McKenna's Pharmacology for Nursing, 2e

715

C H A P T E R 4 6 Antianginal agents

Acute myocardial infarction If a coronary vessel becomes completely occluded and is unable to deliver blood to the cardiac muscle, the area of muscle that depends on that vessel for oxygen becomes ischaemic and then necrotic. This is called a myocardial infarction (MI) . The pain associated with this event can be excruciating. Nausea and a severe sympathetic stress reaction may also be present. A serious danger of an MI is that arrhythmias can develop in nearby tissue that is ischaemic and very irritable. Most of the deaths caused by MI occur as a result of fatal arrhythmias. If the heart muscle has a chance to heal, within 6 to 10 weeks, scar tissue will form in the necrotic area and the muscle will compensate for the injury. If the area of the muscle that is damaged is very large, however, the muscle may not be able to compensate for the loss, and heart failure and even cardiogenic shock may occur. These conditions can be fatal or can leave a person severely limited by the weakened heart muscle. ■■ CAD involves changes in the coronary vessels that promote atheromas (tumours), which narrow the coronary arteries and decrease their elasticity and responsiveness to normal stimuli. ■■ Angina pectoris occurs when the narrowed vessels cannot accommodate the myocardial demand for oxygen. ■■ Stable angina occurs when the heart muscle is perfused adequately except during exertion or increased demand. ■■ Unstable or pre-infarction angina occurs when the vessels are so narrow that the myocardial cells are deprived of sufficient oxygen even at rest. ■■ Variant angina is a spasm of a coronary vessel that decreases the flow of blood through the narrowed lumen. ■■ When a coronary vessel is completely occluded, the cells that depend on that vessel for oxygen become ischaemic, then necrotic and die. The result is known as an MI. ANTIANGINAL AGENTS Antianginal drugs (Table 46.1) are used to help restore the appropriate supply-and-demand ratio in oxygen delivery to the myocardium when rest is not enough. These drugs can work to improve blood delivery to the heart muscle in one of two ways: (1) by dilating blood vessels (i.e. increasing the supply of oxygen) or (2) by decreasing the work of the heart (i.e. decreasing the demand for oxygen). Nitrates, beta-adrenergic blockers KEY POINTS

the intimal lining of the vessels, attracting platelets and immune factors and causing swelling and the develop­ ment of a larger deposit. Over time, these deposits severely decrease the size of the vessel. While the vessel is being narrowed by the deposits in the intima, it is also losing its natural elasticity and becoming unable to respond to the normal stimuli to dilate or constrict to meet the needs of the tissues. The person with atherosclerosis has a classic supply- and-demand problem. The heart may function without a problem until increases in activity or other stresses place a demand on it to beat faster or harder. Normally, the heart would stimulate the vessels to deliver more blood when this occurs, but the narrowed vessels are not able to respond and cannot supply the blood needed by the working heart (Figure 46.1B). The heart muscle then becomes hypoxic. This imbalance between oxygen supply and demand is manifested as pain, or angina pectoris , which literally means “suffocation of the chest”. Angina The body’s response to a lack of oxygen in the heart muscle is pain, called angina. Although the heart muscle does not have any pain fibres, a chemical mediator called factor P is released from ischaemic myocardial cells, and pain is felt wherever factor P reacts with a pain receptor. For many people this is the chest, for some it is the left arm, while others have pain in the jaw and teeth. The basic response to this type of pain is to stop whatever one is doing and to wait for the pain to go away. In cases of minor limitations to the blood flow through vessels, stopping activity may bring the supply and demand for blood back into balance. This predictable condition is called stable angina . There is no damage to heart muscle and the basic reflexes surrounding the pain restore blood flow to the heart muscle. This process can go on for a long time with no resultant myocardial infarction. This is also called chronic angina, and can severely limit a person’s activities and quality of life. If the narrowing of the coronary arteries becomes more pronounced, the heart may experience unpredict- able episodes of ischaemia even when the person is at rest. This condition is called unstable angina or pre-in- farction angina. Although no damage to heart muscle occurs, the person is at increased risk of a complete blockage of blood supply to the heart muscle if the heart needs to work harder or the oxygen demand increases. Variant angina (also known as Prinzmetal angina or vasospastic angina) is an unusual form of angina because it seems to be caused by spasm of the coronary blood vessels and not just by vessel narrowing. The person with this type of angina has angina at rest, often at the same time each day and usually with an associ- ated electrocardiogram (ECG) pattern change.