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696 Cards in this Set
- Front
- Back
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How many leaflets do the semilunar valves have?
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three
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Where is the fibrosa of the valve?
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collagenous core on ventricular side of AV valves, continuous with fibrous skeleton
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Where is the spongiosa of the valve?
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looser connective tissue on either side of the fibrosa
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What are the causes of mitral stenosis?
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rheumatic, congenital, endocarditis, calcification of mitral annulus
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What are the causes of mitral regurgitation?
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mitral prolapse, papillary muscle dysfunction, rheumatic, chordal rupture, LV enlargement, endocarditis
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What are the causes of aortic stenosis?
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congenital, senile calcification, rheumatic
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What are the causes of aortic regurgitation?
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rheumatic, endocarditis, syphilis, ankylosing spondylitis, dissecting aneurysm, Marfan's
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What are the causes of tricuspid stenosis?
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rheumatic, congenital, carcinoid
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What are the causes of tricuspid regurgitation?
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functional, rheumatic, endocarditis, carcinoid, trauma, endomyocardial fibrosis with eosinophilia, congenital
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What are the causes of pulmonic stenosis?
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congenital, carcinoid, rheumatic
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What are the causes of pulmonic regurgitation?
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functional, congenital, endocarditis, rheumatic, trauma
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What causes mitral stenosis?
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rheumatic heart disease
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What are the symptoms of mitral stenosis?
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dyspnea, orthopnea, paroxysmal nocturnal dyspnea
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What is rheumatic fever?
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systemic inflammatory disease
2-3 weeks after strep throat, humoral and cell-mediated immune response to cell membrane antigens, cross-reactive |
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What are the symptoms of rheumatic fever?
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fever, carditis, polyarthritis, chorea, subcu nodules, skin rash
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What is the EKG change in rheumatic fever?
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prolonged PR interval
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What are the heart effects of rheumatic fever?
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scarring of valve leaflets and support structure, valvular stenosis/insufficiency
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What are the gross cardiopath changes with rheumatic fever?
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acute fibrinous pericarditis, cardiomegaly, globular-shaped heart, valve lesions
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Which valve is most likely to be involved in rheumatic fever?
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mitral
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What are the microscopic path changes with rheumatic fever?
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verrucous vegetations on the edge of valve at lines of closure, myocarditis, Aschoff's nodules, inflammation around chordae tendinae
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What are Aschoff nodules?
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fibrinoid degeneration with histiocytes and lymphocytes
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What are the three phases of Aschoff nodules?
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exudative (acute inflammation, edema), proliferative, healed (scar)
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What happens in the chronic changes of rheumatic fever?
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healed inflammation and turbulence-induced fibrosis, diffuse fibrous scarring with progressive bridging across commissures, thickening, fusion and shortening of chordae, fish mouth mitral valve, MacCallum's patch on endocardium
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What does mitral valve prolapse cause?
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isolated mitral insufficiency
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What are symptoms of mitral valve prolapse?
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chest pain, palpitations, syncope, left heart failure, sudden death, systolic click or murmur
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What are the complications of mitral valve prolapse?
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CHF, chordal rupture, infective endocarditis, emboli, sudden death
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What is the pathology of mitral valve prolapse?
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leaflet hooding or redundancy, posterior leaflet is usually involved, dilation of valve anulus, elongated and tortuous chordae, histological expansion and proliferation of spongiosa with increased acid mucopolysaccharides
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What happens to the chordae in mitral valve prolapse?
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become stretched and rupture, resulitng in flail leaflet
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What congenital abnormalities are associated with MVP?
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ASD, hypertrophic cardiomyopathy, Marfan's
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What are the causes of mitral regurgitation?
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mitral valve prolapse, ischemic injury
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How does ischemic injury cause mitral regurgitation?
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secondary to coronary artery atherosclerosis can cause regurgitation by necrosis of mitral support structures
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What are the symptoms of aortic stenosis?
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angina, syncope, CHF symptoms
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What is the most common sign of aortic stenosis?
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systolic ejection murmur radiating to the neck
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What is the most common cause of aortic stenosis?
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bicuspid aortic valve, functions normally at first, then gets scarred and calcified, with resultant stenosis/insufficiency later
can be congenital or acquired |
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What does congenital bicuspid aortic valve look like?
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commissures equal distance from each other, rudimentary 3rd commisure
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What does acquired bicuspid aortic valve look like?
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commissures are not equal distant, fusion between one edge of two leaflets
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How old are patients with calcific aortic stenosis?
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>60 yo
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What is the major problem in calcific aortic stenosis?
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calcium deposition, don't have commissural fusion, deposits near basal attachments near Valsalva's sinuses
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What are the causes of aortic stenosis?
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congenital (bicuspid and unicuspid), rheumatic, degenerative
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How does acquired aortic stenosis happen?
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fusion of commissures and fibrosis, causes stenotic and regurgitant aortic valve
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What is the hemodynamic consequence of aortic stenosis?
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myocardial hypertrophy
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How do you treat aortic stenosis?
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valve replacement, commissurotomy, balloon valvuloplasty
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What causes aortic regurgitation?
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disease of aortic leaflets or aortic root
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What are common causes of leaflet abnormalities?
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infective endocarditis and rheumatic fever
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What are the aortic root causes of aortic regurgitation?
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ectasia, collagen vascular disease, syphilis
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What is carcinoid syndrome?
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complication of carcinoid tumors metastatic to the liver, produces collection of fibrous tissue on endocardium of valve cusps and cardiac chambers
more severe on right side of heart |
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What causes carcinoid syndrome?
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probably biogenic amines produced by the tumor
serotonin is released directly into IVC by carcinoid in liver, acts on right side of heart |
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What causes tricuspid regurgitation (Loeffler's disease)?
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endomyocardial fibrosis with eosinophilia
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What happens in Loeffler's disease?
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fibrous thickening of ventricular inflow tracts, causes severe tricuspid and mitral regurgitation, CHF
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What causes nonbacterial thrombotic endocarditis?
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acute or chronic illness, malformed valves, intracardiac catheters, monitoring devices
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What complications are associated with nonbactieral thrombotic endocarditis?
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valve dysfunction, fragments of thrombus can embolize, vegetations can be infected
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What is the most serious complication of valvular heart disease?
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CHF
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Why do thrombi form in the heart with valve problems?
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stasis in dilated ventricles, thrombi can embolize
atrial fibrillation can also contribute |
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Why do thrombi form in the peripheral circulation with valve problems?
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CHF causes congestion, also embolization of material from valve surfaces
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What causes atrial/ventricular arrhythmias with valve problems?
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chamber dilation, myocardial hypertrophy, MI related to decrease in coronary blood flow
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Why does hemolysis occur with valve problems?
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prosthetic mechanical heart problems
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Why does infective endocarditis occur with valve problems?
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abnormal morphology may predispose to subsequent development of infective endocarditis
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From which cusps of the aortic valve do coronary arteries originate?
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right and left
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At what aortic valve area do you get significant obstruction?
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< 2 cm
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What is the law of LaPlace?
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wall stress = (pressure x radius)/wall thickness
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What is the most common symptom of aortic stenosis?
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dyspnea, related to increased filling pressures an inability to augment CO with exercise
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What do you hear on cardiac exam with aortic stenosis?
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apical impulse: laterall displaced and sustained, palpable S4
A2 is delayed and softer as stenosis progresses crescendo-decrescendo murmur |
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What do you feel with the carotid impulse and aortic stenosis?
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pulsus parvus et tardus: upstroke is weak and delayed, less helpful in elderyly/with vascular disease
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What do you see on ECG with aortic stenosis?
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LV hypertrophy, LAL enlargement, absence of LVH doesn't exclude it
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What do you see on chest XRay with aortic stenosis?
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cardiomegaly: LVH, rounding of hte apex, calcification of the aortic valve and root, dilation of the aorta
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Why would you use cardiac catheterization with aortic stenosis?
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when noninvasive testing is inconclusive or discrepant results between symptoms/noninvasive results
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When do you intervene in aortic stenosis?
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once symptoms develop, high risk of death
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Why do you use valvuloplasty for aortic stenosis?
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as a bridge until surgery, high restenosis rate, can be used in kids and teens with congenital aortic stenosis and pliable valve leaflets
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Why do you have a volume overload state with aortic regurgitation?
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regurgitant volume leaks into LV during diastole is ejected during systole, total stroke volume increased, forward volume is reduced
eccentric hypertrophy and LV dilation |
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Why do you have a pressure overload state with aortic regurgitation?
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pulse pressure widens with increased SV and systolic BP increases, concentric hypertrophy to normalize wall stress
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When does LVEF fall?
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degree of hypertrophy does not compensate for afterload, reduction in contractility
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What do you see on physical exam with chronic aortic regurgitation?
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elevated systolic BP, widened pulse pressure, Hill's sign
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What is Hill's sign?
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leg pressure > arm pressure by more than 40 mm Hg
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What is the cardiac exam of Chronic Aortic Regurgitation?
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apical impulse: displaced laterally, systolic ejection sound, S3: increased LV volume, murmur
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How do you treat chornic aortic regurgiation?
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vasodilators, inotrpic therapy, antibiotics
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What happens in the chronic phase of mitral regurgitation?
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eccentric cardiac hyptertrophy, increase in LV end-diastolic volume, increase in stroke volume and CO
above normal EF |
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What are the most common symptoms of chronic mitral regurgitation?
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dyspnea, fatigue, right sided heart failure
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What do you hear on heart exam wtih chronic mitral regurgitation?
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apical impulse is brisk and displaced laterally S1 is variable, prominent P2, S3 with rapid filling
holosystolic murmur |
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What do you see on ECG with chronic mitral regurgitation?
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left atrial enlargement, LVH, atrial fibrillation
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What do you see on CXR with chronic mitral regurgitation?
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cardiomegaly, left atrial enlargement, calcium in annulus/leaflets
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What do you give for chronic mitral regurgitation?
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vasodilators, surgery
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At what area does the mitral valve change the pressure in the left side of the heart?
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2 cm^2
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How does mitral valve stensosis change the heart rate?
