvivors of a cardiac arrest that is not due to transient factors remain at high risk for recurrent cardiac arrest and sudden cardiac death. An implantable defibrillator improves outcomes in survivors of cardiac arrest. 8

1. Hpfl M, Selig HF, Nagele P. Chest-compression-only versus standard cardiopulmonary resuscita-tion: a meta-analysis. Lancet. 2010;376:1552-1557.

2. Bardy GH, Lee KL, Mark DB, et al. Home use of automated external defibrillators for sudden cardiac arrest. N Engl J Med. 2008;358:1793-1804.

3. Wik L, Hansen TB, Fylling F, et al. Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation: a randomized trial. JAMA. 2003;289:1389-1395.

4. Aung K, Htay T. Vasopressin for cardiac arrest: a systematic review and meta-analysis. Arch Intern Med. 2005;165:17-24.

5. Gueugniaud PY, David JS, Chanzy E, et al. Vasopressin and epinephrine vs. epinephrine alone in cardiopulmonary resuscitation. N Engl J Med. 2008;359:21-30.

6. Dorian P, Cass D, Schwartz B, et al. Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med. 2002;346:884-890.

7. Arrich J, Holzer M, Herkner H, et al. Hypothermia for neuroprotection in adults after cardiopulmo-nary resuscitation. Cochrane Database Syst Rev. 2009;4:CD004128.

8. Connolly SJ, Hallstrom AP, Cappato R, et al. Meta-analysis of the implantable cardioverter defibril-lator secondary prevention trials. AVID, CASH and CIDS studies. Antiarrhythmics vs Implantable Defibrillator study. Cardiac Arrest Study Hamburg. Canadian Implantable Defibrillator study. Eur Heart J. 2000;21:2071-2078.

SUGGESTEDREADINGS

Brooks SC, Bigham BL, Morrison LJ. Mechanical versus manual chest compressions for cardiac arrest. Cochrane Database Syst Rev. 2011;1:CD007260. Review finding no benefit from mechanical devices.

Field JM, Hazinski MF, Sayre MR, et al. Executive summary: 2010 American Heart Association Guide-lines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. Circulation. 2010;122:S640-S656. Review.

Kong MH, Fonarow GC, Peterson ED, et al. Systematic review of the incidence of sudden cardiac death in the United States. J Am Coll Cardiol. 2011;57:794-801. Review.

Maron BJ, Estes NA 3rd. Commotio cordis. N Engl J Med. 2010;362:917-927. Review.Nichol G, Aufderheide TP, Eigel B, et al. Regional systems of care for out-of-hospital cardiac arrest: a

policy statement from the American Heart Association. Circulation. 2010;121:709-729. Advocates national implementation of systems known to be effective.

Stub D, Bernard S, Duffy SJ, et al. Post cardiac arrest syndrome: a review of therapeutic strategies. Circulation. 2011;123:1428-1435. Review.

Bradyarrhythmia/asystole or pulseless electrical activity

Initiate and continue CPR

Pacingexternal or pacing wire

Epinephrine Atropine Sodium bicarbonate 1 mg IV (repeat) 1 mg IV (repeat)

Hypoxia Hyper-/Hypokalemia Severe acidosis Drug overdose Hypothermia Terminal disease

Hypovolemia Pulmonary embolus Hypoxia Drug overdose Tamponade Hyperkalemia Pneumothorax Severe acidosis Hypothermia Massive acute MI Severe CHF Shock Terminal disease

Confirm electricalasystole

Confirm absence of mechanical pulse

Ventilation; IV access

Identify and manage cause(if treatable)

1 mEq/kg IV

FIGURE 63-3. Generalalgorithmforadvancedcardiaclifesupportresponsetobrady-cardicorasystoliccardiacarrestorpulselesselectricalactivity.Formoredetail,seeSug-gested Readings. CHF = congestive heart failure; CPR = cardiopulmonary resuscitation;MI=myocardialinfarction.

63 Approach to Cardiac Arrest and Life-Threatening Arrhythmias ?Predisposing WideQrs Complex TachycardiasManagement of Sustained Ventricular TachycardiaDistinguishing Supraventricular from Ventricular Tachycardias

General Management of Cardiac ArrestBasic Life SupportAutomated External DefibrillatorsIntermediate Life SupportAdvanced Cardiac Life Support

Management of Tachyarrhythmic Cardiac ArrestsDirect Current CardioversionPharmacotherapy for Resistant Arrhythmias

Management of Cardiac Arrest Caused By Asystole, Bradyarrhythmias, or Pulseless Electrical ActivityAdjunctive Therapeutic ActionsLong-Term ManagementGrade ASuggested ReadingsAdditional Suggested Readings