Valvular Diseases Flashcards
(51 cards)
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