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as HR increases, diastole is shortened disproportionately to systole
at a given CO, increases in HR result in an increase in transmitral gradient |
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What do you hear with heart exam of mitral stenosis?
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S1: loud early, S2: single, P2 accentuated, opening snap, diastolic rumble
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What do you see on CXR with mitral stenosis?
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left atrial enlargement, enlarged PA, RA, RV with severe pulmonary HTN
intersitial markings |
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What do you see on ECG with mitral stenosis?
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LA enlargement, atrial fibrillation, RVH
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How long does it take to develop MS after RF?
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at least 2 years, symptoms in 3rd and 4th decades
in underdeveloped nations, develop it earlier |
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What is the medical therapy of mitral stenosis?
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rate slowing, diuretics, anti-coagulation, antiarrhythmics
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What are the symptoms of tricuspid stenosis?
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salt restriction, diuretics, surgery
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What causes functional tricuspid regurgitation?
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dilation of the annulus and RV, not intrinsic valve disease
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What do you see with tricuspid valve disease and pulmonary hyptertension?
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systemic venous congestion, ascites, ab pain, edema, low output with fatigue and dyspnea
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What do you see in the jugular vein with tricuspid regurgitation?
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venous distention, systolic or "v" wave
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What do you hear on heart exam with tricuspid regurgitation?
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RV lift, right sided S3, murmur (pansystolic), pulsatile enlarged liver, ascites, edema
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What causes pulmonic stenosis?
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congenital is most common, carcinoid, rheumatic
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What causes pulmonic valve insuficiency?
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HTN, congenital, endocarditis
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How does pulmonary valve insufficiency present with pulmonary HTN?
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right sided heart failure (edema, hepatomegaly, ascities, jugular vein distension)
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What do you hear on heart exam with pulmonary insufficiency?
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decrescendo diastolic murmur at left sternal border, increased with inspiration
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How does pulmonary stenosis present?
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severe: right sided heart failure
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What is in a vegetation?
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thrombotic debris, inflammatory cells and microorganisms
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What cuases acute endocarditis?
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highly virulent organisms
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Where does acute endocarditis affect?
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normal valves
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What is acute endocarditis associated with?
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metastatic infection
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What causes subacute endocarditis?
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less virulent organisms
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How does endothelial injury contribute to endocarditis?
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high velocity jets striking endothelial surface, flow from high to low pressure, flow across narrow orifice at high velocity, direct injury due to foreign body
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How do blood clots contribute to endocarditis?
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formation of a clot comes into contact with subendothelium forming fibrin-platelet clump
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What is Marantic endocarditis?
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macroscopic clump of platelets in patients with chronic wasting diseases, cancer, burn, DIC
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What is Libman-Sacks endocarditis?
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patients with SLE
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How does the Ventrui effect affect endocarditis?
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blood flow through narrow orifice during bacteremia deposits bacteria at low pressure sink, on atrial side of AV valves and ventricular side of aortic valve
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What are the clinical manifestations of endocarditis?
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fever, malaise, anorexia, back pain
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What are the local effects of endocarditis?
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CHF, conduction system disturbances, fistula formation
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What are the sequelae of the immune response?
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petechia, splinter hemorrhages, splenomegaly, Osler's nodes, glomerulonephritis
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What emoblic phenomena are associated with endocarditis?
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Roth spots, Janeway lesions, renal/mesenteric infarcts, stroke, mycotic aneurysm formation, septic pulmonary emobli
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What are lab findings of endocarditis?
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positive blood clutures, anemia, leukocytosis,
ESR, CRP, RF elevated proteinuria and hematuria |
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Why would you treat endocarditis surgically?
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moderate to severe CHF, failure to clear infection, prosthetic valve, large, recurrent emboli
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What is primary cardiomyopathy?
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etiology of the heart disease is unknown
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What is secondary cardiomyopathy?
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etiology of myocardial abnormality is known or part of a systemic process
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What characterizes dilated cardiomyopathy?
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ventricular dilation, systolic contraction dysfunction, reduced CO
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What are the cardiac results in dilated cardiomyopathy?
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low EF, high end-systolic volume, CHF
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What are the clinical features of dilated cardiomyopathy?
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signs and symptoms of progressive CHF, arrhythmias, conduction defects
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How do you treat dilated cardiomyopathy?
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vasodilators, beta-blockers, positive inotropes, cardiac transplant
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What is the gross pathology of dilated cardiomyopathy?
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enlarged volume and mass, ventricles dilated, normal LV thickness, fibroelastosis, normal valves
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What is the microscopic pathology of dilated cardiomyopathy?
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myocyte hypertrophy, myocyte loss, myocyte atrophy, myofibrillar loss, fibrosis
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In whom does dilated CM occur?
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most common in middle-aged men, alcoholics, diabetics
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What does myocarditis do to dilated CM?
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inflammation of myocardium by Coxsackie B, other viruses, reduced cardiac function
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How does alcohol affect dilated CM?
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reduced contractility, myocardial damage
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How does diabetes affect dilated CM?
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small-vessel disease impairs interactions between capillary endothelial cells and cardiac myocytes, loss of myocytes
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How does heredity affect dilated CM?
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mutations in cytoskeletal or contractile proteins
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How does peripartum affect dilated cardiomyopathy?
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myocardial adaptations during pregnancy, adapt to the need for increased CO, reveresed after birth, can be maladaptive
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How does nutritional deficiency affect dilated cardiomyopathy?
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thiamine deficiency
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How does chemotherapy affect dilated cardiomyopathy?
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tetracyclic anthracyclines leads to myocardial damage due to cell death, myofilament damage, impaired myofilament synthesis
related to cumulative dose |
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What is the mechanism for chemotherapy-related dilated cardiomyopathy?
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antrhacycline-mediated formation of ROS, interruption of transcription and translation, DNA repair
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What happens when you have reduced CO with dilated CM?
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reduced perfusion of vital organs
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How does the body try to restore CO in dilated CM?
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activation of sympathetic NS, increase in circulating catecholamines
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How do catecholamines affect the heart?
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increase HR, increase CO
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How do chronically elevated catecholamines negatively affect the heart?
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arrhythmias, myocyte death, progressive ventricular dilation, reduces beta receptor expression
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What are the peripheral effects of low CO?
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arterial vasoconstriction, increased peripheral vascular resistance, activation of renin-angiotensin, increase in vasopressin
increases afterload and preload |
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How does hypertrophic CM affect the heart?
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impaired myocardial diastolic relaxation, systolic function is normal
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Where can hypertrophic CM occur?
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septum, LV outflow tract, concentric LV
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What is the gross pathology of hypertrophic CM?
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hypertrophy of ventricular septum, reduction in volume of ventricular cavities, endocardial thickening, mural plaque formation in LV outflow, mitral valve thickening, dilated atria
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What are the microscopic changes in hypertrophic CM?
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myofiber disarray in IVS, myocyte hypertrophy with enlarged nuclei, perinuclear halo, narrowed intramyocardial coronary arteries with medial thickening and luminal narrowing
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Who gets hypertrophic cardiomyopathy?
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young adults, may die suddenly, can be familial
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What is the most common pathology associated with hypertrophic CM?
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diastolic dysfunction due to impaired LV relaxation and LV filling
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What is the most common symptom of hypertrophic CM?
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dyspnea due to elevated LV diastolic pressure
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What other symptoms are common to hypertrophic CM?
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angina, fatigue, syncope, palpitations, paroxysmal nocturnal dyspnea, CHF, dizziness
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What is the course of hypertrophic CM?
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variable, can improve, can cause death due to ventricular arrhythmia
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What are the risk factors for sudden death by hypertrophic CM?
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strong family history, persistent syncope, physical findings, enlarged heart, young age at diagnosis, nonsustained ventricular tachycardia
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How do you treat hypertrophic cardiomyopathy?
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automatic implanted cardiac defibrillators, ablation, Ca channel blockers, beta blockers
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What genes are mutated in hypertrophic cardiomyopathy?
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beta-myosin heavy chain, cardiac troponin, myosin binding protein
lead to prolonged IC calcium transients |
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Which type of cardiomyopathy is least common in Western countries?
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restrictive
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How does cardiac function change in restrictive cardiomyopathy?
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decreased stroke volume, inadequate diastolic filling
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What can cause restrictive cardiomyopathy?
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amyloid, hemochromatosis, glycogen deposition, endocardial fibrosis, sarcoidosis, hypereosinophilic syndrome, neoplastic infiltration of the ventricular myocardium
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What are the two diseases that cause primary restrictive CM?
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endomyocardial fibrosis, Loffler's endocarditis parietalis fibroplastica
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What are the signs of restrictive CM?
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increased central venous pressure, hepatomegaly, ascites, dyspnea on exertion, hemoptysis, left heart failure, pulmonary congestion
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What happens in amyloidosis?
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amyloid deposits of transthyretin in elderly people or as part of systemic amyloidosis
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What are the symptoms of amyloidosis?
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exertional dyspnea, orthopnea, CHF, conduction disturbances
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How long does it take for primary amyloidosis to cause death?
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4 months to 2 years following onsets
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What is amyloid?
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homogenous hyaline EC material
beta-pleated sheets of fibrillar proteins |
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What does the heart look like grossly with amyloidosis?
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heavy heart with thick walls, pale color, rubbery
deposits on teh interstitium, conduction tissues, valves, endocardium, pericardium, intramural arteries |
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How do you confirm amyloidosis?
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apple-green birefringence under polarized light after Congo read
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What is endomyocardial fibrosis?
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a type of restrictive/obliterative cardiomyopathy
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What is hypereosinophilic syndrome?
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blood eosiniophilia with diffuse eosinophilic infiltration of organs
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What are the symptoms associated with hypereosinophilic syndrome?
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cardiac murmurs, biventricular failure
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What are the microscopic changes with endomyocardial myocarditis?
