To determine the causes of impaired left ventricular function during hypovolemic shock we measured diastolic and end-systolic pressure-volume relationships and hemodynamics. Left ventricular pressure (Millar catheter) and volume (3 ultrasonic crystal pairs) were measured in six open-chest, chloralose-morphine anesthetized, juvenile pigs. After baseline measurements, the pigs were bled and maintained at a mean aortic pressure of 50 cmH2O for 7 +/- 1 h. After resuscitation with all shed blood, left ventricular function was markedly impaired as indicated by increased end-diastolic pressure (20.3 vs. 8.7 cmH2O at baseline, P less than 0.05), decreased aortic pressure (36% of baseline, P less than 0.01), and decreased stroke volume (50% of baseline, P less than 0.01). Systolic contractility was increased (P less than 0.05), but diastolic compliance was greatly reduced due to decreased diastolic maximum (52% of baseline, P less than 0.01) and equilibrium volumes (57% of baseline, P less than 0.01). We conclude that impaired left ventricular function during hypovolemic shock is due entirely to increased diastolic stiffness. These results can theoretically be accounted for by a 20% reduction in myocardial muscle length with no change in muscle stress-strain characteristics. This may be the physiological expression of morphologically observed myocardial "zonal lesions" of hypovolemic shock.