《心肺复苏指南》参考资料（英文版）Part 7-2 Management of Cardiac Arrest

Frhythms produce pulseless cardiac arrest: ventricular effective for fluid resuscitation, drug delivery, and blood fibrillation (VF), rapid ventricular tachycardia (VT), sampling for laboratory evaluation, and is attainable in all age useless electrical activity(PEA), and asystole. Surviva

团购合买资源类别：文库，文档格式：PDF，文档页数：10，文件大小：563.6KB

Part 7.2: Management of Cardiac Arrest F rhythms produce pulseless cardiac arrest: ventricular effective for fluid resuscitation, drug delivery, and blood fibrillation (VF), rapid ventricular tachycardia (VT), sampling for laboratory evaluation, and is attainable in all age useless electrical activity(PEA), and asystole. Surviva groups. Providers may establish I0 access if IV access is from these arrest rhythms requires both basic life support unavailable( Class IIa). Commercially available kits can (BLS) and advanced cardiovascular life support(ACLS) facilitate IO access in adults The foundation of ACLS care is good BLS care, beginning If spontaneous circulation does not return after defibrilla with prompt high-quality bystander CPR and, for VE/pulse- tion and peripheral venous or I0 drug administration, the less VT, attempted defibrillation within minutes of collapse. provider may consider placement of a central line(unless For victims of witnessed VF arrest, prompt bystander CPr there are contraindications ). Note that central venous cathe and early defibrillation can significantly increase the chance terization is a relative (not absolute) contraindication for for survival to hospital discharge. In comparison, typical fibrinolytic therapy in patients with stroke or acute coronary ACLS therapies, such as insertion of advanced airways and syndromes of the circulation have not be If iv and io access cannot be established. some resusci- shown to increase rate of survival to hospital discharge. This tation drugs may be administered by the endotracheal route section details the general care of a patient in cardiac arrest One study in children(LOE 2), 2 5 studies in adults(LOE and provides an overview of the ACLs Pulseless Arrest 213-15; LOE 316.1), as well as multiple animal studies(LOE 6), 8-20 showed that lidocaine, 14,2I epinephrine, 2 atropine, 23 naloxone, and vasopressin20 are absorbed via the trachea. Access for Medications: Correct Priorities dministration of resuscitation drugs into the trachea, how- During cardiac arrest, basic CPR and early defibrillation are ever, results in lower blood concentrations than the same dose of primary importance, and drug administration is of second- given intravascularly. Furthermore, recent animal studies24 ary importance. Few drugs used in the treatment of cardiac suggest that the lower epinephrine concentrations achieved arrest are supported by strong evidence. After beginning CPR when the drug is delivered by the endotracheal route may and attempting defibrillation, rescuers can establish intrave- produce transient B-adrenergic effects. These effects can be nous (Tv) access, consider drug therapy, and insert an detrimental, causing hypotension, lower coronary artery per dvanced airway. fusion pressure and flow, and reduced potential for return of Central Versus Peripheral Infusions spontaneous circulation (ROSC). Thus, although Central line access is not needed in most resuscitation cheal administration of some resuscitation drugs is attempts. If IV access has not been established, the provide IV or Io drug administration is preferred because should insert a large peripheral venous catheter. Although in provide more predictable drug delivery and pharmacologic effect adults peak drug concentrations are lower and circulation times longer when drugs are administered via peripheral sites In one nonrandomized cohort study of out-of-hospital cardiac arrest in adults (loe 4)28 using a randomized control rather than central sites, the establishment of peripheral administration of atropine and epinephrine by the IV route access does not require interruption of CPR. .2 Drugs typi cally require I to 2 minutes to reach the central circulation was associated with a higher rate of rosc and survival to when given via a peripheral vein but require less time when hospital admission than administration of the drugs by the endotracheal route. Five percent of those who received Iv given via central venous access. venous route, administer the drug by bolus injection and in the group receiving drugs by the endotracheal roule ved If a resuscitation drug is administered by a peripheral drugs survived to hospital discharge, but no patient survived The optimal endotracheal dose of most drugs is unknown, follow with a 20-mL bolus of IV fluid Elevate the extremity but typically the dose given by the endotracheal route is 2 to for 10 to 20 seconds to facilitate drug delivery to the central irculation 3 21 times the recommended iv dose. In 2 CPR studies th Intraosseous(1O)cannulation provides access to a noncol- equipotent epinephrine dose given endotracheally was ap- lapsible venous plexus, enabling drug delivery similar to that proximately 3 to 10 times higher than the IV dose(LOE 52 achieved by central venous access. Two prospective(LOE 3) LOE 630). Providers should dilute the recommended dose in trials, in children and adults 5 and 6 other studies(LOE 46, 5 to 10 mL of water or normal saline and inject the drug LOE 57: LOE 710.1)documented that IO access is safe and directly into the endotracheal tube. 22 Studies with epineph- rine3I and lidocaine showed that dilution with water instead of 0.9%o saline may achieve better drug absorption (Circulation. 2005: 112: lV-58-IV-66) o 2005 American Heart Associa Arrest rhythms This special supplement to Circulation is freely available at The management of pulseless arrest is highlighted in the http://www.circulationaha.org ACLS Pulseless Arrest Algorithm(Figure). Box numbers in DOI: 10.1161/CIRCULATIONAHA 105. 166557 the text refer to the numbered boxes in the algorithm IV-58

Part 7.2: Management of Cardiac Arrest Four rhythms produce pulseless cardiac arrest: ventricular fibrillation (VF), rapid ventricular tachycardia (VT), pulseless electrical activity (PEA), and asystole. Survival from these arrest rhythms requires both basic life support (BLS) and advanced cardiovascular life support (ACLS). The foundation of ACLS care is good BLS care, beginning with prompt high-quality bystander CPR and, for VF/pulseless VT, attempted defibrillation within minutes of collapse. For victims of witnessed VF arrest, prompt bystander CPR and early defibrillation can significantly increase the chance for survival to hospital discharge. In comparison, typical ACLS therapies, such as insertion of advanced airways and pharmacologic support of the circulation, have not been shown to increase rate of survival to hospital discharge. This section details the general care of a patient in cardiac arrest and provides an overview of the ACLS Pulseless Arrest Algorithm. Access for Medications: Correct Priorities During cardiac arrest, basic CPR and early defibrillation are of primary importance, and drug administration is of secondary importance. Few drugs used in the treatment of cardiac arrest are supported by strong evidence. After beginning CPR and attempting defibrillation, rescuers can establish intravenous (IV) access, consider drug therapy, and insert an advanced airway. Central Versus Peripheral Infusions Central line access is not needed in most resuscitation attempts. If IV access has not been established, the provider should insert a large peripheral venous catheter. Although in adults peak drug concentrations are lower and circulation times longer when drugs are administered via peripheral sites rather than central sites, the establishment of peripheral access does not require interruption of CPR.1,2 Drugs typically require 1 to 2 minutes to reach the central circulation when given via a peripheral vein but require less time when given via central venous access. If a resuscitation drug is administered by a peripheral venous route, administer the drug by bolus injection and follow with a 20-mL bolus of IV fluid. Elevate the extremity for 10 to 20 seconds to facilitate drug delivery to the central circulation.3 Intraosseous (IO) cannulation provides access to a noncollapsible venous plexus, enabling drug delivery similar to that achieved by central venous access. Two prospective (LOE 3) trials, in children4 and adults,5 and 6 other studies (LOE 46; LOE 57–9; LOE 710,11) documented that IO access is safe and effective for fluid resuscitation, drug delivery, and blood sampling for laboratory evaluation, and is attainable in all age groups. Providers may establish IO access if IV access is unavailable (Class IIa). Commercially available kits can facilitate IO access in adults. If spontaneous circulation does not return after defibrillation and peripheral venous or IO drug administration, the provider may consider placement of a central line (unless there are contraindications). Note that central venous catheterization is a relative (not absolute) contraindication for fibrinolytic therapy in patients with stroke or acute coronary syndromes. If IV and IO access cannot be established, some resuscitation drugs may be administered by the endotracheal route. One study in children (LOE 2),12 5 studies in adults (LOE 213–15; LOE 316,17), as well as multiple animal studies (LOE 6),18–20 showed that lidocaine,14,21 epinephrine,22 atropine,23 naloxone, and vasopressin20 are absorbed via the trachea. Administration of resuscitation drugs into the trachea, however, results in lower blood concentrations than the same dose given intravascularly. Furthermore, recent animal studies24–27 suggest that the lower epinephrine concentrations achieved when the drug is delivered by the endotracheal route may produce transient -adrenergic effects. These effects can be detrimental, causing hypotension, lower coronary artery perfusion pressure and flow, and reduced potential for return of spontaneous circulation (ROSC). Thus, although endotracheal administration of some resuscitation drugs is possible, IV or IO drug administration is preferred because it will provide more predictable drug delivery and pharmacologic effect. In one nonrandomized cohort study of out-of-hospital cardiac arrest in adults (LOE 4)28 using a randomized control, administration of atropine and epinephrine by the IV route was associated with a higher rate of ROSC and survival to hospital admission than administration of the drugs by the endotracheal route. Five percent of those who received IV drugs survived to hospital discharge, but no patient survived in the group receiving drugs by the endotracheal route. The optimal endotracheal dose of most drugs is unknown, but typically the dose given by the endotracheal route is 2 to 21⁄2 times the recommended IV dose. In 2 CPR studies the equipotent epinephrine dose given endotracheally was approximately 3 to 10 times higher than the IV dose (LOE 529; LOE 630). Providers should dilute the recommended dose in 5 to 10 mL of water or normal saline and inject the drug directly into the endotracheal tube.22 Studies with epinephrine31 and lidocaine17 showed that dilution with water instead of 0.9% saline may achieve better drug absorption. Arrest Rhythms The management of pulseless arrest is highlighted in the ACLS Pulseless Arrest Algorithm (Figure). Box numbers in the text refer to the numbered boxes in the algorithm. (Circulation. 2005;112:IV-58-IV-66.) © 2005 American Heart Association. This special supplement to Circulation is freely available at http://www.circulationaha.org DOI: 10.1161/CIRCULATIONAHA.105.166557 IV-58

Part 7.2: Management of cardiac arrest / v-59 PULSELESS ARREST Artach monitordefibrillator when available Check rhythm Shockable rhythm? VE/T Asystole/PEA ve 1 shock Oie s eretes ef CPR May give 1 dose of vasopressin 40 U IAO to replace first or second dose of epin Consider atropine 1 mg Ino Shockable rhythm? Continue CPR while defibrillator is charging ve 1 shock Manual biphasic device specific AED: device specif ressor during CPR (before or after the shock Repeat every 3 to 5 min May give 1 dose of vasopressin 40 U no to replace first or second dose of epinephrine 12 l asystole, go to Box 10 13 e pulse. If no pulse, got Shockable rhythm? Continue CPA while dehbritator is charging nsure full chest recoil 2 minutes wth rhythm checks Manual biphasic: device specific Minimize interruptions in chest A D: device specific One cycle of CPR: 30 compressions Avoid hy it ation Secure airway and confirm placement consider addtional 150 m0 once, then w ANer an airway in placed (1 to 1.5 mg/kg first dose, then doses or 3 mo/ko) af CPR. Give continous ct ium, loading dose Thrombosis (coronary or Give B to 10 breathe/minute Check After 5 cycles of CPR, ' got to Box 5 above rhythm every 2 minutes ACLS Pulseless Arrest Algorithm. Ventricular fibrillation/Pulseless seconds, the provider should turn on the defibrillator, place Ventricular Tachycardia adhesive pads or paddles, and check the rhythm(Box 2) The most critical interventions during the first minutes of VF If the healthcare provider does not witness the arrest in the or pulseless VT are immediate bystander CPR (Box 1)with out-of-hospital setting (eg, the emergency medical services minimal interruption in chest compressions and defibrillation [EMS] provider arrives at the scene of an arrest), the provider as soon as it can be accomplished( Class D). In cases of may give 5 cycles of CPR before attempting defibrillation. In itnessed arrest with a defibrillator on-site, after delivery of adults with a prolonged arrest, shock delivery may be more 2 rescue breaths the healthcare provider should check for a successful after a period of effective chest pulse. If the provider definitely does not feel a pulse within 10 For further information about the sequence of CPR first

