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41 Cards in this Set
- Front
- Back
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dilated cardiomyopathy pathophysiology
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- --> LV chamber enlargement/minimal hypertrophy
-impaired systolic contraction - EF <35% -initial compensation for impaired myocyte contractility by increasing intravascular volume - F-S mechanism -increase sympathetic input and use renin-angiotensin (angiotensin II bad b/c vasoconstriction and prothrombotic -compensate, but eventually can't any more |
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hypertrophic cardiomyopathy pathophysioogy
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-LV thickening - myofiber disarray
- abnormal diastolic relaxation |
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restrictive cardiomyopathy pathophysioogy
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-stiffened myocardium
-diastolic relaxation impaired/systolic function usually normal |
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etiology of DCM
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-post-viral
-alcohol (reversible) -idiopathic -infiltrative disease -peripartum |
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findings in DCM
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-biventricular congestive HF (L --> R)
-lo forward CO -pulmonary congestion -systemic congestion -end stage: pulsus alternans: alternation of strong and weak beats due to alternate strong and weak ventricular contractions -laterally dysplaced PMI, S3 gallop, mitral/tri regurg murmur, increased JVD -EKG: LVH and LA enlargement (prone to re-entry rhythm), tachy (a and v), conduction abnl (LBBB) -echo: increased LV size, dec LV function, wall hypertrophy, valve regurg, reduced EF |
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prognosis of DCM
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-decline in function
---> heart failure -conduction abnl -ventricular/supraventricular arrhythmias -reduced EF --> increased mortality -defibrillator for DCM, EF <30, post-MI EF <30, II or III HF LVEF <35% -LBBB - myocardial dyssynchrony - abn in electrical activation of myocardium -- mechanical dysfunction |
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treatments for DCM
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-pacemaker/defibrillator
-cardiac resynchronization therapy to improve hemodynamics, reverse LV remodeling/architecture |
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HCM general
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-LV hypertrophy NOT due to pressure overload
-hypertrophy is variable in severity/location -asymmetrical septal hypertrophy --> HOCM -symmetric (non-obstructive) -apical hypertophy (asian) vigorous systolic function, but impaired diastolic most common cause of cardiac death in young people |
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HCM pathophys
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-myocyte hypertrophy --> myofibers in disarray --> ventricular arrythmias --> sudden death, syncope
-myocyte hypertrophy --> LVH --> impaired relaxation, increased MVO2 --> dyspnea, angina -dynamic LV outflow obstructions --> LV systolic pressure increase, mitral regurg, failure to increase CO w/ exertion --> dypnea, syncope |
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HOCM pathophys
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-dynamic LVOT obstruction
-systolic anterior motion of mitral valve |
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HCM findings
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-bisferiens pulse: spike and dome
-S4 gallop -crescendo/descrescendo systolic ejection murmur -holosytolic apical blowing MR murmur -HOCM vs AS - valsalva --> reducing preload --> LV shrinking --> outflow tract much worse (AS the murmur gets softer during valsalva) -EKG: NSR, LVH, septal Q -Echo: septum >1.4x free wall, LVOT gradient by doppler -systolic anterior motion of mitral valve --> regurg -Brockenbrough-Braunwald sign: failure of aortic pressure to rise post PVC --> compensatory pause after PVC |
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treatment of HCM
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- beta blockers to reduce mvO2, decrease gradient, decrease arrhythmias
-Ca channel blockers -antiarrhythmics - amiodarone, disophyramide (afib); -surgical treatment - myomectomy, ETOH ablation |
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how does HCM --> HF?
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-LV not accept adequate volume during diastole at normal pressure --> rise in LVEDP, LAP, PVP/PHTN
-superimposed conditions |
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restrictive cardiomyopathy is characterized by...
