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Background: During the administration of advanced cardiac life support for resuscitation from cardiac arrest, a combination of vasopressin and epinephrine may be more effective than epinephrine or vasopressin alone, but evidence is insufficient to make clinical recommendations., Methods: In a multicenter study, we randomly assigned adults with out-of-hospital cardiac arrest to receive successive injections of either 1 mg of epinephrine and 40 IU of vasopressin or 1 mg of epinephrine and saline placebo, followed by administration of the same combination of study drugs if spontaneous circulation was not restored and subsequently by additional epinephrine if needed. The primary end point was survival to hospital admission; the secondary end points were return of spontaneous circulation, survival to hospital discharge, good neurologic recovery, and 1-year survival., Results: A total of 1442 patients were assigned to receive a combination of epinephrine and vasopressin, and 1452 to receive epinephrine alone. The treatment groups had similar baseline characteristics except that there were more men in the group receiving combination therapy than in the group receiving epinephrine alone (P=0.03). There were no significant differences between the combination-therapy and the epinephrine-only groups in survival to hospital admission (20.7% vs. 21.3%; relative risk of death, 1.01; 95% confidence interval [CI], 0.97 to 1.05), return of spontaneous circulation (28.6% vs. 29.5%; relative risk, 1.01; 95% CI, 0.97 to 1.06), survival to hospital discharge (1.7% vs. 2.3%; relative risk, 1.01; 95% CI, 1.00 to 1.02), 1-year survival (1.3% vs. 2.1%; relative risk, 1.01; 95% CI, 1.00 to 1.02), or good neurologic recovery at hospital discharge (37.5% vs. 51.5%; relative risk, 1.29; 95% CI, 0.81 to 2.06)., Conclusions: As compared with epinephrine alone, the combination of vasopressin and epinephrine during advanced cardiac life support for out-of-hospital cardiac arrest does not improve outcome. (ClinicalTrials.gov number, NCT00127907.), (2008 Massachusetts Medical Society)

Background: In a porcine model, we compared the effect of the combination of vasopressin/epinephrine with that of a lipid emulsion on survival after bupivacaine-induced cardiac arrest., Methods: After administration of 5 mg/kg of a 0.5% bupivacaine solution i.v., ventilation was interrupted for 2 +/- 0.5 (mean +/- SD) min until asystole occurred. Cardiopulmonary resuscitation (CPR) was initiated after 1 min of untreated cardiac arrest. After 2 min of CPR, 10 animals received, every 5 min, either vasopressin combined with epinephrine or 4 mL/kg of a 20% lipid emulsion. Three minutes after each drug administration, up to three countershocks (4, 4, and 6 J/kg) were administered; all subsequent shocks with 6 J/kg. Blood for determination of the plasma bupivacaine concentration was drawn throughout the experiment., Results: In the vasopressor group, all five pigs survived, whereas none of five pigs in the lipid group had restoration of spontaneous circulation (P < 0.01). There was no significant difference between groups in the plasma concentration of total bupivacaine., Conclusion: In this model of a bupivacaine-induced cardiac arrest, the vasopressor combination of vasopressin and epinephrine compared with lipid emulsion resulted in higher coronary perfusion pressure during CPR and survival rates.

Background: Synergistic effects of adrenaline (epinephrine) and vasopressin may be beneficial during cardiopulmonary resuscitation. However, it is unknown whether either adrenaline alone or an alternating administration of adrenaline and vasopressin is better for restoring vital organ perfusion following basic life support (BLS) according to the revised algorithm with a compression-to-ventilation (c/v) ratio of 30:2., Material and Methods: After 4min of ventricular fibrillation, and 6min of BLS with a c/v ratio of 30:2, 16 pigs were randomised to receive either 45microg/kg adrenaline, or alternating 45microg/kg adrenaline and 0.4U/kg vasopressin, respectively., Results: Coronary perfusion pressure (mean+/-S.D.) 20 and 25min after cardiac arrest was 7+/-4 and 5+/-3mm Hg after adrenaline, and 25+/-2 and 14+/-3mm Hg after adrenaline/vasopressin (p<0.001 and <0.01 versus adrenaline), respectively. Cerebral perfusion pressure was 23+/-7 and 19+/-9mm Hg after adrenaline, and 40+/-10 and 33+/-7mm Hg after adrenaline/vasopressin (p<0.001 and <0.01 versus adrenaline), and cerebral blood flow was 30+/-10 and 27+/-11% of baseline after adrenaline, and 65+/-40 and 50+/-31% of baseline after adrenaline/vasopressin (p<0.05 versus adrenaline), respectively. Return of spontaneous circulation (ROSC) did not differ significantly between the adrenaline group (0/8) and the adrenaline/vasopressin group (3/8)., Conclusion: Adrenaline/vasopressin resulted in higher coronary and cerebral perfusion pressures, and cerebral blood flow, while ROSC was comparable.

Epinephrine given during cardiopulmonary resuscitation (CPR) may cause beta-mimetic complications in the postresuscitation phase. Vasopressin may be an alternative vasopressor drug during CPR. A subgroup analysis of a large prospective CPR investigation and of retrospective CPR studies suggests that vasopressin may be especially beneficial when combined with epinephrine. Beneficial effects of adding vasopressin were observed in other catecholamine-refractory shock states as well, such as vasodilatory shock and haemorrhagic shock. In order to maximize effects of any vasopressor during CPR, rapid aggressive chest compressions must be ensured to maximize blood flow and to enable advanced cardiac life support drugs to reach the arterial vasculature. We suggest alternating injections of 1 mg epinephrine i.v. and 40 IU vasopressin i.v. every 3-5 minutes during CPR until spontaneous circulation can be achieved or CPR efforts are terminated.