lV-60 Circulation December 13, 2005 versus shock first, see Part 5: " Electrical Therapies: Auto- rescuers to deliver shocks as efficiently as possible. Pulse and mated External Defibrillators, Defibrillation, Cardioversion, rhythm checks are limited and are not recommended imme diately after shock delivery; instead healthcare providers give If VF/pulseless VT is present(Box 3), providers shoul 5 cycles(about 2 minutes of CPR) immediately after the deliver I shock(Box 4)and then resume CPR immediately, shock and then check the rhythm. Ideally, compression beginning with chest compressions. If a biphasic defibrillator should be interrupted only for ventilation(until an adva is available, providers should use the dose at which that airway is placed), rhythm check, or shock delivery defibrillator has been shown to be effective for terminating Once an advanced airway (eg, endotracheal tube VF(typically a selected energy of 120 J to 200 D). If the esophageal-tracheal combitube [Combitube], laryngeal mask provider is unaware of the effective dose range of the device, airway [LMAD is placed, 2 rescuers no longer deliver cycles the rescuer may use a dose of 200 J for the first shock and of compressions interrupted with pauses for ventilation equal or higher shock dose for the second and subsequent Instead, the compressing rescuer should deliver 100 compres shocks. If a monophasic defibrillator is used, providers sions per minute continuously, without pauses for ventilation. should deliver an initial shock of 360 j and use that dose fo The rescuer delivering the ventilations should give 8 to 10 subsequent shocks. If VF is initially terminated by a shock breaths per minute and should be careful to avoid delivering but then recurs later in the arrest, deliver subsequent shocks at an excessive number of ventilations. Two or more rescuers the previously successful energy level. should rotate the compressor role approximately every 2 Biphasic defibrillators use a variety of waveforms, and minutes(when the victim's rhythm is checked). This change each waveform has been shown to be effective in terminating should prevent compressor fatigue and deterioration in qual VF over a specific dose range. Manufacturers should this effective waveform dose range on the face of the biphasic Establishing IV access is important(see below ) but it device, and providers should use that dose range to attempt should not interfere with CPR and delivery of shocks. As defibrillation with that device. The 200-J default "energy always, the provider should recall the H's and T's to identify level was selected because it falls within the reported range of a factor that may have caused the arrest or may be compli- selected doses that are effective for first and subsequent cating the resuscitative effort(see the green box, During biphasic shocks and can be provided by every biphasic CPR, "at the bottom of the algorithm) manual defibrillator available in 2005. This is a consensus There is inadequate evidence to identify an optimal number default dose and not a recommended ideal dose If biphasic of CPR cycles and defibrillation shocks that should be given devices are clearly labeled and providers are familiar with the before pharmacologic therapy is initiated. The recommended devices they use in clinical care, there will be no need for the sequence depicted in the algorithm is based on expert default 200-J dose. Ongoing research is necessary to firmly consensus. If VF/VT persists after delivery of I or 2 shocks establish the most appropriate initial settings for both plus CPR, give a vasopressor (epinephrine every 3 to 5 monophasic and biphasic defibrillators minutes during cardiac arrest: one dose of vasopressin may Providers should give I shock rather than the 3 successive replace either the first or second dose of epinephrine-se ("stacked")shocks recommended in previous versions of the Box 6). Do not interrupt CPR to give medications ECC guideliness for the treatment of VF/pulseless VT The drug should be administered during cpr and s Soon because the first-shock success rate for biphasic defibrillators as possible after the rhythm is checked. It can be administered is high 36 and it is important to minimize interruptions in chest before or after shock delivery, in a CPR-RHYTHM compressions. Although the l-shock strategy CHECK-CPR (while drug administered and defibrillator directly studied against a 3-shock strategy, the evidence is charged)SHOCK sequence(repeated as needed). This se compelling that interruption of chest compressions reduces quence differs from the one recommended in 200035:it coronary perfusion pressure. The time required to charge a designed to minimize interruptions in chest compressions. defibrillator, deliver a shock, and check a pulse can interrupt The 2000 recommendations In too many interrup- compressions for 37 seconds or longer 37(for further informa- tions in chest compressions. tion see Part 5:"Electrical Therapies: Automated External In these 2005 recommendations. during treatment of car- Defibrillators, Defibrillation, Cardioversion, and Pacing) diac arrest the drug doses should be prepared before the When a rhythm check reveals VF/VT, rescuers should rhythm check so they can be administered as soon as possible provide CPR while the defibrillator charges(when possible), after the rhythm check, but the timing of drug delivery is less until it is time to "clear"the victim for shock delivery. Give important than the need to minimize interruptions in chest the shock as quickly as possible. Immediately after shock compressions. Rhythm checks should be very brief(see delivery, resume CPR(beginning with chest compressions) below ). If a drug is administered immediately after the without delay and continue for 5 cycles (or about 2 minutes rhythm check(before or after the shock) it will be circulated if an advanced airway is in place), and then check the rhyth by the CPR given before and after the shock. After 5 cycles (Box 5). In in-hospital units with continuous monitoring(eg, (or about 2 minutes)of CPR, analyze the rhythm again(Box electrocardiography, hemodynamics), this sequence may be 7)and be prepared to deliver another shock immediately if modified at the physician's discretion(see Part 5) y. The management strategy depicted in the ACLS Pulseless When VF/pulseless VT persists after 2 to 3 shocks plus rest Algorithm is designed to minimize the number of CPR and administration of a vasopressor, consider adminis- times that chest ce ssions are interrupted and to enable tering an antiarrhythmic such as amiodarone (Box 8). If

versus shock first, see Part 5: “Electrical Therapies: Automated External Defibrillators, Defibrillation, Cardioversion, and Pacing.” If VF/pulseless VT is present (Box 3), providers should deliver 1 shock (Box 4) and then resume CPR immediately, beginning with chest compressions. If a biphasic defibrillator is available, providers should use the dose at which that defibrillator has been shown to be effective for terminating VF (typically a selected energy of 120 J to 200 J). If the provider is unaware of the effective dose range of the device, the rescuer may use a dose of 200 J for the first shock and an equal or higher shock dose for the second and subsequent shocks. If a monophasic defibrillator is used, providers should deliver an initial shock of 360 J and use that dose for subsequent shocks. If VF is initially terminated by a shock but then recurs later in the arrest, deliver subsequent shocks at the previously successful energy level. Biphasic defibrillators use a variety of waveforms, and each waveform has been shown to be effective in terminating VF over a specific dose range. Manufacturers should display this effective waveform dose range on the face of the biphasic device, and providers should use that dose range to attempt defibrillation with that device. The 200-J “default” energy level was selected because it falls within the reported range of selected doses that are effective for first and subsequent biphasic shocks and can be provided by every biphasic manual defibrillator available in 2005. This is a consensus default dose and not a recommended ideal dose. If biphasic devices are clearly labeled and providers are familiar with the devices they use in clinical care, there will be no need for the default 200-J dose. Ongoing research is necessary to firmly establish the most appropriate initial settings for both monophasic and biphasic defibrillators. Providers should give 1 shock rather than the 3 successive (“stacked”) shocks recommended in previous versions of the ECC guidelines35 for the treatment of VF/pulseless VT because the first-shock success rate for biphasic defibrillators is high36 and it is important to minimize interruptions in chest compressions. Although the 1-shock strategy has not been directly studied against a 3-shock strategy, the evidence is compelling that interruption of chest compressions reduces coronary perfusion pressure. The time required to charge a defibrillator, deliver a shock, and check a pulse can interrupt compressions for 37 seconds or longer37 (for further information see Part 5: “Electrical Therapies: Automated External Defibrillators, Defibrillation, Cardioversion, and Pacing”). When a rhythm check reveals VF/VT, rescuers should provide CPR while the defibrillator charges (when possible), until it is time to “clear” the victim for shock delivery. Give the shock as quickly as possible. Immediately after shock delivery, resume CPR (beginning with chest compressions) without delay and continue for 5 cycles (or about 2 minutes if an advanced airway is in place), and then check the rhythm (Box 5). In in-hospital units with continuous monitoring (eg, electrocardiography, hemodynamics), this sequence may be modified at the physician’s discretion (see Part 5). The management strategy depicted in the ACLS Pulseless Arrest Algorithm is designed to minimize the number of times that chest compressions are interrupted and to enable rescuers to deliver shocks as efficiently as possible. Pulse and rhythm checks are limited and are not recommended immediately after shock delivery; instead healthcare providers give 5 cycles (about 2 minutes of CPR) immediately after the shock and then check the rhythm. Ideally, compression should be interrupted only for ventilation (until an advanced airway is placed), rhythm check, or shock delivery. Once an advanced airway (eg, endotracheal tube, esophageal-tracheal combitube [Combitube], laryngeal mask airway [LMA]) is placed, 2 rescuers no longer deliver cycles of compressions interrupted with pauses for ventilation. Instead, the compressing rescuer should deliver 100 compressions per minute continuously, without pauses for ventilation. The rescuer delivering the ventilations should give 8 to 10 breaths per minute and should be careful to avoid delivering an excessive number of ventilations. Two or more rescuers should rotate the compressor role approximately every 2 minutes (when the victim’s rhythm is checked). This change should prevent compressor fatigue and deterioration in quality and rate of chest compressions. Establishing IV access is important (see below), but it should not interfere with CPR and delivery of shocks. As always, the provider should recall the H’s and T’s to identify a factor that may have caused the arrest or may be complicating the resuscitative effort (see the green box, “During CPR,” at the bottom of the algorithm). There is inadequate evidence to identify an optimal number of CPR cycles and defibrillation shocks that should be given before pharmacologic therapy is initiated. The recommended sequence depicted in the algorithm is based on expert consensus. If VF/VT persists after delivery of 1 or 2 shocks plus CPR, give a vasopressor (epinephrine every 3 to 5 minutes during cardiac arrest; one dose of vasopressin may replace either the first or second dose of epinephrine—see Box 6). Do not interrupt CPR to give medications. The drug should be administered during CPR and as soon as possible after the rhythm is checked. It can be administered before or after shock delivery, in a CPR–RHYTHM CHECK–CPR (while drug administered and defibrillator charged)–SHOCK sequence (repeated as needed). This sequence differs from the one recommended in 200035: it is designed to minimize interruptions in chest compressions. The 2000 recommendations resulted in too many interruptions in chest compressions. In these 2005 recommendations, during treatment of cardiac arrest the drug doses should be prepared before the rhythm check so they can be administered as soon as possible after the rhythm check, but the timing of drug delivery is less important than the need to minimize interruptions in chest compressions. Rhythm checks should be very brief (see below). If a drug is administered immediately after the rhythm check (before or after the shock) it will be circulated by the CPR given before and after the shock. After 5 cycles (or about 2 minutes) of CPR, analyze the rhythm again (Box 7) and be prepared to deliver another shock immediately if indicated. When VF/pulseless VT persists after 2 to 3 shocks plus CPR and administration of a vasopressor, consider administering an antiarrhythmic such as amiodarone (Box 8). If IV-60 Circulation December 13, 2005

Part 7.2: Management of Cardiac Arrest V-6I amiodarone available, lidocaine may be considered. should insert an advanced airway (eg, endotracheal tube Consider magnesium for torsades de pointes associated with Combitube, LMA). Once the airway is in place, 2 rescuers a long QT interval(see below). You should administer the should no longer deliver cycles of CPr(ie, compressions drug during CPR, as soon as possible after rhythm analysis. If interrupted by pauses when breaths are delivered). Instead the a nonshockable rhythm is present and the rhythm is organized compressing rescuer should give continuous chest compres- (complexes appear regular or narrow), try to palpate a pulse sions at a rate of 100 per minute without pauses for ventila tion. The rescuer delivering ventilation provides 8 to 10 Rhythm checks should be brief, and pulse checks should breaths per minute. The 2 rescuers should change compressor generally be performed only if an organized rhythm is and ventilator roles approximately every 2 minutes(when the observed. If there is any doubt about the presence of a pulse, rhythm is checked) to prevent compressor fatigue and dete- resume CPR. If the patient has ROSC, begin postresuscitation rioration in quality and rate of chest compressions. When care. If the patient's rhythm changes to asystole or PEA, see multiple rescuers are present, they should rotate the compres- Asystole and Pulseless Electrical Activity "below (Boxes 9 and sor role about every 2 minutes. Rescuers should minimize 10) interruptions in chest compressions while inserting the airway If a perfusing rhythm is transiently restored but not and should not interrupt CPR while establishing I or IO successfully maintained between repeated shocks(recurrent access VF/VT), the patient may be a candidate for early treatment If the rhythm check confirms asystole or PEA, resume CPR with antiarrhythmic medications(see Part 7.3: " Management immediately. A vasopressor (epinephrine or vasopressin) may of Symptomatic Bradycardia and Tachycardia") be administered at this time. Epinephrine can be administered During treatment of VF/pulseless VT, healthcare providers approximately every 3 to 5 minutes during cardiac arrest; or must practice efficient coordination between CPR and shock dose of vasopressin may be substituted for either the first or delivery. When VF is present for more than a few minutes, second epinephrine dose(Box 10). For a patient in asystole the myocardium is depleted of oxygen and metabolic sub- slow PEA, consider atropine(see below). Do not interrupt and energy substrates, increasing the likelihood that a possible after the rhythm check. Give the drug as soon as ng rhythm will return after shock delivery.38 Analyses After drug delivery and approximately 5 cycles(or about 2 waveform characteristics predictive of shock success minutes)of CPR, recheck the rhythm(Box 11). If a shockable have documented that the shorter the time between chest rhythm is present, deliver a shock(go to Box 4). If no rhythm compression and shock delivery, the more likely the shock is present or if there is no change in the appearance of the will be successful. 38,39 Reduction in the interval from com- electrocardiogram, immediately resume CPR(Box 10). If an pression to shock delivery by even a few seconds can increase organized rhythm is present(Box 12), try to palpate a pulse. he probability of shock If no pulse is present (or if there is any doubt about the presence of a pulse), continue CPR(Box 10). If a pulse is Asystole and Pulseless Electrical Activity(Box 9) present the provider should identify the rhythm and treat PEA encompasses a heterogeneous group of pulseless appropriately(see Part 7.3: " Management of Symptomatic rhythms that includes pseudo-electromechanical dissociation Bradycardia and Tachycardia"). If the patient appears to have (pseudo-EMD), idioventricular rhythms, ventricular escape an organized rhythm with a good pulse, begin postresuscita- rhythms, postdefibrillation idioventricular rhythms, and bra- dyasystolic rhythms Research with cardiac ultrasonography and indwelling pressure catheters has confirmed that pulse When Should Resuscitative Efforts Stop? less patients with electrical activity have associated mechan- The resuscitation team must make a conscientious and com- ical contractions, but these contractions are too weak to petent effort to give patients a trial of CPR and ACLS duce a blood detectable by palpation or nonin- provided that the patient has not expressed a decision to vasive blood pressure monitoring. PEA is often caused by forego resuscitative efforts. The final decision to stop efforts reversible conditions and can be treated if those conditions can never be as simple as an isolated time interval. Clinical are identified and corrected judgment and respect for human dignity must enter into al rate from cardiac arrest with asystole is decision making. There is little data to guide this decision. dismal. During a resuscitation attempt, brief periods of an Emergency medical response systems should not re rganized complex may appear on the monitor screen, but field personnel to transport every victim of cardiac arrest to a spontaneous circulation rarely emerges. As with PEA, the hospital or emergency department(ED). Transportation with hope for resuscitation is to identify and treat a reversible continuing CPR is justified if interventions are available in cause the ED that cannot be performed in the field, such as Because of the similarity in causes and management of cardiopulmonary bypass or extracorporeal circulation for these two arrest rhythms, their treatment has been combined victims of severe hypothermia( Class IIb) in the second part of the ACLS Pulseless Arrest Algorithm Unless special situations are present(eg, hypothermia), for Patients who have either asystole or PEA will not benefit nontraumatic and blunt traumatic out-of-hospital cardiac from defibrillation attempts. The focus of resuscitation is to arrest, evidence confirms that ACLS care in the ED offers perform high-quality CPR with minimal interruptions and to advantage over ACLS care in the field Stated succinctly, if identify reversible causes or complicating factors. Providers ACLS care in the field cannot resuscitate the victim, ED care

