A 64-year-old man with a long-standing history of hypertension is brought to the emergency department due to a dry cough and shortness of breath. The patient has been unable to sleep in a flat position for the past 2 days. Blood pressure is 192/102 mm Hg and pulse is 92/min and regular. Physical examination reveals an S4 and bibasilar crackles. He is started on a high-dose intravenous nitroglycerin infusion, and soon after he reports significant symptomatic relief. Which of the following physiologic changes most likely occurred in this patient as a result of the infusion?
This patient's clinical presentation is consistent with acute pulmonary edema due to severely elevated blood pressure (hypertensive emergency). Intravenous vasodilators (eg, nitroglycerin, sodium nitroprusside) are often used in the management of acute heart failure due to severe hypertension.
Nitrates (eg, nitroglycerin, isosorbide dinitrate, isosorbide mononitrate) are primarily venodilators that increase peripheral venous capacitance, thereby reducing cardiac preload and left ventricular end-diastolic pressure (LVEDP) and volume. This is the primary mechanism of action for symptom relief in patients with acute pulmonary edema. Lower LVEDP also leads to a reduction in LV systolic wall stress and a decrease in myocardial oxygen demand, resulting in relief of angina symptoms.
At high doses, nitrates also cause some degree of arteriolar dilation (in addition to venodilation), which decreases systemic vascular resistance and may sometimes cause a precipitous decline in blood pressure. Sodium nitroprusside has slightly different effects than nitrates, acting as a balanced vasodilator of venules and arterioles at all dose levels.
Educational objective:
Nitrates are primarily venodilators and increase peripheral venous capacitance, thereby reducing cardiac preload and left ventricular end-diastolic volume and pressure. At high doses, nitrates also cause some degree of arteriolar dilation with a resulting decrease in systemic vascular resistance.