Hypertension & Coronary Artery Disease Q 14

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As an initial step in treating a client with angina, the physician prescribes nitroglycerin tablets, 0.3mg given sublingually. This drug’s principal effects are produced by:

  

     A. Antispasmodic effect on the pericardium.

     B. Causing an increased myocardial oxygen demand.

     C. Vasodilation of peripheral vasculature.

     D. Improved conductivity in the myocardium.

    

    

Correct Answer: C. Vasodilation of peripheral vasculature

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Nitroglycerin produces peripheral vasodilation, which reduces myocardial oxygen consumption and demand. Vasodilation in coronary arteries and collateral vessels may also increase blood flow to the ischemic areas of the heart. Nitroglycerin is a vasodilatory drug used primarily to provide relief from anginal chest pain. It is currently FDA approved for the acute relief of an attack or acute prophylaxis of angina pectoris secondary to coronary artery disease.

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Option A: Although nitroglycerin has a vasodilatory effect in both arteries and veins, the profound desired effects caused by nitroglycerin are primarily due to venodilation. Venodilation causes pooling of blood within the venous system, reducing preload to the heart, which causes a decrease in cardiac work, reducing anginal symptoms secondary to demand ischemia.

Option B: Nitroglycerin decreases myocardial oxygen demand. Arterial vasodilation will still occur as well and contribute towards the relief of anginal symptoms, but its effects are not as significant. Vasodilation of the coronary arteries will cause increased blood flow to the heart, increasing perfusion, but this effect remains minimal compared to the effects of venodilation.

Option D: Nitroglycerin does not have an effect on pericardial spasticity or conductivity in the myocardium. Similar to other nitrates used to treat anginal chest pain, nitroglycerin converts to nitric oxide (NO) in the body. NO then activates the enzyme guanylyl cyclase, which converts guanosine triphosphate (GTP) to guanosine 3′,5′-monophosphate (cGMP) in vascular smooth muscle and other tissues. cGMP then activates many protein kinase-dependent phosphorylations, ultimately resulting in the dephosphorylation of myosin light chains within smooth muscle fibers. This activity causes the relaxation of smooth muscle within blood vessels, resulting in the desired vasodilatory effect.

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