amiodarone is unavailable, lidocaine may be considered. Consider magnesium for torsades de pointes associated with a long QT interval (see below). You should administer the drug during CPR, as soon as possible after rhythm analysis. If a nonshockable rhythm is present and the rhythm is organized (complexes appear regular or narrow), try to palpate a pulse (see Box 12). Rhythm checks should be brief, and pulse checks should generally be performed only if an organized rhythm is observed. If there is any doubt about the presence of a pulse, resume CPR. If the patient has ROSC, begin postresuscitation care. If the patient’s rhythm changes to asystole or PEA, see “Asystole and Pulseless Electrical Activity” below (Boxes 9 and 10). If a perfusing rhythm is transiently restored but not successfully maintained between repeated shocks (recurrent VF/VT), the patient may be a candidate for early treatment with antiarrhythmic medications (see Part 7.3: “Management of Symptomatic Bradycardia and Tachycardia”). During treatment of VF/pulseless VT, healthcare providers must practice efficient coordination between CPR and shock delivery. When VF is present for more than a few minutes, the myocardium is depleted of oxygen and metabolic substrates. A brief period of chest compressions can deliver oxygen and energy substrates, increasing the likelihood that a perfusing rhythm will return after shock delivery.38 Analyses of VF waveform characteristics predictive of shock success have documented that the shorter the time between chest compression and shock delivery, the more likely the shock will be successful.38,39 Reduction in the interval from compression to shock delivery by even a few seconds can increase the probability of shock success.40 Asystole and Pulseless Electrical Activity (Box 9) PEA encompasses a heterogeneous group of pulseless rhythms that includes pseudo-electromechanical dissociation (pseudo-EMD), idioventricular rhythms, ventricular escape rhythms, postdefibrillation idioventricular rhythms, and bradyasystolic rhythms. Research with cardiac ultrasonography and indwelling pressure catheters has confirmed that pulseless patients with electrical activity have associated mechanical contractions, but these contractions are too weak to produce a blood pressure detectable by palpation or noninvasive blood pressure monitoring. PEA is often caused by reversible conditions and can be treated if those conditions are identified and corrected. The survival rate from cardiac arrest with asystole is dismal. During a resuscitation attempt, brief periods of an organized complex may appear on the monitor screen, but spontaneous circulation rarely emerges. As with PEA, the hope for resuscitation is to identify and treat a reversible cause. Because of the similarity in causes and management of these two arrest rhythms, their treatment has been combined in the second part of the ACLS Pulseless Arrest Algorithm. Patients who have either asystole or PEA will not benefit from defibrillation attempts. The focus of resuscitation is to perform high-quality CPR with minimal interruptions and to identify reversible causes or complicating factors. Providers should insert an advanced airway (eg, endotracheal tube, Combitube, LMA). Once the airway is in place, 2 rescuers should no longer deliver cycles of CPR (ie, compressions interrupted by pauses when breaths are delivered). Instead the compressing rescuer should give continuous chest compressions at a rate of 100 per minute without pauses for ventilation. The rescuer delivering ventilation provides 8 to 10 breaths per minute. The 2 rescuers should change compressor and ventilator roles approximately every 2 minutes (when the rhythm is checked) to prevent compressor fatigue and deterioration in quality and rate of chest compressions. When multiple rescuers are present, they should rotate the compressor role about every 2 minutes. Rescuers should minimize interruptions in chest compressions while inserting the airway and should not interrupt CPR while establishing IV or IO access. If the rhythm check confirms asystole or PEA, resume CPR immediately. A vasopressor (epinephrine or vasopressin) may be administered at this time. Epinephrine can be administered approximately every 3 to 5 minutes during cardiac arrest; one dose of vasopressin may be substituted for either the first or second epinephrine dose (Box 10). For a patient in asystole or slow PEA, consider atropine (see below). Do not interrupt CPR to deliver any medication. Give the drug as soon as possible after the rhythm check. After drug delivery and approximately 5 cycles (or about 2 minutes) of CPR, recheck the rhythm (Box 11). If a shockable rhythm is present, deliver a shock (go to Box 4). If no rhythm is present or if there is no change in the appearance of the electrocardiogram, immediately resume CPR (Box 10). If an organized rhythm is present (Box 12), try to palpate a pulse. If no pulse is present (or if there is any doubt about the presence of a pulse), continue CPR (Box 10). If a pulse is present the provider should identify the rhythm and treat appropriately (see Part 7.3: “Management of Symptomatic Bradycardia and Tachycardia”). If the patient appears to have an organized rhythm with a good pulse, begin postresuscitative care. When Should Resuscitative Efforts Stop? The resuscitation team must make a conscientious and competent effort to give patients a trial of CPR and ACLS, provided that the patient has not expressed a decision to forego resuscitative efforts. The final decision to stop efforts can never be as simple as an isolated time interval. Clinical judgment and respect for human dignity must enter into decision making. There is little data to guide this decision. Emergency medical response systems should not require field personnel to transport every victim of cardiac arrest to a hospital or emergency department (ED). Transportation with continuing CPR is justified if interventions are available in the ED that cannot be performed in the field, such as cardiopulmonary bypass or extracorporeal circulation for victims of severe hypothermia (Class IIb). Unless special situations are present (eg, hypothermia), for nontraumatic and blunt traumatic out-of-hospital cardiac arrest, evidence confirms that ACLS care in the ED offers no advantage over ACLS care in the field. Stated succinctly, if ACLS care in the field cannot resuscitate the victim, ED care Part 7.2: Management of Cardiac Arrest IV-61

Iv-62 Circulation December 13. 2005 will not resuscitate the victim. Civil rules, administrative repeated in I study) was compared with epinephrine (I mg, concerns, medical insurance requirements, and even reim- repeated) as the initial vasopressor for treatment of cardiac bursement enhancement have frequently led to requirements arrest. In the large multicenter trial involving 1186 out-of- to transport all cardiac arrest victims to a hospital or ED. If hospital cardiac arrests with all rhythms(LOE 1), 5 a post-hoc these requirements are nonselective, they are inappropriate, analysis of the subset of patients with asystole showed futile, and ethically unacceptable. Cessation of efforts in the significant improvement in survival to hospital discharge but out-of-hospital setting, following system-specific criteria and not neurologically intact survival when 40 U(repeated once under direct medical control, should be standard practice in if necessary) of vasopressin was used as the initial vasopres all EMS systems or compared with epinephrine(I mg, repeated if necessary) A meta-analysis of 5 randomized trials(LOE 1)66 showed Medications for Arrest Rhythms no statistically significant differences between vasopressin Vasopressors and epinephrine for ROSC, 24-hour survival, or survival to To date no placebo-controlled trials have shown that admin- hospital discharge. The subgroup analysis based on initial istration of any vasopressor agent at any stage during man- cardiac rhythm did not show any statistically significant agement of pulseless VT, VE, PEA, or asystole increases the erence in survival to hospital discharge(LOE 1).66 rate of neurologically intact survival to hospital discharge In a large in-hospital study of cardiac arrest, 200 patients were randomly assigned to receive either I mg of epinephrine There is evidence, however, that the use of vasopressor(initial rhythm: 16% VE, 3% VT, 54% PEA, 27% asystole)or agents favors initial ROSC 40 U of vasopressin(initial rhythm: 20% VF, 3% VT, 41% Epinephrine and vasopressin PEA, 34%o asystole). There was no difference in survival to I VF and Pulseless VT hour(epinephrine: 35%, vasopressin: 39%)or to hospital discharge (epinephrine: 14%0, vasopressin: 12%)between Epinephrine groups or subgroup Epinephrine hydrochloride produces beneficial effects A retrospective analysis documented the effects of epi- patients during cardiac arrest, primarily because of its nephrine alone (231 patients)compared with a combination a-adrenergic receptor-stimulating(ie, vasoconstrictor) prop- of vasopressin and epinephrine (37 patients) in out-of erties4The a-adrenergic effects of epinephrine can increase hospital cardiac arrest with VF/T, PEA, or asystole. There coronary and cerebral perfusion pressure during CPR.42 The was no difference in survival or rosc when vf or Pea was value and safety of the B-adrenergic effects of epinephrine are the presenting rhythm, but ROSC was increased in the controversial because they may increase myocardial work epinephrine plus vasopressin group among patients pre- and reduce subendocardial perfusion. 43 senting with asystole. 67 Although epinephrine has been used universally in resus Because vasopressin effects have not been shown to differ itation,there is a paucity of evidence to show that it from those of epinephrine in cardiac arrest, one dose of improves survival in humans. Both beneficial and toxic vasopressin 40 U IV/O may replace either the first or second physiologic effects of epinephrine administration during CPR dose of epinephrine in the treatment of pulseless arrest( Class have been shown in animal and human studies. 44-50 Initial or Indeterminate). escalating high-dose epinephrine has occasionally improved initial ROSC and early survival rates. But in 8 randomized Asystole and Pulseless Electrical Activity clinical studies involving >9000 cardiac arrest patients, high-dose epinephrine produced no improvement in survival The studies described above enrolled patients with PEA and to hospital discharge rates or neurologic outcomes asystole and failed to show that either vasopressin or epi compared with standard doses, even in subgroups give nephrine is superior for treatment of PEA regardless of the tial high-dose epinephrine, 50-57 order of administration. In the case of asystole, a single It is appropriate to administer a I-mg dose of epinephrine post-hoc analysis of a larger study found a survival benefit of IV/O every 3 to 5 minutes during adult cardiac arrest( Class vasopressin over epinephrine but did not find an increase in IIb). Higher doses may be indicated to treat specific prob- intact neurologic survival lems, such as B-blocker or calcium channel blocker overdo On the basis of these findings, providers may consider If IV/O access is delayed or cannot be established, epineph- vasopressin for treatment of asystole, but there is insufficient rine may be given by the endotracheal route at a dose of 2 to evidence to recommend for or against its use in PEA. Further 2.5 mg studies are required. Epinephrine may be administered every 3 to 5 Vasopressin may be substituted for the first or second epinephrine dose Vasopressin is a nonadrenergic peripheral vasoconstrictor that also causes coronary enal vasoconstriction.5859 Atropine Despite I promising randomized study ( LoE 2), 0 additional Atropine sulfate reverses cholinergic-mediated decreases in lower-level studies (LOE 11- heart rate, systemic vascular resistance, and blood pressure performed animal studies, 2 large randomized controlled No prospective controlled studies support the use of atropine human trials (loe 1)64, 65 failed to show an increase in rates in asystole or slow PEA arrest. Administration of atropine for of ROSC or survival when vasopressin(40 U, with the dose asystole is supported by a retrospective review (loe 4)68 of

