Continuous cardiac output monitoring via arterial pressure waveform analysis following severe hemorrhagic shock in dogs*

Abstract

To determine agreement and correlation between cardiac output determined by arterial pressure waveform analysis (PulseCO) and the lithium dilution indicator technique (LiDCO) during severe hemorrhagic shock and after fluid resuscitation in dogs. Prospective experimental study. University research laboratory. Twelve adult mongrel dogs. Dogs were anesthetized, and selected arteries and veins were catheterized. Baseline cardiac output was determined by LiDCO and used to calibrate the PulseCO. Hemorrhagic shock was induced by withdrawing blood to achieve and maintain a mean arterial pressure of 30-40 mm Hg for 60 mins, and cardiac output was measured again using both methods. All dogs were resuscitated by administering lactated Ringer's solution intravenously to achieve and maintain a mean arterial pressure between 60 and 70 mm Hg. PulseCO and LiDCO values were measured at 10 and 120 mins after resuscitation. Mean baseline cardiac output was 2.93 +/- 0.45 L/min. PulseCO values overestimated cardiac output compared with LiDCO during hemorrhagic shock (2.25 vs. 0.78 L/min). There were no differences in cardiac output determined by PulseCO and LiDCO at 10 and 120 mins after fluid resuscitation. Bland-Altman analysis suggested that PulseCO values were inaccurate after hemorrhage, producing significant bias with wide limits of agreement and percentage error (1.47 +/- 1.46 L/min; 97%). Bias was small but the limits of agreement and percentage error were large for cardiac output at 10 and 120 mins after resuscitation (-0.1 +/- 1.88 [98%] and -0.17 +/- 1.32 [71%] L/min, respectively). There appeared to be a negative but not significant correlation after hemorrhage (r = -.45; p = .15). PulseCO determination of cardiac output does not accurately predict rapid decreases in cardiac output or the effects of fluid resuscitation in dogs. Recalibration of PulseCO may be necessary after any apparent or suspected decrease in cardiac preload, afterload, or contractility.