Objective: Synergistic effects of epinephrine and vasopressin may be of benefit during cardiopulmonary resuscitation. However, cerebral perfusion was decreased when epinephrine was combined with vasopressin compared with vasopressin alone. Although a combined infusion of norepinephrine and vasopressin improves hemodynamic variables compared with norepinephrine alone during sepsis, it is unknown whether norepinephrine in addition to vasopressin and epinephrine changes vital organ perfusion during cardiopulmonary resuscitation., Design: Prospective, randomized animal study., Setting: : University hospital research laboratory., Subjects: Twenty-one domestic pigs., Interventions: After 4 mins of ventricular fibrillation and 3 mins of basic life support, the pigs were randomly assigned to receive either 200 microg/kg epinephrine, 0.4 units/kg vasopressin alone, or 45 microg/kg norepinephrine plus 45 microg/kg epinephrine plus 0.4 units/kg vasopressin before defibrillation., Measurements and Main Results: Organ perfusion was determined by radiolabeled microspheres. Myocardial blood flow (mean +/- sem) before and 90 secs and 5 mins after drug administration was 8 +/- 2, 25 +/- 6, and 7 +/- 1 mL/min/100 g after high-dose epinephrine, 12 +/- 1, 75 +/- 7, and 60 +/- 10 mL/min/100 g after vasopressin, and 9 +/- 2, 95 +/- 26, and 46 +/- 15 mL/min/100 g after vasopressin/epinephrine/norepinephrine, respectively (p < .05 at 90 secs and 5 mins vasopressin vs. epinephrine and vasopressin/epinephrine/norepinephrine vs. epinephrine). At the same time points, cerebral blood flow was 8 +/- 2, 23 +/- 3, and 17 +/- 3 mL/min/100 g after epinephrine, 11 +/- 3, 55 +/- 7, and 52 +/- 7 mL/min/100 g after vasopressin, and 11 +/- 4, 67 +/- 13, and 53 +/- 12 mL/min/100 g after vasopressin/epinephrine/norepinephrine, respectively (p < .05 at 90 secs and 5 mins vasopressin vs. epinephrine and vasopressin/epinephrine/norepinephrine vs. epinephrine). Two of seven animals in the epinephrine group, four of seven animals in the vasopressin/epinephrine/norepinephrine group, and seven of seven animals in the vasopressin group could be successfully resuscitated (p < .05 vasopressin vs. epinephrine)., Conclusions: Vasopressin with or without epinephrine and norepinephrine resulted in higher myocardial and cerebral perfusion than epinephrine alone, but there was no benefit in adding norepinephrine to vasopressin and epinephrine with regard to cardiac and cerebral blood flow during cardiopulmonary resuscitation.

Objective: To report a cardiopulmonary resuscitation attempt in a 20-month-old child employing a combination of vasopressin and epinephrine., Design: Case report., Setting: Out-of-hospital cardiopulmonary resuscitation., Patient: A 20-month-old child found in cardiac arrest after submersion., Interventions and Results: Dispatcher-assisted basic life support was initiated immediately after pulling the child out of the water. The emergency medical service crew arrived approximately 6 mins later and found a hypothermic, cyanotic child in cardiocirculatory arrest. The first electrocardiogram showed sinus bradycardia. After intubation and administration of epinephrine and atropine with no effect, an intravenous bolus of 0.2 mg of epinephrine and 10 IU of vasopressin resulted in restoration of spontaneous circulation. The boy was flown to a hospital and was discharged 23 days later to a rehabilitation facility. He returned home 6 months after the accident, where further rehabilitation efforts are pending., Conclusion: Bystander cardiopulmonary resuscitation, early and aggressive advanced life support, rewarming, and the combination of intravenous epinephrine and vasopressin were associated with sustained return of spontaneous circulation following hypothermic submersion-associated cardiac arrest.

Objective: In patients undergoing cardiopulmonary resuscitation, circulating endogenous vasopressin concentrations were significantly higher in successfully resuscitated patients than in patients who died. These observations have prompted several investigations to assess the role of vasopressin to improve cardiopulmonary resuscitation management., Design: Literature review., Results: In the cardiopulmonary resuscitation laboratory, vasopressin improved vital organ blood flow, cerebral oxygen delivery, the probability of restoring spontaneous circulation, and neurologic recovery better than epinephrine. In pediatric preparations with asphyxia, epinephrine was superior to vasopressin, whereas in both pediatric pigs with ventricular fibrillation and adult porcine models with asphyxia, combinations of vasopressin and epinephrine proved to be highly effective. In addition, vasopressin enabled short- and long-term survival in a porcine model of uncontrolled hemorrhagic shock. In a recently published European, multiple-center trial, 1,219 adult patients with out-of-hospital cardiac arrest were randomized to receive two injections of either 40 IU of vasopressin or 1 mg of epinephrine followed by additional epinephrine if needed. The clinical study did not confirm laboratory data showing vasopressin to be more effective than epinephrine in ventricular fibrillation and pulseless electrical activity, but vasopressin was superior to epinephrine in patients with asystole. Vasopressin followed by epinephrine was more effective than epinephrine alone in the treatment of refractory cardiac arrest., Conclusions: According to new data from the European vasopressin study, we suggest, first, the administration of 1 mg of epinephrine, followed alternately by 40 IU of vasopressin and 1 mg of epinephrine every 3 mins in adult cardiac arrest victims, regardless of the initial electrocardiographic rhythm.

Unlabelled: In a porcine model, we compared the efficacy of epinephrine, vasopressin, or the combination of epinephrine and vasopressin with that of saline placebo on the survival rate after bupivacaine-induced cardiac arrest. After the administration of 5 mg/kg of a 0.5% bupivacaine solution i.v., ventilation was interrupted for 3 +/- 1 min (mean +/- SD) until asystole occurred. Cardiopulmonary resuscitation (CPR) was initiated after 1 min of cardiac arrest. After 2 min of CPR, 28 animals received, every 5 min, epinephrine; vasopressin; epinephrine combined with vasopressin; or placebo i.v.. Three minutes after each drug administration, up to 3 countershocks (3, 4, and 6 J/kg) were administered; all subsequent shocks were 6 J/kg. Blood was drawn throughout the experiment for the determination of plasma bupivacaine concentration. In the vasopressin/epinephrine combination group, all pigs survived (P < 0.01 versus placebo); in the vasopressin group 5 of 7, in the epinephrine group 4 of 7, and in the placebo group none of 7 swine survived. The plasma concentration of total bupivacaine showed no significant difference among groups. In this model of bupivacaine-induced cardiac arrest, CPR with a combination of vasopressin and epinephrine resulted in significantly better survival rates than in the placebo group., Implications: Although cardiovascular collapse occurs mostly immediately after rapid injection of a local anesthetic in the presence of anesthesiologists, resuscitation may be difficult, and the outcome is usually poor. In this model of bupivacaine-induced cardiac arrest, cardiopulmonary resuscitation with a combination of vasopressin and epinephrine resulted in significantly better survival rates than in the placebo group.

