[Significance of respiratory compensation in acidosis in calves].
[Significance of respiratory compensation in acidosis in calves].
复制标题
呼吸代偿在犊牛酸中毒中的意义
DOI：
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发表时间：
2000
期刊：
影响因子：
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通讯作者：
W. Hofmann
中科院分区：
文献类型：
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作者：
J. Berchtold;H. Hartmann;W. Hofmann
在n = 36头患有新生儿腹泻和酸中毒（静脉血pH值：< 7.30; x +/- s = 7.08 +/- 0.15）的小牛（年龄：x +/-s = 8.7 +/- 5.0 d）中观察到酸碱状态的呼吸组分PvCO 2。在n = 10头（28%）患有重度代谢性酸中毒（pH：x +/- s = 7.03 +/- 0.12; BE：x +/- s = -22.1 +/- 5.3 mmol/l）的小牛中，PvCO 2降低< 5.3 kPa（x +/- s = 4.5 +/- 0.5 kPa），并显示出明显的呼吸代偿。在n = 16（44%）头酸中毒小牛中观察到PvCO 2介于5.3-6.7 kPa（x +/- s = 6.0 +/- 0.4 kPa）之间（pH：x +/- s = 7.11 +/- 0.13; BE：x +/- s = -15.2 +/- 7.4 mmol/l）。这些n = 26（72%）小牛表现出简单的代谢性酸中毒，这是新生儿腹泻小牛的常见症状。其余n = 10头（28%）小牛显示PvCO 2增加> 6.7 kPa（x +/- s = 8.0 +/- 1.5 kPa）。这些动物存在混合性代谢性酸中毒（pH：x +/- s = 7.08 +/- 0.20; BE：x +/- s = -13.9 +/- 10.3 mmol/l），因为pH值降低无法通过酸碱状态的代谢组分HCO 3-降低单独确定。在住院期间死亡的小牛和PvCO 2> 6.7 kPa的小牛往往更年轻，并显示出部分显着较低的供氧参数PvO 2和SvO 2值。乳酸盐在垂死小牛中显着较高，但在混合性酸中毒小牛中不高，另一方面，混合性酸中毒小牛脱水程度更高。研究的小牛酸中毒性疾病的呼吸补偿功能能力几乎与狗和人相同。一些小牛呼吸补偿失败的原因之一可能是更严重的血容量不足。使用“静脉低氧血症”（降低PvO 2和降低SvO 2）检测组织缺氧比乳酸浓度更容易。
The respiratory component PvCO2 of acid-base-status was observed in n = 36 calves (age: x +/- s = 8.7 +/- 5.0 d) with neonatal diarrhea and an acidosis (venous blood-pH: < 7.30; x +/- s = 7.08 +/- 0.15). In n = 10 (28%) calves with a severe metabolic acidosis (pH: x +/- s = 7.03 +/- 0.12; BE: x +/- s = -22.1 +/- 5.3 mmol/l) the PvCO2 was decreased < 5.3 kPa (x +/- s = 4.5 +/- 0.5 kPa) and showed a distinct respiratory compensation. A PvCO2 between 5.3-6.7 kPa (x +/- s = 6.0 +/- 0.4 kPa) was observed in n = 16 (44%) acidotic calves (pH: x +/- s = 7.11 +/- 0.13; BE: x +/- s = -15.2 +/- 7.4 mmol/l). These n = 26 (72%) calves showed a simple metabolic acidosis which is well known for calves with neonatal diarrhea. The remaining n = 10 (28%) calves showed an increase of the PvCO2 > 6.7 kPa (x +/- s = 8.0 +/- 1.5 kPa). These animals had a mixed respiratory-metabolic acidosis (pH: x +/- s = 7.08 +/- 0.20; BE: x +/- s = -13.9 +/- 10.3 mmol/l), as the decrease of the pH could not be determined by the decreased metabolic component HCO3- of acid-base-status alone. Calves which died during hospitalization and calves with a PvCO2 > 6.7 kPa tended to be younger and showed partially significant lower values for the parameters of oxygen-supply PvO2 and SvO2. Lactate was significantly higher in dying calves but not in calves with a mixed acidosis which on the other hand were more dehydrated. The functional capacity of respiratory compensation of acidotic disorders in the calves studied promised to be almost the same as in dog and man. One reason for the failure of respiratory compensation in some calves could be a more severe hypovolemia. With the use of "venous hypoxemia" (decrease PvO2 and decrease SvO2) the detection of tissue hypoxia was easier than with lactate concentration.