Like most other American pit vipers, the venom contains proteolytic enzymes. Proteolytic venoms are concentrated secretions that destroy tissues as a result of catabolism of structural and other proteins, which help in disabling prey. The venom of C. atrox is primarily hemotoxic, affecting mainly the blood vessels, blood cells and the heart. The venom contains hemorrhagic components called zinc metalloproteinases. The venom also contains cytotoxins and myotoxins which destroy cells and muscles that add to the failure of the cardiovascular system. In addition to hemorrhage, venom metalloproteinases induce myonecrosis (skeletal muscle damage), which seems to be secondary to the ischemia that ensues in muscle tissue as a consequence of bleeding and reduced perfusion. Microvascular disruption by metalloproteinases also impairs skeletal muscle regeneration, being therefore responsible for fibrosis and permanent tissue loss after bites from this species. General local effects include pain, heavy internal bleeding, severe swelling, severe muscle damage, bruising, blistering, and necrosis; systemic effects are variable and not specific, but may include headache, nausea, vomiting, abdominal pain, diarrhea, dizziness, and convulsions. Hemorrhagins causing bleeding is a major clinical effect. This species has LD50 values of 2.72 mg/kg intravenous, 20 mg/kg intramuscular and 18.5 mg/kg subcutaneous, which is far less toxic than many other rattlesnakes. However, because of its large venom glands and specialized fangs, the western diamondback rattlesnake can deliver a significant amount of venom in a single bite. The average venom yield per bite is usually between 250 and 350 mg, with a maximum of 700–800 mg. Severe envenomation is rare, but possible, and can be lethal. Mortality rate of untreated bites is between 10 and 20%.
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