Valvular Diseases Flashcards
Rapid Review: AORTIC STENOSIS
pressure builds up in:
resulting hypertrophy:
2˚ effects
Auscultation:
pressure builds up in: LV
resulting hypertrophy: concentric
2˚ effects: LAE + pulmonary venous congestion
Auscultation: creshendo/decreshendo systolic mumur with S4
Rapid Review: MITRAL STENOSIS
pressure builds up in:
resulting hypertrophy:
2˚ effects
Auscultation:
pressure builds up in: LA + pulmonary venous bed
resulting hypertrophy: LAE + pulmonary venous congestion
2˚ effects: decrease LV pressure + size “underloading”
Auscultation: late diastolic mumur with crescendo pattern
Rapid Review: AORTIC REGURGITATION
resulting hypertrophy:
where the extra blood is pumped into:
2˚ effects
Auscultation:
resulting hypertrophy: eccentric LVH
where the extra blood is pumped into: aorta
2˚ effects: aortic dilatation
Auscultation: diastolic decrescendo murmur
Rapid Review: MITRAL REGURGITATION
pressure builds up in:
resulting hypertrophy:
2˚ effects
Auscultation:
resulting hypertrophy: eccentric LVH
where the extra blood is pumped into: LA
2˚ effects: LAE
Auscultation: systolic murmur (blood pumped back into LA during systole)
Rapid Review: ATRIAL SEPTAL DEFECT
Type of shunt: Flow due to: Resulting hypertrophy Auscultation: Reverse flow?
ECG:
CXR?
Complications?
Treatment?
Type of shunt: L-R
Flow due to: increased pressure in LA
Resulting hypertrophy: eccentric RV hypertrophy (to pump out the extra blood in addition to the normal CO)
Auscultation: crescendo/decrescendo murmur
Reverse flow? Yes; the pulmonary arteriolar reaction to the increased pulmonary flow results in pulmonary HTN, which causes the flow to reverse into a R–>L shunt “Eisenmenger’s Syndrome”
ECG: R axis deviation
CXR? cardiomeagly with prominent RA contour and pulmonary artery segment
Complications? CHF, Pulmonary HTN
Treatment? surgical closure
Rapid Review: Patent Ductus Arteriosus
Type of shunt: Flow due to: Resulting hypertrophy Auscultation: Reverse flow?
Type of shunt: L-R Flow due to: increased pressure in aorta Resulting hypertrophy: eccentric LV + aortic root dilation (to pump out the extra blood in addition to the normal CO) Auscultation: continuous murmur Reverse flow? No
Rapid Review: VENTRICULAR SEPTAL DEFECT
Type of shunt: Flow due to: Resulting hypertrophy Auscultation: Reverse flow?
ECG:
CXR?
Complications?
Treatment?
Type of shunt: L-R
Flow due to: increased pressure in LV
Resulting hypertrophy: eccentric RV hypertrophy (to pump out the extra blood in addition to the normal CO) and LV eccentric hypertrophy due to increased pulmonary venous return to the LV
Auscultation: holosystolic murmur with split S2
Reverse flow? Yes; the pulmonary arteriolar reaction to the increased pulmonary flow results in pulmonary HTN, which causes the flow to reverse into a R–>L shunt “Eisenmenger’s Syndrome”
ECG: R axis deviation (RVH) or biventricular hypertrophy
CXR: cardiomeagly with increased pulmonary vascularity
Complications:
- CHF due to pulmonary overcirculation
- pulmonary vascular obstructive dz due to pulmonary HTN
Treatment:
- valve closure
Rapid Review: TETRAOLOGY OF FALLOT (VSD, pulmonic stenosis, RVH, overriding aorta)
Type of shunt: Flow due to: Resulting hypertrophy Auscultation: Reverse flow?
Type of shunt: R->L (due to pulmonic stenosis and VSD)
Flow due to: increase RV pressure
Resulting hypertrophy: concentric RV hypertrophy
Auscultation: crescendo/decrescendo systolic murmur
Reverse flow? No, but because there is a decreased pulmonary blood flow and the fact that deoxygenated blood enters directly into the LV outflow tract, this results in cyanosis.
