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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 ofwill 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