will not resuscitate the victim. Civil rules, administrative concerns, medical insurance requirements, and even reimbursement enhancement have frequently led to requirements to transport all cardiac arrest victims to a hospital or ED. If these requirements are nonselective, they are inappropriate, futile, and ethically unacceptable. Cessation of efforts in the out-of-hospital setting, following system-specific criteria and under direct medical control, should be standard practice in all EMS systems. Medications for Arrest Rhythms Vasopressors To date no placebo-controlled trials have shown that administration of any vasopressor agent at any stage during management of pulseless VT, VF, PEA, or asystole increases the rate of neurologically intact survival to hospital discharge. There is evidence, however, that the use of vasopressor agents favors initial ROSC. Epinephrine and Vasopressin VF and Pulseless VT Epinephrine Epinephrine hydrochloride produces beneficial effects in patients during cardiac arrest, primarily because of its -adrenergic receptor-stimulating (ie, vasoconstrictor) properties.41 The -adrenergic effects of epinephrine can increase coronary and cerebral perfusion pressure during CPR.42 The value and safety of the -adrenergic effects of epinephrine are controversial because they may increase myocardial work and reduce subendocardial perfusion.43 Although epinephrine has been used universally in resuscitation, there is a paucity of evidence to show that it improves survival in humans. Both beneficial and toxic physiologic effects of epinephrine administration during CPR have been shown in animal and human studies.44–50 Initial or escalating high-dose epinephrine has occasionally improved initial ROSC and early survival rates. But in 8 randomized clinical studies involving 9000 cardiac arrest patients, high-dose epinephrine produced no improvement in survival to hospital discharge rates or neurologic outcomes when compared with standard doses, even in subgroups given initial high-dose epinephrine.50–57 It is appropriate to administer a 1-mg dose of epinephrine IV/IO every 3 to 5 minutes during adult cardiac arrest (Class IIb). Higher doses may be indicated to treat specific problems, such as -blocker or calcium channel blocker overdose. If IV/IO access is delayed or cannot be established, epinephrine may be given by the endotracheal route at a dose of 2 to 2.5 mg. Vasopressin Vasopressin is a nonadrenergic peripheral vasoconstrictor that also causes coronary and renal vasoconstriction.58,59 Despite 1 promising randomized study (LOE 2),60 additional lower-level studies (LOE 5),61–63 and multiple wellperformed animal studies, 2 large randomized controlled human trials (LOE 1)64,65 failed to show an increase in rates of ROSC or survival when vasopressin (40 U, with the dose repeated in 1 study) was compared with epinephrine (1 mg, repeated) as the initial vasopressor for treatment of cardiac arrest. In the large multicenter trial involving 1186 out-ofhospital cardiac arrests with all rhythms (LOE 1),65 a post-hoc analysis of the subset of patients with asystole showed significant improvement in survival to hospital discharge but not neurologically intact survival when 40 U (repeated once if necessary) of vasopressin was used as the initial vasopressor compared with epinephrine (1 mg, repeated if necessary). A meta-analysis of 5 randomized trials (LOE 1)66 showed no statistically significant differences between vasopressin and epinephrine for ROSC, 24-hour survival, or survival to hospital discharge. The subgroup analysis based on initial cardiac rhythm did not show any statistically significant difference in survival to hospital discharge (LOE 1).66 In a large in-hospital study of cardiac arrest, 200 patients were randomly assigned to receive either 1 mg of epinephrine (initial rhythm: 16% VF, 3% VT, 54% PEA, 27% asystole) or 40 U of vasopressin (initial rhythm: 20% VF, 3% VT, 41% PEA, 34% asystole). There was no difference in survival to 1 hour (epinephrine: 35%, vasopressin: 39%) or to hospital discharge (epinephrine: 14%, vasopressin: 12%) between groups or subgroups.64 A retrospective analysis documented the effects of epinephrine alone (231 patients) compared with a combination of vasopressin and epinephrine (37 patients) in out-ofhospital cardiac arrest with VF/VT, PEA, or asystole. There was no difference in survival or ROSC when VF or PEA was the presenting rhythm, but ROSC was increased in the epinephrine plus vasopressin group among patients presenting with asystole.67 Because vasopressin effects have not been shown to differ from those of epinephrine in cardiac arrest, one dose of vasopressin 40 U IV/IO may replace either the first or second dose of epinephrine in the treatment of pulseless arrest (Class Indeterminate). Asystole and Pulseless Electrical Activity Vasopressors The studies described above enrolled patients with PEA and asystole and failed to show that either vasopressin or epinephrine is superior for treatment of PEA regardless of the order of administration. In the case of asystole, a single post-hoc analysis of a larger study found a survival benefit of vasopressin over epinephrine but did not find an increase in intact neurologic survival. On the basis of these findings, providers may consider vasopressin for treatment of asystole, but there is insufficient evidence to recommend for or against its use in PEA. Further studies are required. Epinephrine may be administered every 3 to 5 minutes during the attempted resuscitation; vasopressin may be substituted for the first or second epinephrine dose. Atropine Atropine sulfate reverses cholinergic-mediated decreases in heart rate, systemic vascular resistance, and blood pressure. No prospective controlled studies support the use of atropine in asystole or slow PEA arrest. Administration of atropine for asystole is supported by a retrospective review (LOE 4)68 of IV-62 Circulation December 13, 2005

Part 7.2: Management of cardiac arrest / v-63 intubated patients with refractory asystole who showed im- Lidocaine proved survival to hospital admission with atropine. A case The use of lidocaine for ventricular arrhythmias was sup- series (LoE 5)69 of adults in cardiac arrest documented orted by initial studies in animals(LoE 6)80. 8I and extrap- onversion from asystole to sinus rhythm in 7 of 8 patients olation from the historic use of the drug to suppress prema- Literature to refute the use of atropine is equally sparse and ture ventricular contractions and prevent VF after acute of limited quality. A small prospective controlled nonan- myocardial infarction. 2 Although lidocaine improved short- domized study (LOE 3)70 of patients with out-of-hospital term survival in I prehospital study (OE 4),833 randomized cardiac arrest found no difference versus control when trials comparing amiodarone and lidocaine found lower rates atropine 1 to 2 mg was given as the initial resuscitation of ROSC73 84 and a higher incidence of asystoleS with use of medication, but subtherapeutic dosing and delay to epineph lidocaine. The out-of-hospital double-blind randomized con rine administration may have had an impact on survival in the trolled trial (Loe 1)73 that compared amiodarone with lido- study. In an animal model of PEA(LOE 6), 7I no difference caine found that amiodarone improved rate of survival to was noted in resuscitation outcome between standard-dose hospital admission and that lidocaine was associated with atropine and placebo groups more asystole after defibrillation. Asystole can be precipitated or exacerbated by excessive In summary, lidocaine is an alternative antiarrhythmic of vagal tone, and administration of a vagolytic medication is long standing and widespread familiarity with fewer imme- consistent with a physiologic approach. Atropine is inexpen- diate side effects than may be encountered with other antar sive, easy to administer, and has few side effects and rhythmics. Lidocaine, however, has no proven short-term or therefore can be considered for asystole or PEA. The recom- long-term efficacy in cardiac arrest. Lidocaine should be mended dose of atropine for cardiac arrest is I mg IV, which considered an alternative treatment to amiodarone(Class be repeated every 3 to 5 minutes(maximum total of 3 Indeterminate). The initial dose is I to 1.5 mg/kg Iv. If doses or 3 mg) if asystole persists( Class Indeterminate) VF/pulseless VT persists, additional doses of 0.5 to 0.75 mg/kg IV push may be administered at 5-to 10-minute Antiarrhythmics intervals, to a maximum dose of 3 mg/kg. This is the same There is no evidence that any antiarrhythmic drug given dose that was recommended in the ECC Guidelines 2000 routinely during human cardiac arrest increases survival to hospital discharge. Amiodarone, however, has been shown to Magnesium increase short-term survival to hospital admission when Two observational studies (LOE 5)86,87 showed that IV compared with placebo or lidocaine magnesium can effectively terminate torsades (irregular/polymorphic VT associated with prolonged vf and Pulseless vt interval). One small adult case series in adults(LoE 5)88 Amiodarone showed that isoproterenol or ventricular pacing can be effec IV amiodarone affects sodium, potassium, and calcium chan tive in terminating torsades de pointes associated with bra nels as well as a- and B-adrenergic blocking properties. It can dycardia and drug-induced QT prolongation. Magnesium is be considered for the treatment of VF or pulseless VT not likely to be effective in terminating irregular/polymorphic esponsive to shock delivery, CPR, and a vasopressor VT in patients with a normal In blinded randomized controlled clinical trials in adults When VF/pulseless VT cardiac arrest is associated with with refractory VF/pulseless VT in the out-of-hospital setting torsades de pointes, providers may administer magnesium (LOE 1), 72.73 paramedic administration of amiodarone(300 sulfate at a dose of I to 2 g diluted in 10 mL D, W IV/O push mg72 or 5 mg/kg)improved survival to hospital admission typically over 5 to 20 minutes( Class Ila for torsades). When rates when compared with administration of placebo or 1.5 torsades is present in the patient with pulses, the same I to 2 g mg/kg of lidocaine. 73 Additional studies(LOE 7)74-78 docu is mixed in 50 to 100 mL of D,W and given as a loading dose. mented consistent improvement in defibrillation response an be given more slowly (eg, over 5 to 60 minutes I) when amiodarone was given to humans or animals with VFor under these conditions. See Part 7.3: " Management of Symp- hemodynamically unstable VT. tomatic Bradycardia and Tachycardia" for additional infor Amiodarone produced vasodilation and hyp ion in l of mation about management of torsades de pointes not associ the out-of-hospital studies. 2 A canine study (LOE 6)79 noted ated with cardiac arrest that administration of a vasoconstrictor before amiodarone prevented hypotension. A new aqueous formulation of ami- Potentially Beneficial Therapies odarone does not contain the vasoactive solvents(polysorbate Fibrinolysis 80 and benzyl alcohol) of the standard formulation. In an Adults have been successfully resuscitated following admin- analysis of the combined data of 4 prospective clinical trials istration of fibrinolytics(tPA) after initial failure of standard of patients with VT(some included hemodynamically unsta- CPR techniques, particularly when the condition leading to ble patients), aqueous amiodarone produced no more hypo- the arrest was acute pulmonary embolism or other presumed tension than lidocaine. 77 cardiac cause (LOE 389: LOE 490-92: LOE 593-97). Evidence In summary, amiodarone may be administered for VF or from I large clinical trial (LOE 2),98 however, failed to show pulseless VT unresponsive to CPR, shock, and a ssor any significant treatment effect when a fibrinolytic(tPA) (Class IIb). An initial dose of 300 mg IV/O can be followed given to out-of-hospital patients with undifferentiated PEA by one dose of 150 mg IV/O cardiac arrest unresponsive to initial interventions

intubated patients with refractory asystole who showed improved survival to hospital admission with atropine. A case series (LOE 5)69 of adults in cardiac arrest documented conversion from asystole to sinus rhythm in 7 of 8 patients. Literature to refute the use of atropine is equally sparse and of limited quality. A small prospective controlled nonrandomized study (LOE 3)70 of patients with out-of-hospital cardiac arrest found no difference versus control when atropine 1 to 2 mg was given as the initial resuscitation medication, but subtherapeutic dosing and delay to epinephrine administration may have had an impact on survival in the study. In an animal model of PEA (LOE 6),71 no difference was noted in resuscitation outcome between standard-dose atropine and placebo groups. Asystole can be precipitated or exacerbated by excessive vagal tone, and administration of a vagolytic medication is consistent with a physiologic approach. Atropine is inexpensive, easy to administer, and has few side effects and therefore can be considered for asystole or PEA. The recommended dose of atropine for cardiac arrest is 1 mg IV, which can be repeated every 3 to 5 minutes (maximum total of 3 doses or 3 mg) if asystole persists (Class Indeterminate). Antiarrhythmics There is no evidence that any antiarrhythmic drug given routinely during human cardiac arrest increases survival to hospital discharge. Amiodarone, however, has been shown to increase short-term survival to hospital admission when compared with placebo or lidocaine. VF and Pulseless VT Amiodarone IV amiodarone affects sodium, potassium, and calcium channels as well as - and -adrenergic blocking properties. It can be considered for the treatment of VF or pulseless VT unresponsive to shock delivery, CPR, and a vasopressor. In blinded randomized controlled clinical trials in adults with refractory VF/pulseless VT in the out-of-hospital setting (LOE 1),72,73 paramedic administration of amiodarone (300 mg72 or 5 mg/kg73) improved survival to hospital admission rates when compared with administration of placebo72 or 1.5 mg/kg of lidocaine.73 Additional studies (LOE 7)74–78 documented consistent improvement in defibrillation response when amiodarone was given to humans or animals with VF or hemodynamically unstable VT. Amiodarone produced vasodilation and hypotension in 1 of the out-of-hospital studies.72 A canine study (LOE 6)79 noted that administration of a vasoconstrictor before amiodarone prevented hypotension. A new aqueous formulation of amiodarone does not contain the vasoactive solvents (polysorbate 80 and benzyl alcohol) of the standard formulation. In an analysis of the combined data of 4 prospective clinical trials of patients with VT (some included hemodynamically unstable patients), aqueous amiodarone produced no more hypotension than lidocaine.77 In summary, amiodarone may be administered for VF or pulseless VT unresponsive to CPR, shock, and a vasopressor (Class IIb). An initial dose of 300 mg IV/IO can be followed by one dose of 150 mg IV/IO. Lidocaine The use of lidocaine for ventricular arrhythmias was supported by initial studies in animals (LOE 6)80,81 and extrapolation from the historic use of the drug to suppress premature ventricular contractions and prevent VF after acute myocardial infarction.82 Although lidocaine improved shortterm survival in 1 prehospital study (LOE 4),83 3 randomized trials comparing amiodarone and lidocaine found lower rates of ROSC73,84 and a higher incidence of asystole85 with use of lidocaine. The out-of-hospital double-blind randomized controlled trial (LOE 1)73 that compared amiodarone with lidocaine found that amiodarone improved rate of survival to hospital admission and that lidocaine was associated with more asystole after defibrillation. In summary, lidocaine is an alternative antiarrhythmic of long standing and widespread familiarity with fewer immediate side effects than may be encountered with other antiarrhythmics. Lidocaine, however, has no proven short-term or long-term efficacy in cardiac arrest. Lidocaine should be considered an alternative treatment to amiodarone (Class Indeterminate). The initial dose is 1 to 1.5 mg/kg IV. If VF/pulseless VT persists, additional doses of 0.5 to 0.75 mg/kg IV push may be administered at 5- to 10-minute intervals, to a maximum dose of 3 mg/kg. This is the same dose that was recommended in the ECC Guidelines 2000. Magnesium Two observational studies (LOE 5)86,87 showed that IV magnesium can effectively terminate torsades de pointes (irregular/polymorphic VT associated with prolonged QT interval). One small adult case series in adults (LOE 5)88 showed that isoproterenol or ventricular pacing can be effective in terminating torsades de pointes associated with bradycardia and drug-induced QT prolongation. Magnesium is not likely to be effective in terminating irregular/polymorphic VT in patients with a normal QT interval.87 When VF/pulseless VT cardiac arrest is associated with torsades de pointes, providers may administer magnesium sulfate at a dose of 1 to 2 g diluted in 10 mL D5W IV/IO push, typically over 5 to 20 minutes (Class IIa for torsades). When torsades is present in the patient with pulses, the same 1 to 2 g is mixed in 50 to 100 mL of D5W and given as a loading dose. It can be given more slowly (eg, over 5 to 60 minutes IV) under these conditions. See Part 7.3: “Management of Symptomatic Bradycardia and Tachycardia” for additional information about management of torsades de pointes not associated with cardiac arrest. Potentially Beneficial Therapies Fibrinolysis Adults have been successfully resuscitated following administration of fibrinolytics (tPA) after initial failure of standard CPR techniques, particularly when the condition leading to the arrest was acute pulmonary embolism or other presumed cardiac cause (LOE 389; LOE 490–92; LOE 593–97). Evidence from 1 large clinical trial (LOE 2),98 however, failed to show any significant treatment effect when a fibrinolytic (tPA) was given to out-of-hospital patients with undifferentiated PEA cardiac arrest unresponsive to initial interventions. Part 7.2: Management of Cardiac Arrest IV-63