Background: Vasopressin is an alternative to epinephrine for vasopressor therapy during cardiopulmonary resuscitation, but clinical experience with this treatment has been limited., Methods: We randomly assigned adults who had had an out-of-hospital cardiac arrest to receive two injections of either 40 IU of vasopressin or 1 mg of epinephrine, followed by additional treatment with epinephrine if needed. The primary end point was survival to hospital admission, and the secondary end point was survival to hospital discharge., Results: A total of 1219 patients underwent randomization; 33 were excluded because of missing study-drug codes. Among the remaining 1186 patients, 589 were assigned to receive vasopressin and 597 to receive epinephrine. The two treatment groups had similar clinical profiles. There were no significant differences in the rates of hospital admission between the vasopressin group and the epinephrine group either among patients with ventricular fibrillation (46.2 percent vs. 43.0 percent, P=0.48) or among those with pulseless electrical activity (33.7 percent vs. 30.5 percent, P=0.65). Among patients with asystole, however, vasopressin use was associated with significantly higher rates of hospital admission (29.0 percent, vs. 20.3 percent in the epinephrine group; P=0.02) and hospital discharge (4.7 percent vs. 1.5 percent, P=0.04). Among 732 patients in whom spontaneous circulation was not restored with the two injections of the study drug, additional treatment with epinephrine resulted in significant improvement in the rates of survival to hospital admission and hospital discharge in the vasopressin group, but not in the epinephrine group (hospital admission rate, 25.7 percent vs. 16.4 percent; P=0.002; hospital discharge rate, 6.2 percent vs. 1.7 percent; P=0.002). Cerebral performance was similar in the two groups., Conclusions: The effects of vasopressin were similar to those of epinephrine in the management of ventricular fibrillation and pulseless electrical activity, but vasopressin was superior to epinephrine in patients with asystole. Vasopressin followed by epinephrine may be more effective than epinephrine alone in the treatment of refractory cardiac arrest., (Copyright 2004 Massachusetts Medical Society)

Unlabelled: We sought to determine the effects of a combination of vasopressin and epinephrine on neurologic recovery in comparison with epinephrine alone and saline placebo alone in an established porcine model of prolonged cardiopulmonary resuscitation (CPR). After 4 min of cardiac arrest, followed by 3 min of basic life support CPR, 17 animals were randomly assigned to receive, every 5 min, either a combination of vasopressin and epinephrine (vasopressin [IU/kg]/epinephrine [ micro g/kg]: 0.4/45, 0.4/45, and 0.8/45; n = 6), epinephrine alone (45, 45, and 200 micro g/kg; n = 6), or saline placebo alone (n = 5). After 22 min of cardiac arrest, including 18 min of CPR, defibrillation was attempted to achieve the return of spontaneous circulation. Aortic diastolic pressure was significantly (P < 0.01) increased 90 s after each of 3 vasopressin/epinephrine injections versus epinephrine alone versus saline placebo alone (mean +/- SEM: 69 +/- 3 mm Hg versus 45 +/- 3 mm Hg versus 29 +/- 2 mm Hg, 63 +/- 4 mm Hg versus 27 +/- 3 mm Hg versus 23 +/- 1 mm Hg, and 52 +/- 4 mm Hg versus 21 +/- 3 mm Hg versus 16 +/- 3 mm Hg, respectively). Spontaneous circulation was restored in six of six vasopressin/epinephrine pigs, whereas six of six epinephrine and five of five saline placebo pigs died (P < 0.01). Neurologic evaluation 24 h after successful resuscitation revealed only an unsteady gait and was normal 5 days after the experiment in all vasopressin/epinephrine-treated animals. In conclusion, in this porcine model of prolonged CPR, repeated vasopressin/epinephrine administration, but not epinephrine or saline placebo alone, ensured long-term survival with full neurologic recovery., Implications: We present a study to evaluate the effects of a combination of vasopressin and epinephrine during prolonged cardiopulmonary resuscitation on neurological outcome in pigs. We found that all pigs treated with a combination of vasopressin and epinephrine could be resuscitated and had full neurologic recovery observed over an entire period of 5 days.

Objective: Epinephrine is widely used for treatment of life-threatening hypotension, although new vasopressor drugs may merit evaluation. The purpose of this study was to determine the effects of vasopressin vs. epinephrine vs. saline placebo on hemodynamic variables, regional blood flow, and short-term survival in an animal model of uncontrolled hemorrhagic shock and delayed fluid resuscitation., Design: Prospective, randomized, laboratory investigation that used a porcine model for measurement of hemodynamic variables and regional abdominal organ blood flow., Setting: University hospital laboratory., Subjects: A total of 21 pigs weighing 32 +/- 3 kg., Interventions: The anesthetized pigs were subjected to a penetrating liver injury, which resulted in a mean +/- sem loss of 40% +/- 5% of estimated whole blood volume within 30 mins and mean arterial pressures of <20 mm Hg. When heart rate declined progressively, pigs randomly received a bolus dose and continuous infusion of either vasopressin (0.4 units/kg and 0.04 units.kg-1.min-1, n = 7), or epinephrine (45 microg/kg and 5 microg.kg(-1).min(-1), n = 7), or an equal volume of saline placebo (n = 7), respectively. At 30 mins after drug administration, all surviving animals were fluid resuscitated while bleeding was surgically controlled., Measurements and Main Results: Mean +/- sem arterial blood pressure at 2.5 and 10 mins was significantly (p <.001) higher after vasopressin vs. epinephrine vs. saline placebo (82 +/- 14 vs. 23 +/- 4 vs. 11 +/- 3 mm Hg, and 42 +/- 4 vs. 10 +/- 5 vs. 6 +/- 3 mm Hg, respectively). Although portal vein blood flow was temporarily impaired by vasopressin, it was subsequently restored and significantly (p <.01) higher when compared with epinephrine or saline placebo (9 +/- 5 vs. 121 +/- 3 vs. 54 +/- 22 mL/min and 150 +/- 20 vs. 31 +/- 17 vs. 0 +/- 0 mL/min, respectively). Hepatic and renal artery blood flow was significantly higher throughout the study in the vasopressin group; however, no further bleeding was observed. Despite a second bolus dose, all epinephrine- and saline placebo-treated animals died within 15 mins after drug administration. By contrast, seven of seven vasopressin-treated animals survived until fluid replacement, and 60 mins thereafter, without further vasopressor therapy (p <.01). Moreover, blood flow to liver, gut, and kidney returned to normal values in the postshock phase., Conclusions: Vasopressin, but not epinephrine or saline placebo, improved short-term survival in a porcine model of uncontrolled hemorrhagic shock after liver injury when surgical intervention and fluid replacement was delayed.

