Cardiovascular Responses to Rattlesnake Venom

Abstract

The immediate response to small amts. of rattlesnake venom is a vasodilation sufficient to produce a rapid decline in arterial pressure; a cardioacceleration with an evanescent increase in cardiac output probably reflecting a direct action of the venom on the heart; splenic contraction with resulting increase in cell/blood ratio and in blood specific gravity; cardiac damage, as reflected electrocardiographically by a depression in the S-T segment, increased T waves, a shift of the QRS axis, premature ventricular systoles and bundle branch block; and possible myocardial weakness, as reflected in prolonged ejection times. The cardiac output is decreased, the resistance reduced. An interruption of the venom infusion is followed by a slow reversal of the above changes, and recovery. If venom admn. is continued, a second set of signs appear, of dire prognosis. The arterial pressure remains low, petechial hemorrhages appear, the mucosa of the lower intestine becomes congested with hemorrhage into the lumen, there is mild respiratory distress and hyperexcitablllty, there is a failure of the blood clotting.mechanism, and a decline in cardiac output Specific gravity values furnish no evidence of a preferential loss of plasma. The amt. of blood loss was not enough to represent a lethal hemorrhage in a normal dog, although it might in a dog with maintained vasodilation. It is probable that ollgemla, myocardial weakness and biochemical changes in the blood all contributed in variable amts. to the total collapse.