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eosinophilic infiltrates and necrosis in acute phase, fibrosis and scar in healed stage
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What is the gross pathology with endomyocardial myocarditis?
|
posterior mitral leaflet adherent to the left ventricular free wall by thrombus
thrombus in apex of left ventricle endocardial fibrosis, esp at apex of RV, can extend to mitral valve |
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What happens in idiopathic restrictive cardiomyopathy?
|
not associated with abnormal deposition of material in the myocardium
marked interstitial myocardial fibrosis, impedes diastolic relaxation and systolic dysfunction |
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What happens in arrhythmogenic right ventricular cardiomyopathy/dysplasia?
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loss of myocytes in RV, fatty/fibrofatty tissue replacement
LV involvement in 75% of patients |
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What is the gross pathology of arrhythmogenic right ventricular cardiomyopathy/dysplasia?
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dilated RV, aneurysmal thinning of RV wall
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What is the microscopic pathology of arrhythmogenic RV cardiomyopathy/dysplasia?
|
fatty infiltration in the RV, fibrosis, chronic inflammation
can also be in LV |
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How is arrhythmogenic RV cardiomyopathy/dysplasia transmitted?
|
autosomal dominant trnasmission
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What are the presenting symptoms of arrhythmogenic RV cardiomyopathy/dysplasia?
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arrhythmias, syncope, cardiac arrest, focal/global chamber dilation, wall motion abnormalities
sudden death |
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What is ischemic cardiomyopathy?
|
CHF due to CAD and myocardial ischemic fibrosis
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What is the pathology of ischemic cardiomyopathy?
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LV contractile dysfunction secondary to fibrosis as a result of myocardial infarction and CAD
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What are the causes of aneurysms?
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atherosclerosis, Marfan's, dissections, annuloaortic ectasia, traumatic, pregnancy, fibromuscular dysplasia, vasculitis, infectious, pancreatitis
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Where do atherosclerotic aneurysms occur?
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abdominal aorta, politeal, splenic, axillary, renal, iliac, femoral, coronary arteries
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Where do ab aortic aneurysms usually occur?
|
below renal arteries, above bifurcation
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What do you usually find in the dilated part of an aortic aneurysm?
|
mural thrombus
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What are the histologic features of atherosclerotic aneurysms?
|
atheromas, fibroatheromas, plaques, hemorrhage, calcification, bony metaplasia, inflammatory infiltrate
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What are the complications of ab aortic aneurysms?
|
rupture, occlusion of branch vessels, emboli, compress adjacent structures
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How do ab aortic aneurysms present?
|
pulsatile abdominal mass
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What predicts the risk of rupture of an ab aneurysm?
|
size of aneurysm
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What is an aortic dissection?
|
accumulation of blood between planes of arterial media or between media and adventitia, associated with intimal and medial tear
|
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Where do spontaneous aortic dissections occur?
|
almost any arterial bed
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Which conditions are associated with aortic dissection?
|
HTN, atherosclerosis, vasculitis, CT disorders, fibromuscular dysplasia, trauma, pregnancy, iatrogenic procedures, bicuspid/unicuspid aortic valve, coarctation of the aorta
|
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What are the initial histo characteristics of an aortic dissection?
|
lining of platelets with/without fresh blood in the dissection plane
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What are the chronic histo characteristics of an aortic dissection?
|
dissection plane lined by granulation tissue, fibrous tissue, distortion of the arterial wall, can have a false lumen
|
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What is cystic medial degeneration?
|
in many diseases
large areas of mucinous material with loss of elastic fibers |
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Which disease causes severe medial degeneration?
|
Marfan's
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What happens in death by aortic dissection?
|
rupture into pericardial, pleural, peritoneal cavities
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What are the symptoms of aortic dissection?
|
sudden onset of excruciating pain, usually beginning in anterior chest, radiating to the back and moving downward
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What is Takayasu's arteritis?
|
necrotizing, granulomatous inflammatory disease that evolves into fibrointimal thickening and adventitial fibrosis
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Where does Takayasu's affect?
|
aorta, coronary, renal, subclavian, L common carotid, mesenteric, innominate arteries
|
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What are the early clinical features of Takayasu's arteritis?
|
malaise, weakness, fever, night sweats, arthralgias, arthritis, myalgias, weight loss, pleuritic pain, anorexia
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|
|
What are the signs/symptoms of late phase Takayasu's artertitis?
|
no pulses, bruits, HTN, heart failure, retinopathy, aortic insufficiency, coronary ostial stenosis
|
|
|
What are the early histo phases of Takayasu's?
|
vascular edema and inflammation, lymphocytes, plasma cells, giant cells, histiocytes
inflammation most severe in outer 2/3rds of media, extends to adventitia, coagulation necrosis of media with surrounding histiocytes and giant cells |
|
|
How do you treat early acute Takayasu's?
|
corticosteroids or cyclophosphamide
|
|
|
How do you treat late Takayasu's?
|
surgical bypass
|
|
|
What are the gross path changes of late Takayasu's?
|
narrowing of arteries, esp arch vessels, descending thoracic aorta, ab aorta
intima has "tree bark appearance" |
|
|
What are the histo changes of late Takaysu's?
|
intimal smooth muscle cell proliferation, increased EC matrix, medial destruction and fibrosis, stenosis
|
|
|
What are the eye changes of Marfan's?
|
myopia, retinal detachment, elongated globe
|
|
|
What are the skeletal changes of Marfan's Syndrome?
|
joint hypermobility, tall stature, pectus excavatum, scoliosis
|
|
|
What is the mutation in Marfan's?
|
gene that encodes fibrillin-1 on chromosome 15
|
|
|
What does Fibrillin-1 do?
|
component of microfibrils that form elastin
|
|
|
What are the CV problems with Marfan's?
|
aortic root dissection, aortic dissections, mitral valve prolapse, cystic medial necrosis of the aorta
|
|
|
What are the risk factors for PAD?
|
diabetes, smoking, age
|
|
|
Where is atherosclerosis most commonly?
|
arms rather than legs
|
|
|
Where does PAD usually occur in people under 40?
|
aortoiliac
|
|
|
Where does PAD usually occur in people over 40?
|
femoropopliteal
|
|
|
What is the hallmark of PAD?
|
intermittent claudication
|
|
|
What is intermittent claudication?
|
reproducible cramping discomfort of the legs, hips, butt, produced by exertion and relieved by sitting or standing still
|
|
|
What should you do to check out PAD?
|
BP in both arms, palpate pulses, auscultate for bruits, check out extremities
|
|
|
What is the ankle brachial index?
|
noninvasive assessment of PAD
ratio of BP in lower legs to that in the arms |
|
|
In what patients is the ABI artificially high?
|
patients with arterial calcification, diabetes
|
|
|
What is the gold standard for imaging in PAD?
|
invasive angiography
|
|
|
What drug do you use for intermittent claudication?
|
Cilostazol
|
|
|
How does Cilostazol work?
|
inhibits PDE3, relaxes smooth muscle
|
|
|
For what do you use Tizanidine?
|
treatment of muscular spasm with diseases like MS
|
|
|
Upon what receptors does Tizanidine act?
|
alpha2 agonist
|
|
|
What are the side effects associated with Tizanidine?
|
vasoconstriction, Traynaud's, sedation, loss of energy, depression, reduced sex drive, dry mouth
|
|
|
Upon what receptors does Brimonidine act?
|
alpha2 agonist
|
|
|
Why do you use Brimonidine?
|
opthalmic solution to lower intra-ocular pressure in glaucoma
|
|
|
What are the side effects of Brimonidine?
|
vasoconstriction, Raynaud's
|
|
|
Which receptor does Teradosin affect?
|
alpha1 blocker
|
|
|
Which receptor does Doxazosin affect?
|
alpha1 blocker
|
|
|
Why are terazosin and doxazosin better than prazosin?
|
longer half life than prazosin
less swing in levels and blood pressure |
|
|
What does terazosin act like?
|
prazosin and doxazosin
|
|
|
What does doxazosin act like?
|
prazosin and terazosin
|
|
|
Which receptor does Labetalol affect?
|
selective alpha1 antagonist, beta1 antagonist, partial beta 2agonist
|
|
|
What determines cardiac function?
|
preload, afterload, HR, contractility
|
|
|
What happens when you have impaired contractility?
|
less caridac work generated for a given fiber length/pressure
|
|
|
How do drugs that increase Ca concentration affect the heart?
|
increase in contractility and in mortality
|
|
|
How do you reduce preload?
|
restrict Na intake, diuretics, venodilators
|
|
|
How do you reduce afterload?
|
vasodilators
|
|
|
How do you reduce HR?
|
reflex with sympathetic withdrawal as CO improves
|
|
|
What drug is preferred for IV therapy in atrial fibrillation?
|
diltiazem
|
|
|
What causes PVST?
|
reentrant circuit in/near AV node or retrograde conduction over accessory AV conduction
|
|
|
What is mild hypertension?
|
140-159 systolic
90-99 diastolic |
|
|
What is moderate hypertension?
|
160-179 systolic
100-109 diastolic |
|
|
What is severe hypertension?
|
>180 systolic
>110 diastolic |
|
|
What is labile hypertension?
|
intermittently-elevated pressures
|
|
|
What is secondary hypertension?
|
has a known cause
|
|
|
Which renal diseases cause secondary hypertension?
|
chronic glomerulonephritis, chronic pyelonephritis, congenital polycystic renal disease
ostial atherosclerosis, fibromuscular dysplasia, thromboemoblism, ateriovenous fistula |
|
|
Which endocrine diseases cause secondary hyptertension?
|
hypothyroidism, hyperthyroidism, adrenal disease (primary aldosteronism, pheochromocytoma)
|
|
|
What are the other causes of secondary hypertension?
|
coarctation of the aorta, pregnancy, stress
|
|
|
What can cause systolic hypertension?
|
rigidiity and dilation of the aorta, increasing age
increased CO |
|
|
What are the symptoms of hypertension?
|
headache, nosebleed, tinnitus, dizziness, syncope
|
|
|
What happens in benign hypertension?
|
benign nephrosclerosis: medial hypertrophy, proliferation of intimal smooth muscle cells, increase in elastic tissue, hyalinization of arterioles and small arteries
|
|
|
What happens in malignant hypertension?
|
benign nephrosclerosis plus "onion-skin" lesions, fibrinoid necrosis, glomoid or plexiform lesions
|
|
|
What are gross changes of benign hypertension?
