Effects of thermal trauma on cardiac force of contraction

Previous studies have reported that administration of potent peripheral vasodilating drugs will significantly increase thermal trauma-induced depression of cardiac output. This finding suggests that most of the depression in cardiac output after thermal trauma is due to an increase in peripheral resistance and a decrease in venous return rather than a direct depression of myocardial contractile force. Studies have been carried out using a strain gauge arch sewn on the left ventricle to measure myocardial force of contraction in the mongrel dog anaesthetized with sodium pentobarbital and receiving a 15 per cent total body surface area full skin thickness flame burn. The results of this study showed a significant decrease in cardiac output immediately after burn, which persisted for 7 h. Myocardial force of contraction, measured in grams, fell immediately after burn and returned to pre-burn values by 3 h post-burn. In one series of animals, verapamil, a calcium-channel-blocking substance, was administered. In these animals cardiac output returned to pre-burn levels following the administration of the drug, but myocardial force of contraction remained significantly lower than pre-burn value for the duration of the experiment. Correlation coefficients comparing cardiac output and myocardial force of contraction showed no significant relationship between values in either untreated or verapamil-treated animals.