Objective: Despite the important role of the adrenal gland during cardiac arrest, little is known about changes in the adrenal medullary or cortical blood flow in this setting. This study was designed to assess regional adrenal gland perfusion in the medulla and cortex during cardiopulmonary resuscitation (CPR), and after administration of adrenaline (epinephrine) versus vasopressin versus saline placebo., Methods: After 4 min of untreated ventricular fibrillation, and 3 min of basic life support CPR, 19 animals were randomly assigned to receive either vasopressin (0.4 U/kg; n=7), adrenaline (45 microg/kg; n=6) or saline placebo (n=6), respectively. Haemodynamic variables, adrenal, and renal blood flow were measured after 90 s of CPR, and 90 s and 5 min after drug administration., Results: All values are given as mean+/-S.E.M. Blood flow in the adrenal medulla was significantly higher 90 s after adrenaline when compared with saline placebo in the right adrenal medulla (210+/-14 vs. 102+/-5 ml/min per 100 mg), and in the left adrenal medulla (218+/-14 vs. 96+/-3 ml/min per 100 mg). Blood flow in the adrenal medulla was significantly higher 90 s and 5 min after vasopressin when compared with adrenaline in the right (326+/-22 mg vs. 210+/-14 ml/min per 100 mg, and 297+/-17 vs. 103+/-5 ml/min per 100 mg), and in the left medulla (333+/-25 vs. 218+/-14 ml/min per 100 mg, and 295+/-14 vs. 111+/-7 ml/min per 100 mg). Ninety seconds and five minutes after vasopressin, and 90 s after adrenaline, adrenal cortex blood flow was significantly higher when compared with saline placebo. After 12 min of cardiac arrest, including 8 min of CPR, seven of seven pigs in the vasopressin group, one of six pigs in the adrenaline group, but none of six placebo were successfully defibrillated., Conclusion: Both vasopressin and adrenaline produced significantly higher medullary and cortical adrenal gland perfusion during CPR than did a saline placebo; but vasopressin resulted in significantly higher medullary adrenal gland blood flow when compared with adrenaline.

Objective: It is well established that epinephrine administered during cardiopulmonary resuscitation results in pulmonary gas exchange disturbances. It is uncertain how vasopressin affects gas exchange after cardiopulmonary resuscitation., Design: Prospective, randomized experimental study., Setting: Animal research laboratory., Subjects: Twenty domestic pigs., Interventions: Animals were subjected to ventricular fibrillation and cardiopulmonary resuscitation by using either vasopressin or epinephrine. Hemodynamic and pulmonary gas exchange (multiple inert gas elimination technique) variables were recorded before cardiopulmonary resuscitation and 10, 30, 60, and 120 mins after return of spontaneous circulation when either epinephrine (control) or vasopressin was used., Measurements and Main Results: At 10 mins after return of spontaneous circulation, blood flow to low V /Q lung units was increased in animals treated with epinephrine (17.8 +/- 6 vs. 2.6 +/- 3%, mean +/- sd, p<.01). Resulting carbon dioxide elimination was impaired in animals treated with epinephrine but not in animals treated with vasopressin (PaCO2, 55 +/- 2 vs. 46 +/- 4 torr, p<.05). Thirty minutes after return of spontaneous circulation, blood flow to lung units with a normal VA /Q ratio was reduced in animals treated with epinephrine (79 +/- 1 vs. 84 +/- 12%, p<.05), resulting in a depressed PaO2 (147 +/- 4 vs. 127 +/- 10 torr, p<.05)., Conclusion: Vasopressin compared with epinephrine for cardiopulmonary resuscitation resulted in better gas exchange variables in the early postresuscitation phase.

There is increasing evidence that the combination of epinephrine (adrenaline) with vasopressin may be superior to either epinephrine or vasopressin alone for treatment of cardiac arrest. However, the optimal combination, and dosage of cardiovascular drugs to minimize side effects, and to improve outcome has yet to be found. We therefore evaluated whether the combination of vasopressin plus epinephrine plus nitroglycerin (EVN), would improve vital organ blood flow during cardiopulmonary resuscitation (CPR) when compared with epinephrine (EPI) alone. After 4 min of ventricular fibrillation (VF) and 4 min of standard CPR, pigs were randomized to the combination of epinephrine (45 microg/kg) plus vasopressin (0.4 U/kg) plus nitroglycerin (7.5 microg/kg; n=12), or epinephrine (40 microg/kg; n=12) alone. Cerebral and myocardial blood flow was measured with radiolabeled microspheres. Defibrillation was attempted after 19 min of VF including 15 min of CPR. Mean+/-SEM coronary perfusion pressures were significantly (P < 0.01) higher 5 min after EVN vs. EPI alone (34+/-3 vs. 24+/-3 mmHg, respectively). At the same time, mean+/-SEM left ventricular, and global cerebral blood flow was also significantly (P < 0.05) higher after EVN vs. EPI alone (0.78+/-0.11 vs. 0.48+/-0.08 ml/min/g; and 0.37+/-0.05 vs. 0.22+/-0.0 3 ml/min/g, respectively). Spontaneous circulation was restored in 11 of 12 animals in the EVN group vs. 6 of 12 swine after EPI alone (P = N.S.). In conclusion, the combination of EVN significantly improved vital organ blood flow during CPR compared with EPI alone. Addition of nitroglycerin to the combination of low dose epinephrine with vasopressin during cardiac arrest may be beneficial.