|
granular outer surface, ill-defined corticomedullary junction
|
|
|
What are the microscopic changes of benign hypertension?
|
thick, hyalinized vascular walls iwth homogenous eosinophilic appearance, elastosis
|
|
|
How does malignant hypertension develop?
|
runs rapid course, can develop in the setting of benign hypertension or de novo
|
|
|
What is the gross kidney pathology of malignant hypertension?
|
focal, petechial hemorrhages on outer surface of the kidney
|
|
|
What are the microscopic kdiney changes of malignant hypertension?
|
arterioles have fibrin deposition, thickening due to intimal proliferation, thrombosis, fibrinoid necrosis, hemorrhage, glomoid lesions, glomerular necrosis/necrotizing glomeruloneprhitis
|
|
|
What are the non-renal effects of malignant hypertension?
|
dissecting aneurysms, necrotizing vasculitis in medium and large arteries
|
|
|
How does malignant hypertension affect the heart?
|
heart has to work harder since peripheral resistance increases, ends up with LV hypertrophy, RV hypertrophy, heart failure
promotes CAD |
|
|
What is the calcium concentration in vascular smooth muscle cells?
|
10^-6 M
|
|
|
What does intracellular Ca bind in vascular smooth muscle cells?
|
calmodulin
|
|
|
What does Ca-calmodulin activate?
|
myosin kinase
|
|
|
What does myosin kinase do?
|
phosphorylates light chain of myosin
|
|
|
What does phosphorylated myosin do?
|
interacts with actin, leads to contraction of smooth muscle cell and arteriolar constriction
|
|
|
What is electric potential in resting myocardium?
|
negative
|
|
|
What is electric potential in fast conducting tissue?
|
negative
|
|
|
What happens in phase 0?
|
brief depolarization, inward Na current
|
|
|
What happens in phase 1?
|
Ca enters the cell, plateau
|
|
|
What happens in phase 2?
|
Ca enters the cell, plateau
|
|
|
What does Ca bind when intracellular Ca binds?
|
binds subunit of troponin
|
|
|
Which Ca channel is more prominent in sinus and AV nodes?
|
slow channel
|
|
|
What happens in phase 4?
|
fall in K in nodal cells
slow rise in Ca in nodal cells pacemaker cells spontaneously depolarize |
|
|
How do L-type calcium channels work?
|
like volt-dep Na channel
|
|
|
What do T calcium channels do?
|
low-voltage activated Ca channels
start to open at a more negative potential and close more slowly than other Ca channels |
|
|
What type of calcium channels are overexpressed in proliferating cells?
|
T Ca channels
|
|
|
Which CCB would you use for subarachnoid hemorrhage?
|
nimodipine
|
|
|
What is the cut off for desirable total cholesterol?
|
200
|
|
|
What is the cut off for high total cholesterol?
|
240
|
|
|
What is the cut off for normal triglycerides?
|
140
|
|
|
What is the cut off for high triglycerides?
|
200
|
|
|
What is the cut off for low HDL?
|
40
|
|
|
What is the cut off for good HDL level?
|
50
|
|
|
How much saturated fat should be in your diet?
|
< 7%
|
|
|
How much of your diet should be fat?
|
25-35%
|
|
|
How much cholesterol should you get daily?
|
< 200
|
|
|
What should you worry about with Rosuvastatin?
|
use caution when combined with warfarin, do not combine with gemfibrozil
|
|
|
What should you combine Rosuvastatin with?
|
bile acid resins or ezetimibe to lower LDL
|
|
|
Which drugs are fibrates?
|
fenofibrate, fenofibric acid, gemfibrozil
|
|
|
What are the side effects of fenofibrate?
|
nausea, skin rash, myopathy
|
|
|
What percentage of primary cardiac tumors are benign?
|
75%
|
|
|
What is a cardiac myxoma?
|
benign proliferation of primitive cells that differentiate among endothelial lines
|
|
|
Where do cardiac myxomas generally occur?
|
left side of interatrial septum
|
|
|
When do cardiac myxomas present?
|
50 years
|
|
|
What is the most common clinical presentation of cardiac myxomas?
|
mitral stenosis
|
|
|
How else can cardiac myxomas present?
|
strokes, TIAs, claudication, MI, renal insufficiency
|
|
|
What are the symptoms of cardiac myxoma?
|
weakness, malaise, fevers
|
|
|
What is myxoma syndrome?
|
cardiac myxoma, pigmentation, endocrine overactivity, neurofibromas
|
|
|
How do myxomas attach?
|
to the atrial septum by stalk or pedicle
|
|
|
What do myxomas look like?
|
variegated with hemorrhagic, fibrous, myxoid areas
can be smooth and gelatinous |
|
|
What is the microscopic pathology of myxomas?
|
"myxoma" cells which are stellate - ovoid, form rings, nests and can merge with capillaries
background infiltrated by histiocytes, plasma cells, mast cells, lymphocytes can see degenerative changes |
|
|
When do cardiac fibromas occur?
|
infancy or childhood
|
|
|
What is the most common pediatric cardiac tumor?
|
cardiac fibroma
|
|
|
What are the symptoms of cardiac fibromas?
|
heart failure, arrhythmias, sudden death, chest pain
|
|
|
What do cardiac fibromas look like grossly?
|
bulging, whorled masses of rubbery white tissue, mural elsions that can bulge into LV outflow tract
|
|
|
Where do cardiac fibromas occur?
|
ventricles and atria
|
|
|
What do cardiac fibromas look like microscopically?
|
cellular or with extensive collagen
can also show up with calcification |
|
|
Where do most cardiac sarcomas arise?
|
within cardiac muscle
|
|
|
What are the most common types of caridac sarcomas?
|
angiosarcoma and malignant fibrous histiocytoma
|
|
|
Where are most cardiac sarcomas located?
|
left atrium
|
|
|
How do cardiac sarcomas in the LA present?
|
dyspnea secondary to LV inflow obstruction
|
|
|
What is the prognosis for cardiac sarcomas?
|
poor, measured in months
|
|
|
What is the most common tumor that metastisizes to the heart?
|
lung carcinoma
|
|
|
What is lymphocytic myocarditis?
|
inflammatory process that results in lymphocytic inflammation and myocyte necrosis
|
|
|
What causes lymphocytic necrosis?
|
enteroviral infection
|
|
|
What kind of necrosis is involved in lymphocytic myocarditis?
|
single cells or clusters
|
|
|
What are the clinical features of myocarditis?
|
flulike syndromew ith fever, arthralgias, malaise
|
|
|
What are the ECG abnormalities with myocarditis?
|
arrythmias or heart block
|
|
|
What are the lab abnormalities with myocarditis?
|
leukocytosis, elevated sed rate, elevated in cardiac creatinine kinase
|
|
|
What are the gross pathologic changes with myocarditis?
|
cna be normal or enlarged, soft, discolored with dilated ventricles
|
|
|
What are the histologic changes with lymphocytic myocarditis?
|
inflammation of myocardium, necrosis, degeneration of adjacent myocytes
focal inflammation/necrosis lymphocytes, macrophages, plasma cells, neutrophils eventually fibrosis |
|
|
What is the most common form of lymphocytic myocarditis worldwide?
|
Chagas disease
|
|
|
How does virally-induced lymphocytic myocarditis form?
|
RNA virus taken up by the cell, replicates in the cytoplasm, released taken up by macrophages, cytokine expression can continue after the virus is cleared and cause cardiomyopathy
|
|
|
How do you treat lymphocytic myocarditis?
|
supportive care
|
|
|
How does giant cell myocarditis present?
|
CHF, ventricular arrhythmia, heart block
|
|
|
What is the histo presentation of giant cell myocarditis?
|
inflammatory infiltrate of lymphocytes, giant cells, eosinophils
|
|
|
What causes hypersensitivity myocarditis?
|
hypersensitivity to medications
|
|
|
How does hypersensitivity myocarditis present?
|
mild eosinophilia, arrhythmia, sudden death, CHF
|
|
|
What is the histo presentation of hypersensitivity myocarditis?
|
interstitial inflammation, necrosis is not prominent
|
|
|
What happens in hypereosinophilic myocarditis?
|
persistent peripheral eosiniophlia, multiorgan infiltration by eosinophils
affects both ventricles eosinophilia gose to necrosis and mural thrombus |
|
|
Which vessel is usually used for CA bypass graft of LAD and RCA?
|
internal mammary artery
|
|
|
What vessel is used for most other grafts?
|
greater saphenous vein
|
|
|
What causes early occlusion of vein grafts?
|
thrombosis from damage, poor run-off due to severe distal CAD, twisting/kinking
|
|
|
What does fibrointimal proliferation in vein grafts look like?
|
thickening of the intima by cellular tissue with collagen and proteoglycan ground substance
|
|
|
What does atherosclerosis in vein grafts look like?
|
friable foam cell-rich lesions with large lipid cores, thin fibrous cap, intraplaque hemorrhage can happen
can have acute plaque rupture |
|
|
What is the vasculopathy of internal mammary artery grafts?
|
fibrointimal proliferation of smooth muscle cells in proteoglycan-rich EC matrix
|
|
|
What is the major complication of PTCA?
|
elastic recoil
|
|
|
What happens immediately after PTCA?
|
thrombus deposition and acute inflammation on the injured endothelial surface
|
|
|
What happens a few weeks after PTCA?
|
chronic inflammation, migration of smooth muscle cells, forms neointima
|
|
|
At what point are stents covered by endothelial cells?
|
3 months
|
|
|
What facilitates in-stent restenosis?
|
increased inflammation and more severe arterial injury, damage to media
|
|
|
What is an orthotopic allograft?
|
recipient heart is totally replaced by donor heart
|
|
|
What is a heterotropic transplant?
|
diseased heart is left in place to which donor heart is connected
|
|
|
When does hyperacute rejection occur?
|
hours
|
|
|
What happens with hyperacute rejection?
|
diffuse interstitial hemorrhage with neutrophils marginating in vessels and microthrombi
|
|
|
When does reperfusion or ischemic injury happen?
