Validation study of PulseCO system for continuous cardiac output measurement.

Ultrasonic flow probes have been used to optimize biventricular pacing immediately after cardiopulmonary bypass, improving cardiac output (CO) by 10%; however, flow probes must be removed with chest closure. The PulseCO system (LiDCO Limited, Cambridge, UK) may extend optimization into the postoperative period, but controlled validations have not been reported. Six anesthetized pigs were instrumented for right heart bypass. Flow was varied from 3 to 1 L/min and then back to 3 in 0.5 L/min increments for 60 second intervals. CO was measured by ultrasonic flow probe on the aorta and by PulseCO using a femoral arterial line. PulseCO and flow probe accurately measured CO (PulseCO R2: 0.79-0.95; flow probe R2: 0.96-0.99). At flow of 2 L/min, when the heart was paced 30 bpm over the sinus rate, PulseCO falsely indicated an increase in CO (2.13 vs. 2.30 L/min, p = 0.014). When mean arterial pressure was increased by 20% using a phenylephrine infusion, PulseCO falsely indicated an increase in CO (2.13 vs. 2.47 L/min, p = 0.014). When mean arterial pressure was decreased by 20% using a nitroprusside infusion, PulseCO falsely indicated a decrease in CO (2.13 vs. 1.79 L/min, p = 0.003). PulseCO appears to be useful for assessing acute changes in CO if its limitations are recognized.

High-flow venovenous rewarming for the correction of hypothermia in a canine model of hypovolemic shock.

BACKGROUND: Continuous arteriovenous rewarming (CAVR) has been shown to effectively reverse hypothermia; however, its use is limited in the setting of profound hypotension. We have evaluated the effectiveness of high-flow venovenous rewarming (HFVR) using bypass for the correction of hypothermia in a hypotensive canine model and compared these results to CAVR. METHODS: Eight dogs, randomly assigned to either HFVR or CAVR, were cooled to a core temperature of 29.5 degrees C and then bled to a mean arterial pressure of 55 mm Hg. Rewarming was then initiated and the time required for blood, liver parenchyma, and esophageal (core) temperature to reach 36 degrees C was recorded. RESULTS: Mean flow rates were 1,536 +/- 667 mL/min for HFVR and 196 +/- 35 mL/min for CAVR (p = 0.007). Time in minutes to rewarm to 36 degrees C for the HFVR versus the CAVR groups, respectively, were as follows: blood, 12 +/- 2 versus 99 +/- 19; liver, 21 +/- 3 versus 102 +/- 16; and esophageal, 25 +/- 6 versus 125 +/- 17 (all < 0.001). CONCLUSION: HFVR is an effective method for rapid rewarming in a profoundly hypothermic, hypotensive animal model and may have clinical utility in patients presenting with hypovolemia/hypotension complicated by hypothermia.

Intracranial complications of preinjury anticoagulation in trauma patients with head injury.

BACKGROUND: We have evaluated our recent experience as a Level I trauma center to test the hypothesis that preinjury anticoagulation adversely affects the morbidity and mortality of trauma patients with an intracranial injury. METHODS: Records of 380 patients admitted to the trauma service from January 1997 to December 1998 who at the time of admission were taking warfarin, low-molecular-weight heparin, aspirin, nonsteroidal anti-inflammatory drugs, clopidogrel, dipyridamole, pentoxifylline, or naproxen were reviewed. Thirty-seven patients with intracranial injuries were identified and compared with a matched (age, gender, mechanism, and severity of injury) control group of 37 patients with similar head injury but not taking any anticoagulant randomly selected from the trauma registry for that same time period. RESULTS: The control and anticoagulated groups were comparable in terms of age, 75 +/- 8 versus 74 +/- 11 years (p = 0.655); gender, 22 men/15 women versus 21 men/16 women; mechanism of injury, 30 falls/7 motor vehicle crashes versus 30 falls/7 motor vehicle crashes; and length of hospital stay, 11 +/- 14 versus 10 +/- 11 days (p = 0.853). In the anticoagulated group, the mean Injury Severity Score was 17.0 +/- 7.8 and the mean Glasgow Coma Scale score was 11.8 +/- 4.0; these were not significantly different from the control group, which had a mean Injury Severity Score of 19.8 +/- 8.1 (p = 0.143) and a Glasgow Coma Scale score of 12.5 +/- 2.6 (p = 0.378). There were 14 deaths (38%) in the anticoagulation group, versus 3 deaths in the control group (8%) (p = 0.006). In the anticoagulation group, 4 of 12 patients (33%) taking warfarin died, whereas 9 of 19 patients (47%) taking aspirin died (p = 0.285). All deaths were secondary to head injuries; all deaths in the control group and all but one in the anticoagulated group were the result of a fall; 6 of 10 anticoagulated patients who fell on stairs died, and 5 of these were taking aspirin only. CONCLUSION: These data indicate that the trauma patient with preinjury anticoagulation such as warfarin or even aspirin who has an intracranial injury has a four- to fivefold higher risk of death than the nonanticoagulated patient. The efficacy of reversing the anticoagulant effect at the time of hospital admission remains to be evaluated.