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 (\(\dot Q\)) and tissue oxygenation. This paper compares the effect of improving\(\dot Q\) 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,\(Pmv = P\overline {LA} + 0.4(P\overline {PA} - P\overline {LA} )\) from 2.53 ± 0.27to3.35 ± 0.13 kPa, p < 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 oxygénation and create the least need for interventions to improve Q.
Résumé
Les microembolies pulmonaires peuvent créer chez les chiens un état identique au syndrome de détresse respiratoire de l’adulte (résistance vasculaire pulmonaire élevée, œdème pulmonaire et hypoxémie artérielle). La ventilation à pression positive continue peut corriger l’hypoxémie dû aux microembolies pulmonaires mais réduit le débit cardiaque (\(\dot Q\)) et l’oxygénation tissulaire. Cette étude compare les effets d’une amélioration du débit cardiaque (\(\dot Q\)) par la perfusion de volume, la réduction de la post-charge ou l’augmentation de la contractilité myocardique. Quatre groupes de sept chiens chaque, ont été étudiés. Tous ont reçu 0.125 g·kg-1 de particules d’amidon (63–74 microns) en perfusion et une ventilation à pression positive continue à 15cm H2O. Pour le groupe contrôle aucun traitement ne fut appliqué. Dans les trois autres groupes du volume (dextran) ou dobutamine ou nitroprussiate (NTP) a étéperfusé afin de retourner le débit cardiaque (\(\dot Q\)) au niveau initial avant l’application de ventilation à pression positive continue. Tous les traitements (volume, dobutamine et NTP) ont amélioré le débit cardiaque ainsi que le transport d’oxygène. Seul le groupe “volume” a démontré une augmentation significative dans la\(Pmv = P\overline {LA} + 0.4(P\overline {PA} - P\overline {LA} )\) de2.53±0.27à3.35±0.13 kPa,p< 0.05. Seul le groupe traité par du volume a démontre une augmentation significative de l’eau pulmonaire qui a doublé par rapport au contrôle tel que mesuré par la technique de dilution à double indicateur (ETVl) et la pesée des poumons post-mortem. On conclut que la perfusion de volume afin d’améliorer un débit cardiaque déprimé suite â la ventilation à pession positive continue peut augmenter l’eau pulmonaire. Un meilleur traitement serait l’administration de nitroprussiate ou de dobutamine afin de maintenir un Pmv bas et ainsi empêcher la rétention de l’eau dans le poumon. Comme corollaire on devra utiliser avec précaution la ventilation à pression positive continue pour maintenir une bonne oxygénation tissulaire, afin de ne point être obliger de créer le besoin d’altérer le débit cardiaque.
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This study was funded by the Medical Research Council of Canada.
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Noble, W.H., Kay, J. The effects of dobutamine, nitroprusside, or volume expansion on cardiac output and lung water after CPPV. Can Anaesth Soc J 33, 48–56 (1986). https://doi.org/10.1007/BF03010908
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DOI: https://doi.org/10.1007/BF03010908