|
up to 4 weeks following transplantation
|
|
|
What happens in reperfusion/ischemic injury?
|
myocyte necrosis and sparse inflammation
|
|
|
How do you diagnose acute rejection?
|
endomyocardial biopsy
grade extent and pattern of inflammation |
|
|
What happens in vascular rejection?
|
endothelial cells stimulated by activated T cells mediate it
|
|
|
What do you see in vascular rejection?
|
activated endothelial cells, perivascular edema and inflammation
IG or complement on blood vessels |
|
|
What is the major limitation to long term successful cardiac transplant?
|
graft coronary artery disease
|
|
|
What does graft coronary artery disease look like histologically?
|
proliferative lesions with circumferential and longitudinal increases in intimal fibrous tissue and myointimal cells
|
|
|
What are long term changes of graft coronary artery disease?
|
can look like conventional atherosclerosis with intra/extracellualar lipid, calcium, plaque hemorrhage
|
|
|
What is the mechanism of VT in patients without structural heart disease?
|
DADs triggered by increased sympathetic tone
|
|
|
What is the distribution half life of lidocaine?
|
8 min
|
|
|
What is the elimination 1/2 life of lidocaine?
|
108 min
|
|
|
What does volume of distribution determine?
|
size of loading dose
|
|
|
How do you calculate volume of distribution?
|
C0 = dose/Vd
|
|
|
How do you calculate elimination half life?
|
elimination half life = 0.693(Vd/clearance)
|
|
|
What is Amiodarone's structure?
|
lipophilic, structural analog of thyroid hormone
|
|
|
What are the goals of antiarrhythmia treatment?
|
termination of arrhythmia, prevention of recurrence
|
|
|
What are symptoms of arrhythmias?
|
palpitations, lightheadedness, loss of consciousness, chest pain, shortness of breath
|
|
|
What are premature beats?
|
ectopic beats can occur anywhere in excitable tissue of the heart, basic mechanism is unclear
|
|
|
What is Paroxysmal supraventricular tachycardia?
|
common in otherwise healthy people
due to reentry near AV node or accessory PW |
|
|
What causes atrial flutter?
|
structural heart disease, multiple reentrant circuits in the atria
|
|
|
What is the problem with atrial flutter?
|
risk of blood clot formation in the atria with embolism
|
|
|
What is the problem with ventricular tachycardia?
|
usually life-threatening, esp in the setting of significant disease
|
|
|
What is the pathology of ventricular tachycardia?
|
most types are probably reentrant with triggered activity likely in patients with normal hearts
|
|
|
What is Torsades de Pointes?
|
in the setting of marked QT prolongation due to drugs or electrolyte abnormalities, polymorphic
|
|
|
What happens in ventricular fibrillation?
|
common cause of sudden cardiac death, significant coronary disease present, multiple wavelets of reentry
|
|
|
What are the metabolic reversible causes of arrhythmias?
|
hypoxia, hypo/hyperkalemia, hypomagnesia, acidosis
|
|
|
What are the reversible drug causes of arrhythmias?
|
antiarrhythmics, digitalis
|
|
|
What are the reversible disease cauess of arrhythmias?
|
acute ischemia, heart failure
|
|
|
How do Na channel blockers terminate/prevent arrhythmias?
|
slow conduction to interrupt a reentrant circuit, increase refractoriness to terminate reentry, allow "less room" for premature beats to occur
shift membrane responsiveness curve to more negative potentials |
|
|
What is the result of Na channel blockers?
|
increases refractoriness, slowed action potentials
|
|
|
What happens in state-dependent Na channel blockers?
|
specific receptor site for binding of blockers, as ion channel changes conformation, affinity is changed
drugs bind Na channel and block conductance in state-specific manner |
|
|
What are the mechanisms of atrial fibrillation?
|
disorganized "functional" reentry
or continual AV node stimulation, which leads to irregular, often rapid, ventricular rate |
|
|
How do you treat atrial fibrillation acutely?
|
control ventricular response: AV nodal block
restore sinus rhythm: DC cardioversion |
|
|
What is the chronic therapy for atrial fibrillation?
|
control ventricular response: AV node block
maintain normal rhythm: K channel block, Na channel block with recovery > 1 second |
|
|
What are the mechanisms of atrial flutter?
|
stable reentrant circuit in right atrium, ventricular rate often rapid and irregular
|
|
|
What is the acute therapy for atrial flutter?
|
control ventricular response: AV nodal block
Restore sinus rhythm: DC cardioversion |
|
|
What is the chronic therapy for atrial flutter?
|
control ventricular response: AV nodal block
maintain normal rhythm: K channel block, Na channel block with recovery > 1 second AV nodal blocking drugs are especially good, can also do ablation |
|
|
What is atrial tachycardia?
|
enhanced automaticity, DAD-related automaticity, reentry within the atrium
|
|
|
What is the acute therapy for atrial tachycardia?
|
control ventricular response: AV node block
restore sinus rhythm: DC cardioversion |
|
|
What is the chronic therapy for atrial tachycardia?
|
control ventricular response: AV node block
maintain normal rhythm: K channel block, Na channel block with recovery time > 1 second ablation of tachycardia "focus" |
|
|
What is the cardiac cell membrane potential at rest?
|
-90 mV
|
|
|
What is the potassium concentration in cardiac cells?
|
4 mM external and 150 mM internal
|
|
|
What kind of equilibrium potential depolarizes a cardiac cell?
|
positive equilibrium potential (Na and Ca)
|
|
|
What kind of equilibrium potential repolarizes a cell?
|
negative (K+)
|
|
|
What happens with inward movement of positive ions?
|
depolarization
|
|
|
What happens with outward movement of positive ions?
|
repolarization
|
|
|
What happens during phase 4?
|
resting phase
|
|
|
What determines potential in phase 4?
|
equilibrium potential for K due to high K channel conductance
|
|
|
What is the automaticity in Phase 4?
|
normal
|
|
|
What is phase 0?
|
rapid depolarization
|
|
|
What causes phase 0?
|
fast inward Na current, rapidly activates and inactivates in most cells
cuases other channels to open or activate |
|
|
In what phase is there maximum upstroke velocity?
|
Phase 0
|
|
|
What causes maximum upstroke velocity?
|
Na conductance
|
|
|
What is Phase 1?
|
early rapid repolarization
|
|
|
What causes Phase 1?
|
outward K currents which rapidly inactivate
|
|
|
What is Phase 2?
|
plateau
|
|
|
What causes Phase 2?
|
inward current through Ca channels
inward current is approximately equivalent to outward K current channels, keeps voltage constant |
|
|
What is Phase 3?
|
repolarization
|
|
|
What causes Phase 3?
|
decreasing inward Ca current
increasing outward currents ("delayed rectifier" K current) |
|
|
Where does electrical activity originate?
|
SA node
|
|
|
What causes atrial depolarization?
|
activity in the SA node
|
|
|
What does the heart rate reflect?
|
sinus node automaticity
|
|
|
What does most of hte PR interval consist of?
|
time for atrial contraction to dump blood into the ventricles
|
|
|
Why is conduction slow over AV node?
|
to allow time for atrial contraction to dump blood into the ventricles
|
|
|
What modulates the AV node?
|
autonomic NS
|
|
|
What does the His-Purkinje system do?
|
permits rapid impulse conduction, allows synchronized ventricular depolarization
|
|
|
What does the QRS complex measure?
|
ventricular depolarization
|
|
|
What determines the width of the QRS?
|
speed of impulse conduction through ventricles
|
|
|
What does ventricular depolarization cause?
|
contraction
|
|
|
What does the T wave measure?
|
ventricular repolarization
|
|
|
What causes ventricular contraction?
|
ventricular depolarization
|
|
|
What does the QT measure?
|
ventricular action potential duration
|
|
|
What is the action potential like in endocardial ventricular cells?
|
little phase 1 notch (early rapid repolarization)
|
|
|
What is hte action potential like in midmyocardial cells?
|
long action potential
|
|
|
What is the action potential in atrial cells?
|
very short, Ito is larger (K+ transient outward current), Ikach is presen
|
|
|
What is the action potential like in SA, AV nodes?
|
little Na current, intrinsic pacemaker activity
|
|
|
What are the three states of Na channel?
|
rested, activated, inactivated
|
|
|
When does the rested state of Na channels occur?
|
phase 4
|
|
|
What happens during the rested state of Na channel?
|
no Na current, but channels are available to open
|
|
|
When does the activated stage of Na channels occur?
|
phase 0
|
|
|
What happens in the activated stage of Na channels?
|
10^7 ions/sec enter the cell, short lived
|
|
|
When does the inactivated stage of Na channel occur?
|
phases 1-3
|
|
|
What happens in the inactivated stage of Na channels?
|
non-conducting state that occurs rapidly after opening, recovery from inactivation is voltage dependent and determines refractoriness
|
|
|
What is proportional to the magnitude of Na current present?
|
maximal Phase 0 upstroke velocity
|
|
|
What is conduction?
|
speed of impulse propagation through cardiac tissues, depends on magnitude of depolarizing current and geometry of cell-cell electric connections
|
|
|
Where is conduction fastest?
|
along the length of cells rather than across them, more rapid in fast response tissue
|
|
|
What reflects conduction velocity in fast response tissue?
|
Na current (Vmax)
|
|
|
Where is fast response tissue?
|
atria and bundle branches
|
|
|
Where is slow response tissue?
|
AV node
|
|
|
How fast is fast response tissue?
|
1-4 m/sec
|
|
|
How fast is slow response tissue?
|
20 mm/sec
|
|
|
Upon what do Na current and Vmax depend?
|
membrane potential from which they are initiated
|
|
|
What depresses Ina?
|
antiarrhythmic drugs, depolarization of resting potential, premature beats
|
|
|
What does depression of Ina do?
|
slowed conduction
|
|
|
What reflects conduction velocity in His-Purkinje system?
|
duration of QRS complex
|
|
|
What determines conduction velocity in atrium and ventricle?
|
magnitude of Na current and fiber orientation
|
|
|
Upon what does fast response tissue depend?
|
Na channels
|
|
|
What is the conduction like in fast response tissue?