Objective: We recently demonstrated that vasopressin alone resulted in a poorer outcome in a pediatric porcine model of asphyxial cardiac arrest when compared with epinephrine alone or with epinephrine plus vasopressin in combination. Accordingly, this study was designed to differentiate whether the inferior effects of vasopressin in pediatrics were caused by the type of cardiac arrest., Design: Prospective, randomized laboratory investigation that used an established porcine model for measurement of hemodynamic variables and organ blood flow., Setting: University hospital laboratory., Subjects: Eighteen piglets weighing 8-11 kg., Interventions: After 8 mins of ventricular fibrillation and 8 mins of cardiopulmonary resuscitation, either 0.4 units/kg vasopressin (n = 6), 45 microg/kg epinephrine (n = 6), or a combination of 45 microg/kg epinephrine with 0.8 units/kg vasopressin (n = 6) was administered. Six minutes after drug administration, a second respective bolus dose of 0.8 units/kg vasopressin, 200 microg/kg epinephrine, or a combination of 200 microg/kg epinephrine with 0.8 units/kg vasopressin was given. Defibrillation was attempted 20 mins after initiating cardiopulmonary resuscitation., Measurements and Main Results: Mean +/- sem left ventricular myocardial blood flow 2 mins after each respective drug administration was 65 +/- 4 and 70 +/- 13 mL x min(-1) x 100 g(-1) in the vasopressin group; 83 +/- 42 and 85 +/- 41 mL x min(-1) x 100 g(-1) in the epinephrine group; and 176 +/- 32 and 187 +/- 29 mL x min(-1) x 100 g(-1) in the epinephrine-vasopressin group (p <.006 after both doses of epinephrine-vasopressin vs. vasopressin and after the first dose of epinephrine-vasopressin vs. epinephrine, respectively). At the same times, mean +/- sem total cerebral blood flow was 73 +/- 3 and 47 +/- 5 mL x min(-1) x 100 g(-1) after vasopressin; 18 +/- 2 and 12 +/- 2 mL x min(-1) x 100 g(-1) after epinephrine; and 79 +/- 21 and 41 +/- 8 mL x min(-1) x 100 g(-1) after epinephrine-vasopressin (p <.025 after both doses of vasopressin and epinephrine-vasopressin vs. epinephrine). Five of six vasopressin-treated, two of six epinephrine-treated, and six of six epinephrine-vasopressin treated animals had return of spontaneous circulation (nonsignificant)., Conclusions: In this pediatric porcine model of ventricular fibrillation, the combination of epinephrine with vasopressin during cardiopulmonary resuscitation resulted in significantly higher levels of left ventricular myocardial blood flow than either vasopressin alone or epinephrine alone. Both vasopressin alone and the combination of epinephrine with vasopressin, but not epinephrine alone, improved total cerebral blood flow during cardiopulmonary resuscitation. In stark contrast to asphyxial cardiac arrest, vasopressin alone or in combination with epinephrine appears to be of benefit after ventricular fibrillation in the pediatric porcine model.

The importance of vital organ perfusion in patients suffering cardiac arrest makes arterial vasomotor tone, and the resultant perfusion pressure, critical in resuscitation from sudden death. Although there are multiple mechanisms that may affect arterial vascular tone, historically, the therapy most commonly used has been catecholamine-induced adrenergic receptor stimulation, with catecholamine epinephrine being the commonest drug used. Over the last decade, however, it has become widely known that the utility of epinephrine during cardiopulmonary resuscitation is undefined. This has led to research into alternative agents, in particular nonadrenergic vasoactive peptides. Other agents appear promising. This article addresses pressor drugs and adrenergic agonists, including a review of their history, basic science, mechanism of action, and efficacy. Epinephrine is reviewed.

Objective: The aim of the current study was to assess the effects of epinephrine in a pig model of hypothermic cardiac arrest followed by closed-chest cardiopulmonary resuscitation combined with active rewarming, simulating the clinical management of an arrested hypothermic patient in a hospital without cardiopulmonary bypass facilities., Design: Prospective, randomized animal study., Setting: University research laboratory., Subjects: Twelve 12- to 16-week-old domestic pigs., Interventions: Pigs were surface cooled to a body core temperature of 28 degrees C. After 4 min of untreated cardiac arrest, manual closed-chest CPR and thoracic lavage with 40 degrees C warmed fluid were started. After 3 min of external chest compression animals were randomly assigned to receive epinephrine (45, 45 and 200 microg/kg) or saline placebo in 5-min intervals., Measurements and Main Results: Coronary perfusion pressure was about 15 mmHg in placebo group pigs. Coronary perfusion pressure was significantly higher after epinephrine, but restoration of spontaneous circulation was not more frequent (one of six epinephrine versus three of six saline placebo pigs, P=0.34). After 45 microg/kg epinephrine the arterial PO(2) was significantly lower when compared to the saline placebo. The third 200 microg/kg epinephrine dose resulted in a significantly enhanced mixed venous hypercarbic acidosis., Conclusions: After a short 4-min period of hypothermic cardiac arrest, epinephrine may not be necessary to maintain coronary perfusion pressure around the threshold usually correlating with successful defibrillation, even during prolonged closed-chest CPR combined with active rewarming. The enhanced mixed venous hypercarbic acidosis in epinephrine-treated animals may support the argument against repeated or high dose epinephrine administration during hypothermic CPR.

Cardiopulmonary resuscitation (CPR) during epidural anesthesia is considered difficult because of diminished coronary perfusion pressure. The efficacy of epinephrine and vasopressin in this setting is unknown. Therefore, we designed this study to assess the effects of epinephrine versus vasopressin on coronary perfusion pressure in a porcine model with and without epidural anesthesia and subsequent cardiac arrest. Thirty minutes before induction of cardiac arrest, 16 pigs received epidural anesthesia with bupivacaine while another 12 pigs received only saline administration epidurally. After 1 min of untreated ventricular fibrillation, followed by 3 min of basic life-support CPR, Epidural Animals and Control Animals randomly received every 5 min either epinephrine (45, 45, and 200 microg/kg) or vasopressin (0.4, 0.4, and 0.8 U/kg). During basic life-support CPR, mean +/- SEM coronary perfusion pressure was significantly lower after epidural bupivacaine than after epidural saline (13 +/- 1 vs 24 +/- 2 mm Hg, P < 0.05). Ninety seconds after the first drug administration, epinephrine increased coronary perfusion pressure significantly less than vasopressin in control animals without epidural block (42 +/- 2 vs 57 +/- 5 mm Hg, P < 0.05), but comparably to vasopressin after epidural block (45 +/- 4 vs 48 +/- 6 mm Hg). Defibrillation was attempted after 18 min of CPR. After return of spontaneous circulation, bradycardia required treatment in animals receiving vasopressin, especially with epidural anesthesia. Systemic acidosis was increased in animals receiving epinephrine than vasopressin, regardless of presence or absence of epidural anesthesia. We conclude that vasopressin may be a more desirable vasopressor for resuscitation during epidural block because the response to a single dose is longer lasting, and acidosis after multiple doses is less severe compared with epinephrine.

