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Heart Diseases, Heart Disease Congestive Heart Failure mortᡪ% inɝyr Cardiac Hypertrophy-response to inc. work or trophic signals (hyperthyroidism->beta-ad) -hyperplasia does not occur (adult myo can't divide) Pressure overload(HTN, Ao stenosis)->HCM, new sarcs ->pressure(concentric) hypertrophy-reduce diameter -gene expression sim to fetus, some apoptosis ->dec. cap density, deposit fibrous tissue Volume overload(mitral, Ao valve regurg) ->dilation, inc. vent diameter (DCM) If induced by NL strenuous exercise, no negative results -physiologic hypertrophy Forward findings-poor organ perfusion Backward-peripheral edema Usually results in global heart failure, Most from faulty wk 3-8 embryogenesis -most common type of HD in kids, higher in premies -can ->endocarditis, hyperviscosity CAUSE-genetic, trisomies 13, 15, 18, 21, XO -env - congenital rubella infx -cause identified in only 10% -familial ASD linked to chrom 5q 3 Major Categories Right-to-left Shunt -early cyanosis -paradoxical embolism->brain ToF-most common cyanotic-reparable 1)VSD 2)subpulm stenosis 3)overriding Ao 4)RV hypertrophy -all from displacement of mm. septum ->enlarged, boot-shaped heart -if mild (2)->like isolated VSD-pink ToF -as (2) increases-> R->L shunt-cyanosis -worse w/ age b/c pulm orifice still small Transposition of Great Arteries-A to V NL -ABNL formation of truncal, aortopulm septa ->anterior Ao ->two parallel circuits->death unless shunt -35% w/ VSD-stable -65% w/ ASD or patent F.O.-unstable -degree of mixing->outcome Tx-most w/ transection, and switch Truncus Arteriosus-single great artery w/ VSD -mixing, so systemic cyanosis+high pulm blood flow->pulm HTN Tricuspid Atresia-complete occlusion -unequal division of AV canal->big mitral valve -usually have RV hypoplasia -R->L shunt maintains (ASD, PFO), VSD to lungs -cyanosis from birth Total Anomalous Pulmonary Venous Connection -no pulm vv to LA -will drain to cor sinus, left innominate vein ->vol/pressure hypertrophy of RA/V -shunt at ASD, so mixing->body -NL LV, hypoplastic LA, Heart Disease Valvular Disease Artificial Valve Complications -Thromboembolic-MAJOR PROBLEM -thus use long-term anticoags -Infective Endocarditis-infrequent -at prosthesis-tissue interface ->ring abscess->leaks -or on bioprosthetic cusps -esp Staph and Strep -Structural deterioration-esp bio valves -calcify, cuspal tear->regurg -Other-hemolysis (blood shear), -fibrous overgrowth, mech obstruct., Heart Disease Ischemic Heart Disease 80-90% of deaths See IHD Map, Heart Disease Nonischemic (primary) HD See Primary Heart Disease Map, Heart Disease General Principles Heart Failure-most frequent -dmged mm-weak, inadequate contractions -or can't relax sufficiently -Compensatory Mechs-1)Frank-Starling, 2)Myocardial hypertrophy 3)Neurohumoral system-release NE ->inc. HR, contractility -activate renin-AT-aldo axis; release ANP Flow Obstruction-prevents valve opening, etc. -inc. vent pressure->overwork chamber Regurgitant Flow-valve regurgitation-reflux -volume workload on mm. Conduction D/o-heart block, arrhythmias -nonuniform, inefficient contractions Disruption of circulation-gunshot thru Ao -blood escapes, Heart Disease Valvular Disease Carcinoid HD-mostly on RIGHT vent, T/P valves 1/2 of carcinoid syndrome pts -episodic flushing, cramps, nausea, vomiting, diarrhea MORPHOLOGY-fibrous intimal thickenings on inside of cardiac chambers, leaflets -endocardial plaques -mostly sm. mm. cells, collagen -in acid-mucopolysacc matrix ->expands endocardium -underlying structures intact Due to tumor's serotonin, kallikrein, brady, histamine, PGs, tachykinins -esp in non-portal-draining organs -in rt side b/c sero, brady inactivated in lungs -some in left side w/ migraine Tx, fen-phen, Heart Disease Hypertensive Heart Disease -heart's response to HTN Pulmonary HTN HD (Cor Pulmonale) -RV hypertrophy, dilation, failure -2ndary to pulm HTN from lung d/o -can be acute or chronic based on lung d/o Acute after pulm embolism->only DILATION Chronic-hypertrophy due to prolonged P overload -from pulm aa, a'oles obstruction; cap compression əcm wall hypertrophy-can be size of LV -can ->obstruction of outflow tract -can ->tricuspic regurg(fibrous), compression of LV, Heart Disease Valvular Disease Rheumatic Fever, HD -most frequent cause of mitral stenosis -Mostly in kids 5-15 yo -usually after group A Strep-hypersensitivity -triggers immunologic etiology-M proteins ASCHOFF Body-focal interstitial inflam -in myocardium, everywhere in acute -Anitschkow myocytes in here (PATHOGNO) -some Aschoff cells (giant cells) -replaced w/ fibrous scar later Pancarditis->effusions, Aschoff present in acute Pericarditis-bread & butter Myocarditis->cardiac failure -cause of death in most acute cases Endocarditis->valvular dmg -areas of greatest hymodynamic stress -mitral (50%), aortic valves mostly -M-fishmouth buttonhole &/or insuff -Ao-stenosis or insuff -gradual changes, so well-tolerated -valve closure points, posterior LA ->MacCallum plaque-irreg thickening Early-red, swollen leaflets -tiny, rubbery, warty verrucae -nonfriable (not source of emboli) Healing->thickened, fibrotic, deformed -fusion of cusps, thickened cords RHD-calcifications+above dmg in late dz Other RF problems (2+recent infx=Dx) 2)migratory polyarthritis of large jts 3)subcutaneous nodules 4)erythema marginatum 5)Sydenham chorea, Most from faulty wk 3-8 embryogenesis -most common type of HD in kids, higher in premies -can ->endocarditis, hyperviscosity CAUSE-genetic, trisomies 13, 15, 18, 21, XO -env - congenital rubella infx -cause identified in only 10% -familial ASD linked to chrom 5q 3 Major Categories Obstruction Coarctation of Ao-MALE>F -F w/ XO syn; 50% w/ biocuspid Ao valve Infantile-tubular hypoplasia of arch -proximal to PDA->S/Sx early-more severe -if w/out PDA-HTN in UL, weak pulses in LL Adult-ridgelike infolding distal to ligamentum -form collaterals w/ incostals, int. mammary -murmurs through systole, LV hypertrophy Surgical Tx successful w/ graft, resection Pulmonary Stenosis, Atresia-relatively freq -obstruction at PV-mild to severe -can be w/ ToF, TGA->RV hypertrophy ->post-stenotic dilation of PA -if atretic-hypoplastic RV->ASD/PDA help Aortic Stenosis/Atresia Valvular-cusps hypoplastic, dysplastic, abnl # Supra-, Sub- Severe-hypoplastic LV, Ascending Ao, PDA -fatal when ductus closes in 1st week Subaortic-fibrous below valve-discrete or tunnel Supravalv-asc Ao thickened-due to elastin defect -can be due to hyperCa of infancy (Williams) -systolic murmur-good prognosis -possible sudden death w/ exertion