ECG: R axis deviation + RVH
CXR? “boot-shaped heart”
Complications? cyanotic spells, bacterial endocarditis, polycythemia, brain abscess
Treatment? closure of VSD, cardiopulmonary bypass for pulmonic stnosis
Aortic stenosis has many etiologies. Comment on how these can play a role in development of AS:
congenital
degenerative
rheumatic
hypertrophic obstructive cardiomyopathy
congenital
1) bicuspid aortic valve alters flow characteristics around the valve, which accelerates the normal degenerative processes (thickening, scarring, calcification), which can lead to significant stenosis.
2) sub/supra-vavular aortic stenosis can lead to LV outflow obstruction, associated with hypercalcemia
degenerative - hemodynamic wear and tear; leads to gradual thickening + calcification of the valve leaflets
rheumatic - occurs after an episode of rheumatic fever, where the aortic valves become stenotic by gradual fusion; coexists with aortic regurgitation
hypertrophic obstructive cardiomyopathy - due to severe asymmetrical septal hypertrophy, which produces a dynamic obstruction to LV outflow below the aortic valve
Why does the transvalvular pressure gradient increase in aortic stenosis?
to overcome the resistance to outflow, the LV increases its contractile force, which increases systolic pressures in the LV, resulting in a transvavular pressure gradient >40mmHg
LV pressure –> concentric LV hypertrophy. How does this happen?
What is the result of this hypertrophy?
increased systolic LV pressure is achieved by an increase in LV wall tension, which the heart responds by increasing WALL THICKNESS, which allows an INCREASE IN TOTAL WALL TENSION without increasing the tension developed PER individual wall sarcomere.
Concentric hypertrophy
- > decreased compliance
- > ischemia
- > myocardial failure
Concentric hypertrophy leads to:
- > decreased compliance
- > ischemia
- > myocardial failure
What are the clinical outcomes of these changes?
decreased compliance
- diastolic LV dysfunction; hypertrophied myocardium resists ventricular filling; results in an S4 atrial kick
ischemia
- angina + syncope as a result of decreased O2 supply/increased O2 demand
myocardial failure
- systolic LV dysfunction; deterioration of individual sarcomeres or replacement of hypoxic fibers with fibrosis
What do patients with aortic stenosis experience?
asymptomatic
typical angina
syncope
dyspnea, orthopnea, PND
What are some of the physical findings of aortic stenosis?
physical exam:
ECG:
ECHO:
CXR:
1) parvus et tardus carotid pulse - slow upstroke + delayed peak
2) creschendo/decreschendo murmur
3) concentric LVH
- s4 gallop
- ECG: L axis deviation (ECG)
- ECHO: increased wall thickness, abnormal aortic valve leaflets
- CXR: cardiac dilation, pulmonary congestion
What is the purpose of aortic stenosis cardiac catherization?
records LV pressure and aortic root pressure to measure the mean pressure gradient (should increase with aortic stenosis)
What are the etiologies of aortic regurgitation? (2)
disease of aortic valve: congenital + rheumatic
disease of aortic root: widening that prevents the aortic leaflets to close properly (syphilis, marfans, HTN, HLA/inflammation)
What can cause aortic root dilation? (4)
Syphilis
Marfan’s syndrome
HLAB27
HTN
What is the pathophysiology of AR?
LV volume overload due to regurgitation during DIASTOLE, the heart compensates via eccentric hypertrophy so that it can pump the same volume load against high pressures repeatedly
LV volume –> eccentric LV hypertrophy. How does this happen?
What is the result of this hypertrophy?
sarcomeres are added in series so that the LV can accomodate the extra volume load AND eject a constant stroke volume with the usual amount of sarcomere shortening
Eccentric hypertrophy leads to:
- > ischemia
- > myocardial failure
What are the clinical outcomes of these changes?
ischemia - due to increased oxygen demand (increased preload, myocardial mass, increase shortening), but decreased oxygen supply (decreased diastolic pressure, compression of intramural arteries)
myocardial failure - systolic dysfunction may develop and lead to pulmonary congestion
What do patients with AS experience?
