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 im￾proved 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 nonran￾domized 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 epineph￾rine 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 inexpen￾sive, easy to administer, and has few side effects and therefore can be considered for asystole or PEA. The recom￾mended 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 chan￾nels 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 docu￾mented 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 ami￾odarone 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 unsta￾ble patients), aqueous amiodarone produced no more hypo￾tension 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 sup￾ported by initial studies in animals (LOE 6)80,81 and extrap￾olation from the historic use of the drug to suppress prema￾ture ventricular contractions and prevent VF after acute myocardial infarction.82 Although lidocaine improved short￾term 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 con￾trolled trial (LOE 1)73 that compared amiodarone with lido￾caine 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 imme￾diate side effects than may be encountered with other antiar￾rhythmics. 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 effec￾tive in terminating torsades de pointes associated with bra￾dycardia 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 Symp￾tomatic Bradycardia and Tachycardia” for additional infor￾mation about management of torsades de pointes not associ￾ated with cardiac arrest. Potentially Beneficial Therapies Fibrinolysis Adults have been successfully resuscitated following admin￾istration 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