|
all or none, recovery of excitability, voltage-dependent
|
|
|
Where is fast response tissue?
|
atria, ventricles, His-Purkinje
|
|
|
Upon what does slow response tissue depend?
|
Ca channels
|
|
|
What is conduction like in slow response tissue?
|
slow, decremental, more time-dependent
|
|
|
Where is slow response tissue?
|
sinus, AV nodes, depolarized tissue
|
|
|
What is decremental conduction?
|
conduction in tissue that is time-dependent, slowed conduction with premature stimuli or rapid rates, probably due to slow recovery from inactivation
|
|
|
What is effective refractory period?
|
minimal interval between two propagating impulses, assessed by seeing if premature stimuli result in propagated impulses
|
|
|
Upon what does ERP depend?
|
action potential duration
recovery of Na channels from inactivation is voltage dependent and parallels repolarization |
|
|
What is the membrane responsiveness relationship?
|
relationship between upstroke of premature stimulus arising during phase 3 and voltage at which it arises, measures Na channel availability at that voltage
|
|
|
How does refractoriness change in slow response tissue?
|
can outlast full repolarization because Ca channels recover more slowly from inactivation, also time dependent, propagation is decremental
|
|
|
What causes automaticity?
|
spontaneous Phase 4 depolarization
|
|
|
What cells have automaticity?
|
SA and AV nodal cells, His-Purkinje system
|
|
|
What is the dominant pacemaker?
|
SA node
|
|
|
What is the first backup pacemaker?
|
AV node
|
|
|
What is the last backup pacemaker?
|
His-Purkinje cells
|
|
|
How fast is the SA node?
|
60-100 bpm
|
|
|
How fast is the aV node?
|
40-60 bpm
|
|
|
How fast is the His-Purkinje system?
|
30-40 bpm
|
|
|
What is the pacemaker current?
|
inward, cation-mediated, may be driven by cyclic Ca release from sarcoplasmic reticulum
|
|
|
How does depolarization signal in an EKG lead?
|
depolarization moving toward an electrode is positive
depolarization moving away from an electrode is negative |
|
|
What does one small square horizontally equal?
|
.04s
|
|
|
What does one large square horizontally equal?
|
.2s
|
|
|
What does one small square vertically equal?
|
.1 mV
|
|
|
What does the P waves ignal?
|
sequential depolarization of right/left atria
|
|
|
What is the PR interval?
|
time from the onset of atrial depolarization to ventricular depolarization, reflects AV nodal conduction
|
|
|
What is the QRS complex?
|
right/left ventricular depolarization, speed of conduction through the ventricles
|
|
|
What are the S-T waves?
|
ventricular repolarization
|
|
|
What is the U wave?
|
final phase of ventricular repolarization
|
|
|
What is the QT interval?
|
duration of ventricular dpolarization and repolarization, reflects action potential duration in the ventricles
|
|
|
What is the RR interval?
|
duration of ventricular cardiac cycle, indicates ventricular rate
|
|
|
Which leads are inferior?
|
II, III, aVF
|
|
|
Which leads are lateral?
|
I, aVL
|
|
|
Where is V1?
|
right 4th IC space
|
|
|
Where is V2?
|
left 4th IC space
|
|
|
Where is V3?
|
halfway between V2 and V4
|
|
|
Where is V4?
|
left 5th IC space, mid clavicular line
|
|
|
Where is V5?
|
horizontal to V4, anterior axillary line
|
|
|
Where is V6?
|
horizontal to V5, mid-axillary line
|
|
|
What is teh normal PR interval?
|
.12-.2s
|
|
|
What is the normal QRS complex?
|
.06-.1s
|
|
|
What is the normal QT interval?
|
depends on HR, normal < .44s
|
|
|
How do you calculate normal QT interval?
|
QT/sqrt(RR interval)
|
|
|
How does QT change with heart rate?
|
as HR increases, QT shortens
|
|
|
What is the normal QRS axis?
|
+90 - -30 degrees
|
|
|
How do you measure the QT interval?
|
from the first part of the deflection of the Q wave to the
end of T wave is the intersection of a tangent to the steepest slope of the last limb of the T wave |
|
|
What does it mean when you have right axis deviation?
|
chronic obstructive lung disease, pulmonary hypertension
|
|
|
What does it mean if you have left axis deviation?
|
hypertension or aortic stenosis with major LV predominance
|
|
|
Where is the P wave normally negative?
|
lead II, aVR
|
|
|
Where is the QRS normally "septal"?
|
I, aVL, V5-V6
|
|
|
Where does the QRS transition normally?
|
V3-V4
|
|
|
Where is the QRS normally negative?
|
aVR
|
|
|
Where is the T wave normally upright?
|
I, II, V3-V6
|
|
|
What does the T wave normally follow?
|
QRS direction
|
|
|
What is the best source for detecting atrial abnormalities?
|
P wave in V1
|
|
|
What happens with atrial enlargement?
|
P wave in V1 is often biphasic
|
|
|
What happens with a right atrial abnormality?
|
P wave positive deflection in lead V1
P wave amplitude can increase in II, III, aVF |
|
|
What happens to the EKG with a left atrial abnormality?
|
terminal component of P wave in V1 is negative, increased in size and wide
P wave can be notched and prolonged (usually in lead II) |
|
|
What happens when you have left ventricular hypertrophy?
|
increased electric predominance of LV over RV
increased WRS complex amplitude, ST-T changes (opposite of QRS) leftward shift in QRS complex left atrial abnormality |
|
|
What can cause LV hypertrophy?
|
life-threatening pressure or volume overload state, like valvular heart disease, hypertrophic CM
|
|
|
What are the ECG features of RV hypertrophy?
|
electric predominance of LV is overcome by RV, tall R waves in RV leads, deep S waves in LV leads, ST changes with T wave inversion in right mid precordial leads
rightward shift of QRS axis, evidence for LAL abnormality can often be accompanied by RV abnormality |
|
|
What can cause RV hypertrophy?
|
congenital heart disease, pulmonary artery hypertension, mitral stenosis
NOT with COPD, emphysema |
|
|
What signifies RBBB?
|
QRS duration > .12s, usually in V1 and V6
|
|
|
What neurochemicals are activated with initial myocardial injury?
|
renin-angiotensin, aldosterone, endothelins, vasopressin
|
|
|
What else is shown wtih RBBB?
|
late R wave in V1 indicating late anterior forces
late S wave in V6 indicating late rightward forces |
|
|
What does the initial neurochemical activation do to the body?
|
increases HR, increases retention of salt and water
|
|
|
Where are ST-T waves oriented in RBBB?
|
opposite to the direction of the terminal QRS forces
|
|
|
What is the purpose of volume expansion in initial cardiac failure?
|
augments preload, increases cardiac contractility by Starling's law, increases blood pressure, improves blood flow to organs
|
|
|
What can cause RBBB?
|
can have otherwise normal heart, aging of conduction system, coronary artery disease, cardiac disease that affects right side of heart
|
|
|
What are the negative effects of elevated capillary pressures?
|
promotes pulmonary congestion and peripheral edema
|
|
|
How do you diagnose LBB?
|
QRS > .12s in leads V1 and V6
|
|
|
What are the negative effects of increased vasoconstriction?
|
increases afterload, depresses cardiac function
|
|
|
What does left bundle branch block affect in the heart?
|
early phase of ventricular activataion (depolarizes from right to left, stimulation of LV is prolonged)
|
|
|
What are the negative effects of neurohomronal activation?
|
increased myocardial workload, myocardial ischemia, apoptosis, maladaptive fetal contractile protein isoforms, myocyte hypertrophy, cardiac arrythmias
|
|
|
What does LBBB affect in the heart?
|
late forces of QRS are oriented leftward and posteriorly,
late S waves in lead V1 indicating late posterior forces later R waves in lead V6 (and I, aVL) indicating late leftward forces, usually broad, monophasic R waves in these leads |
|
|
What are the negative effects of vasopressin release?
|
hyponatremia
|
|
|
In what direction should the ST-T waves be in LBBB?
|
opposite to the direction of terminal QRS forces (in leads with late R forces, ST-T should be downwards)
|
|
|
What is cor pulmonale?
|
RV dilation and hypertrophy caused by pulmonary pathology
|
|
|
What causes LBBB?
|
sign of organic heart disease, patients with long-standing hypertensive heart disease, aging of conduction system, CAD, valvular heart disease, cardiomyopathy
|
|
|
What is the primary cause of right-sided heart failure?
|
left-sided failure
|
|
|
What is myocardial infarction?
|
necrosis of the myocardium caused by severe ischemia
|
|
|
What are the symptoms of right sided heart failure?
|
peripheral edema, abdominal pain, abdominal distension, fatigue
|
|
|
What shows up on the ECG during acute transmural MI?
|
ST segment elevation, tall positive T waves, ST depression in alternate waves
|
|
|
What causes left-sided heart failure?
|
disease of the left ventricle
|
|
|
What shows up on the ECG during evolving phase of MI?
|
deeply inverted T waves in leads that showed hyperacute T waves and ST elevations
|
|
|
What are the symptoms of left sided heart failure?
|
fatigue, weakness, dyspnea on exertion or rest, orthopnea, paroxysmal nocturanl dyspnea, nocturnal cough
|
|
|
What shows up on the ECG during the first day or so after MI?
|
new abnormal Q waves appear in 1+ leads
|
|
|
What are the symptoms of CHF caused by inadequate cardiac output?
|
poor perfusion of tissues, fatigue, weakness
|
|
|
Why do Q waves appear?
|
with transmural infarction, necrosis of heart muscle occurs in a localized area of hte ventricle, voltages produced by this area disappear, end up with Q waves over infarcted area instead of R waves
|
|
|
What are the symptoms of CHF caused by excess fluid accumulation?
|
dyspnea on exertion or rest, orthopnea, paroxysmal nocturnal dyspnea, nocturnal cough, peripheral edema, abdominal pain, abodminal distension
|
|
|
How long do ST-T changes show after MI?
|
changes occur over hours or days, resolve over weeks to months
|
|
|
What causes paroxysmal nocturnal dyspnea?
