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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:The effects of dobutamine, nitroprusside, or volume expansion on cardiac output and lung water after CPPV. 351 43

Pulmonary microemboli may play a role in the adult respiratory distress syndrome, creating both pulmonary oedema and hypoxaemia. We measured the time course of pulmonary oedema and hypoxaemia after pulmonary microemboli of 63-74 mu starch were infused into dogs. Dogs were divided into two groups: six dogs that did not develop pulmonary oedema, and seven that did. Immediately after emboli there was no difference between groups in the large fall in PaO2 or the rise in Qs/Qt. Therefore the hypoxaemia of pulmonary embolism is not created by pulmonary oedema. As pulmonary oedema increased with time in the oedematous dogs, PaO2 fell further. There was no further reduction in PaO2 in the dogs who did not develop pulmonary oedema. We conclude that hypoxaemia after pulmonary embolism may be worsened if pulmonary oedema occurs, but the immediate large reduction in PaO2 after embolism is not created by pulmonary oedema.
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PMID:Hypoxaemia created by pulmonary oedema after pulmonary microemboli in dogs. 683 Dec 90