Experimental amniotic fluid embolism in animals produces profound pulmonary hypertension and acute cor pulmonale without evidence of left ventricular compromise. Hemodynamic alterations associated with clinicl amniotic fluid embolism were traditionally explained within this experimental framework. A reanalysis of the 5 published cases of amniotic fluid embolism, which include hemodynamic data derived from pulmonary artery catheterization as well as a report of a 6th case suggests a hemodynamic interpretation different from the traditional one based on the animal model. Left ventricular failure is the only hemodynamic abnormality consistently observed in humans and the published data are most readily explained on this basis alone. A theoretical model of hemodynamic changes accompanying amniotic fluid embolism that incorporates both experimental and clincial observations is presented. Therapeutic implications are discussed.