|
reflexes initiated by vascular distention, increased rigidity of lungs and impaired gas exchange from interstitial edema, accumulation of fluid in alveoli
|
|
|
What does it mean if ST segment elevations persist after acute MI?
|
if they last for more than 2-3 weeks, signifies a ventricular aneurysm
|
|
|
What are the most specific signs of heart failure?
|
jugular venous distention, third/fourth heart sound
|
|
|
What are the ECG changes with an acute anterior MI?
|
ST elevations and abnormal Q waves in 1+ of V1-V4
reciprocal ST elevations in II, III, and aVF |
|
|
What causes S3?
|
atrial pressure >20 mm and increased ventricular end diastolic pressure >15 mm
|
|
|
What are ECG changes with lateral MI?
|
ST elevations and Q waves in I and aVL
ST depressions in inferior leads (II, III, aVF) |
|
|
What do you check for in blood tests in CHF?
|
hyponatremia, renal dysfunction, fasting lipids, ANP, brain natriuretic peptide, TSH, iron, ferritin, low albumin
|
|
|
What are ECG changes with anterolateral MI?
|
ST elevations and abnormal Q waves in I, aVL, V1-V6
ST depression sin II, III, aVF |
|
|
What do you look for in EKG for heart failure?
|
ischemia, LV hypertrophy, LBBB, arrhythmias
|
|
|
What are ECG changes with inferior myocardial infarction?
|
ST elevations and Q waves in II, III, and aVF
ST depressions in I, aVL, V1-V6 |
|
|
What do you look for in chest X-Ray for heart failure?
|
cardiomegaly, pulmonary edema, Kerley's B lines, pleural effusions
|
|
|
What are the ECG changes with posterior MI?
|
ST elevations may not appear
tall R waves and ST depressions in V1 and V2 |
|
|
What do you look for in unexplained heart failure?
|
Mg, Ca, Phosphorus, Selenium, Thiamine problems
|
|
|
What happens in the evolving phase of ECG with posterior MI?
|
deep T wave inversions appear in posterior leads, anterior leads may show tall positive T waves (V1-V4)
|
|
|
What are the short term treatment goals of CHF?
|
increase CO and decrease ventricular filling pressures
|
|
|
What usually occurs with posterior MI?
|
inferior MI
|
|
|
What are the routine goaals of CHF therapy?
|
reduce weight, control HTN, restrict salt and fluid, daily weights
|
|
|
What besides MI can cause Q waves in V1-V3?
|
LBBB, left ventricular hypertrophy, chronic lung disease in absence of MI
hypertrophic cardiomyopathy |
|
|
How do diuretics affect CO?
|
not clinically significant
|
|
|
How do you pick up a non-ST elevation MI?
|
evolving ST-T changes over time in patient with typical symptoms/elevated enzymes
ST segment depression, T wave inversion, convex upwards/straight ST segment don't localize the MI by ST-T changes |
|
|
What are the common loop diuretics used in heart failure?
|
furosemide, bumetamide, torsemide
|
|
|
Why is the subenodcardium particularly vulnerable to MI?
|
most distant from coronary blood supply, highest pressure of ventricle
|
|
|
Upon what transporter do loop diuretics act?
|
Na/K/2Cl symporter
|
|
|
What is the most common change with subendocardial ischemia?
|
flat/down-sloping ST-T depression
|
|
|
Upon which cells do loop diuretics act?
|
renal epithelial cells in ascending limb of loop of Henle
|
|
|
What else can cause ST segment elevation?
|
normal variant, pericarditis, Brugada syndrome, left ventricular hypertrophy, LBBB
|
|
|
Upon which transporters do thiazide diuretics act?
|
Na/Cl cotransporter
|
|
|
What else can cause ST segment depression?
|
MI, left/right ventricular hypertrophy, left/right BBB, drugs, etc.
|
|
|
Where do thiazide diuretics act?
|
renal tubular epithelial cells in distal convoluted tubule
|
|
|
What is an arrhythmia?
|
abnormal cardiac rhythm by virtue of site of origin, rate, regularity, conduction
|
|
|
With what do you use Thiazide diuretics?
|
loop diuretics, true synergy
|
|
|
What are palpitations?
|
sensation that cardiac rhythm is not normal
|
|
|
what kind of drug is Spironolactone?
|
aldosterone antagonist
|
|
|
What is paroxysmal?
|
abrupt onset
|
|
|
Where does Spironolactone act?
|
collecting duct
|
|
|
How does noraml sinus rhythm spread?
|
from right to left and downward towards the AV node
|
|
|
What are the adverse side effects of diuretics?
|
hyponatremia, hypokalemia, hypochloremic alkalosis
|
|
|
What is heart block?
|
failure of impulses to propagate from atrium to ventricle, dropped beats
|
|
|
What can cause sinus pause or arrest?
|
increased parasympathetic tone, drugs, aging, hypoxemia, MI
|
|
|
Where do escape beats come from?
|
atria, AV node, ventricles
|
|
|
What is escape?
|
response of automatic focus to pause in pacemaking activity
can occur as a single beat or as a rhythm |
|
|
What happens in atrial fibrillation?
|
disorganized, rapid, ineffective atrial contraction, variable and rapid ventricular response
|
|
|
What does atrial fibrillation cause?
|
blood stasis and thrombus formation
stroke in the elderly |
|
|
What is first-degree heart block?
|
uniformly prolonged PR interval > .2s, impulse from atria to ventricles is delayed, not blocked
|
|
|
What is ventricular fibrillation?
|
disorganized, rapid ventricular contractions
immediately fatal |
|
|
What is the major drawback of ARB?
|
failure to augment bradykinin production
|
|
|
What is triggered automaticity?
|
under some pathological conditions, a normal cardiac AP can be interrupted or followed by an abnormal depolarization, if it reaches threshold, can cause secondary upstrokes and arrhythmias
|
|
|
What happens in second-degree heart block?
|
intermediate AV conduction disturbance, impulse transmission fails intermittently
|
|
|
Through which receptor does angiotensin II cause bad effects in heart failure?
|
AT1
|
|
|
What happens in third-degree heart block?
|
AV node does not conduct any stimuli between atria and ventricles
|
|
|
What aggrevates EADs?
|
slow rate
|
|
|
How do beta-blockers help in heart failure?
|
increases ejection fraction, prevents adverse effects of NE on myocardium
|
|
|
What aggrevates DADs?
|
rapid rate
|
|
|
What is the ECG change with first degree AV block?
|
uniformly prolonged PR interval >.2s
|
|
|
When do EADs happen?
|
interrupt phase 3
|
|
|
What do cardiac glycosides inhibit and how does this affect the myocardium?
|
active transport of Na/K across cell membranes, increase IC Ca2 and increase myocardial contractility
|
|
|
When do DADs happen?
|
after phase 3 repolarization
|
|
|
What are the symptoms of first degree AV block?
|
usually none
|
|
|
What reverses EADs?
|
rapid rates: pacing, isoproterenol, magnesium
|
|
|
What are the hemodynamic responses to heart failure?
|
tachycardia, increase in venous and arterial vasoconstriction, shunting of blood towards the thorax and brain and away from the periphery and splanchnic and renal vascular beds
|
|
|
What is the underlying mechanism of EADs?
|
increased action potential duration, probably increased inward current
|
|
|
How does increased preload affect heart failure?
|
really doesn't help, can't accommodate the increased load, flat Frank-Starling
|
|
|
What is the underlying mechanism of DADs?
|
intracellular Ca overload (myocardial ischemia, adrenergic stress, digitalis intoxication) inward current
|
|
|
What are the ECG changes with second degree AV block?
|
some P waves conduct tot he ventricles --> QRS, some are blocked, leaving lone P waves without QRS
|
|
|
What is paroxysmal supraventricular tachycardia?
|
abrupt onset of regular, narrow-complex tachycardia
|
|
|
How does increased filling pressure affect the body?
|
transmission of increased pressure into pulmonary and systemic venous beds
|
|
|
What are the symptoms of PSVT?
|
rapid palpitations, dyspnea, chest pain, lightheadedness, fainting
|
|
|
What happens in ECG of second degree AV block: Mobitz I?
|
progressive lengthening of PR interval from beat to beat, until a beat is dropped
PR after nonconducted P wave is shorter than PR interval just before nonconducted P wave gropu beating |
|
|
What is the most common caues of PSVT?
|
reentry within the AV node using an accessory AV connection or pathway
|
|
|
What can you do to decrease ventricular filling pressures?
|
decrease intravascular volume with diuretics, increase venous capacitance with venodilators
|
|
|
What else can cause PSVT?
|
enhanced automaticity causing atrial tachycardia
|
|
|
Where is the AV block in Wenckebach?
|
usually within the AV node
|
|
|
How do you treat PVST?
|
medications or catheter ablation
|
|
|
For whom should you not lower preload?
|
patients with poorly compliant hypertrophied ventricles
reducing preload could reduce cardiac output |
|
|
What happens in AV nodal reentrant tachycardia?
|
cardiac stimulus originates in wave of excitation that spins around the AV nodal area
|
|
|
What are the symptoms of Wenckebach?
|
usually none unless ventricular rate is very slow
|
|
|
How does AVNRT change the ECG?
|
P waves may be buried in QRS or appear immediately before or just after QRS complex
nearly simultaneous stimulation of atria and ventricles |
|
|
How does reducing afterload affect heart failure?
|
helps it, prevents hypertrophy of ventricular muscle
improves stroke volume reduces mitral regurgitation |
|
|
What happens in atrial tachycardia?
|
focus outside the SA node fires off automaticity at a rapid rate
|
|
|
What can cause Wenckebach?
|
increased vagal tone, drugs, acute inferior MI
|
|
|
What is the recovery time of fast conduction tissue?
|
long
|
|
|
What is the recovery time of slow conduction tissue?
|
slow
|
|
|
What happens in the ECG in Second Degree Mobitz II?
|
sudden appearance of nonconducted sinus P wave without progresssive prolongation of PR interval and shortening after nonconducted P wave
|
|
|
How does AVNRT manifest during normal sinus rhythm?
