This document provides information on the management of clients with functional cardiac disorders, specifically coronary heart disease (CHD). It discusses the causes, risk factors, pathophysiology, diagnostic tests, and treatment for various types of CHD including stable angina, unstable angina, and myocardial infarction. Diagnostic tests covered include ECG, cardiac enzymes, stress testing, cardiac catheterization, and imaging modalities. Treatment focuses on lifestyle modifications, medications, activity restrictions, and diet instructions to prevent further cardiac events.

1. Management of Clients with Functional Cardiac Disorders

3. Risk Factors Non-modifiable Modifiable Age, gender, race, heredity Endothelial injury Stress, diet, sedentary living, Smoking, Alcohol, HPN, DM, Obesity, Contraceptive pills, Hyperlipidemia/hypercholesterolemia Desquamation of endothelial lining (peeling off)

4. Increased permeability/ adhesion of molecules LDLs & platelets assimilate into the area Plaques begins to form Decreased coronary tissue perfusion Coronary ischemia Decreased myocardial oxygenation ANGINA PECTORIS MYOCARDIAL INFARCTION

20. CHD Chronic Ischemic Heart Disease Acute Coronary Syndrome Stable Angina Variant Angina Silent Myocardial Ischemia Non ST-segment Elevation MI (Unstable Angina) ST-segment Elevation MI

22. Causes: Atherosclerosis, HPN, DM, Buerger’s Disease, Polycythemia Vera, Aortic regurgitation Reduced coronary tissue perfusion Decreased myocardial oxygenation Anaerobic metabolism Increased lactic acid production (lactic acidosis) Chest pain

33. Causes: atherosclerotic heart disease, thrombosis/embolism, shock &/or hemorrhage, direct trauma Myocardial ischemia ↑ cellular hypoxia ↓ myocardial O 2 supply ↓ myocardial contractility ↓ cardiac output ↓ arterial pressure Stimulation of sympathetic receptors ↑ peripheral vasoconstriction ↑ myocardial contractility ↑ afterload ↑ myocardial O 2 demand ↑ HR ↑ diastolic filling ↓ myocardial tissue perfusion

34. Time after Onset Type of Injury & Gross Tissue Changes 0-0.5hrs Reversible injury 1-2hrs Onset of irreversible injury 4-12hrs Beginning of coagulation necrosis 18-24hrs Continued necrosis; gross pallor of infected tissue 1-3days Total necrosis; onset of acute inflammatory process 3-7days Infarcted area becomes soft with a yellow-brown center & hyperemic edges 7-10days Minimally soft & yellow with vascularized edges; scar tissue generation begins (fibroplastic activity) 8 th week Complete scar tissue replacement

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