Changes in left ventricular preload and contractility following severe burns in the dog

To examine the effects of severe burns on preload and left ventricular (LV) contractility, we continuously measured LV pressures and dimensions in severely burned dogs throughout the early part of the postburn period. Hemodynamic parameters, including cardiac output (CO), mean aortic pressure (MAP), heart rate (HR), LV pressures and their first derivatives (dP/dt), and the LV regional dimension, were measured and compared before and every 30 min after burns were produced (up to 360 min) in four groups: group A (n=7), dogs with sham burns; group B (n=5), dogs with nonresuscitated full-thickness burns involving 50% of the total body surface area; group C (n=6), dogs with burns resuscitated with lactated Ringer's solution at 4 ml × kg × % burn/24 h; and group D (n=6), dogs with burns resuscitated with 1.5% dextran in lactated Ringer's solution at 2 ml × kg × % burn/24 h. From these measurements, we obtained the LV end-diastolic segment length (EDL) as an index of preload and three indices of cardiac contractility, i.e., peak dP/dt, the percentage of shortening (%ΔL), and mean Vcf. Our results showed that CO, MAP, and preload (i.e., EDL) decreased significantly more in the three burn groups (groups B, C, and D) than in the sham burn group, but that there were no significant differences in CO, MAP, and EDL among the three burn groups. The three indices of contractility also decreased significantly more in the three burn groups than in the sham burn group. When changes in LV end-diastolic pressure (LVEDP) and EDL during the experiment were examined, apparent discrepancies were found in the changes between LVEDP and EDL in the burn-resuscitated groups (C and D); the postburn decreases in LVEDP in the burn-resuscitated groups were significantly smaller than those in the burn-nonresuscitated group, but there were no significant differences in the postburn decreases in EDL among the three burn groups. These findings indicate that: (1) the fall in cardiac output following severe burns was due to both the decreased preload and decreased LV contractility; (2) the decreased preload and LV contractility could not be restored to preburn levels by conventional fluid therapy during the 6-h experimental period; and (3) the possible decrease in LV compliance was more prominent in the burn-resuscitated groups.