Same as AR -
asymptomatic
typical angina
syncope
dyspnea, orthopnea, PND
What are some of the physical findings of AS?
physical exam:
ECG:
ECHO:
CXR:
1) widened pulse pressure
2) blowing decrescendo, early diastolic murmur best heard at sternum
max intensity @ L sternal border = valvular dz
max intensity @ R sternal border = aortic root dz
3) Eccentric LVH
- ECG: L axis deviation (ECG) but no STRAIN pattern
- ECHO: aortic valve deformity +/- aortic root dilation
- CXR: LV enlargement, +/- aortic root dilation, +/-pulmonary congestion
What is the purpose of AR cardiac catherization?
measures degree of regurgitation/LV function using a dye. An increase in LV diastolic pressure indicates significant regurgitation
What are the etiologies of acute AR? (3)
What do these result in?
1) bacterial endocarditis leading to valve perforation
2) aortic dissection, resulting in separation/disruption of aortic valve leaflets
3) congenital - ruptured sinus of Valsalva aneurysm
results in: acute diastolic volume overload, which causes LV to increase wall shortening by increasing sympathetic tone. This leads to a dramatic increase in wall tension (decreased compliance) and subsequent increase in LV diastolic pressure and pulmonary congestion
Compare & contrast acute AR with chronic AR in terms of:
LV size
LV compliance
LA size
LA/LV pressure
Acute AR:
LV size - normal
LV compliance - low due to increased wall tension/sympathetic tone
LA size - normal
LA/LV pressure - very high; leads to pulmonary congestion
Chronic AR: LV size - eccentric hypertrophy LV compliance - high LA size - enlarged LA/LV pressure - normal to high
How do you treat acute AR?
vasodilatory therapy with emergency valve replacement
What are the common diseases of the mitral valve? (5)
1) myxomatous degeneration - weakening of CT that prevents leaflets from closing properly
2) IHD
3) infectious endocarditis
4) CT disease (ie Marfan’s)
5) LV dilation/eccentric hypertrophy
The majority of mitral stenosis is caused by:
what is the etiology of this?
rheumatic heart disease; due to molecular mimicry of streptococcal group A antigens with cardiac myocardium (Type II Hypersensitivity - antibodies against own cells)
What is the pathophysiology of mitral stenosis?
mitral valve narrows and restricts blood flow from LA->LV, leads to impaired LV filling and increased pulmonary pressures
Ultimately leads to pulmonary HTN and right heat failure
What are the physical findings of mitral stenosis?
What are the symptoms of mitral stenosis?
PE exam:
increased JVP
crackles
Auscultation:
loud S1; palpable at the apex.
Opening snap (OS) often follows S2 and initiates the murmur.
Loud P2 if there is pulmonary HTN; RV impulse becomes palpable.
CXR: increase LA + RV size
ECHO: LAE + abnormal mitral valve
ECG: LAE, RVH, a-fib
Symptoms: dyspnea, orthopnea, hemoptysis, and anything related to RHF (edema, ascites, a-fibs)
How would you treat mitral stenosis?
Class II b-blockers Class IV Ca blockers diuretics anti-coagulation surgery
What are the etiologies of mitral regurgitation? (2 main ones, one has 5 subtypes)
rheumatic
non-rheumatic
- prolapse
- ischemia
- infectious endocarditis
- LV dilation
- mitral annular calcification
What is the pathophysiology of rheumatic mitral regurgitation?
systolic regurgitation of blood back into the LA, LV compensates by increasing ventricular volume to maintain a constant CO (volume overload).
Dilated LV may eventually fail, leading to increased pulmonary pressures
What are some of the physical signs of mitral regurgitation?
What would a CXR/ECG show?
physical findings:
low carotid pulse
laterally displaced apex (due to LV dilation)
normal S1/S2, presence of S3 gallop
pansystolic mumur at apex that radiates to axilla
CXR: LV/LA enlargement, calcified valves
ECG: LV/LA enlargement (L axis deviation); atrial fibrillation
What are some of the etiologies of mitral valve prolapse? How does it lead to mitral regurgitation?
What do these cause?
What patients is this common in?
floppy valve due to
- myxomatous degeneration of valve tissue
- elongated chordinae tendinae
thickened + elongated leaflets (usually posterior leaflet) balloon into the LA during systole, may be associated with a mitral regurgitation
Common in Marfan’s syndrome
What are the physical findings of mitral valve prolapse?
