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Cardiac Pathology Heart Failure, Ischemic Heart Disease and more Cardiac Pathology Outline • Blood Vessels • Heart I • Heart II Cardiac Pathology Outline • Blood Vessels • Heart I • Heart Failure • Ischemic Heart Disease • Hypertensive Heart Disease • Congenital Heart Disease Cardiac Pathology Outline • Blood Vessels • Heart I • Heart Failure Heart failure Definition It is the pathophysiological process in which the heart as a pump is unable to meet the metabolic requirements of the tissue for oxygen and substrates despite venous return to the heart being normal or increased Factors effecting heart pump effectiveness Preload • Preload can be defined as the initial stretching of the cardiac myocytes prior to contraction. • Preload, therefore, is related to the sarcomere length. • Preload is also related to the volume of blood in ventricles at the end of diastole – Depends on venous return – Depends on compliance Afterload • Force needed to eject blood into circulation • Arterial B/P, pulmonary artery pressure • Valvular disease increases afterload Heart Failure • End point of many heart diseases • Common! • 5 million affected each year • 300,000 fatalities • Heart can’t pump blood fast enough to meet the needs of the body – The heart can’t fill with enough blood or – The heart doesn’t have enough force Heart Failure • System responds to failure by • Releasing hormones (e.g., norepinephrine) • Frank-Starling mechanism • Hypertrophy • Initially, this works • Eventually, it doesn’t • Myocytes degenerate • Heart needs more oxygen • Myocardium becomes vulnerable to ischemia Heart Failure • Heart failure develops over time – Can affect right side of heart or both sides • Right-side heart failure occurs if the heart can't pump enough blood to the lungs to pick up oxygen. • Left-side heart failure occurs if the heart can't pump enough blood to the rest of the body. • Also known as Congestive Heart Failure Heart Failure (AKA-congestive heart failure) • Pathophysiology – Cardiac compensatory mechanisms • Tachycardia • Ventricular dilation-Starling’s law • Myocardial hypertrophy – Hypoxia leads to decreased contractility R L cyanosis pulmonary edema hepatomegaly Clinical consequences of left and right heart failure peripheral edema splenomegaly ascites Left Heart Failure • Left ventricle fails; blood backs up in lungs • Most Common Causes • Ischemic heart disease (IHD) • Systemic hypertension • Mitral or aortic valve disease • Primary heart diseases • Heart changes • LV hypertrophy, dilation • LA may be enlarged too (risk of atrial fibrillation) Left Heart Failure • Dyspnea (shortness of breath) • Orthopnea, paroxysmal nocturnal dyspnea too • Enlarged heart, increased heart rate, fine rales at lung bases • Later: mitral regurgitation, systolic murmur • If atrium is big, “irregularly irregular” heartbeat Right Heart Failure • Right-side heart failure may cause fluid to build up in the feet, ankles, legs, liver, abdomen, and the veins in the neck. • Right-side and left-side heart failure also may cause shortness of breath and fatigue • Leading cause of heart failure is due to diseases that damage the heart – Diabetes – High blood pressure – Coronary heart disease Right Heart Failure • Right ventricle fails; blood backs up in body • Most Common Causes • Left heart failure • Lung disease (“cor pulmonale”) • Failure of the right side of the heart brought on by long-term high blood pressure in the pulmonary arteries and right ventricle of the heart • Caused by long term hypoxia, ie. chronic bronchitis or obesity • Some congenital heart diseases • Heart changes • Right ventricular hypertrophy, dilation • Right atrial enlargement Right Heart Failure • Peripheral edema • Big, congested liver (“nutmeg liver”) • Big spleen • Most chronic cases of heart failure are bilateral Cause What is it? How does it cause right sided heart failure? Left-sided heart failure The left ventricle does not pump blood efficiently, leading to pressure building behind the left side of the heart that eventually causes the right side of the heart to