Wk 3 notes 4 - TREATMENT OF ISCHEMIC HEART DISEASE The...

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TREATMENT OF ISCHEMIC HEART DISEASE The Pathophysiology of Angina In its simplest terms, angina is chest pain that results from anaerobic metabolism occurring in the myocardial cells. The anaerobic metabolism is, in turn, a result of an imbalance between myocardial oxygen supply and myocardial oxygen demand. Conditions that decrease supply are coronary occlusive disease (usually associated with atherosclerosis), coronary artery vasospasm, and extreme tachycardia. Conditions that cause an increase in myocardial oxygen demand are increased heart rate, increased force of myocardial contractility, increased ventricular wall strain from either increased intra-ventricular volume [i.e. increased ventricular preload]) or increased ventricular strain from hypertension [i.e., increased ventricular afterload]). The three types of angina are: - Chronic stable angina (also called effort or classic angina) - Variant angina (also called vasospastic or Prinzmetal angina) - Unstable angina (also called pre-infarction angina) The main objectives of antianginal therapy are to: - Decrease myocardial oxygen demand - Increase myocardial oxygen supply - Decrease the workload on the heart by decreasing the force of myocardial contraction, decreasing heart rate, and/or decreasing wall stress. The following categories of drugs are used in managing ischemic heart disease: Nitrates ACE inhibitors Beta blockers Calcium Channel Blockers Antithrombotic Drugs Statins List of Available Nitrate Drugs nitroglycerin (Nitrostat) (Nitrogard) (NitroBid) (NitroDur) (Transderm-Nitro) (Minitran) (many others) isosorbide mononitrate (Monoket)(Imdur) isosorbide dinitrate (Isobid) (Isordil) (Sorbitrate) 1
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TREATMENT OF ISCHEMIC HEART DISEASE Pharmacodynamics of the Nitrate Drugs The nitrate drugs act directly on vascular smooth muscle. They increase the release of nitric oxide in the smooth muscle cells of arterioles and veins. In doing so, they cause the activation of a smooth muscle relaxing factor which produces vasodilatation in veins primarily and also in arteries. This results in an increase in capacitance of the venous system, decrease in venous return to the heart, and a marked decrease in left ventricular preload. As a consequence of reduction in left ventricular preload, there is a redistribution of coronary blood flow to the subendocardial tissues. The vasodilatation that occurs on the arterial side of the vascular system results in a decrease in peripheral resistance and a modest decrease in left ventricular afterload. Decreases in both preload and afterload will result in a significant reduction in myocardial oxygen consumption by decreasing left ventricular filling pressure, left ventricular wall stress, and myocardial contractility. Nitrates also have the additional effects of producing coronary artery vasodilatation and interfering with platelet agglutination. Coronary vasodilatation occurs primarily in those patients who have a vasospastic component to their angina; not in patients with coronary occlusive forms of the disease. Interference with platelet agglutination
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