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持续气道正压通气(CPPV)后多巴酚丁胺、硝普钠或容量扩充对心输出量和肺水的影响。

The effects of dobutamine, nitroprusside, or volume expansion on cardiac output and lung water after CPPV.

作者信息

Noble W H, Kay J C

出版信息

Can Anaesth Soc J. 1986 Jan;33(1):48-56. doi: 10.1007/BF03010908.

Abstract

Pulmonary microemboli can create an ARDS-like state in dogs (high pulmonary vascular resistance, pulmonary oedema and arterial hypoxemia). CPPV can correct the hypoxemia of pulmonary microemboli but reduces cardiac output (Q) and tissue oxygenation. This paper compares the effect of improving Q by infusing volume, reducing afterload, or increasing myocardial contractility. Four groups of seven dogs were studied. All had 0.125 g . kg-1 of starch microemboli (63-74 microns) infused and then CPPV at 15 cm H2O applied. The control group had no further treatment applied. In three other groups volume (dextran) or dobutamine or nitroprusside (NTP) was infused to return Q to the level before CPPV was applied. All treatments (volume, dobutamine and NTP) improved Q and O2 transport. Only the volume group had a significant increase in pulmonary microvascular pressure, Pmv = PLA + 0.4 (PPA - PLA) from 2.53 +/- 0.27 to 3.35 +/- 0.13 kPa, p less than 0.05. Only the volume group demonstrated a significant increase in lung water above (double) the control group as measured by a double indicator dilution technique (ETVL) and post mortem lung weights. We conclude volume infusions to improve a CPPV depressed Q may increase lung water and that better treatment would be to infuse NTP or dobutamine, thus maintaining a lower Pmv and therefore lung water. As a corollary the least CPPV should be applied to maintain adequate oxygenation and create the least need for interventions to improve Q.

摘要

肺微栓塞可在犬类中引发类似急性呼吸窘迫综合征的状态(高肺血管阻力、肺水肿和动脉血氧不足)。持续气道正压通气(CPPV)可纠正肺微栓塞导致的低氧血症,但会降低心输出量(Q)和组织氧合。本文比较了通过输注液体、降低后负荷或增加心肌收缩力来提高心输出量的效果。研究了四组,每组七只犬。所有犬均输注0.125 g·kg-1的淀粉微栓子(63 - 74微米),然后施加15 cm H2O的持续气道正压通气。对照组未进行进一步治疗。在其他三组中,输注液体(右旋糖酐)、多巴酚丁胺或硝普钠(NTP)以使心输出量恢复到施加持续气道正压通气之前的水平。所有治疗(输注液体、多巴酚丁胺和硝普钠)均提高了心输出量和氧输送。只有输注液体组的肺微血管压力有显著升高,肺微血管压力Pmv = PLA + 0.4(PPA - PLA)从2.53±0.27 kPa升高至3.35±0.13 kPa,p < 0.05。通过双指示剂稀释技术(ETVL)和死后肺重量测量,只有输注液体组的肺水含量显著高于(两倍于)对照组。我们得出结论,输注液体以改善因持续气道正压通气降低的心输出量可能会增加肺水含量,更好的治疗方法是输注硝普钠或多巴酚丁胺,从而维持较低的肺微血管压力,进而降低肺水含量。由此推论,应采用最低的持续气道正压通气来维持足够的氧合,并尽量减少改善心输出量的干预措施的需求。

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