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lecture 26 brickner

definition: cardiomyopathy myocardial disorder in which the heart muscle is structurally or functionally abnormal in the absence of CAD, HTN, valve or congenital heart dz sufficient to have caused said abnormality
3 types of cardiomyopathy hypertrophic obstructive, restrictive and dilated
dilated cardiomyopathy LV dilatation and dec systolic function in the absence of abnormal loading conditions like HTN or valve dz
primary vs secondary cardiomyopathy primary: not associated with another type of heart dz // secondary: specific etiology is known like post-partum cardiomyopathy
common etiologies of dilated cardiomyopathy up to 20% are familial or hereditary like Duchenne muscular dystrophy, idiopathic, post-partum, post-viral or caused by toxins like EtOH
presentation of pt with dilated cardiomyopathy sx of heart failure: left - DOE, PND, orthopnea and fatigue // right - pedal edema, inc abd girth, anorexia and/or nausea
systolic vs diastolic dysfunction inability to maintain sufficient CO vs inability of ventricles to receive incoming blood
sx seen occasionally in pt with dilated cardiomyopathy palpitations or CP without evidence of CAD, syncope or embolic event from thrombus formation in LA or LV
PEx of pt with dilated cardiomyopathy resting tachy, narrow pulse pressure, S3/4 JVD with prominent v waves (reflects tricuspid regurg - tender pulsatile liver if so), CM with lateral PMI. R heart failure sx 50% of the time
best prognostic indicator in pt with dilated cardiomyopathy who are in heart failure NOT LVEF but maximal oxygen consumption at peak exercise (measures systemic oxygen delivery or consumption)
clinical course of pt with dilated cardiomyopathy usually deteriorate until the point of sudden death from ventricular arrhythmias, progressive heart failure or thromboembolic events to pulmonary or systemic circulations
CXR and EKG of pt with dilated cardiomyopathy CXR: mod-severe CM with pulmonary vascular congestion, pleural effusions // EKG: sinus tach with atrial or ventricular ectopy, Q waves ("pseudoinfarction pattern"), non-specific ST changes, LAE & LVH
findings on Echo for pt with dilated cardiomyopathy large dilated and poorly contractile ventricle, possible thrombus in the ventricular apex, associated mitral/tricuspid regurg, elevated intracardiac filling pressures
why risk of thromboembolic events is so high in pts with dilated cardiomyopathy LVEF is usually less than 45% and there is stasis of blood in the ventricle, predisposing to thrombus formation
hypertrophic cardiomyopathy characterized by an increased left ventricular wall thickness in the absence of any apparent etiology that causes diastolic dysfunction. usually involved the interventricular septum, LV free wall or the apex
HOCM 25% of hypertophic cardiomyopathies - usually asymmetric thickening and causes an obstruction to outflow from the LV and resultant pressure gradient btwn LV cavity and aorta. in addition to restriction of LV filling
2 biggest causes of HCM cardiac myosin heavy chain beta mutation and myosin binding protein C mutation (next are troponin I and tropomyosin mutations)
maneuvers and HCM Valsalva or nitrates make HCM worse b/c the RV is filling more and providing less space for the LV to fill. isometric contraction or squatting makes it better b/c it stops venous return of blood to the LV
presenting signs and sx of pt with HCM all typical sx from pulmonary congestion due to inc end-diastolic LV, LA and pulmonary vascular pressures. dyspnea, orthopnea, PND, angina, palpitations & syncope from ventricular or atrial arrhythmias
leading cause of sudden death in young athletes (<35 y/o) hypertrophic cardiomyopathy - either from fatal ventricular arrhythmia or MI from inability to perfuse thickened myocardium especially when with exertion outflow vol can't inc appropriately
PEx of pt with HCM bisfiriens pulse (double carotid), forceful and lateral PMI, apical systolic thrill, prominent S4, systolic murmur that changes with maneuvers
PEx in pt with aortic stenosis vs HOCM both will have harsh crescendo-decrescendo systolic murmur and abnormal carotid pulses. AS: pulsus parvus et tardens, murmur radiates to carotids // HCM: murmur radiates to base of heart, bisfiriens pulse
structural phenomenon that worsens HOCM anterior leaflet of mitral valve can be pulled into the outflow tract further obstructing flow of blood
common complications in pts with hypertrophic cardiomyopathy 10-15% of pts develop dilated cardiomyopathy, ventricular or atrial arrhythmias, infective endocarditis from turbulent flow about the outflow tract
CXR & EKG of pt with hypertrophic cardiomyopathy CXR: usually nl, maybe some pulmonary vascular redistribution // EKG: LVH with septal Q waves (due to myofibrillar disarray), giant inverted T waves in precordial leads
Echo findings in hypertrophic cardiomyopathy LVH, a normal LVEF, LV outflow tract obstruction/MR possible. asymmetric septal hypertrophy is septum to LV free wall ratio exceeds 1.3:1, possible systolic anterior motion of mitral leaflet = HOCM
tx of hypertrophic cardiomyopathy diuretics to relieve pulmonary congestion, beta blockers or CCBs help with ventricular filling, resection of septum, iatrogenic septal MI, treating arrhythmias with amiodarone
Created by: sirprakes