fail. Blood backs up behind the left ventricle into the left atrium, in the lungs, and then eventually into the right ventricle, which also eventually fails, allowing blood to then back up farther into the extremities, the liver, and the other organs. Chronic lung disease Includes emphysema, pulmonary embolism, and other causes of pulmonary hypertension High blood pressure in the pulmonary arteries increases the workload of the right ventricle, eventually causing the right ventricle to fail. Coronary artery disease Blockage of the arteries that supply blood to your heart CAD can cause left-sided heart failure leading to right-sided heart failure or can directly cause right-sided heart failure by blocking blood supply to the right ventricle. Pulmonic Stenosis Narrowing of the pulmonic valve that limits blood flow out of the right ventricle Increases the work of the right ventricle; similar to chronic lung disease Cardiomegaly/ventricular remodeling occurs as heart overworked> changes in size, shape, and function of heart after injury to left ventricle. Injury due to acute myocardial infarction or due to causes that inc. pressure or volume overload as in Heart failure American Heart Assn-Media files Animations Hepatic blood flow “Nutmeg” liver Nutmeg Symptoms Cardiac Pathology Outline • Blood Vessels • Heart I • Heart Failure • Ischemic Heart Disease • Hypertensive Heart Disease • Congenital Heart Disease Ischemic Heart Disease • Myocardial perfusion can’t meet demand • Usually caused by decreased coronary artery blood flow (“coronary artery disease”) • Four syndromes: • angina pectoris • acute MI • chronic IHD • sudden cardiac death • http://www.youtube.com/watch?v=2 2bDs8teiZA Angina Pectoris • Intermittent chest pain caused by transient, reversible ischemia • Typical (stable) angina • pain on exertion • fixed narrowing of coronary artery • Prinzmetal (variant) angina • pain at rest • coronary artery spasm of unknown etiology • Unstable (pre-infarction) angina • increasing pain with less exertion • plaque disruption and thrombosis Myocardial Infarction • Necrosis of heart muscle caused by ischemia • 1.5 million people have MIs each year • Most due to acute coronary artery thrombosis • sudden plaque disruption • platelets adhere • coagulation cascade activated • thrombus occludes lumen within minutes • irreversible injury/cell death in 20-40 minutes • Prompt reperfusion can salvage myocardium • https://www.youtube.com/watch?v=zeS0au8ij4 Morphologic Changes in Myocardial Infarction Time Gross changes Microscopic changes 0-4h None None 4-12h Mottling Coagulation necrosis 12-24h Mottling More coagulation necrosis; neutrophils come in 1-7 d Yellow infarct center Neutrophils die, macrophages come to eat dead cells 1-2 w Yellow center, red borders Granulation tissue 2-8 w Scar Collagen Acute Myocardial Infarction MI: day 1, day 3, day 7 Myocardial Infarction • Clinical features • Severe, crushing chest pain ± radiation • Not relieved by nitroglycerin, rest • Sweating, nausea, dyspnea • Sometimes no symptoms • Laboratory evaluation • Troponins increase within 2-4 hours and remains elevated for a week. • CK/MB increases within 2-4 hours, returns to normal within 72 hours. Myocardial Infarction • Complications • Contractile dysfunction • Arrhythmias • Rupture of muscle • Chronic progressive heart failure • Prognosis • Depends on remaining function and perfusion • Overall 1 year mortality: 30% • 3-4% mortality per year thereafter Rupture of papillary muscle after MI Cardiac Pathology Outline • Blood Vessels • Heart I • Heart Failure • Congenital Heart Disease • Ischemic Heart Disease • Hypertensive Heart Disease Hypertensive Heart Disease • Can affect either L or R ventricle • Cor pulmonale is RV enlargement due to pulmonary hypertension caused by primary lung disorders • Result: myocyte hypertrophy • Reasons for heart failure in hypertension are poorly understood Left ventricular hypertrophy (L) and cor pulmonale (R) Drugs • Chronotropic – Alters heart rate • Ionotropic – Alters myocardial contractility – Digitalis is a positive ionotropic drug • Diuretics – Loop – reduces sodium reabsorption – Thiazide – increases sodium loss , water loss • ACE Inhibitors • Nitrates – Induces NO release by vessels = vasodilation Cardiac Pathology Outline • Blood Vessels • Heart I • Heart Failure • Ischemic Heart Disease • Hypertensive Heart Disease • Congenital Heart Disease Congenital Heart Disease • Abnormalities of heart/great vessels present from birth • Faulty embryogenesis, weeks 3-8 • Broad spectrum of severity • Cause unknown in 90% of cases Congenital Heart Disease • Left-to-right shunts • atrial septal defects • ventricular septal defects • Patent ductus arteriosus • Right-to-left shunts • tetralogy of fallot • transposition of the great arteries • Obstructions • aortic coarctation Atrial Septal Defects • Initially, left-to-right shunt (asymptomatic) • Eventually, pulmonary vessels may become constricted (“pulmonary hypertension”), leading to right-to-left shunt (“Eisenmenger syndrome”) • Surgical repair prevents irreversible pulmonary changes and heart failure Ventricular Septal Defects • Most common congenital cardiac anomaly • Most close spontaneously in childhood • Small VSD: asymptomatic • Large VSD: big left-to-right shunt, may become right-to-left Patent Ductus Arteriosus • Ductus: allows flow from PA to aorta • Closes spontaneously by day 1-2 of life • Small PDA: asymptomatic • Large PDA: shunt becomes right-to-left PDA Tetralogy of Fallot • Most common cause of cyanotic congenital heart disease • Four features: • VSD- ventricular septal defect • obstruction to RV outflow tract • overriding aorta • RV hypertrophy • Cyanosis, erythrocytosis, clubbing of fingertips, paradoxical emboli • http://www.cincinnatichildrens.org/health /t/tof/ Clubbing of fingertips Normal (L) and clubbed (R) fingertips Transposition of Great Arteries • Aorta arises from R ventricle; pulmonary artery arises from L ventricle • Outcome: separation of systemic and pulmonary circulations • Incompatible with life unless there is a big shunt (VSD) • http://www.cincinnatichildrens.org/health /t/transposition/ Aortic Coarctation • Coarctation = narrowing “Infantile” (preductal) and “adult” (postductal) forms • Cyanosis and/or low blood pressure in lower extremities • Severity depends on degree of coarctation • Coarctation of the aorta The End Essential functions of the heart are secured by integration of electrical and mechanical functions of the heart Cardiac output (CO) = heart rate (HR) x stroke vol.(SV) - changes of the heart rate - changes of stroke volume • Control of HR: - autonomic nervous system - hormonal (humoral) control • Control of SV: - preload - contractility - afterload Adaptive mechanisms of the heart to increased load • Frank - Starling mechanism • Ventricular hypertrophy – increased mass of contractile elements strength of contraction • Increased sympathetic adrenergic activity – increased HR, increased contractility • Increased activity of R–A–A system Causes leading to changes of number and size of cardiomyocytes Heart Failure Etiology and Pathophysiology • Systolic failure- most common cause – Hallmark finding: in *Decrease in left ventricular ejection fraction (EF) • Due to – Impaired contractile function (e.g., MI) – Increased afterload (e.g., hypertension) – Cardiomyopathy – Mechanical abnormalities (e.g., valve disease) Heart Failure Etiology and Pathophysiology • Diastolic failure – Impaired ability of ventricles to relax and fill during diastole > decreased stroke volume and CO – Diagnosis based on presence of pulmonary congestion, pulmonary hypertension, ventricular hypertrophy Heart Failure Etiology and Pathophysiology • Mixed systolic and diastolic failure – Seen in disease states such as dilated cardiomyopathy (DCM) – High pulmonary pressures • Biventricular failure (both ventricles may be dilated and have poor filling and emptying capacity) Heart Failure Etiology and Pathophysiology • Primary risk factors – Coronary artery disease (CAD) – Advancing age • Contributing risk factors – – – – – – – – Hypertension Diabetes Tobacco use Obesity High serum cholesterol African American descent Valvular heart disease Hypervolemia