IV-6 Circulation December 13. 2005 There is insufficient evidence to recommend for or against arrest, and the results of 4 animal studies (loe 623-126 were the routine use of fibrinolysis for cardiac arrest. It may be neutral. There is insufficient evidence to recommend routine considered on a case-by-case basis when pulmonary embolus administration of fluids to treat cardiac arrest(Class Indeter is suspected( Class Ila). Ongoing CPR is not a contraindica minate). Fluids should be infused if hypovolemia is tion to fibrinolysis. Interventions Not Supported by Summary Outcome evidence Ideally ACLS providers will prevent pulseless arrest if they Pacing in Arrest are able to intervene in the prearrest period. If arrest occurs, Several randomized controlled trials(LOE 2)99-101 failed good ACLS begins with high-quality BLS. During resuscita- show benefit from attempted pacing for asystole. At this time tion rescuers must provide good chest compressions(ade use of pacing for patients with asystolic cardiac arrest is not quate rate and depth), allow complete recoil of the chest between compressions, and minimize interruptions in chest compressions. Rescuers should be careful to avoid provision Procainamide in VF and Pulseless vt of excessive ventilation, particularly once an advanced ai Use of procainamide in cardiac arrest is supported by 1 way is in place. Resuscitation drugs have not been shown to retrospective comparison study of 20 patients. o2Administra- increase rate of survival to hospital discharge, and none has tion of procainamide in cardiac arrest is limited by the nee the impact of early and effective CPR and prompt for slow infusion and by uncertain efficacy in emergent defibrillation. References Norepinephrine I. Barsan WG. Levy RC. Weir H. Lidocaine levels during CPR: differences Norepinephrine has been studied in only a limited fashion for ater p mph., sentral venous, and intracardiac injections. treatment of cardiac arrest. human data is limited. but it 2. Kuhn G, White BC, Swetnam RE. Mumey JF, Rydesky MF, Tintinalli JE, suggests that norepinephrine produces effects equivalent epinephrine in the initial resuscitation of cardiac arrest. 53.10 3. Emerman CL, Pinchak AC, Hancock D. Hagen JF. Effect of injection site In the only prospective human trial comparing standard-dose epinephrine, high-dose epinephrine, and high-dose norepi- 4. Banerjee S, Singhi SC, Singh S, Singh M. The intraosseous route is a nephrine, the norepinephrine was associated with no benefit editor.1994:31:1511-1520 and a trend toward worse neurologic outcome (LOe 1).53 5. Brickman KR, Krupp K, Rega P, Alexander J, Guinness M. Typing and reening of blood from intraosseous access. Ann Emerg Med. 1992: 2 Precordial Thump for VF or Pulseless VT 6. Fiser RT, Walker WM, Seibert J, McCarthy R, Fiser DH. Tibial length There are no prospective studies that evaluated the use of 1997: 13: 186-188ospective, radiographic analysi precordial(chest) thump. In 3 case series(LOE 5), 04-06 VF 7. Ummenhofer w, Frei F, Urwyler A, Drewe J. Are laboratory values in or pulseless VT was converted to a perfusing rhythm by a editable for venous blood in paediatric patients? precordial thump. In contrast, other case series documented 8. Glaeser Pw, Hellmich TR, Szewczuga D, Losek JD, Smith DS Five-yea deterioration in cardiac rhythm, such as rate acceleration of 19-1124 VT, conversion of VT to VF, or development of complete heart block or asystole following the use of the thump (lOe Pediatr Surg. 1993: 28: 158-161 Phillips K, Pollack C Jr, Robinson DJ, Rumball C, Stair T. Tiffan The precordial thump is not recommended for BLS pro viders. In light of the limited evidence in support of its 11.EI H efficacy and reports of potential harm, no recommendation reterm and full term neonates. Arch Dis Child Fetal Neonatal Ed. 1999 80:F74-F75. can be made for or against its use by AClS providers(Class 12. Howard RF, Bingham RM. Endotrack mpared with intravenous 13. Lee PL, Chung YT, Lee BY, Yeh CY, Lin SY, Chao CC. Th the endotracheal route. Ma zui xue Za Zhi. 1989- 27:35-38 14. Prengel Aw. Lindner KH, Hahnel J. Ahn Electrolyte Therapies in Arrest Rhythms ma lidocaine cos eldt KK. Endobronchial application of In-hospital and out-of-hospital studies in adult cardiac arrest of hospital cardiopulmon Resuscitation. 2000: 47 (LOE 23-16: LOE 37; LOE 78)and animal studies ( lOe 6)119-l22 showed no increase in the rate of RoSC when ne in patients with severe cardiac disease. magnesium was routinely given during CPR. Administration Ann Intern Med. 2000: 132: 800-80 of magnesium can be considered for treatment of torsades de pointes( Class Ila-see above), but it is not effective for treatment of cardiac arrest from other causes 18. Brown LK. Diamond J. The ue to coronary art neal vs intravenous use. Proc West Routine Administration of Iv Fluids During endotracheal epinephrin Cardiac arrest of routine luin published human studies evaluating the effect 20. Wenzel V, Lindner KH, Prengel AW, Lurie KG, Strohmenger HU Endo- There were administration during normovolemic cardiac ation in pigs. Anesthesiology. 1997; 86: 1375-138

There is insufficient evidence to recommend for or against the routine use of fibrinolysis for cardiac arrest. It may be considered on a case-by-case basis when pulmonary embolus is suspected (Class IIa). Ongoing CPR is not a contraindication to fibrinolysis. Interventions Not Supported by Outcome Evidence Pacing in Arrest Several randomized controlled trials (LOE 2)99–101 failed to show benefit from attempted pacing for asystole. At this time use of pacing for patients with asystolic cardiac arrest is not recommended. Procainamide in VF and Pulseless VT Use of procainamide in cardiac arrest is supported by 1 retrospective comparison study of 20 patients.102 Administration of procainamide in cardiac arrest is limited by the need for slow infusion and by uncertain efficacy in emergent circumstances. Norepinephrine Norepinephrine has been studied in only a limited fashion for treatment of cardiac arrest. Human data is limited, but it suggests that norepinephrine produces effects equivalent to epinephrine in the initial resuscitation of cardiac arrest.53,103 In the only prospective human trial comparing standard-dose epinephrine, high-dose epinephrine, and high-dose norepinephrine, the norepinephrine was associated with no benefit and a trend toward worse neurologic outcome (LOE 1).53 Precordial Thump for VF or Pulseless VT There are no prospective studies that evaluated the use of precordial (chest) thump. In 3 case series (LOE 5),104–106 VF or pulseless VT was converted to a perfusing rhythm by a precordial thump. In contrast, other case series documented deterioration in cardiac rhythm, such as rate acceleration of VT, conversion of VT to VF, or development of complete heart block or asystole following the use of the thump (LOE 5105,107–111; LOE 6112). The precordial thump is not recommended for BLS providers. In light of the limited evidence in support of its efficacy and reports of potential harm, no recommendation can be made for or against its use by ACLS providers (Class Indeterminate). Electrolyte Therapies in Arrest Rhythms Magnesium In-hospital and out-of-hospital studies in adult cardiac arrest (LOE 2113–116; LOE 3117; LOE 7118) and animal studies (LOE 6)119–122 showed no increase in the rate of ROSC when magnesium was routinely given during CPR. Administration of magnesium can be considered for treatment of torsades de pointes (Class IIa—see above), but it is not effective for treatment of cardiac arrest from other causes. Routine Administration of IV Fluids During Cardiac Arrest There were no published human studies evaluating the effect of routine fluid administration during normovolemic cardiac arrest, and the results of 4 animal studies (LOE 6)123–126 were neutral. There is insufficient evidence to recommend routine administration of fluids to treat cardiac arrest (Class Indeterminate). Fluids should be infused if hypovolemia is suspected. Summary Ideally ACLS providers will prevent pulseless arrest if they are able to intervene in the prearrest period. If arrest occurs, good ACLS begins with high-quality BLS. During resuscitation rescuers must provide good chest compressions (adequate rate and depth), allow complete recoil of the chest between compressions, and minimize interruptions in chest compressions. Rescuers should be careful to avoid provision of excessive ventilation, particularly once an advanced airway is in place. Resuscitation drugs have not been shown to increase rate of survival to hospital discharge, and none has the impact of early and effective CPR and prompt defibrillation. References 1. Barsan WG, Levy RC, Weir H. Lidocaine levels during CPR: differences after peripheral venous, central venous, and intracardiac injections. Ann Emerg Med. 1981;10:73–78. 2. Kuhn GJ, White BC, Swetnam RE, Mumey JF, Rydesky MF, Tintinalli JE, Krome RL, Hoehner PJ. Peripheral vs central circulation times during CPR: a pilot study. Ann Emerg Med. 1981;10:417–419. 3. Emerman CL, Pinchak AC, Hancock D, Hagen JF. Effect of injection site on circulation times during cardiac arrest. Crit Care Med. 1988;16: 1138–1141. 4. Banerjee S, Singhi SC, Singh S, Singh M. The intraosseous route is a suitable alternative to intravenous route for fluid resuscitation in severely dehydrated children. Indian Pediatr. 1994;31:1511–1520. 5. Brickman KR, Krupp K, Rega P, Alexander J, Guinness M. Typing and screening of blood from intraosseous access. Ann Emerg Med. 1992;21: 414–417. 6. Fiser RT, Walker WM, Seibert JJ, McCarthy R, Fiser DH. Tibial length following intraosseous infusion: a prospective, radiographic analysis. Pediatr Emerg Care. 1997;13:186–188. 7. Ummenhofer W, Frei FJ, Urwyler A, Drewe J. Are laboratory values in bone marrow aspirate predictable for venous blood in paediatric patients? Resuscitation. 1994;27:123–128. 8. Glaeser PW, Hellmich TR, Szewczuga D, Losek JD, Smith DS. Five-year experience in prehospital intraosseous infusions in children and adults. Ann Emerg Med. 1993;22:1119–1124. 9. Guy J, Haley K, Zuspan SJ. Use of intraosseous infusion in the pediatric trauma patient. J Pediatr Surg. 1993;28:158–161. 10. Macnab A, Christenson J, Findlay J, Horwood B, Johnson D, Jones L, Phillips K, Pollack C Jr, Robinson DJ, Rumball C, Stair T, Tiffany B, Whelan M. A new system for sternal intraosseous infusion in adults. Prehosp Emerg Care. 2000;4:173–177. 11. Ellemunter H, Simma B, Trawoger R, Maurer H. Intraosseous lines in preterm and full term neonates. Arch Dis Child Fetal Neonatal Ed. 1999; 80:F74–F75. 12. Howard RF, Bingham RM. Endotracheal compared with intravenous administration of atropine. Arch Dis Child. 1990;65:449–450. 13. Lee PL, Chung YT, Lee BY, Yeh CY, Lin SY, Chao CC. The optimal dose of atropine via the endotracheal route. Ma Zui Xue Za Zhi. 1989;27:35–38. 14. Prengel AW, Lindner KH, Hahnel J, Ahnefeld FW. Endotracheal and endobronchial lidocaine administration: effects on plasma lidocaine concentration and blood gases. Crit Care Med. 1991;19:911–915. 15. Schmidbauer S, Kneifel HA, Hallfeldt KK. Endobronchial application of high dose epinephrine in out of hospital cardiopulmonary resuscitation. Resuscitation. 2000;47:89. 16. Raymondos K, Panning B, Leuwer M, Brechelt G, Korte T, Niehaus M, Tebbenjohanns J, Piepenbrock S. Absorption and hemodynamic effects of airway administration of adrenaline in patients with severe cardiac disease. Ann Intern Med. 2000;132:800–803. 17. Hahnel JH, Lindner KH, Schurmann C, Prengel A, Ahnefeld FW. Plasma lidocaine levels and PaO2 with endobronchial administration: dilution with normal saline or distilled water? Ann Emerg Med. 1990;19:1314–1317. 18. Brown LK, Diamond J. The efficacy of lidocaine in ventricular fibrillation due to coronary artery ligation: endotracheal vs intravenous use. Proc West Pharmacol Soc. 1982;25:43–45. 19. Jasani MS, Nadkarni VM, Finkelstein MS, Hofmann WT, Salzman SK. Inspiratory-cycle instillation of endotracheal epinephrine in porcine arrest. Acad Emerg Med. 1994;1:340–345. 20. Wenzel V, Lindner KH, Prengel AW, Lurie KG, Strohmenger HU. Endobronchial vasopressin improves survival during cardiopulmonary resuscitation in pigs. Anesthesiology. 1997;86:1375–1381. IV-64 Circulation December 13, 2005