Objective: The intraosseous route is an emergency alternative for the administration of drugs and fluids if vascular access cannot be established. However, in hemorrhagic shock or after vasopressors are given during resuscitation, bone marrow blood flow may be decreased, thus impairing absorption of intraosseously administered drugs. In this study, we evaluated the effects of vasopressin vs. high-dose epinephrine in hemorrhagic shock and cardiac arrest on bone marrow blood flow., Design: Prospective, randomized laboratory investigation that used an established porcine model for measurement of hemodynamic variables and organ blood flow., Setting: University hospital laboratory., Subjects: Fourteen pigs weighing 30 +/- 3 kg., Interventions: Radiolabeled microspheres were injected to measure bone marrow blood flow during a prearrest control period and during hypovolemic shock produced by rapid hemorrhage of 35% of the estimated blood volume. In the second part of the study, ventricular fibrillation was induced; after 4 mins of untreated cardiac arrest and 4 mins of standard cardiopulmonary resuscitation, a bolus dose of either 200 microg/kg epinephrine (n = 6) or 0.8 units/kg vasopressin (n = 6) was administered. Defibrillation was attempted 2.5 mins after drug administration, and blood flow was assessed again at 5 and 30 mins after successful resuscitation., Measurements and Main Results: Mean +/- sem bone marrow blood flow decreased significantly during induction of hemorrhagic shock from 14.4 +/- 4.1 to 3.7 +/- 1.8 mL.100 g-1.min-1 in the vasopressin group and from 18.2 +/- 4.0 to 5.2 +/- 1.0 mL.100 g-1.min-1 in the epinephrine group (p =.025 in both groups). Five minutes after return of spontaneous circulation, mean +/- sem bone marrow blood flow was 3.4 +/- 1.1 mL.100 g-1.min-1 after vasopressin and 0.1 +/- 0.03 mL.100 g-1.min-1 after epinephrine (p =.004 for vasopressin vs. epinephrine). At the same time, bone vascular resistance was significantly (p =.004) higher in the epinephrine group when compared with vasopressin (1455 +/- 392 vs. 43 +/- 19 mm Hg. mL-1.100 g.min, respectively)., Conclusions: Bone blood flow responds actively to both the physiologic stress response of hemorrhagic shock and vasopressors given during resuscitation after hypovolemic cardiac arrest. In this regard, bone marrow blood flow after successful resuscitation was nearly absent after high-dose epinephrine but was maintained after high-dose vasopressin. These findings emphasize the need for pressurized intraosseous infusion techniques, because bone marrow blood flow may not be predictable during hemorrhagic shock and drug therapy.

Objective: This study was designed to compare the effects of vasopressin vs. epinephrine vs. the combination of epinephrine with vasopressin on vital organ blood flow and return of spontaneous circulation in a pediatric porcine model of asphyxial arrest., Design: Prospective, randomized laboratory investigation using an established porcine model for measurement of hemodynamic variables, organ blood flow, blood gases, and return of spontaneous circulation., Setting: University hospital laboratory., Subjects: Eighteen piglets weighing 8-11 kg., Interventions: Asphyxial cardiac arrest was induced by clamping the endotracheal tube. After 8 mins of cardiac arrest and 8 mins of cardiopulmonary resuscitation, a bolus dose of either 0.8 units/kg vasopressin (n = 6), 200 microg/kg epinephrine (n = 6), or a combination of 45 microg/kg epinephrine with 0.8 units/kg vasopressin (n = 6) was administered in a randomized manner. Defibrillation was attempted 6 mins after drug administration., Measurements and Main Results: Mean +/- SEM coronary perfusion pressure, before and 2 mins after drug administration, was 13 +/- 2 and 23 +/- 6 mm Hg in the vasopressin group; 14 +/- 2 and 31 +/- 4 mm Hg in the epinephrine group; and 13 +/- 1 and 33 +/- 6 mm Hg in the epinephrine-vasopressin group, respectively (p = NS). At the same time points, mean +/- SEM left ventricular myocardial blood flow was 44 +/- 31 and 44 +/- 25 mL x min-(1) x 100 g(-1) in the vasopressin group; 30 +/- 18 and 233 +/- 61 mL x min(-1) x 100 g(-1) in the epinephrine group; and 36 +/- 10 and 142 +/- 57 mL x min(-1) x 100 g(-1) in the epinephrine-vasopressin group (p < .01 epinephrine vs. vasopressin; p < .02 epinephrine-vasopressin vs. vasopressin). Total cerebral blood flow trended toward higher values after epinephrine-vasopressin (60 +/- 19 mL x min(-1) x 100 g(-1)) than after vasopressin (36 +/- 17 mL x min(-1) x 100 g(-1)) or epinephrine alone (31 +/- 7 mL x min(-1) x 100 g(-1); p = .07, respectively). One of six vasopressin, six of six epinephrine, and four of six epinephrine-vasopressin-treated animals had return of spontaneous circulation (p < .01, vasopressin vs. epinephrine)., Conclusions: Administration of epinephrine, either alone or in combination with vasopressin, significantly improved left ventricular myocardial blood flow during cardiopulmonary resuscitation. Return of spontaneous circulation was significantly more likely in epinephrine-treated pigs than in animals resuscitated with vasopressin alone.

Objective: Vasopressin is a possible stimulus for both adrenocorticotropin (ACTH) and endothelin-1 release. The aim of this study was to compare plasma concentrations of ACTH, cortisol, and endothelin-1 after epinephrine or vasopressin administration in an experimental animal model of cardiopulmonary resuscitation (CPR)., Design: Prospective, randomized, controlled animal study., Setting: A university research laboratory., Subjects: Fourteen 12- to 14-wk-old domestic pigs., Interventions: After 4 mins of cardiac arrest and 3 mins of external chest compression, the pigs were randomly assigned to receive either 0.045 mg/kg epinephrine (n = 7) or 0.4 units/kg vasopressin (n = 7). At 5 mins after drug administration, defibrillation was attempted., Measurements and Main Results: Coronary perfusion pressure, ACTH, cortisol, and endothelin-1 were measured before cardiocirculatory arrest, during CPR before drug administration, and at 90 secs and 5 mins after drug administration. Coronary perfusion pressure was comparable between groups. All seven animals in the vasopressin group survived, but only one pig in the epinephrine group survived (p = .005). ACTH and cortisol concentrations remained unchanged in epinephrine-treated animals, but increased significantly after vasopressin administration and were significantly higher than in epinephrine-treated animals 5 mins after drug administration. Endothelin-1 concentrations remained unchanged during the study period and were comparable between both groups., Conclusions: Vasopressin is a potent stimulus for ACTH secretion, but does not trigger endothelin-1 release from vascular cells during cardiac arrest and CPR. The increased plasma cortisol concentrations caused by the enhanced ACTH release after vasopressin may be one factor contributing to the improved outcome repeatedly observed with vasopressin in animal models of CPR.

