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人工通气仔猪高血容量的循环和通气效应

Circulatory and ventilatory effects of hypervolaemia in artificially ventilated piglets.

作者信息

Lindahl S

出版信息

Can Anaesth Soc J. 1981 Jul;28(4):356-62. doi: 10.1007/BF03007803.

DOI:10.1007/BF03007803
PMID:7260714
Abstract

The influence of hypervolaemia upon circulation and pulmonary ventilation was studied in six piglets (body weights 8.5-10.5 kg). A new functional principle for artificial ventilation was used. The alveolar ventilation was unchanged at normovolaemia and hypervolaemia. Arterial blood gases were sampled and end-tidal carbon dioxide concentrations were measured continuously. Central circulation was followed by pressure recordings and an electromagnetic flow meter for cardiac output measurements. Mean values +/- SEM of end-inspiratory tracheal pressures increased from 0.98 +/- 0.06 kPa at normovolaemia to 1.57 +/- 0.06 kPa at hypervolaemia (p less than 0.02). In all animals total compliance decreased (p less than 0.02). Simultaneously the insufflation time for the tidal volume decreased by 13 per cent (p less than 0.05). Arterial oxygen tensions decreased from 8.5 +/- 0.48 kPa to 7.0 +/- 0.77 kPa (p less than 0.05). During hypervolaemia aortic pressures increased from 13.1 +/- 1.3 kPa to 14.9 +/- 0.8 kPa (p less than 0.05), pulmonary artery pressures from 2.8 +/- 0.33 kPa to 5.0 +/- 0.53 kPa (p less than 0.02) and cardiac output from 1.07 +/- 0.17 1 . min-1 to 1.5 +/- 0.19 1 . min-1 (p less than 0.02). The stroke work for the right heart increased by 74 per cent (p less than 0.02) and for the left heart by 62 per cent (p less than 0.02). Pulmonary vascular resistance was unchanged, while systemic vascular resistance was significantly decreased (p less than 0.05). The positive effect upon systemic circulation gained by the use of excessive fluid therapy resulted in an overcirculation within the lungs which reduced pulmonary ventilation. This reduction could most probably be related to a closure of terminal airways secondary to lung hyperperfusion, increasing the pulmonary shunt.

摘要

对6只仔猪(体重8.5 - 10.5千克)研究了血容量过多对循环和肺通气的影响。采用了一种新的人工通气功能原理。在血容量正常和血容量过多时,肺泡通气量不变。采集动脉血气样本并持续测量呼气末二氧化碳浓度。通过压力记录和电磁流量计测量心输出量来跟踪中心循环。吸气末气管压力的平均值±标准误从血容量正常时 的0.98±0.06千帕增加到血容量过多时的1.57±0.06千帕(p<0.02)。在所有动物中,总顺应性降低(p<0.02)。同时,潮气量的吹气时间减少了13%(p<0.05)。动脉血氧张力从8.5±0.48千帕降至7.0±0.77千帕(p<0.05)。在血容量过多期间,主动脉压力从13.1±1.3千帕增加到14.9±0.8千帕(p<0.05),肺动脉压力从2.8±0.33千帕增加到5.0±0.53千帕(p<0.02),心输出量从1.07±0.17升·分钟⁻¹增加到1.5±0.19升·分钟⁻¹(p<0.02)。右心的每搏功增加了74%(p<0.02),左心增加了62%(p<0.02)。肺血管阻力不变,而体循环血管阻力显著降低(p<0.05)。过度液体治疗对体循环产生的积极作用导致肺内循环过度,从而降低了肺通气。这种降低很可能与肺过度灌注继发的终末气道关闭有关,增加了肺内分流。

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