What would a CXR/ECG show?
mid-systolic click (due to sudden tensing of the leaflets + chordae tendinae) followed by a late systolic mitral regurgitation murmur
ECG: ST segment + T wave changes, ventricular arrhythmias
How would you treat mitral valve prolapse?
b-blockers
valve replacement
antibiotics for prophylaxis
What are some of the etiologies of ischemic heart disease that result in mitral regurgitation?
ischemia of the papillary muscles or chordinae tendinae can result in rupture or dysfunction; due to blockage of the RCA or LAD/LCX arteries.
What are some of the pathophysiology of ischemic heart disease that result in mitral regurgitation?
increased LA pressure due to regurgitation; leads to acute pulmonary congestion –> pulmonary edema
What are some of the signs of mitral regurgitation caused by ischemic heart disease?
mild: insignificant systolic murmur during angina
severe/acute: murmur is shorter and diamond shape with prominent S4
Compare & contrast acute mitral regurgitation with chronic MR in terms of:
LV size
LA size
LA pressure
Acute MR:
LV size: normal
LA size: normal
LA pressure: high
Chronic AR:
LV size: eccentric hypertrophy to maintain normal SV
LA size: enlarged
LA pressure: normal
What are the histological features present in the heart as result of rheumatic heart disease?
pericardium myocardium endocardium valves chordae tendinae
pericardium - diffuse fibrinous inflammation with adhesion of the two layers “bread and butter”
myocardium - scattered pale foci that contains Aschoff nodes (fibrinoid collagen necrosis w. surrounding granulmatous tissue)
endocardium - scarring, vegetations, and nodules
valves - thickened and deformed with fibrinous bridges that may fuse the valve cusps
chordae tendinae - thickened and fused
What is infective endocarditis?
What causes it?
inflammation of the endocardium with superimposed thrombus formation.
bacterial: strep (sub-acute), stAph (Acute)
fungal: candida, aspergillus histoplasma
rickettsial: coxiella brunetii
routes of entry: oropharynx, GU, GI, lungs, skin
What is the leading cause of death as a result of infective endocarditis?
cardiac failure as a result of:
- cusp destruction
- rupturing of chordae tendinae
- myocardial infarction
What is the pathogenesis of infective endocarditis?
1) endothelial damage -> exposes collagen
2) formation of fibrin/platelet thrombotic vegetations
3) bacteremia w. infection of thrombus and vegetation formation
What is the pathology of infective endocarditis?
vegetations on valves
“blue haze” observed on histological specimens
What are complications associated with infective endocarditis?
heart
kidneys
brain
emboli from the vegetations can break off and cause:
heart - minute infarcts + focal abscesses that can lead to valvular insufficiency, suppurative pericarditis, dehiscence of artificial valves
kidney - immune complex disease + glomerulonephritis
brain - mycotic aneurysms (due to bacterial-induced degeneration of the arterial wall) in the brain
What is Marantic endocarditis? What is it caused by?
Non-bacterial thrombotic endocarditis (NBTE)
formation of small fibrin clots on normal valves due to hyper-coagulable state (cancer, renal failure)
NOT associated with bacterial infection or inflammation (STERILE; no signs of inflammatory cells)
clots are loosely attached and prediposes to endocarditis/embolization as a result of the secondary reaction to rheumatic fever.
What is Libmann Sack’s Endocarditis?
wart-like sterile vegetations on valves that may result in fibrinous pericarditis or myocarditis
usually not serious unless secondarily infected
Which valves are commonly affected with
IV drug users?
carcinoid tumors originating from the gut?
rheumatic heart disease?
IV drug users: tricuspid
carcinoid tumors originating from the gut: tricuspid
rheumatic heart disease: aortic + mitral
RAPID REVIEW: Transposition of the great vessels
Type of shunt:
Flow due to:
ECG:
CXR?
Clinical presentation?
Treatment?
Type of shunt: aorta arises from RV and pulmonary arises from LV; NOT compatible with life unless there is a shunt present to allow adequate mixing of blood (PDA, ASD, VSD)
Flow due to: failure of the aorticopulmonary septum to spiral
ECG: normal
CXR: cardiomeagly w. increased pulmonary vascularity “eggs on a strong”
Clinical presentation? intensely cyanotic baby that is unresponsive to 100% oxygen
Treatment? arterial switch surgery to connect the aorta with LV and pulmonary with RV.