Part 7.2: Management of Cardiac Arrest V-65 21. Prengel Aw, Rembecki M, Wenzel V, Steinbach G. A comparison of the 48. Tang W, Weil MH, Sun S, Noc M, Yang L, Gazmuri R. Pine ndotracheal tube and the laryngeal mask airway as a route for end increases the severity of postresuscitation myocardial dysfunction. M平 akelstein MS. Mandell GA, Salzman SK4.图W时 MY, Blake HC, McGeorge FT, Buderer NM. test. crit care med 19o4:22:1174-1180 g delivery. Pediatr Emerg Care. 1992: 8: 0. Lindner KH, Ahnefeld FW. Prengel Aw. Comparison of standard and Efrati O, Lotan D, Barzilay Z Scand.1991:35:253-256 aret G. Is endotracheal adrenaline deleterious because of the beta 23.mm2图 otan D. Berkovitch Endotracheal epinephrin 52. Stidy Group. N Engl J Med. 1992: 327: 1051-10% 52. Stiell IG. Hebert PC, Weitzman BN. Wells GA, Raman S. Stark RM rten A, Man- lay Z, Paret arinc an es n Med igg2 3 2: 04g-dss epinephrine in aduit 27. Elizn. 2003: 59: 117_esponse and haemodynamic effect in dogs. Resusci 53. Callaham M. Madsen CD. Barton Cw. Saunders CE. Pointer J. A Ben-Abraham R, Manisterski Y, Barak A. Efrati O. Lotan D, ard-dose epinephrine in prehospital cardiac arrest. JAMA. 1992: 268 beta blockade in a o71_276 beta blockade bestow any benefi 54 wilson w, Kobilski S, Scribante J, Lee C, Kraus P, Cooper J. 28. Niemann JT, Stratton SJ, Cruz B, Lewis R. Endotracheal drug adminis- diopulmonary resuscitation: a double-blind randomised trial. Anaesth 55. Choux C. Gueugniaud PY, Barbieux A. Pham E Lae C. Dubien PY, Petit eling BJ, Hornchen U, Kulka P. Suhling B, 56. Sherman BW, Munger MA, Foulke GE, Rutherford WF, Panacek EA High-dose versus standard-dose epinephrine treatment J. Stoeckel H. Eichelkraut tation ergnion M, Petit P, Carli P. A compa of repeated high 31. Naganobu K, Hasebe Y, Uchiyama Y, Hagio M, Ogawa H A comparison as9pLatoturopean Epinephrine Study Group. N Engl /Med.1998: 339 nest analg.200091:317-321. 58. Oyama H, Suzuki Y, Satoh S, Kajita Y, Takayasu M. Shibuya M, M so aid oky khn strdhgse ncr reb. eons per p P93325 er H. Hetzel WD. Ahnefe wy GA, Ou no Cw. Taren DL. Moon TE. Influence of d therapy on ventricular defibrillation in dogs. Crit Care Med. 1980: 8 157-163 60. Lindner KH. Dirks B Strg) 992: 77: 662-668 hmenger hu. prengel aw. Lindner IM. Lurie 34. Wik L, Hansen TB, Fylling F. Steen T, Vaagenes P, Auestad BH, Steen with ith out-of-hospital ventricular fibrillation: a randomized trial 61. Lindner KH, Prengel Aw, Brinkmann A Strohmenger HU, Lindner IM. AMA.2003:289:1389-1 35. American Heart Association in collaboration with the International liaison ommittee on Resuscitation Guidelines 2000 for Car ation and Emergency Cardiovascular Care: International Consensus on 6. Martens PR, Russell JK. Wolcke B. Paschen H, Kuisma M. Gliner BE 63. Morris DC. Der BE, Grzybowski M, Martin GB, Rivers EP Weaver WD. Bossaert L, Chamberlain D Wortsman J, Amico JA. Vasopressin can cardiac Arrest study: defibrillation waveform effects. Resuscitation. pressure during human cardiopulmonary resuscitation. Acad Emerg Med 01:49:233-243 37. Yu T, Weil MH, Tang W. Sun S, Klouche K, Povoas H, Bisera J. Adverse 64. Stiell IG. Hebert PC. Wells GA. Vandemheen KL, Tang AS, Higginson compression during automated defibrin- I I. Mason s. Klass Eftestol T, wik L, Sunde K, Steen PA. Effects of cardiopulmonary resus- 65. Wenzel V. Krismer AC. Amtz HR Sitter H, Stadlbauer KH, Lindner KH. 3 ea ing out-of-hospital cardiac arrest. Circulation. 2004: 1 10:10-15.cess resuscitation. N Engl J Med. 2004: 350: 105-113 hospital cardio- 66. Aung K, Htay pres a systematic review and tients with hospital cardiac arrest Circulation.2000102:1523-1529 67. Guyette FX, Guimond GE, Hostler D, Callaway CW. Vasopressin admin- 40. Eftestol T, Sunde K, Steen PA. Effects of interrupting precordial com rdiac arest res ss ted with a retum of a pulse in Bh(CD.k102103202d obability 8. Stueven HA, Tonsfeldt DJ, Thompson BM, Whitcomb J, 41. Yakaitis of a and B Aprahamian C. Atropine in asystole: human studies. Ann Emerg Med. 69. Brown DC. Lewis Aj. Cril iedermeyer E, Rogers MC, Traystman R, Weisfeldt ML Mechanisms by hich epinephrine augments cerebral and myocardial perfusion during 1979: 8: 448-p52mpalheaey JM. Asystole and its treatment: the possible 70. Coon GA, Clinton JE, Ruiz E. Use of atropine for bradyasystolic pre- 71. DeBehnke DJ, Swart GL, Spreng D, Aufderheide TP. Standard and higher oses of atropine in a canine model of pulseless electrical activity. Acad 72. Kudenchuk PJ, Cobb LA, Copass MK, Cummins RO, Doherty AM, Fahr GA. A randomized, blinded trial of high-dose epinephrine P, Ewy bruch CE. Hallstrom AP, Murray WA. Olsufka M. Walsh T. Amiod epinephrine in a swine model of pediatric asphyxial itation after out-of-hospital cardiac arrest due to ventri arrest. Crit Care Med. 1996: 24: 16 ardial 73. Dorian P Cass D, Schwartz B, Cooper R, Gelaznikas R. Barr A. Amiod- CG. Effect of standard-dose versus high-dose epinephrine on myoca fibrillation and closed-ck NEr 346: 884r shock-resistant ventricular fibril- 46. Hormchen U, Lussi C, Schuttler J. Potential risks of high-dose epinephrine 74. Skrifvars MB, Kuisma M, Boyd J, Maatta T, Repo J, Rosenberg Pl or resuscitation from ventricular fibrillation in a porcine model. JCar- thorac Vasc Anesth. 1993- 7. 1 75. Pe-hospital cardiac arrest. Acta Anaesthesiol Scand. 2004: 48: 582-587. rma J. Lewis R. Treatment 76. Levine JH. Massumi A. Scheinman MM, Winkle RA, Platia EV. Chilso rine and CPR preceding countershock. Circulation. 1992: 85: 281-2 A, Gomes A, Woosley RL Intravenous amiodarone for recurrent sus-

