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 It is the pathophysiological process in which the heart as a pump is unable to meet the heart as a pump is unable to meet the metabolic requirements of the tissue for the metabolic requirements of the tissue for oxygen and substrates despite venous oxygen and substrates despite venous return to the heart being normal or increased return to the heart being normal or increased

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 Factors effecting heart pump effectiveness

Afterload Force needed to eject blood into circulation Arterial B/P, pulmonary artery pressure Valvular disease increases afterload

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

Heart Failure (AKA-congestive heart failure) Pathophysiology – Cardiac compensatory mechanisms Tachycardia Ventricular dilation-Starling’s law Myocardial hypertrophy –Hypoxia leads to decreased contractility

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Clinical consequences of left and right heart failure peripheral edema ascites hepatomegaly cyanosis pulmonary edema splenomegaly

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 Left 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 Right Heart Failure

CauseWhat is it?How does it cause right sided heart failure? Left-sided heart failureThe 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 diseaseIncludes 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 diseaseBlockage 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 StenosisNarrowing 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 failureleft ventricleacute myocardial infarction

American Heart Assn-Media files Animations

Hepatic blood flow

“ Nutmeg ” liver Nutmeg

Symptoms

Blood Vessels Heart I Heart Failure Ischemic Heart Disease Hypertensive Heart Disease Congenital Heart Disease Cardiac Pathology Outline

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 2bDs8teiZA 2bDs8teiZA Ischemic Heart Disease

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 Angina Pectoris

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 minutes Prompt reperfusion can salvage myocardium Myocardial Infarction

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TimeGross changesMicroscopic changes 0-4hNone 4-12hMottlingCoagulation necrosis 12-24hMottlingMore coagulation necrosis; neutrophils come in 1-7 dYellow infarct centerNeutrophils die, macrophages come to eat dead cells 1-2 wYellow center, red bordersGranulation tissue 2-8 wScarCollagen Morphologic Changes in Myocardial Infarction

Acute Myocardial Infarction

MI: day 1, day 3, day 7

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 Myocardial Infarction

Rupture of papillary muscle after MI

Blood Vessels Heart I Heart Failure Congenital Heart Disease Ischemic Heart Disease Hypertensive Heart Disease Cardiac Pathology Outline

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 Hypertensive Heart Disease

Left ventricular hypertrophy (L) and cor pulmonale (R)

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 Drugs

Blood Vessels Heart I Heart Failure Ischemic Heart Disease Hypertensive Heart Disease Congenital Heart Disease Cardiac Pathology Outline

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 Congenital Heart Disease

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 Atrial 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 Ventricular Septal Defects

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 Patent Ductus Arteriosus

PDA

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 /t/tof/ /t/tof/ Tetralogy of Fallot

Clubbing of fingertips

Normal (L) and clubbed (R) fingertips

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) /t/transposition/ /t/transposition/ Transposition of Great Arteries

Coarctation = narrowing “ Infantile ” (preductal) and “ adult ” (postductal) forms Cyanosis and/or low blood pressure in lower extremities Severity depends on degree of coarctation Aortic Coarctation

Coarctation of the aorta

The End

Essential functions of the heart are secured Essential functions of the heart are secured by integration of electrical and mechanical by integration of electrical and mechanical functions of the heart 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: Control of HR: - autonomic nervous system - hormonal (humoral) control Control of SV: 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) –CardiomyopathyCardiomyopathy –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 hypertrophypulmonary hypertension

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