Biancolini C A, Del Bosco C G, Jorge M A, Poderoso J J, Capdevila A A
Intensive Care Division, University Hospital, Buenos Aires, Argentina.
Crit Care Med. 1993 Aug;21(8):1164-8. doi: 10.1097/00003246-199308000-00015.
To determine in hypothermic patients if a) the decrease in oxygen consumption (VO2) is exclusively dependent on the decrease in metabolic rate, or b) as a consequence of the greater hemoglobin affinity for oxygen, hypothermic tissues have impaired oxygen extraction.
Clinical, prospective study; sequential measurements of oxygen-related variables during active core rewarming.
Intensive care unit of a university hospital.
Twelve patients (44 +/- 16 yrs of age) admitted to the intensive care unit with a core temperature of < 34 degrees C due to severe neurologic damage.
Rewarming (with heated enemas, gastric infusions, and heated blankets) to increase body temperature at a rate of approximately 1 degree C/hr. Measurements of oxygen-related variables were performed at a baseline of 31.0 +/- 1.1 degrees C, and repeated at each 1 degree C increase to reach a core temperature of approximately 35 degrees C.
Oxygen-related variables of rewarmed patients were allocated into two groups, above or below the observed mean core temperature of 33.1 degrees C recorded for all measurements (n = 45). Comparison of the low core temperature group (31.1 +/- 1.4 degrees C; n = 20) with the high core temperature group (34.7 +/- 0.9 degrees C; n = 25) showed that the group with the lower core temperatures had a significant increase in VO2 index (67 +/- 22 vs. 103 +/- 38 mL/min/m2 [p < .001]), oxygen delivery index (183 +/- 73 vs. 290 +/- 123 mL/min/m2 [p < .001]), and the PO2 value at which hemoglobin was half-saturated with oxygen ([P50] 23 +/- 5.7 vs. 27.7 +/- 5.7 torr [3.0 +/- 0.7 vs. 3.6 +/- 0.7 kPa] [p < .02]). An increase in metabolic acidosis could be observed in the lower temperature group: arterial pH 7.47 +/- 0.15 vs. 7.34 +/- 0.13 (p < .01); base deficit -3.7 +/- 6.7 vs. -8.2 +/- 4.9 mEq/L (p < .02). The oxygen extraction ratio remained unchanged: 0.39 +/- 0.10 vs. 0.38 +/- 0.10 (NS).
These data show that VO2 was reduced to half of normal values during hypothermia. Active core rewarming produced an average 4.5% increase in VO2 per 1 degree C that was characterized by the wide variation observed in this metabolic response between different patients and for individual cases. Despite the rightward shift of P50 observed during rewarming (mainly due to the Bohr effect), no change was reflected on the oxygen extraction ratio.
确定在体温过低的患者中,a)氧耗量(VO₂)的降低是否仅取决于代谢率的降低,或者b)由于血红蛋白对氧的亲和力增加,体温过低的组织是否存在氧摄取受损的情况。
临床前瞻性研究;在主动复温过程中对与氧相关的变量进行连续测量。
大学医院的重症监护病房。
12名患者(年龄44±16岁)因严重神经损伤入住重症监护病房,核心体温<34℃。
通过加热灌肠、胃内灌注和加热毛毯进行复温,使体温以约1℃/小时的速度升高。在基线体温31.0±1.1℃时测量与氧相关的变量,并在体温每升高1℃时重复测量,直至核心体温达到约35℃。
将复温患者的与氧相关的变量分为两组,高于或低于所有测量记录的观察到的平均核心体温33.1℃(n = 45)。将低核心体温组(31.1±1.4℃;n = 20)与高核心体温组(34.7±0.9℃;n = 25)进行比较,结果显示,核心体温较低的组VO₂指数显著升高(67±22 vs. 103±38 mL/min/m² [p <.001])、氧输送指数显著升高(183±73 vs. 290±123 mL/min/m² [p <.001]),以及血红蛋白氧饱和度为一半时的PO₂值显著升高([P50] 23±5.7 vs. 27.7±5.7 torr [3.0±0.7 vs. 3.6±0.7 kPa] [p <.02])。在低温组中可观察到代谢性酸中毒增加:动脉pH 7.47±0.15 vs. 7.34±0.13(p <.01);碱剩余-3.7±6.7 vs. -8.2±4.9 mEq/L(p <.02)。氧摄取率保持不变:0.39±0.10 vs. 0.38±0.10(无显著差异)。
这些数据表明,体温过低期间VO₂降至正常值的一半。主动复温使VO₂平均每升高1℃增加4.5%,其特征是不同患者之间以及个别病例的这种代谢反应存在广泛差异。尽管在复温过程中观察到P50向右移动(主要由于波尔效应),但氧摄取率没有变化。