Chapter 11: The Heart 1. Heart Failure: systolic dysfunction or diastolic a.

Inadequate CO (forward failure); Increased venous congestion (backward failure) b. Concentric hypertrophy: ventricular wall increased without increase in size of the chamber c. Eccentric hypertrophy: increase in heart size and increase in wall thickness d. Right Heart Failure i. Pathophys: intrinsic DDx of lung parenchyma/pulm vasculature; congenital heart disease; TRANSUDATE! ii. Histo: Systemic edema, nutmeg liver, centrilobular necrosis (w/ long term passive congestion), cardiac cirrhosis, congestive splenomegaly, pleural effusions; atelectasis, anasarca; congestion in liver, kidneys, and spleen iii. Sx: pitting edema of the lower extremities and JVD e. Left Heart Failure i. Pathophys: IHD; systemic hypertension; mitral or aortic valve disease; primary disease of myocardium ii. Histo: Pulmonary edema, heart failure cells in alveoli iii. Sx: dyspnea, PND, orthopnea, cough, cardiomegaly, tachycardia, S3, rales, mitral regurg, chronic LA dilation (atrial fibrillation) 2. Congenital Heart Disease a. Left-to-Right Shunts i. ASD 1. Most common type is ostium secundum 2. Down Syndrome 3. Present Eisenmengers in adulthood because takes longer to develop pulmonary hypertension ii. VSD 1. Can be muscular or membranous; if muscular, can spontaneously close 2. Jet stream effect can cause bacterial endocarditis, even if small VSD is closed 3. Holosystolic murmur throughout systole; Eisenmengers as a kid iii. PDA 1. Closes because of high O2 content or prostaglandins 2. Usually seen in premature kids under condition of hypoxia/respiratory distress syndrome 3. Machine-like murmur 4. Rx: indomethacin, ligate duct b. Right-to-Left Shunt i. Tetralogy of Fallot: pulmonary hypotension! 1. Pulmonary Stenosis 2. Right ventricular hypertrophy

3. VSD 4. Overriding Aorta 5. May get bacterial endocarditis because of VSD ii. Transposition of the Great Arteries 1. Need PDA or patient will die 2. AORTA IS ANTERIOR TO PULMONARY TRUNK 3. Early cyanosis 4. RVH 5. Associated with maternal diabetes 6. Want shunts!!! iii. Truncus arteriosus: cyanosis because pulmonary artery & aorta did not separate iv. Tricuspid atresia: tricuspid membrane did not form into a valve, so blood from the RA is shunted via and ASD to the LA and into the systemic circulation v. Total anomalous pulmonary venous return 1. Pulmonary veins with oxygenated blood is not connected to the LA, and instead to somewhere else. Thus, baby becomes quickly cyanotic c. Obstructive Lesions i. Aortic Coarctation: 1. Preductal: infantile, cyanosis in lower half of body a. Aortic narrowing is pre-ductus arteriosus: aorta that is postnarrowing will have lower pressure than pulmonary arteries, so lower extremities can be cyanotic!!! & right ventricular hypertrophy!! b. Upper limbs = high pressure c. Lower limbs = lower pressure 2. Postductal: upper extremity hypertension, claudication, and coldness of lower extremities (lower pressure); a. Ductus arteriosus is closed (ligamentum arteriosum) b. LVH c. No cyanosis! d. Notching of ribs from intercostals trying to shunt blood to the lower extremities e. Complications: CHF, intracerebral hemorrhage, dissecting aortic aneurysm 3. Ischemic Disease a. Angina pectoris b. MI c. Chronic IHD d. Sudden Cardiac Death 4. Hypertensive Heart Disease a. Pathophysiology of Cardiac hypertrophy b. Systemic Hypertensive Heart Disease