This study evaluated ventricular fibrillation mean frequency and amplitude to predict defibrillation success in a porcine cardiopulmonary resuscitation (CPR) model using repeated administration of vasopressin or epinephrine. After 4 min of cardiac arrest and 3 min of CPR, 10 pigs were randomly assigned to receive either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 units/kg, respectively, n = 5) or epinephrine (early epinephrine: 45, 45, and 200 microg/kg, respectively, n = 5). Another 11 animals were randomly allocated after 4 min of cardiac arrest and 8 min of CPR to receive every 5 min either vasopressin (late vasopressin: 0.4 and 0. 8 units/kg, respectively, n = 5) or epinephrine (late epinephrine: 45 and 200 microg/kg, n = 6). Ventricular fibrillation mean frequency and amplitude on defibrillation were significantly higher in the vasopressin groups than in the epinephrine groups, respectively. In vasopressin versus epinephrine animals, mean frequency immediately before defibrillation was 9.6 +/- 1.5 Hz vs 7. 0 +/- 0.7 Hz (P < 0.001), mean amplitude was 0.65 +/- 0.26 mV vs 0. 21 +/- 0.14 mV (P < 0.001, and coronary perfusion pressure was 27 +/- 9 mm Hg vs 8 +/- 4 mm Hg (P < 0.00001), respectively. In contrast to no epinephrine animals, all vasopressin animals were successfully defibrillated and survived 1 h (P < 0.05). Mean fibrillation frequency and amplitude predicted successful defibrillation and may serve as noninvasive markers to monitor continuing CPR efforts. Furthermore, vasopressin was superior to epinephrine in maintaining these variables above a threshold necessary for successful defibrillation.

Objective: To compare the effects of vasopressin versus epinephrine on splanchnic blood flow during and after cardiopulmonary resuscitation (CPR), and to evaluate the effects of these vasopressors on renal function in the postresuscitation phase., Design: Prospective, randomized laboratory investigation using an established porcine CPR model with instrumentation for continuous measurement of splanchnic and renal blood flow., Setting: University hospital experimental laboratory., Subjects: A total of 12 anesthetized, 12- to 16-wk-old domestic pigs weighing 30-35 kg., Interventions: After 4 mins of cardiac arrest, and 3 mins of CPR, 12 pigs were randomly assigned to receive either 0.4 units/kg vasopressin (n = 6) or 45 microg/kg epinephrine (n = 6). Defibrillation was performed 5 mins after drug administration; all animals were observed for 6 hrs after return of spontaneous circulation (ROSC)., Measurements and Main Results: Mean +/- SEM superior mesenteric artery blood flow was significantly (p < .05) lower after vasopressin compared with epinephrine at 90 secs after drug administration (13+/-3 vs. 129+/-33 mL/min); at 5 mins after drug administration (31+/-18 vs. 155+/-39 mL/min); at 5 mins after ROSC (332+/-47 vs. 1087+/-166 mL/min); and at 15 mins after ROSC (450+/-106 vs. 1130+/-222 mL/min); respectively. Mean +/- SEM left renal and hepatic artery blood flow after ROSC was comparable in both groups ranging between 120-290 mL/min (renal blood flow), and 150-360 mL/min (hepatic blood flow), respectively. Median urine output after ROSC showed no difference between groups, and highest values (180-220 mL/hr) were observed in the first 60 mins after ROSC. Median calculated glomerular filtration rate showed no difference between groups with values ranging between 30 and 80 mL/min in the postresuscitation phase. Calculated fractional sodium excretion and osmolar relationship between urea and plasma indicated no evidence for renal tubular dysfunction., Conclusions: In the early postresuscitation phase, superior mesenteric blood flow was temporarily impaired by vasopressin in comparison with epinephrine. With respect to renal blood flow and renal function after ROSC, there was no difference between either vasopressor given during CPR. Vasopressin given during CPR did not result in an antidiuretic state in the postresuscitation phase.

Unlabelled: The American Heart Association does not recommend epinephrine for management of hypothermic cardiac arrest if body core temperature is below 30 degrees C. Furthermore, the effects of vasopressin administration during hypothermic cardiac arrest are totally unknown. This study was designed to assess the effects of vasopressin and epinephrine on coronary perfusion pressure in a porcine model during hypothermic cardiac arrest cardiopulmonary resuscitation (CPR). Pigs were surface-cooled until their body core temperature was 26 degrees C. After 30 min of untreated cardiac arrest, followed by 3 min of basic life support CPR, 15 animals were randomly assigned to receive, at 5-min intervals, either vasopressin (0.4, 0.4, and 0.8 U/kg; n = 5), epinephrine (45, 45, and 200 microg/kg; n = 5), or saline placebo (n = 5). Compared with epinephrine, mean +/- SEM coronary perfusion pressure was significantly higher (P < 0.05) 90 s and 5 min after the first (35+/-4 vs 22+/-3 mm Hg and 37+/-2 vs 16+/-2 mm Hg) and the second vasopressin administration (40+/-5 vs 26+/-5 mm Hg and 36+/-5 vs 18+/-2 mm Hg, respectively). After the third drug administration, coronary perfusion pressure in the epinephrine group increased dramatically and was comparable to vasopressin. In the saline placebo group, coronary perfusion pressure was significantly lower (P < 0.05) than in the vasopressin and epinephrine groups. Six animals treated with epinephrine or vasopressin had transient return of spontaneous circulation, whereas all placebo animals died (P < 0.05). During CPR in severe hypothermia, administration of both vasopressin and epinephrine resulted in significant increases in coronary perfusion pressure when compared with placebo., Implications: Our study was designed to assess the effects of vasopressin and epinephrine in a porcine model simulating cardiac arrest during severe hypothermia. This study demonstrates that the administration of both emergency drugs results in an increased perfusion pressure in the heart.

Background: It is unknown whether repeated dosages of vasopressin or epinephrine given early or late during basic life support cardiopulmonary resuscitation (CPR) may be able to increase coronary perfusion pressure above a threshold between 20 and 30 mm Hg that renders defibrillation successful., Methods and Results: After 4 minutes of cardiac arrest, followed by 3 minutes of basic life support CPR, 12 animals were randomly assigned to receive, every 5 minutes, either vasopressin (early vasopressin: 0.4, 0.4, and 0.8 U/kg, respectively; n=6) or epinephrine (early epinephrine: 45, 45, and 200 microg/kg, respectively; n=6). Another 12 animals were randomly allocated after 4 minutes of cardiac arrest, followed by 8 minutes of basic life support CPR, to receive, every 5 minutes, either vasopressin (late vasopressin: 0.4 and 0.8 U/kg, respectively; n=6), or epinephrine (late epinephrine: 45 and 200 microg/kg, respectively; n=6). Defibrillation was attempted after 22 minutes of cardiac arrest. Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after early vasopressin compared with early epinephrine (50+/-4 versus 34+/-3 mm Hg, P<0.02; 42+/-5 versus 15+/-3 mm Hg, P<0.0008; and 37+/-5 versus 11+/-3 mm Hg, P<0. 002, respectively). Mean+/-SEM coronary perfusion pressure was significantly higher 90 seconds after late vasopressin compared with late epinephrine (40+/-3 versus 22+/-4 mm Hg, P<0.004, and 32+/-4 versus 15+/-4 mm Hg, P<0.01, respectively). All vasopressin animals survived 60 minutes, whereas no epinephrine pig had return of spontaneous circulation (P<0.05)., Conclusions: Repeated administration of vasopressin but only the first epinephrine dose given early and late during basic life support CPR maintained coronary perfusion pressure above the threshold that is needed for successful defibrillation.

