During normothermic cardiac arrest, a combination of active compression-decompression (ACD) cardiopulmonary resuscitation (CPR) with the inspiratory threshold valve (ITV) significantly improves vital organ blood flow, but this technique has not been studied during hypothermic cardiac arrest. Accordingly, we evaluated the hemodynamic effects of ACD + ITV CPR before, and after, the administration of vasopressin in a porcine model of hypothermic cardiac arrest. Pigs were surface-cooled until their body core temperature was 26°C. After 10 min of untreated ventricular fibrillation, 14 animals were randomly assigned to either ACD CPR with the ITV (n = 7) or to standard (STD) CPR (n = 7). After 8 min of CPR, all animals received 0.4 U/kg vasopressin IV, and CPR was maintained for an additional 10 min in each group; defibrillation was attempted after 28 rnin of cardiac arrest, including 18 rnin of CPR. Before the administration of vasopressin, mean ± SEM Tcommon carotid blood flow was significantly higher in the ACD + ITV group compared with STD CPR (67 ± 13 versus 26 ± 5 mL/min, respectively; P < 0.025). After vasopressin was given at Minute 8 during CPR, mean ± SEM coronary perfusion pressure was significantly higher in the ACD + ITV group, but did not increase in the STD group (29 ± 3 versus 15 ± 2 mm Hg, and 25 ± 1 versus 14 ± 1 mm Hg at minute 12 and 18, respectively; P < 0.001); mean ± SEM common carotid blood flow remained higher at respective time points (33 ± 8 versus 10 ± 3 mL/min, and 31 ± 7 versus 7 ± 3 mL/min, respectively; P < 0.01). Without active rewarming, spontaneous circulation was restored and maintained for 1 h in three of seven animals in the ACD + ITV group versus none of seven animals in the STD CPR group (not significant). During hypothermic cardiac arrest, ACD CPR with the ITV improved common carotid blood flow compared with STD CPR alone. Moreover, after the administration of vasopressin, coronary perfusion pressure was significantly higher during ACD + ITV CPR, but not during STD CPR.