Pulmonary edemaformation withmyocardial infarction andleft atrial hypertension: intravascular and extravascular pulmonary fluid volumes

Theresponseofpulmonary blood volume(PBV)andextravascular lung water(EVLW) was examined byindicator-diluti on techniques in14"openchest"dogs, seven thatunderwent coronaryocclusion (group 2)andseventhatserved ascontrols (group 1).Datawere obtained ina control stage(control stage1)45minafter coronaryligation (control stage 2),and90minafter theleft atrial pressurehadbeenincreased to-35mm Hgwithaleft atrial balloon. Ingroup2animals, EVLW increased after coronaryligation without amarkedchange inleft atrial pressure(6.9+ 0.4to8.2+ 0.5ml/kg mean + SD;p < .05) andincreased to20.1± 1.4ml/kg after theproduction ofleft atrial hypertension (p< .005vs control andvs coronaryligation). Inthecontrol dogs, EVLW was un- changed 45minafter theinitial datahadbeencollected (7.1 ± 0.7to7.0± 0.8ml/kg). After the production ofleft atrial hypertension inthese dogs, EVLW rose(14.8 ± 1.2ml/kg; p< .005 vscontrol stage 1 andcontrol stage2,p < .01vsgroup2dogs). PBVdidnotchange significantly withligation andincreased similarly inbothgroupsduring left atrial hypertension. We conclude that coronary ligation canincrease EVLW,independent ofmicrovascular hydrostatic pressure. During theproduc- tion ofleft atrial hypertension there was greater transcapillary fluid fluxingroup2dogsatmatched levels ofleft atrial pressureelevation. Thismay beduetoan alteration inthepermeability ofthe pulmonary capillary membrane during myocardial infarction andprovides apartial explanation forthe occasional disparity between left heart dynamics andthechest radiograph inacutemyocardial infarc- tion.