Hopster K, Wogatzki A, Geburek F, Conze P, Kästner S B R
Equine Clinic, University of Veterinary Medicine Hanover, Foundation, Germany.
Center for Systems Neuroscience Hanover, University of Veterinary Medicine Hanover, Foundation, Germany.
Equine Vet J. 2017 Mar;49(2):250-256. doi: 10.1111/evj.12555. Epub 2016 Mar 2.
High airway pressures, necessary to keep equine lungs open, can have a detrimental impact on central and peripheral perfusion.
The aim of this study was to assess the effects of stepwise increasing airway pressure recruitment on central and intestinal perfusion and oxygenation during isoflurane anaesthesia in horses.
In vivo experimental study.
Ten anaesthetised horses were ventilated using intermittent positive pressure ventilation immediately after induction. After 90 min, end-expiratory pressure (PEEP) was increased by steps of 5 cmH O every 10 min up to a PEEP of 30 cmH O and decreased back to zero maintaining a constant airway pressure difference of 20 cmH O. Mean arterial blood pressure (MAP), heart rate, central venous pressure, pulmonary artery pressure, expiratory isoflurane concentration and cardiac output (thermodilution method) were measured. Cardiac index (CI) was calculated. Arterial blood gases were taken to measure arterial partial oxygen pressure (PaO ) and calculate arterial oxygen saturation (SaO ). Intestinal microperfusion and oxygenation were measured by laser Doppler flowmetry and white-light spectrophotometry. After ventral median laparotomy, a probe was placed on the stomach, jejunum and pelvic flexion of the colon. An ANOVA for repeated measurements and Tukey's post hoc test were used for statistical analysis (α = 5%).
Recruitment of the lungs resulted in a significant increase in PaO from 201 ± 58 mmHg (baseline) to a maximum of 495 ± 75 mmHg. The CI and MAP decreased continuously with increasing airway pressures. When CI and MAP were 37 ± 9 ml/kg/min and 52 ± 8 mmHg (at PEEP of 25 cmH O), respectively, a sudden decrease in intestinal perfusion followed by a delayed decrease in oxygenation occurred.
There was linear correlation between airway pressures and CI and MAP but not between central and gastrointestinal perfusion. Despite improvement of arterial oxygenation the decrease in CI and, therefore, in oxygen delivery PEEP resulted in a decrease in gastrointestinal oxygenation.
为使马肺保持张开状态而需要的高气道压力，可能会对中枢和外周灌注产生不利影响。
本研究旨在评估在马异氟烷麻醉期间，逐步增加气道压力复张对中枢和肠道灌注及氧合的影响。
体内实验研究。
10匹麻醉后的马在诱导后立即采用间歇正压通气进行通气。90分钟后，呼气末正压（PEEP）每10分钟以5 cmH₂O的步长增加，直至PEEP达到30 cmH₂O，然后再降至零，同时保持气道压差恒定为20 cmH₂O。测量平均动脉血压（MAP）、心率、中心静脉压、肺动脉压、呼气末异氟烷浓度和心输出量（热稀释法）。计算心脏指数（CI）。采集动脉血气以测量动脉血氧分压（PaO₂）并计算动脉血氧饱和度（SaO₂）。通过激光多普勒血流仪和白光分光光度法测量肠道微灌注和氧合。在腹正中剖腹术后，将探头置于胃、空肠和结肠盆腔弯曲处。采用重复测量方差分析和Tukey事后检验进行统计分析（α = 5%）。
肺复张导致PaO₂从201±58 mmHg（基线）显著增加至最高495±75 mmHg。CI和MAP随着气道压力增加而持续下降。当CI和MAP分别为37±9 ml/kg/min和52±8 mmHg（PEEP为25 cmH₂O时），肠道灌注突然下降，随后氧合延迟下降。
气道压力与CI和MAP之间存在线性关系，但中枢与胃肠道灌注之间不存在线性关系。尽管动脉氧合有所改善，但CI降低，进而氧输送减少，PEEP导致胃肠道氧合下降。
