McKenna's Pharmacology for Nursing, 2e

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P A R T 8  Drugs acting on the cardiovascular system

ANTIANGINAL AGENTS Nitrates glyceryl trinitrate isosorbide dinitrate isosorbide mononitrate

Beta-blockers metoprolol propranolol

Calcium channel blockers amlodipine diltiazem nifedipine perhexiline verapamil

Potassium channel opener nicorandil

A ntianginal agents are used to help restore the appropri- ate supply-and-demand ratio in oxygen delivery to the myocardium. An imbalance in this ratio, manifested by pain, is most commonly due to coronary artery disease (CAD) . CAD has, for many years, been a leading cause of death in Australia and New Zealand and most Western nations. Despite great strides in understanding the con- tributing causes of this disease and ways to prevent it, CAD claims more lives than any other disease. The drugs discussed in this chapter are used to prevent myo- cardial cell death when the coronary vessels are already seriously damaged and are having trouble maintaining the blood flow to the heart muscle. Chapters 47 and 48 discuss drugs that are used to prevent the blocking of the coronary arteries before they become narrowed and damaged or to restore blood flow through narrowed vessels. CORONARY ARTERY DISEASE The myocardium must receive a constant supply of blood to have the oxygen and nutrients needed to maintain a constant pumping action. The myocardium receives all of its blood from two coronary arteries that exit the sinuses of Valsalva at the base of the aorta. These vessels

divide and subdivide to form the capillaries that deliver oxygen to heart muscle fibres. Unlike other tissues in the body, the heart muscle receives its blood supply during diastole, while it is at rest. This is important because when the heart muscle contracts, it becomes tight and clamps the blood vessels closed, rendering them unable to receive blood during systole, which is when all other tissues receive fresh blood. The openings in the sinuses of Valsalva, which are the beginnings of the coronary arteries, are posi- tioned so that they can be filled when the blood flows back against the aortic valve when the heart is at rest. The pressure that fills these vessels is the pulse pressure (the systolic pressure minus the diastolic pressure)—the pressure of the column of blood falling back onto the closed aortic valve. The heart has just finished contract- ing and using energy and oxygen. The acid and carbon dioxide built up in the muscle cause a local vasodilation, and the blood flows freely through the coronary arteries and into the muscle cells. In CAD, the lumen of the blood vessels becomes narrowed so that blood is no longer able to flow freely to the muscle cells. The narrowing of the vessels is caused by the development of atheromas , or fatty tumours in the intima of the vessels, in a process called atheroscle- rosis (Figure 46.1A). These deposits cause damage to

Artery

Intima

Atheroma A FIGURE 46.1  A. Schematic illustration of atheromatous plaque. B. Thrombosis of atherosclerotic plaque. It may partially or completely occlude the lumen of the vessel. Plaque B Thrombus