Extra hemodynamic energy is one of the major benefits of pulsatile flow, improving blood flow to vital organs. But most (80%) of the hemodynamic energy generated from pulsatile flow is damped by the extracorporeal circuit. Most models devised to minimize hemodynamic energy loss have been in vitro pediatric models. The purpose of this study was to measure hemodynamic energy in different vessels of different organs with an in vivo adult swine model. An extracorporeal circuit was constructed for seven Yorkshire swine using a pulsatile pump (Twin-Pulse Life Support). The mean arterial pressure (MAP), energy equivalent pressure (EEP), and surplus hemodynamic energy (SHE) at the renal artery, carotid artery, aortic cannula site, and postoxygenator site were measured simultaneously before starting the pump and at the pump rates of 25, 35, and 45 bpm. The MAP of the renal or carotid artery was 40.0%-51.2% of the postoxygenator site. The EEP and SHE of both arteries were 11.6%-13.0% and 5.5%-7.4% of the postoxygenator site, respectively. The MAP and EEP of both arteries after starting the pump were lower than at baseline. The SHE of the renal artery after starting the pump was significantly higher than at baseline. The SHE of the carotid artery increased substantially after starting the pump although not statistically significantly. There was a significant hemodynamic energy loss in both arterial sites compared with the postoxygenator site. Also, a difference in hemodynamic energy loss was observed in vessel-to-vessel or vessel-to-circuit site comparison. This difference creates a bias in studying pulsatility and its effects. Therefore, the measurement method of hemodynamic energy must be standardized and the measurement site clarified to yield accurate study results.