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-impaired v filling due to stiff ventricle
-normal systolic function -intraventricular pressure rising with small increases in volume |
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causes of RCM
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-infiltration by abnormal substances
myocardial causes: -amyloidosis - primary, secondary, -radiation -hemochromatosis -storage diseases endomyocardial conditions: -endomyocardial fibrosis (fibrous tissue on myocardium) -Loefflers endomyocarditis -endocardial fibroelastosis (lined w/ fibrous tissue and elastic tissue) |
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pathophys of RCM
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-elevated systemic & pulmonary venous pressures --> R/L congestion --> reduced ventricular cavity size + reduced SV and reduced CO
-hemodynamic issues - infiltration --> increased stiffness and chamber not accept volume with rise in pressures -severe diastolic dysfunction |
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RCM findings
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-right > left HF
-dyspne, orthopnea, PND -peripheral edema -ascites -fatigue, reduced exercise tolerance -mimics constrictive pericarditis -echo: mitral in flow velocity, rapid early diastolic filling |
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treatment of RCM
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-treat disease - rule out contriction, amyloid, endomyocardial fibrosis, hemochromatosis, sarcoid
-diuretics for congestive symptoms but reduce LV/RV filling --> reduced CO -dig for a fib rate control - antiarrhythmics -pacemaker -anticoag |
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other cardiomyopathies
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- arrhythmogenic right ventricular dysplasia (ARVD)
- isolated LV non-compaction - stress cardiomyopathy - takosubo's - non-structural - ion channelopathies |
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gross pathology of DCM
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-heavy (2-3x nl)
-large, flabby, dilated -walls thinned, but out of proportion to dilation of chamber -valves intrinsically normal -coronary arteries normal or any atherosclerosis insufficient and can't explain myocardial disease |
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histology of DCM
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-non diagnosic
-myocytes hypertrophied w/ enlarged nuclei -some myocytes atrophied & stretched -interstitial fibrosis & myocyte dropout |
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heart muscle stained with trichrome for collagen. Note non-specific fibrotic staining in between. Non-diagnostic for DCM.
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gross path of HCM
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-massive hypertrophy without chamber dilation
-90% with septal/ventricular ratio > 1.3 -shape - banana-like -possible endocardial thickening with mural plaque due to --contact with anterior mitral valve leaflet |
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histology HCM
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-is diagnostic
-marked myocyte HYPERTROPHY -DISARRAY of myocytes |
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histology of RCM
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-pathy interstitial fibrosis
-appearance of endocardium & myocardium diagnostic of specific disease process |
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amyloid --> restrictive cardiomyopathy
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-arrhythmogenic right ventricular cardiomyopathy aka AVRD
-part of RV thin and lack myocytes, usually contain only fatty infiltration and fibrosis -caused by muscle degeneration, inflammation, infectious, autoimmune, genetic causes |
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-arrhythmogenic right ventricular cardiomyopathy aka AVRD
-part of RV thin and lack myocytes, usually contain only fatty infiltration and fibrosis -caused by muscle degeneration, inflammation, infectious, autoimmune, genetic causes |
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hemocromotosis --> RCM
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-isolated LV non-compaction
- --> prominent trabeculations - thick endocardial layer of trabecular meshwork -deep recesses in apex of LV |
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lysosomal storage diseases --> RCM
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RCM
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takotsubo
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myocarditis definition
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inflammatory cardiomyopathies
presence of inflammatory infiltrate myocyte necrosis or damage not ischemic |
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3 types of myopathy
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- infection (viruses most common)
- immune-mediated - unknown (sarcoid, giant cell) |
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myopathy pathology
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-gross: may be normal, chambers may be dilated, may have pale foci or hemorrhage lesions
-histology: inflammatory infiltrate cells |
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3 phases of myocarditis
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-initial direct insult to myocardium
-subsequent autoimmunity triggered, extensive myocardial injury -development of dilated cardiomyopathy |
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non-infectious myocarditis causes
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1) allergic, hypersensitive, immune: antibiotics, post-strep, transplant reject, EOSINOPHILS
2) giant cell: myocardial necrosis of uncertain cause; mixed inflammatory cells w/ multinucleate giant cells |
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eosinophils -- allergic, hypersensitive, or immune myocarditis
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giant cell myocarditis
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diagnosing myocarditis
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-biopsy (but HUGE false negative rate)
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