21. Prengel AW, Rembecki M, Wenzel V, Steinbach G. A comparison of the endotracheal tube and the laryngeal mask airway as a route for endobronchial lidocaine administration. Anesth Analg. 2001;92:1505–1509. 22. Jasani MS, Nadkarni VM, Finkelstein MS, Mandell GA, Salzman SK, Norman ME. Effects of different techniques of endotracheal epinephrine administration in pediatric porcine hypoxic-hypercarbic cardiopulmonary arrest. Crit Care Med. 1994;22:1174–1180. 23. Johnston C. Endotracheal drug delivery. Pediatr Emerg Care. 1992;8: 94–97. 24. Vaknin Z, Manisterski Y, Ben-Abraham R, Efrati O, Lotan D, Barzilay Z, Paret G. Is endotracheal adrenaline deleterious because of the beta adrenergic effect? Anesth Analg. 2001;92:1408–1412. 25. Manisterski Y, Vaknin Z, Ben-Abraham R, Efrati O, Lotan D, Berkovitch M, Barak A, Barzilay Z, Paret G. Endotracheal epinephrine: a call for larger doses. Anesth Analg. 2002;95:1037–1041. 26. Efrati O, Ben-Abraham R, Barak A, Modan-Moses D, Augarten A, Manisterski Y, Barzilay Z, Paret G. Endobronchial adrenaline: should it be reconsidered? Dose response and haemodynamic effect in dogs. Resuscitation. 2003;59:117–122. 27. Elizur A, Ben-Abraham R, Manisterski Y, Barak A, Efrati O, Lotan D, Barzilay Z, Paret G. Tracheal epinephrine or norepinephrine preceded by beta blockade in a dog model: can beta blockade bestow any benefits? Resuscitation. 2003;59:271–276. 28. Niemann JT, Stratton SJ, Cruz B, Lewis RJ. Endotracheal drug administration during out-of-hospital resuscitation: where are the survivors? Resuscitation. 2002;53:153–157. 29. Schuttler J, Bartsch A, Ebeling BJ, Hornchen U, Kulka P, Suhling B, Stoeckel H. [Endobronchial administration of adrenaline in preclinical cardiopulmonary resuscitation.] Anasth Intensivther Notfallmed. 1987;22: 63–68. 30. Hornchen U, Schuttler J, Stoeckel H, Eichelkraut W, Hahn N. Endobronchial instillation of epinephrine during cardiopulmonary resuscitation. Crit Care Med. 1987;15:1037–1039. 31. Naganobu K, Hasebe Y, Uchiyama Y, Hagio M, Ogawa H. A comparison of distilled water and normal saline as diluents for endobronchial administration of epinephrine in the dog. Anesth Analg. 2000;91:317–321. 32. Cobb LA, Fahrenbruch CE, Walsh TR, Copass MK, Olsufka M, Breskin M, Hallstrom AP. Influence of cardiopulmonary resuscitation prior to defibrillation in patients with out-of-hospital ventricular fibrillation. JAMA. 1999;281:1182–1188. 33. Yakaitis RW, Ewy GA, Otto CW, Taren DL, Moon TE. Influence of time and therapy on ventricular defibrillation in dogs. Crit Care Med. 1980;8: 157–163. 34. Wik L, Hansen TB, Fylling F, Steen T, Vaagenes P, Auestad BH, Steen PA. Delaying defibrillation to give basic cardiopulmonary resuscitation to patients with out-of-hospital ventricular fibrillation: a randomized trial. JAMA. 2003;289:1389–1395. 35. American Heart Association in collaboration with the International Liaison Committee on Resuscitation. Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care: International Consensus on Science. Circulation. 2000;102:I1–I384. 36. Martens PR, Russell JK, Wolcke B, Paschen H, Kuisma M, Gliner BE, Weaver WD, Bossaert L, Chamberlain D, Schneider T. Optimal Response to Cardiac Arrest study: defibrillation waveform effects. Resuscitation. 2001;49:233–243. 37. Yu T, Weil MH, Tang W, Sun S, Klouche K, Povoas H, Bisera J. Adverse outcomes of interrupted precordial compression during automated defibrillation. Circulation. 2002;106:368–372. 38. Eftestol T, Wik L, Sunde K, Steen PA. Effects of cardiopulmonary resuscitation on predictors of ventricular fibrillation defibrillation success during out-of-hospital cardiac arrest. Circulation. 2004;110:10–15. 39. Eftestol T, Sunde K, Aase SO, Husoy JH, Steen PA. Predicting outcome of defibrillation by spectral characterization and nonparametric classification of ventricular fibrillation in patients with out-of-hospital cardiac arrest. Circulation. 2000;102:1523–1529. 40. Eftestol T, Sunde K, Steen PA. Effects of interrupting precordial compressions on the calculated probability of defibrillation success during out-of-hospital cardiac arrest. Circulation. 2002;105:2270–2273. 41. Yakaitis RW, Otto CW, Blitt CD. Relative importance of and adrenergic receptors during resuscitation. Crit Care Med. 1979;7:293–296. 42. Michael JR, Guerci AD, Koehler RC, Shi AY, Tsitlik J, Chandra N, Niedermeyer E, Rogers MC, Traystman RJ, Weisfeldt ML. Mechanisms by which epinephrine augments cerebral and myocardial perfusion during cardiopulmonary resuscitation in dogs. Circulation. 1984;69:822–835. 43. Ditchey RV, Lindenfeld J. Failure of epinephrine to improve the balance between myocardial oxygen supply and demand during closed-chest resuscitation in dogs. Circulation. 1988;78:382–389. 44. Berg RA, Otto CW, Kern KB, Hilwig RW, Sanders AB, Henry CP, Ewy GA. A randomized, blinded trial of high-dose epinephrine versus standard-dose epinephrine in a swine model of pediatric asphyxial cardiac arrest. Crit Care Med. 1996;24:1695–1700. 45. Hoekstra JW, Griffith R, Kelley R, Cody RJ, Lewis D, Scheatzle M, Brown CG. Effect of standard-dose versus high-dose epinephrine on myocardial high-energy phosphates during ventricular fibrillation and closed-chest CPR. Ann Emerg Med. 1993;22:1385–1391. 46. Hornchen U, Lussi C, Schuttler J. Potential risks of high-dose epinephrine for resuscitation from ventricular fibrillation in a porcine model. J Cardiothorac Vasc Anesth. 1993;7:184–187. 47. Niemann JT, Cairns CB, Sharma J, Lewis RJ. Treatment of prolonged ventricular fibrillation: immediate countershock versus high-dose epinephrine and CPR preceding countershock. Circulation. 1992;85:281–287. 48. Tang W, Weil MH, Sun S, Noc M, Yang L, Gazmuri RJ. Epinephrine increases the severity of postresuscitation myocardial dysfunction. Circulation. 1995;92:3089–3093. 49. Rivers EP, Wortsman J, Rady MY, Blake HC, McGeorge FT, Buderer NM. The effect of the total cumulative epinephrine dose administered during human CPR on hemodynamic, oxygen transport, and utilization variables in the postresuscitation period. Chest. 1994;106:1499–1507. 50. Lindner KH, Ahnefeld FW, Prengel AW. Comparison of standard and high-dose adrenaline in the resuscitation of asystole and electromechanical dissociation. Acta Anaesthesiol Scand. 1991;35:253–256. 51. Brown CG, Martin DR, Pepe PE, Stueven H, Cummins RO, Gonzalez E, Jastremski M. A comparison of standard-dose and high-dose epinephrine in cardiac arrest outside the hospital: the Multicenter High-Dose Epinephrine Study Group. N Engl J Med. 1992;327:1051–1055. 52. Stiell IG, Hebert PC, Weitzman BN, Wells GA, Raman S, Stark RM, Higginson LA, Ahuja J, Dickinson GE. High-dose epinephrine in adult cardiac arrest. N Engl J Med. 1992;327:1045–1050. 53. Callaham M, Madsen CD, Barton CW, Saunders CE, Pointer J. A randomized clinical trial of high-dose epinephrine and norepinephrine vs standard-dose epinephrine in prehospital cardiac arrest. JAMA. 1992;268: 2667–2672. 54. Lipman J, Wilson W, Kobilski S, Scribante J, Lee C, Kraus P, Cooper J, Barr J, Moyes D. High-dose adrenaline in adult in-hospital asystolic cardiopulmonary resuscitation: a double-blind randomised trial. Anaesth Intensive Care. 1993;21:192–196. 55. Choux C, Gueugniaud PY, Barbieux A, Pham E, Lae C, Dubien PY, Petit P. Standard doses versus repeated high doses of epinephrine in cardiac arrest outside the hospital. Resuscitation. 1995;29:3–9. 56. Sherman BW, Munger MA, Foulke GE, Rutherford WF, Panacek EA. High-dose versus standard-dose epinephrine treatment of cardiac arrest after failure of standard therapy. Pharmacotherapy. 1997;17:242–247. 57. Gueugniaud PY, Mols P, Goldstein P, Pham E, Dubien PY, Deweerdt C, Vergnion M, Petit P, Carli P. A comparison of repeated high doses and repeated standard doses of epinephrine for cardiac arrest outside the hospital. European Epinephrine Study Group. N Engl J Med. 1998;339: 1595–1601. 58. Oyama H, Suzuki Y, Satoh S, Kajita Y, Takayasu M, Shibuya M, Sugita K. Role of nitric oxide in the cerebral vasodilatory responses to vasopressin and oxytocin in dogs. J Cereb Blood Flow Metab. 1993;13:285–290. 59. Lindner KH, Strohmenger HU, Ensinger H, Hetzel WD, Ahnefeld FW, Georgieff M. Stress hormone response during and after cardiopulmonary resuscitation. Anesthesiology. 1992;77:662–668. 60. Lindner KH, Dirks B, Strohmenger HU, Prengel AW, Lindner IM, Lurie KG. Randomised comparison of epinephrine and vasopressin in patients with out-of-hospital ventricular fibrillation. Lancet. 1997;349:535–537. 61. Lindner KH, Prengel AW, Brinkmann A, Strohmenger HU, Lindner IM, Lurie KG. Vasopressin administration in refractory cardiac arrest. Ann Intern Med. 1996;124:1061–1064. 62. Mann K, Berg RA, Nadkarni V. Beneficial effects of vasopressin in prolonged pediatric cardiac arrest: a case series. Resuscitation. 2002;52: 149–156. 63. Morris DC, Dereczyk BE, Grzybowski M, Martin GB, Rivers EP, Wortsman J, Amico JA. Vasopressin can increase coronary perfusion pressure during human cardiopulmonary resuscitation. Acad Emerg Med. 1997;4:878–883. 64. Stiell IG, Hebert PC, Wells GA, Vandemheen KL, Tang AS, Higginson LA, Dreyer JF, Clement C, Battram E, Watpool I, Mason S, Klassen T, Weitzman BN. Vasopressin versus epinephrine for inhospital cardiac arrest: a randomised controlled trial. Lancet. 2001;358:105–109. 65. Wenzel V, Krismer AC, Arntz HR, Sitter H, Stadlbauer KH, Lindner KH. A comparison of vasopressin and epinephrine for out-of-hospital cardiopulmonary resuscitation. N Engl J Med. 2004;350:105–113. 66. Aung K, Htay T. Vasopressin for cardiac arrest: a systematic review and meta-analysis. Arch Intern Med. 2005;165:17–24. 67. Guyette FX, Guimond GE, Hostler D, Callaway CW. Vasopressin administered with epinephrine is associated with a return of a pulse in out-ofhospital cardiac arrest. Resuscitation. 2004;63:277–282. 68. Stueven HA, Tonsfeldt DJ, Thompson BM, Whitcomb J, Kastenson E, Aprahamian C. Atropine in asystole: human studies. Ann Emerg Med. 1984;13:815–817. 69. Brown DC, Lewis AJ, Criley JM. Asystole and its treatment: the possible role of the parasympathetic nervous system in cardiac arrest. JACEP. 1979;8:448–452. 70. Coon GA, Clinton JE, Ruiz E. Use of atropine for bradyasystolic prehospital cardiac arrest. Ann Emerg Med. 1981;10:462–467. 71. DeBehnke DJ, Swart GL, Spreng D, Aufderheide TP. Standard and higher doses of atropine in a canine model of pulseless electrical activity. Acad Emerg Med. 1995;2:1034–1041. 72. Kudenchuk PJ, Cobb LA, Copass MK, Cummins RO, Doherty AM, Fahrenbruch CE, Hallstrom AP, Murray WA, Olsufka M, Walsh T. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation. N Engl J Med. 1999;341:871–878. 73. Dorian P, Cass D, Schwartz B, Cooper R, Gelaznikas R, Barr A. Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation. N Engl J Med. 2002;346:884–890. 74. Skrifvars MB, Kuisma M, Boyd J, Maatta T, Repo J, Rosenberg PH, Castren M. The use of undiluted amiodarone in the management of outof-hospital cardiac arrest. Acta Anaesthesiol Scand. 2004;48:582–587. 75. Petrovic T, Adnet F, Lapandry C. Successful resuscitation of ventricular fibrillation after low-dose amiodarone. Ann Emerg Med. 1998;32:518–519. 76. Levine JH, Massumi A, Scheinman MM, Winkle RA, Platia EV, Chilson DA, Gomes A, Woosley RL. Intravenous amiodarone for recurrent susPart 7.2: Management of Cardiac Arrest IV-65

lV-66 Circulation December 13, 2005 tained hypotensive ventricular tac Amiodarone 77. Somberg JC, Bailin SJ, Haffajee CI Paladino Wp. 99. Hedges JR, Syverud SA, Dalsey wC, Feero S, Easter R, Shultz B. Pre 98776:1337-1343 100. Barthel E. Troiano P, Olson D, Stueven HA, a prospective, controlled clinical Med.1988:17:1221-1 78. Somberg JC, Timar S, Bailin SJ, Lakatos F, Haffajee CI, Tarjan J Paladino en MP WP. Sarosi I. Kerin NZ, Borbola J, Bridges DE, Molnar J. Lack of J. Nicola RM. Horan S. Out-o aqueous f n.m下P3 V Engle med. 1993- 328: 1377-1382 lic card man S Cardoso LF 102. Stiell IG. Wells bert PC, Laupacis A, Weitzman BN. Association of drug therapy with survival in cardiac arrest: limited role of advanced lac life support drugs. Acad Emerg Med. 1995: 2: 264-273 103. Lindner KH. Ahnefeld FW. Bowd suscitation succe resuscitation in a pig model. Am J Emerg Ma.1919 during experimental myocardial infarction. Am j Cardiol.1976:37:860-863. 104. Befeler B. Mechanical stimulation of the heart; its therapeutic value in fibrillation threshold in the dog during acute ischemia and prematur Allege R, Arnberg 公Am)90边 heart stimulation ngI J Med.1974291:1324-13 fence of the precordial thump and cough version. BMJ. 1985 83. Herlitz J, Bang A, Holmberg M, Axelsson A. Lindkvist J. Holmberg S. 107. Morgera T, Baldi N, Chersevani D, Medugno G, Camerini F Chest thump elation to delay until 108. Rahner E, Z chlag ycardias by 84. Kentsch M. Berkel H. Bleifeld w. Intravenose Amio plication bei 85. Weaver WD. Fahrenbruch CE. Johnson DD, Hallstrom AP, Cobb LA. 109. Gertsch M, Hottinger S, Hess T. Serial chest thumps for the treatment of ar tachycardia in patients with coronary artery disease. Clin I11. Sclarovsky S, Kracoff OH, Agmon J. Acceleration of ventricular magnesium in recurrent persistent ventricular tachycardia. New Trends in Tzivoni D. Banai S, Schuger C, Benhorin J, Keren A, Gottlieb S, Stern S. Treatment of torsade de pointes with magnesium sulfate. Circulation 113. Thel MC, Armstrong AL. McNulty SE, Califf RM, O"Connor CM. R: von D. Gavish D. Levi Gottlieb S. Benhonin J. Stern sspitazcarzz6 amrest. Duke Etiology, warning signs and therapy of torsade de pointes: a study of 10 I 14. Allegra J, Lavery R, Cody R, Birnbaum G. Brennan J, Har atients. Circulation. 1981: 64 Bode C, Kern S Gries A, Gust R, Glatzer R. Bauer H ctory ventricular fibrillation in the prehospital setting itially unsuccessful cardiopulmonary resuscitation: a prospective clinica 1 15. Fatovich D, Prentice D, Dobb G. Magnesium in in-hospital cardiac arrest. 以红2邮 Kroesen G. Aubin M. Recom-16mm段到BmB人m trial to investigate the in 108 patients with out-of-hospital cardiac arrest. Resuscitation. 2001: 50- phate for refractory ventricular fibrillation 91. Lederer W. Lichtenberger C, Pechlaner C, Kinzl J, Kroesen G, Baubin M. 1Cm已 Pilot study of intravenous magnesium sulfate in refractory cardiac arrest: safety data and recommendations for activator during oul-of-hospital cardiac 118. Longstreth WT Jr, Fahrenbruch CE, Olsulka M. Walsh TR, Copass MK, 119. Siemkowicz E 93. Scholz KH, Hilmer T, Schuster S. Wojcik J, Kreuzer H, Tebbe U.Throm- 120. Brown Ce faith RF, Neely D, Hobson J, Mill uscitated patients with pulmonary embolism. Dtsch Mec coronary Wochenschr.1990:115:930-935 94. Klefisch F, et al. Praklinische ultima-ratio thrombolyse bei therap 21. Seaberg DC. Menegazzi JJ, Check B, MacLeod BA, Yealy DM. kardiopulmonaler reanimation. Intensivmedizin 5-162. 95. Tiffany PA, Schultz M, Stueven H. Bolus thrombolytic infusions during 122 ctory arrest rhythms: outcome of a agnesium reduces free radical concentration and preserves left ventric Thrombolytika in der Reanimation als Ultima ratio zur Uberwindung des 123. Ditchey RV, Lindenfeld J. Potential adverse effects of volum perfusion of vital organs during closed-chest resuscitation. Circulation behandlung.1991;16:134-1 le NT, Martin GB, Appleton TJ, Moeggenberg J, Paradis NA. Nowak coronary perfuse thrombolysis in patients with acute myocardial infarction requiring cardio- pressures during canine CPR Resuscitation. 1991: 22: 55-63 125. Jameson eek CA. Wanger KP, useless electrical activity. N Engl J Med. 2002 346: 1522-1528. taton.1987:15:11

