Incidence of Hypertriglyceridemia in Patients on Propofol, Clevidipine, or Both.

BACKGROUND: Propofol and clevidipine (PC) are commonly used in the treatment of critically ill patients. While both medications are lipid emulsions, there is limited evidence concerning the incidence of hypertriglyceridemia (HTG) when these agents are used individually or concurrently. OBJECTIVE: The objective of this study is to determine the effects of propofol, clevidipine, or concurrent PC on triglycerides (TGs) and related outcomes in critically ill adults. METHODS: This was a retrospective cohort study conducted at an academic medical center. Patients were included if they received ≥24 hours of continuous propofol and/or clevidipine. Excluded were those without TG levels after ≥24 hours of infusion, baseline HTG, acute pancreatitis at admission, or receiving total parenteral nutrition with lipids. The primary outcome was incidence of HTG (defined as a TG level >400 mg/dL). Secondary outcomes included median and peak TG levels, hospital length of stay, intensive care unit length of stay, total lipid infused, time to peak TG level, peak lipase level, and development of pancreatitis. RESULTS: In total, 190 patients were studied: 109 in the propofol group, 50 in the clevidipine group, and 31 in the PC group. Incidence of HTG was similar (19 [17.4%] vs 6 [12%] vs 4 [12.9%] patients, P = 0.6246). Peak and median TG levels were similar for propofol, clevidipine, and PC groups (216 mg/dL vs 189.5 mg/dL vs 205 mg/dL, P = 0.7069; 177 mg/dL vs 185.5 mg/dL vs 177 mg/dL, P = 0.6791). CONCLUSIONS AND RELEVANCE: There was a similar incidence of HTG in all groups. The results of this study suggest that the concurrent use of PC should not modify the frequency of TG level monitoring.

Effect of an aerodynamic helmet on head temperature, core temperature, and cycling power compared with a traditional helmet.

Nonvented "aerodynamic helmets" reduce wind resistance but may increase head (Th) and gastrointestinal (Tgi) temperature and reduce performance when worn in hot conditions. This study tested the hypothesis that Th and Tgi would be greater during low-intensity cycling (LIC) in the heat while wearing an aero helmet (AERO) vs. a traditional vented racing helmet (REG). This study also tested the hypothesis that Th, Tgi, and finish time would be greater, and power output would be reduced during a self-paced time trial in the heat with AERO vs. REG. Ten highly trained heat-acclimated endurance athletes conducted LIC (50% V[Combining Dot Above]O2max, LIC) and a high-intensity 12-km self-paced time trial (12-km TT) on a cycle ergometer in 39° C on 2 different days (AERO and REG), separated by >48 hours. During LIC, Th was higher at minute 7.5 and all time points thereafter in AERO vs. REG (p < 0.05). Similarly, during the 12-km TT, Th was higher at minutes 12.5, 15, and 17.5 in AERO vs. REG (p < 0.05). Heart rate (HR) and Tgi increased during LIC and during 12-km TT (both p < 0.001); however, no significant interaction (helmet × time) existed for HR or Tgi at either intensity (all p > 0.05). No group differences existed for finish time or power output during the 12-km TT (both p > 0.05). In conclusion, Th becomes elevated during cycling in the heat with an aero helmet compared with a traditional vented racing helmet during LIC and high-intensity cycling, yet Tgi and HR responses are similar irrespective of helmet type and Th. Furthermore, the higher Th that develops when an aero helmet is worn during cycling in the heat does not affect power output or cycling performance during short-duration high-intensity events.

The magnitude of heat stress-induced reductions in cerebral perfusion does not predict heat stress-induced reductions in tolerance to a simulated hemorrhage.

The mechanisms responsible for heat stress-induced reductions in tolerance to a simulated hemorrhage are unclear. Although a high degree of variability exists in the level of reduction in tolerance amongst individuals, syncope will always occur when cerebral perfusion is inadequate. This study tested the hypothesis that the magnitude of reduction in cerebral perfusion during heat stress is related to the reduction in tolerance to a lower body negative pressure (LBNP) challenge. On different days (one during normothermia and the other after a 1.5°C rise in internal temperature), 20 individuals were exposed to a LBNP challenge to presyncope. Tolerance was quantified as a cumulative stress index, and the difference in cumulative stress index between thermal conditions was used to categorize individuals most (large difference) and least (small difference) affected by the heat stress. Cerebral perfusion, as indexed by middle cerebral artery blood velocity, was reduced during heat stress compared with normothermia (P < 0.001); however, the magnitude of reduction did not differ between groups (P = 0.51). In the initial stage of LBNP during heat stress (LBNP 20 mmHg), middle cerebral artery blood velocity and end-tidal PCO(2) were lower; whereas, heart rate was higher in the large difference group compared with small difference group (P < 0.05 for all). These data indicate that variability in heat stress-induced reductions in tolerance to a simulated hemorrhage is not related to reductions in cerebral perfusion in this thermal condition. However, responses affecting cerebral perfusion during LBNP may explain the interindividual variability in tolerance to a simulated hemorrhage when heat stressed.