Assume the patient was taking no other drugs except the NTG and a beta-blocker. Cyanide, or toxic metabolite of NTG, accumulated. NTG directly induced coronary vasoconstriction. NTG lowered arterial (coronary perfusion) pressure excessively Beta-blocker counteracted the effects of NTG and increased the risk of ischemia
A patient with chronic-stable angina is on prophylactic beta-blocker therapy, with sublingual nitroglycerin used PRN (as needed) for managing acute angina. One day he experiences particularly severe angina and takes the usually recommended dose of sublingual nitroglycerin (NTG). His discomfort is not reduced at all. Seeking relief, he repeats the usual recommended dose of NTG dose 6 times over a period of about 10 minutes, and now has taken far too much of the nitrovasodilator. An electrocardiogram taken by the paramedics, who were called for the patient’s emergency, shows changes consistent with myocardial ischemia. The patient incurs a massive infarction, goes into cardiac arrest, and cannot be resuscitated. Which of the following is the most likely cause of or contributing factor to the patient’s ultimately fatal response to the excessive dosage of NTG? Assume the patient was taking no other drugs except the NTG and a beta-blocker.
- Cyanide, or toxic metabolite of NTG, accumulated.
- NTG directly induced coronary vasoconstriction.
- NTG lowered arterial (coronary perfusion) pressure excessively
- Beta-blocker counteracted the effects of NTG and increased the risk of ischemia
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