Ischemic heart disease (CHD), factors affecting myocardial oxygen supply/demand, myocardial infarction, endocardial and valvular diseases, valve disorders, infective endocarditis, cardiomyopathy, DCM, HCM, pericarditis

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Department
Biomedical Science
Course
BMS 460
Professor
D.Rao Veeramachaneni
Semester
Fall

Description
8 November Ischemic Heart Disease (CHD) Ischemic heart disease: imbalance between myocardial oxygen supply and demand → hypoxia and metabolic build-up Cause: atherosclerotic lesions of coronary arteries Major symptom is angina pectoris or “strangling in the heart” Stable angina – classic, predictable Variant (Prinzmetal) angina – vasospasm Unstable angina – preinfarctional, active clots on vulnerable plaque Silent angina – diabetes, not very painful due to subdued nerve endings Decreased supply Coronary plaque ↓ Perfusion pressure ↓ Arterial oxygen content Increased demand ↑ HR ↑ Preload ↑ Afterload ↑ Contractility Factors affecting myocardial oxygen supply/demand Supply: Q = P/R Perfusion pressure: predominance of flow during diastole vs. systole Vascular resistance External compression during systole: subendocardium most prone to ischemia Intrinsic tone via autoregulation: local metabolites, mediators of tone from EC’s, neural innervation Demand (Px R) Ventricular wall stress = 2h h – wall thickness Heart rate (↑ ATP) Contractility (inotropy) Mismatching occurs between supply and demand in coronary artery disease when poor perfusion (plaque, platelet aggregation, vasospasm) occurs or vascular tone doesn’t decrease (dysfunctional endothelium) to meet demands Myocardial Infarction Two basic types: subendocardial and transmural Time course 0 – 30 min: cell swelling; reversible 1 – 2 hr: sarcolemmal changes; irreversible 4 – 12 hr: necrosis, hemorrhage 2 – 3 days: coagulation; necrosis 7 – 8 weeks: fibrosis Compensatory Changes after Myocardial Infarction SNS enhanced → venoconstriction and ↑ HR and ↑ CO RAAS enhanced → fluid retention → ↑ HR and ↑ CO Result: ↑ SV and ↑ CO but this increases workload of compromised heart as afterload, heart rate and contractility increase Outcome of Myocardial Infarction First day: sudden death, arrhythmia First week: early complications Arrhythmia (90%) CHF (60%) Shock (12%) Heart rupture (1%) First year: late complications CHF (70%) Arrhythmia (20%) Aneurysm (10%) Thromboemboli (10%) 10 years: chronic left heart weakness CHF (70%) Recurrent infarcts Arrhythmia Endocardial and Valvular Diseases Endocarditis primarily affects left sided valves Stenosis: narrowing Regurgitation: leaking st 1 heart sound: closure of AV valves nd 2 heart sound: closure of semilunar valves rd If 3 sound present: filling of ventricles If 4 sound present: atrial contraction Valve Disorders Aortic valve stenosis Aortic pansystolic murmur Aortic valve incomplete opening during systole Forward heart failure Hypotension Hypoperfusion of major organs Syncope Left ventricular hypertrophy Left heart failure Backpressure into lungs Right heart failure Mitral valve regurgitation Mitral systolic murmur Reflux in systole Right heart failure Right ventricular hypertrophy Peripheral edema Left ventricular hypertrophy Pulmonary hypertension Aortic valve regurgitation Aortic diastolic murmur Left atrial dilation Left ventricular hypertrophy Pulmonary hypertension Hyperdynamic heart action Palpitations Thrusting apex Peripheral pulsations Angina Mitral valve stenosis Mitral mid-diastolic murmur Reduced cardiac output Mitral valve incomplete opening Peripheral edema Right heart hypertrophy Right heart failure Pulmonary hypertension Infective Endocarditis Bacterial disease (Staphylococcus aureus, Streptococcus viridans) Affects endocardium of heart and valves 6 month mortality rate of 25% and if untreated – death Requirements Endocardial injury Thrombus formation Bacterial entry to circulation Bacterial adherence to endocardium Lesions leading to endocarditis Rheumatic heart disease Other acquired valve defects Hypertrop
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