Nitroglycerin may interfere with the anticoagulant activity of heparin, necessitating increased heparin doses to achieve therapeutic results. When nitroglycerin is discontinued, excessive anticoagulation may occur.
1A patient is admitted with unstable angina. Cardiac catheterization demonstrates triple-vessel coronary artery disease. He subsequently develops several episodes of chest pain at rest treated with increasing high doses of intravenous nitroglycerin, calcium blockers, heparin, and aspirin. On rounds the following morning, he appears cyanotic and also complains of weakness, headache, and shortness of breath. His lungs are clear, he has no murmurs, and his chest x-ray is normal. How would you treat this syndrome? Are these findings related to his therapy?
High doses of nitroglycerin can result in clinically significant methemoglobinemia. Cyanosis occurs when the level of methemoglobin (HbFe+3) exceeds 10%. When the level exceeds 35%, symptoms of dyspnea, headache, and weakness appear. The treatment for toxic methemoglobinemia is intravenous methylene blue at 2 mg/kg. Methemoglobin levels become significantly reduced, and symptoms substantially improve within 1 hour.
The opinions and assertions contained herein are the private views of the authors and are not to be construed as official or reflecting the views of the Department of the Army or Department of Defense.
Why are vasodilators useful in congestive heart failure due to left ventricular systolic dysfunction?
In patients with low cardiac output, the arterial and venous beds are inappropriately constricted. This is the body’s response to a low flow state in order to maintain adequate blood flow to vital organs. Some compensatory mechanisms responsible for this constriction are increased catecholamine levels, increased sympathetic tone, and increased activity of the renin-angiotensin-aldosterone system. These compensatory mechanisms work against the failing heart, causing a vicious cycle of decreasing cardiac output and increasing vasoconstriction. Vasodilators break this cycle by decreasing vascular resistance, thus improving cardiac output.