tained hypotensive ventricular tachyarrhythmias. Intravenous Amiodarone Multicenter Trial Group. J Am Coll Cardiol. 1996;27:67–75. 77. Somberg JC, Bailin SJ, Haffajee CI, Paladino WP, Kerin NZ, Bridges D, Timar S, Molnar J. Intravenous lidocaine versus intravenous amiodarone (in a new aqueous formulation) for incessant ventricular tachycardia. Am J Cardiol. 2002;90:853–859. 78. Somberg JC, Timar S, Bailin SJ, Lakatos F, Haffajee CI, Tarjan J, Paladino WP, Sarosi I, Kerin NZ, Borbola J, Bridges DE, Molnar J. Lack of a hypotensive effect with rapid administration of a new aqueous formulation of intravenous amiodarone. Am J Cardiol. 2004;93:576–581. 79. Paiva EF, Perondi MB, Kern KB, Berg RA, Timerman S, Cardoso LF, Ramirez JA. Effect of amiodarone on haemodynamics during cardiopulmonary resuscitation in a canine model of resistant ventricular fibrillation. Resuscitation. 2003;58:203–208. 80. Borer JS, Harrison LA, Kent KM, Levy R, Goldstein RE, Epstein SE. Beneficial effect of lidocaine on ventricular electrical stability and spontaneous ventricular fibrillation during experimental myocardial infarction. Am J Cardiol. 1976;37:860–863. 81. Spear JF, Moore EN, Gerstenblith G. Effect of lidocaine on the ventricular fibrillation threshold in the dog during acute ischemia and premature ventricular contractions. Circulation. 1972;46:65–73. 82. Lie KI, Wellens HJ, van Capelle FJ, Durrer D. Lidocaine in the prevention of primary ventricular fibrillation: a double-blind, randomized study of 212 consecutive patients. N Engl J Med. 1974;291:1324–1326. 83. Herlitz J, Bang A, Holmberg M, Axelsson A, Lindkvist J, Holmberg S. Rhythm changes during resuscitation from ventricular fibrillation in relation to delay until defibrillation, number of shocks delivered and survival. Resuscitation. 1997;34:17–22. 84. Kentsch M, Berkel H, Bleifeld W. Intravenose Amiodaron-Applikation bei therapierefraktarem Kammerflimmern. Intensivmedizin. 1988;25:70–74. 85. Weaver WD, Fahrenbruch CE, Johnson DD, Hallstrom AP, Cobb LA, Copass MK. Effect of epinephrine and lidocaine therapy on outcome after cardiac arrest due to ventricular fibrillation. Circulation. 1990;82: 2027–2034. 86. Manz M, Pfeiffer D, Jung W, Lueritz B. Intravenous treatment with magnesium in recurrent persistent ventricular tachycardia. New Trends in Arrhythmias. 1991;7:437–442. 87. Tzivoni D, Banai S, Schuger C, Benhorin J, Keren A, Gottlieb S, Stern S. Treatment of torsade de pointes with magnesium sulfate. Circulation. 1988;77:392–397. 88. Keren A, Tzivoni D, Gavish D, Levi J, Gottlieb S, Benhorin J, Stern S. Etiology, warning signs and therapy of torsade de pointes: a study of 10 patients. Circulation. 1981;64:1167–1174. 89. Bottiger BW, Bode C, Kern S, Gries A, Gust R, Glatzer R, Bauer H, Motsch J, Martin E. Efficacy and safety of thrombolytic therapy after initially unsuccessful cardiopulmonary resuscitation: a prospective clinical trial. Lancet. 2001;357:1583–1585. 90. Lederer W, Lichtenberger C, Pechlaner C, Kroesen G, Baubin M. Recombinant tissue plasminogen activator during cardiopulmonary resuscitation in 108 patients with out-of-hospital cardiac arrest. Resuscitation. 2001;50: 71–76. 91. Lederer W, Lichtenberger C, Pechlaner C, Kinzl J, Kroesen G, Baubin M. Long-term survival and neurological outcome of patients who received recombinant tissue plasminogen activator during out-of-hospital cardiac arrest. Resuscitation. 2004;61:123–129. 92. Janata K, Holzer M, Kurkciyan I, Losert H, Riedmuller E, Pikula B, Laggner AN, Laczika K. Major bleeding complications in cardiopulmonary resuscitation: the place of thrombolytic therapy in cardiac arrest due to massive pulmonary embolism. Resuscitation. 2003;57:49–55. 93. Scholz KH, Hilmer T, Schuster S, Wojcik J, Kreuzer H, Tebbe U. Thrombolysis in resuscitated patients with pulmonary embolism. Dtsch Med Wochenschr. 1990;115:930–935. 94. Klefisch F, et al. Praklinische ultima-ratio thrombolyse bei therapierefraktarer kardiopulmonaler reanimation. Intensivmedizin. 1995;32: 155–162. 95. Tiffany PA, Schultz M, Stueven H. Bolus thrombolytic infusions during CPR for patients with refractory arrest rhythms: outcome of a case series. Ann Emerg Med. 1998;31:124–126. 96. Gramann J, Lange-Braun P, Bodemann T, Hochrein H. Der Einsatz von Thrombolytika in der Reanimation als Ultima ratio zur Überwindung des Herztodes. Intensiv-und Notfallbehandlung. 1991;16:134–137. 97. Ruiz-Bailen M, Aguayo de Hoyos E, Serrano-Corcoles MC, DiazCastellanos MA, Ramos-Cuadra JA, Reina-Toral A. Efficacy of thrombolysis in patients with acute myocardial infarction requiring cardiopulmonary resuscitation. Intensive Care Med. 2001;27:1050–1057. 98. Abu-Laban RB, Christenson JM, Innes GD, van Beek CA, Wanger KP, McKnight RD, MacPhail IA, Puskaric J, Sadowski RP, Singer J, Schechter MT, Wood VM. Tissue plasminogen activator in cardiac arrest with pulseless electrical activity. N Engl J Med. 2002;346:1522–1528. 99. Hedges JR, Syverud SA, Dalsey WC, Feero S, Easter R, Shultz B. Prehospital trial of emergency transcutaneous cardiac pacing. Circulation. 1987;76:1337–1343. 100. Barthell E, Troiano P, Olson D, Stueven HA, Hendley G. Prehospital external cardiac pacing: a prospective, controlled clinical trial. Ann Emerg Med. 1988;17:1221–1226. 101. Cummins RO, Graves JR, Larsen MP, Hallstrom AP, Hearne TR, Ciliberti J, Nicola RM, Horan S. Out-of-hospital transcutaneous pacing by emergency medical technicians in patients with asystolic cardiac arrest. N Engl J Med. 1993;328:1377–1382. 102. Stiell IG, Wells GA, Hebert PC, Laupacis A, Weitzman BN. Association of drug therapy with survival in cardiac arrest: limited role of advanced cardiac life support drugs. Acad Emerg Med. 1995;2:264–273. 103. Lindner KH, Ahnefeld FW, Bowdler IM. Comparison of different doses of epinephrine on myocardial perfusion and resuscitation success during cardiopulmonary resuscitation in a pig model. Am J Emerg Med. 1991;9: 27–31. 104. Befeler B. Mechanical stimulation of the heart; its therapeutic value in tachyarrhythmias. Chest. 1978;73:832–838. 105. Volkmann HK, Klumbies A, Kühnert H, Paliege R, Dannberg G, Siegert K. [Terminating ventricular tachycardias by mechanical heart stimulation with precordial thumps.] Z Kardiol. 1990;79:717–724. 106. Caldwell G, Millar G, Quinn E. Simple mechanical methods for cardioversion: defence of the precordial thump and cough version. BMJ. 1985; 291:627–630. 107. Morgera T, Baldi N, Chersevani D, Medugno G, Camerini F. Chest thump and ventricular tachycardia. Pacing Clin Electrophysiol. 1979;2:69–75. 108. Rahner E, Zeh E. Die Regularisierung von Kammertachykardien durch präkordialen Faustschlag [The regularization of ventricular tachycardias by precordial thumping]. Medizinsche Welt. 1978;29:1659–1663. 109. Gertsch M, Hottinger S, Hess T. Serial chest thumps for the treatment of ventricular tachycardia in patients with coronary artery disease. Clin Cardiol. 1992;15:181–188. 110. Krijne R. Rate acceleration of ventricular tachycardia after a precordial chest thump. Am J Cardiol. 1984;53:964–965. 111. Sclarovsky S, Kracoff OH, Agmon J. Acceleration of ventricular tachycardia induced by a chest thump. Chest. 1981;80:596–599. 112. Yakaitis RW, Redding JS. Precordial thumping during cardiac resuscitation. Crit Care Med. 1973;1:22–26. 113. Thel MC, Armstrong AL, McNulty SE, Califf RM, O’Connor CM. Randomised trial of magnesium in in-hospital cardiac arrest. Duke Internal Medicine Housestaff. Lancet. 1997;350:1272–1276. 114. Allegra J, Lavery R, Cody R, Birnbaum G, Brennan J, Hartman A, Horowitz M, Nashed A, Yablonski M. Magnesium sulfate in the treatment of refractory ventricular fibrillation in the prehospital setting. Resuscitation. 2001;49:245–249. 115. Fatovich D, Prentice D, Dobb G. Magnesium in in-hospital cardiac arrest. Lancet. 1998;351:446. 116. Hassan TB, Jagger C, Barnett DB. A randomised trial to investigate the efficacy of magnesium sulphate for refractory ventricular fibrillation. Emerg Med J. 2002;19:57–62. 117. Miller B, Craddock L, Hoffenberg S, Heinz S, Lefkowitz D, Callender ML, Battaglia C, Maines C, Masick D. Pilot study of intravenous magnesium sulfate in refractory cardiac arrest: safety data and recommendations for future studies. Resuscitation. 1995;30:3–14. 118. Longstreth WT Jr, Fahrenbruch CE, Olsufka M, Walsh TR, Copass MK, Cobb LA. Randomized clinical trial of magnesium, diazepam, or both after out-of-hospital cardiac arrest. Neurology. 2002;59:506–514. 119. Siemkowicz E. Magnesium sulfate solution dramatically improves immediate recovery of rats from hypoxia. Resuscitation. 1997;35:53–59. 120. Brown CG, Griffith RF, Neely D, Hobson J, Miller B. The effect of intravenous magnesium administration on aortic, right atrial and coronary perfusion pressures during CPR in swine. Resuscitation. 1993;26:3–12. 121. Seaberg DC, Menegazzi JJ, Check B, MacLeod BA, Yealy DM. Use of a cardiocerebral-protective drug cocktail prior to countershock in a porcine model of prolonged ventricular fibrillation. Resuscitation. 2001;51: 301–308. 122. Zhang Y, Davies LR, Martin SM, Bawaney IM, Buettner GR, Kerber RE. Magnesium reduces free radical concentration and preserves left ventricular function after direct current shocks. Resuscitation. 2003;56:199–206. 123. Ditchey RV, Lindenfeld J. Potential adverse effects of volume loading on perfusion of vital organs during closed-chest resuscitation. Circulation. 1984;69:181–189. 124. Gentile NT, Martin GB, Appleton TJ, Moeggenberg J, Paradis NA, Nowak RM. Effects of arterial and venous volume infusion on coronary perfusion pressures during canine CPR. Resuscitation. 1991;22:55–63. 125. Jameson SJ, Mateer JR, DeBehnke DJ. Early volume expansion during cardiopulmonary resuscitation. Resuscitation. 1993;26:243–250. 126. Voorhees WD, Ralston SH, Kougias C, Schmitz PM. Fluid loading with whole blood or Ringer’s lactate solution during CPR in dogs. Resuscitation. 1987;15:113–123. IV-66 Circulation December 13, 2005

点击进入文档下载页（PDF格式）

已到末页，全文结束

点击下载（PDF格式）

浏览记录