c. Pulmonary Hypertensive Heart Disease (Cor Pulmonale) 5. Valvular Heart Disease a. Calcific Aortic Stenosis: i. Sx: ischemic, causes angina, syncope, etc. ii. Rx: valve replacement b. Myoxmatous Mitral Valve: Mitral valve prolapse; young female c. Rheumatic Valvular Disease i. Acute: 1. Young child, Strep A beta-hemolytic pyrogenes 2. Type2 hypersensitivity; ASO titers; a. Pericarditis: Friction rub b. Endocarditis: valvular problems; McCallum plaques in LA c. Myocarditis: Aschoff bodies; worst prognosis 3. Jones criteria a. Pancarditis b. Subcutaneous nodules c. Syndenham chorea d. Skin rash e. Fever, acute phase proteins, arthalgias Minor criteria ii. Chronic: 1. Infectious Endocarditis: subacute form (valvular problem) 2. Fibrosis leads to commissural fusion, short tendinae, mitral stenosis/regurg, etc d. Infective Endocarditis: Strep viridans, S. aureus i. Acute: highly virulent organism (S. aureus) attacking a previously normal valve 1. If IV Rx abuse, then go to venous side & tricuspid valve ii. Subacute: low virulent organism (Strep. viridians) on a previously abnormal heart 1. Murmurs, systemic emboli 2. Roth spots: retinal deposits 3. Osler nodes: painful subcutaneous nodules on fingers and feet 4. Janeway lesions: painless lesions on soles of foot and palms of hand 5. Splinter nail hemorrhages iii. Friable lesions, possible abscess cavity (ring) iv. Sx: 1. Acute: Fever 2. Subacute: splenomegaly, murmurs; associated with previously damaged valves v. Complications: glomerulonephritis, mycotic/brain abscess, valve damage, opening of prosthetic valve, rupture of papillary muscles e. Noninfected Vegetations

i. Nonbacterial Thrombotic Endocarditis (NBTE) or marantic endocarditis: immune-mediated during hypercoagulable states (sepsis with DIC); hyperestrogenic states; Trousseau syndrome 1. Tumorous mass somewhere else in the body, but causes body to be in a hypercoagulable state, allowing for vegetations/thrombi (aka RBCs, fibrin, platelets) to form on the closure lining of valves ii. Libman-Sacks Endocarditis: SLE f. Carcinoid Heart Disease i. Right sided endocardial and valvular obstruction; L-side is spared because MAO degrades serotonin in the lungs before getting to the LA ii. Flushing of the face is associated carcinoid syndrome with R-sided heart problems iii. GI tract neural crest tumor metastasizing into liver and heart iv. SMCs and sparse collagen fibers embedded in an acid mucopolysaccharide-rich matrix v. Pathogenesis: 5Ht, kalkikrein, bradykinin, histamine, prostaglandins, tachykinins vi. Fen-hen affects systemic serotonin metabolism vii. Left side plaques occur following methysergide or ergotamine therapy g. Prosthetic Cardiac Valves 6. Cardiomyopathies a. Dilated Cardiomyopathy i. Arrhythmogenic RV Cardiomyopathy ii. Viral (Coxsackie b), pregnancy, adromyacin, alcohol, genetics iii. Decreased CO/contractility, decreased EF, CHF b. Hypertrophic Cardiomyopathy i. Genetically related ii. Young male athlete/exercise + passing out iii. Septum & LV hypertrophy; septum obstructs outflow from ventricle into aorta iv. Myofibril disarray, and interstitial fibrosis c. Restrictive Cardiomyopathy i. Ventricles cant fill properly (lose compliance); contractility is OK ii. Amyloidosis iii. Sarcoidosis iv. Endocardial fibroelastosis v. Loeffler endomyocarditis vi. Note: patients with constrictive pericarditis present like restrictive cardiomyopathy d. Myocarditis i. Lymphocitic myocarditis ii. Hypersensitivity myocarditis iii. Giant-cell myocarditis myocarditis iv. Chagas myocarditis

7. Pericardial Disease a. Pericarditis i. Inflammation of the pericardium b. Pericardial Effusions i. Can lead to cardiac tamponade? 8. Cardiac Tumors a. Metastatic Neoplasms b. Primary Neoplasms i. Myxoma: mucous depositing tumor 1. LA a. On stalk: pedunculated b. Looks like a ball, and will bounce around, and sometimes into the valve, causing insufficiency c. Grow on the LA itself, causing damage by lysing red cells d. If large enough, can press against esophagus giving dysphagia e. May break off and become a tumor embolus ii. Rhabdomyoma: mixed type cell deposits (hamartomas); tuberous sclerosis can affect brain and heart 1. Seen in children w/ spider cells (glycogen laden vacuoles separated by strands of cytoplasm) 9. Cardiac Transplantation a. Leads to infections