|
conduction by fast PW, conduction via slow PW is blocked
|
|
|
What do accessory AV pathways do?
|
conduct electrical impulses only in a backwards or "retrograde" direction from V to A
|
|
|
Where does Mobitz II typically have a block?
|
below the AV node in His-Purkinje system
|
|
|
What is ventricular preexcitation?
|
accessory AV pathways conduct in anterograde direction, causes ventricles to be excietd by both AV node and accessory PW
|
|
|
What do organic nitrates do molecularly?
|
activate soluble guanylyl cyclase and relaxes vascular smooth muscle, mimics NO
|
|
|
What does ventricular excitation do to teh ECG?
|
short PR interval, wide QRS complex
|
|
|
What is bad about Mobitz II?
|
sign of severe disease with high risk of progression to complete heart block
|
|
|
What is Wolff-Parkinson-White Syndrome?
|
ventricular preexcitationa and arrhythmias
|
|
|
What do organic nitrates do systemically?
|
dilate coronary arteries, decline pulmonary and SVR, reduce ventricular filling pressure
|
|
|
What happens with rapid atrial fibrillation with rapid conduction over accessory PW?
|
sudden death!
|
|
|
What do you do for Mobitz II?
|
maybe pacemaker
|
|
|
What is the most common sustained cardiac arrhythmia?
|
atrial fibrillation
|
|
|
Where do pacing leads go with left ventricular conduction system delay?
|
pacing leads in R atrium/ventricle, one in lateral L ventricular wall
|
|
|
What is the ECG manifestation of atrial fibrillation?
|
atria are beating at a very rapid rate due to multiple wavelets of reentry
makes irregular wavy pattern instead of P waves |
|
|
What causes Mobitz II?
|
aging, sometimes acute anterior MI
|
|
|
What is the mean ventricular rate in atrial fibrillation?
|
between 110-180 bpm
|
|
|
What does Sodium Nitroprusside do?
|
reduces ventricular preload and afterload
|
|
|
What is the ventricular response in atrial fibrillation?
|
irregularly irregular
|
|
|
What does not cause Mobitzz II?
|
increased vagal tone, drugs, inferior MI
|
|
|
What is the clinical presentation of atrial fibrillation?
|
reduction in CO, heart failure, can form thrombi
|
|
|
What are symptoms of atrial fibrillation?
|
rapid palpitations, dyspnea, chest pain, fatigue, stroke
|
|
|
What are the ECG changes of Advanced AV block?
|
two or more consecutive nonconducted sinus P waves, not necessarily Mobitz II
|
|
|
What is the clinical course of atrial fibrillation?
|
progressive: short, self-terminating episodes can progress to persistant and even permanent forms despite therapy
|
|
|
What causes atrial fibrillation?
|
structural heart disease, aging, cardiac surgery, hyperthyroidism
can occur with gene mutation |
|
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How do you treat Advanced AV block?
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pacemaker unless you can find the reversible cause
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What is the point of medications for AF?
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slow AV nodal conduction, terminate arrhythmia, prevent recurrences, prevent blood clots
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What is the atrial rate in atrial flutter?
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300 bpm
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What happens in Third Degree AV block?
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no stimuli from the atria are transmitted to the ventricles
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What does the ECG look like with atrial flutter?
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"sawtooth" pattern, best seen in inferior leads (II, III, aVF)
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What is the ventricular rate in atrial flutter?
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150 bpm (2:1 conduction)
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What paces the ventricles in Third Degree AV block?
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escape pacemaker somewhere below the point of block in AV node
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What are the symptoms of atrial flutter?
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rapid palpitations, dyspnea, chest pain, fatigue, stroke
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What does IV nitroglycerin do for heart failure?
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reduces ventricular filling pressures, reduce peripheral venous capacitance and preload
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What is the clinical presentation of atrial fibrillation?
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risk of thromboembolic events, ventricular response is difficult to control
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What is the resting rate in Third Degree AV block?
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ventricular: <30 bpm - 50-60 bpm
atrial: generally faster than ventricular |
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What is tachy-brady syndrome?
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node dysfunction that causes marked sinus bradycardia or sinus arrest
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What are the symptoms of tachy-brady syndrome?
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light-headedness and syncope
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What can cause Third Degree AV block?
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aging, drugs, MI, cardiac surgery, aortic valve endocarditis
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What is the heart rate like in tachy-brady syndrome?
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bradycardia episodes interspersed with paroxysms of tachycardia (atrial fibrillation/flutter)
bradycardia often after termination of tachycardia |
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What are Dobutamine's effects on the heart in CHF?
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positive inotrope, reduces aortic impedance, SVR, reduces afterload
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How do you treat sick sinus syndrome?
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permanent pacemaker to prevent sinus arrest, antiarrhythmic drugs to control tachycardias
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What happens in AV dissociation?
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any arrhythmia in which the atria and ventricles are controlled by independent pacemakers
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What does the ECG look like with premature ventricular beats?
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wide QRS complexes (>.12s)
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How do premature ventricular beats manifest themselves?
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one or multiple foci, can occur in pairs, 3+ consecutive beats, or repetitive grouping
R on T can precipitate VT or VF |
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What paces the atria in AV dissociation?
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SA node
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How do you treat premature ventricular beats?
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no data that treatment prolongs life
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What does sustained ventricular tachycardia look like in ECG?
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rapid rhythm with wide QRS (>.12s), can be monomorphic or polymorphic
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What paces the ventricles in AV dissociation?
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AV junction
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What is the course of sustained ventricular tachycardia?
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can be life threatening due to reduced CO or degenerate into VF
often initial rhythm during cardiac arrest |
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What does dopamine do at intermediate IV rates?
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stimulates beta-adren receptors in heart, induces NE release from vascular sympathetic neurons
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What does ventricular flutter signal?
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hemodynamic collapse
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What is the difference between complete heart block and AV dissociation?
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properly timed P wave through AV node, with complete block, no P wave reaches the ventricles
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What causes ventricular fibrillation?
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underlying heart disease: MI or non-ischemic cardiomyopathy, reentry
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What does DA do at high IV rates?
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peripheral vasoconstriction by alpha-adrenergic receptor stimulation
supports blood pressure |
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What is the acute therapy for sustained ventricular tachycardia?
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antiarrhythmic drugs or defib
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What are the mechanisms of tachyarrhythmias?
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enhanced automaticity, reentry, triggered automaticity
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What is the long term therapy for sustained ventricular tachycardia?
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implantable cardioverter-defib
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What is the ECG like in polymorphic VT?
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rapidly changing morphology of VT beats
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What happens in enhanced automaticity?
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normal features of sinus node, some parts of AV node, infra-nodal conduction system
features that increase the slope of phase 4 depolarization enhance automaticity, modulated by sympathetic and autonomic NS |
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What causes polymorphic VT with a normal QT interval?
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critical coronary blockages
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What causes polymorphic VT with prolonged QT interval?
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genetic mutations in ion channel genes or drug toxicity from QT-prolonging drugs
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What drives the heart in enhanced automaticity?
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pacemaker with fastest spontaneous rate
can also be cells that do not function as pacemakers (AV node, Purkinje, atrial, ventricular) |
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What does Torsades de Pointes look like on ECG?
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polymorphic, marked QT prolongation on the beat after a pause
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What happens in ventricular fibrillation?
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ventricles don't beat in coordinated fashion, but fibrillate or quiver asynchronously and ineffectively
no CO, patient is unconscious iwth no pulse |
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What is the most common mechanism of clinical arrhtyhmias?
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reentry
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What does the ECG look like with ventricular fibrillation?
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fibrillatory waves with an irregular pattern that may be coarse or fine
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What is the most common cause of sudden cardiac death in patients with acute MI?
|
ventricular fibrillation
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What happens in reentry?
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impulses travel by more than one pathway between two points in teh heart, those pathways have heterogeneous electrophysiologic properties
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How do you fix VF?
|
immediate defibrillation with shock
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What can cause VF?
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ischemia, drugs
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What has to happen for reentry?
|
functionally/anatomically at least 2 pathways
conditions create a unidirectional block in one PW and impulse continues in the other resulting conduction is slow enough that the area of initial impulse block recovers excitability and can be "reentered" by the impulse traveling in the second PW |
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What is accelerated idioventricular rhythm?
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HR between 50-100 bpm, benign "escape" rhythm that competes with underlying sinus mechanism
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What do you give to a patient with CHF and elevated SVR?
|
nitroprusside
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What does the ECG of accelerated idioventricular rhythm look like?
|
wide QRS complexes that are ventricular without associated sinus P waves
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How are reentry and unidirectional or bidirectional block related?
|
if the conduction is too slow, end up with bidirectional block and reentry is abolished
if they have different refractory periods and conduction velocity characteristics |
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What is accelerated idioventricular rhythm associated with?
|
acute MI, sign of reperfusion after use of thrombolytic agents or after interventional coronary artery procedures
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How long does accelerated idioventricular rhythm last?
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minutes or less
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What causes a unidirectional block to start a reentrant rhythm?
|
usually a premature beat
impulse may arrive too early to be propagated in one site, but can be conducted in a different PW because it's no longer refractory |
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How do you treat accelerated idioventricular rhythm?
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no specific therapy
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What do you give for a patient with severe heart failure?
|
pulmonary artery catheter, hemodynamic monitoring
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What is the differential for wide complex tachycardias?
|
ventricular tachy, supravetnricular tachy with aberrancy, WPW syndrome
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What is fibrillation?
|
extreme reentry, multiple reentrant wavelets present simulataneously
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What is the most common wide complex tachycardia?
|
ventricular tachycardia
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In whom do you see supraventricular tachycardia with aberrancy?
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younger, healthier patients
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What signs with wide complex tachycardia point to VT?
|
AV dissociation, fusion/capture beats, wide QRS complexes, weird QRS complexes
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What is cardiac arrest?
|
heart stops contracting effectively and ceases to pump blood
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What are the ECG patterns with cardiac arrest?
|
ventricular tachyarrhythmias (VF and pulseless VT), ventricular asystole or brady-asystolic rhythm with slow rate, pulseless electrical activity
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