Objective: Although a benefit of vasopressin when compared with epinephrine was shown during cardiopulmonary resuscitation (CPR) after a short duration of ventricular fibrillation cardiac arrest, the effect of vasopressin during prolonged cardiac arrest with pulseless electrical activity is currently unknown., Design: Prospective, randomized laboratory investigation using an established porcine model with instrumentation for measurement of hemodynamic variables, vital organ blood flow, blood gases, and return of spontaneous circulation., Setting: University hospital laboratory., Subjects: Eighteen domestic pigs., Interventions: After 15 mins of cardiac arrest and 3 mins of chest compressions, 18 animals were randomly treated with either 0.8 units/kg vasopressin (n = 9) or 200 microg/kg epinephrine (n = 9)., Measurements and Main Results: Compared with epinephrine, vasopressin resulted, at both 90 secs and 5 mins after drug administration, in significantly higher (p < .05) median (25th-75th percentiles) left ventricular myocardial blood flow (120 [range, 96-193] vs. 54 [range, 11-92] and 56 [range, 41-80] vs. 21 [range, 11-40] mL/min/100 g, respectively) and total cerebral blood flow (85 [78-102] vs. 24 [18-41] and 50 [44-52] vs. 8 [5-23] mL/min/100 g, respectively). Spontaneous circulation was restored in eight of nine animals in the vasopressin group and in one of nine animals in the epinephrine group (p = .003)., Conclusions: Compared with a maximum dose of epinephrine, vasopressin significantly increased left ventricular myocardial and total cerebral blood flow during CPR and return of spontaneous circulation in a porcine model of prolonged cardiac arrest with postcountershock pulseless electrical activity.

Background and Purpose: It is unknown whether a combination of vasopressin and epinephrine may be superior to vasopressin alone by targeting both nonadrenergic and adrenergic receptors., Methods: After 15 minutes of cardiac arrest (13 minutes of ventricular fibrillation and 2 minutes of pulseless electrical activity) and 3 minutes of chest compressions, 16 animals were randomly treated with either 0.8 U/kg vasopressin (n = 8) or 0.8 U/kg vasopressin combined with 200 microg/kg epinephrine (n = 8)., Results: Comparison of vasopressin with vasopressin and epinephrine at 90 seconds and 5 minutes after drug administration resulted in comparable mean (+/-SEM) coronary perfusion pressure (54+/-3 versus 57+/-5 and 36+/-4 versus 35+/-4 mm Hg, respectively), cerebral perfusion pressure (59+/-6 versus 65+/-8 and 40+/-6 versus 39+/-6 mm Hg, respectively), and median (25th to 75th percentiles) left ventricular myocardial blood flow [116 (81 to 143) versus 108 (97 to 125) and 44 (35 to 81) versus 62 (42 to 74) mL x min(-1) x 100 g(-1), respectively], but significantly increased (P<0.05) total cerebral blood flow [81 (77 to 95) versus 39 (34 to 58) and 50 (43 to 52) versus 28 (16 to 35) mL x min(-1) x 100 g(-1), respectively]. Return of spontaneous circulation rates in both groups were comparable (vasopressin, 7 of 8; vasopressin and epinephrine, 6 of 8)., Conclusions: Comparison of vasopressin with vasopressin and epinephrine resulted in comparable left ventricular myocardial blood flow but significantly increased cerebral perfusion.

In laboratory investigations, vasopressin given during CPR resulted in improved vital organ blood flow when compared with epinephrine. Given the profound and long lasting vasopressor effects of vasopressin, we tested the hypothesis that vasopressin given during CPR would result in renal and splanchnic hypoperfusion in the post-resuscitation period when compared with epinephrine. After 4 min of ventricular fibrillation, 16 pigs were randomly assigned to receive either 0.045 mg x kg(-1) epinephrine or 0.4 U X kg(-1) vasopressin before defibrillation. Splanchnic and renal blood flow were measured 30, 90, and 240 min after restoration of spontaneous circulation (ROSC) in the epinephrine and vasopressin groups and in a control group of eight pigs using radiolabeled microspheres. Hepatic blood flow was measured before arrest and 30, 90, and 240 min after ROSC by means of indocyanine green infusion. Thirty minutes after ROSC, renal and adrenal blood flow were significantly lower in the vasopressin group (300 [273-334] and 256 [170-284] ml X min(-1) x 100 g(-1)) (median and 25th and 75th percentile) as compared with the epinephrine group (370 [346-429] and 360 [326-420] ml x min(-1) x 100 g(-1); P < 0.05). Pancreatic, intestinal, and hepatic blood flow were not significantly different in animals after receiving epinephrine or vasopressin. In comparison to epinephrine, vasopressin given during cardiac arrest impairs renal and adrenal perfusion temporarily but does not lead to intestinal or hepatic hypoperfusion in the post-resuscitation phase.

Recent animal data have challenged the common clinical practice to avoid vasopressor drugs during hypothermic cardiopulmonary resuscitation (CPR) when core temperature is below 30 degrees C. In this report, we describe the case of a 19-year-old-female patient with prolonged, hypothermic, out-of-hospital cardiopulmonary arrest after near drowning (core temperature, 27 degrees C) in whom cardiocirculatory arrest persisted despite 2 mg of intravenous epinephrine; but, immediate return of spontaneous circulation occurred after a single dose (40 IU) of intravenous vasopressin. The patient was subsequently admitted to a hospital with stable haemodynamics, and was successfully rewarmed with convective rewarming, but died of multiorgan failure 15 h later. To the best of our knowledge, this is the first report about the use of vasopressin during hypothermic CPR in humans. This case report adds to the growing evidence that vasopressors may be useful to restore spontaneous circulation in hypothermic cardiac arrest patients prior to rewarming, thus avoiding prolonged mechanical CPR efforts, or usage of extracorporeal circulation. It may also support previous experience that the combination of both epinephrine and vasopressin may be necessary to achieve the vasopressor response needed for restoration of spontaneous circulation, especially after asphyxial cardiac arrest or during prolonged CPR efforts. [ABSTRACT FROM AUTHOR]