Nitroglycerin primarily produces which physiologic effect that lowers myocardial oxygen demand?

Nitroglycerin primarily produces which physiologic effect that lowers myocardial oxygen demand?

• A. Relaxes vascular smooth muscle, causing systemic vasodilation with reduced preload and afterload
• B. Increases heart rate
• C. Causes vasoconstriction
• D. Inhibits platelet aggregation

Answer: (A)

Nitroglycerin lowers myocardial oxygen demand mainly by relaxing vascular smooth muscle to cause venodilation, which reduces preload (and to some extent afterload). This venous pooling lowers venous return to the heart, decreasing LV end-diastolic volume and pressure, which in turn reduces wall stress on the heart. Since myocardial oxygen consumption is tightly tied to wall tension (the stress the heart has to work against), this reduction in preload lowers the heart’s oxygen needs. Arterial dilation also helps by reducing afterload, but preload reduction is the dominant factor in lowering oxygen demand. This is why we see relief of angina with nitrates—the heart doesn’t have to work as hard to pump against a lower filling pressure. The other options don’t fit the mechanism: nitrates don’t increase heart rate (they can cause a reflex tachycardia, but that’s not how they primarily reduce oxygen demand), they don’t cause vasoconstriction, and they aren’t primarily antiplatelet agents.

Nitroglycerin lowers myocardial oxygen demand mainly by relaxing vascular smooth muscle to cause venodilation, which reduces preload (and to some extent afterload). This venous pooling lowers venous return to the heart, decreasing LV end-diastolic volume and pressure, which in turn reduces wall stress on the heart. Since myocardial oxygen consumption is tightly tied to wall tension (the stress the heart has to work against), this reduction in preload lowers the heart’s oxygen needs. Arterial dilation also helps by reducing afterload, but preload reduction is the dominant factor in lowering oxygen demand.

This is why we see relief of angina with nitrates—the heart doesn’t have to work as hard to pump against a lower filling pressure. The other options don’t fit the mechanism: nitrates don’t increase heart rate (they can cause a reflex tachycardia, but that’s not how they primarily reduce oxygen demand), they don’t cause vasoconstriction, and they aren’t primarily antiplatelet agents.