Valvular Heart Disease

Question 1

Obstruction to LV outflow due to stenosis changes of aortic valve

Answer 1

Aortic stenosis

Question 2

Can an obstruction above the supravavlular or below the HOCM valve cause aortic stenosis?

Answer 2

Yep

Question 3

Aortic stenosis at age 50-60

Answer 3

Biscupid

Question 4

Aortic stenosis at age 60-70

Answer 4

Rheumatic

Question 5

Aortic stenosis at age >70

Answer 5

Senile degenerative

Question 6

Pathology of the aortic stenosis

Answer 6

LV pressure overload

Question 7

Compensation for an aortic stenosis?

Answer 7

Concentric hypertrophy, to keep wall stress normal

Question 8

Wall stress

Answer 8

Pressure x radius / 2x width

Question 9

Chambers size at normal in concentric hypertrophy

Answer 9

Yep

Question 10

Consequences of pressure overload hypetrophy (3)

Answer 10

1. Increased stiffness— higher pressures needed to fill LV
2. Increase MVO2 diminished ability to supply coronary flow leading to a O2 supply demand mismatch
3. Susceptibility to Arrhythmias

Question 11

Symptoms of aortic stenosis: (2)

Answer 11

1. None for many years- LVH normalizes tension
2. Eventually we see:
   • Dyspnea due to high filling pressures
   • Angina- oxygen supply/demand mismatch
   • Syncope due to inability to raise C.O. Arrhythmia
   • CHF due to high filling pressures and LV dysfunction

Question 12

Physical findings (2)

Answer 12

1. Diamond shape murmur: there is a small /delayed carotid upstroke and a Late peaking on systolic aortic murmur - cresecendo + decrescendo
2. Absence of second heart sound

Question 13

Aortic stenosis has a short or long aortic stenosis?

Answer 13

Long with increasing obstruction and myocardial overload

Question 14

Aortic stenosis treatment

Answer 14

There are really no medications and the best option is surgery in which AVR is recommended for severe and symptomatic patients. For those where surgery is not recommended, the Balloon AVP is done.

Question 15

Aortic regurgitation:

1. What is it?
2. Creates
3. Etiology (1) primary valve (2) primary aortic root dilatation
4. Pathophysiology and impact on chambers
5. What happens to wall stress?
6. Pathophysiology
7. Eventual outcome
8. Symptoms
9. Physical exam: (1) what type of murmur? (2) pulses? (3) pressure?
10. Therapy
11. Indications for AVR

Answer 15

1. Regurgitation of a significant portion of the SV back into the LV through the incompetent aortic valve during systole
2. Created chronic volume overload of the LV
3. (1) primary valve etiology: congenital, rheumatic, endocarditis or trauma (2) Primary aortic root dilation: rheumatoid syndromes, CMN, Marfan’s, atherosclerotic
4. Due to the volume overload there is an adaptation that leads to dilatation and hypetrophy to normalize the wall stress = eccentric hypetrophy
5. Both the radius and wall thickness increase leading to an overall increase in wall stress
6. The Pathophysiology of this condition: huge EDV allows ejection of large FSV in face of large regurgitate volume
7. Eventual outcome due to increase wall stress is CHF
8. Symptoms: none for years, dyspnea on exertion. There is increased symptoms as forward SV decreases and LV pressures rise
9. Physical exam: (1) loud long diastolic murmur, Austin-flint murmur (2) bounding pulses (3) wide pulse pressure (due to a lot of blood coming backwards)
10. Therapy: med to reduce afterload such as nifedipine or an ACEi and slow down LV deterioration
11. AVR when it is symptomatic and asymptomatic with severe AR and LV systolic dysfunction

Question 16

Mitral Stenosis:

1. Etiology
2. What occurs?
3. Pathology
4. What do we see later?
5. Pathophysiology and impact on chambers
6. Eventual consequence
7. Large LA leads to
8. Symptoms
9. Physical exam: (1) S1 (2) diastolic (3) enlargement of (4) severity of M.S. can be estimated by
10. Latent period
11. therapy

Answer 16

1. Always rheumatic in adults
2. Progressive narrowing of the mitral orifice- requires increasing LA pressure to maintain flow and C.O
3. inflammation results in deformity and fibrosis of leaflets, fusion of commissaries and chordae
4. Calcification and further stiffening
5. MV obstruction results in increased LAP and LA dilation And there is an increase in back pressure to lungs leading to increased interstitial fluid and stiffness —>SOB
6. RV and RA dilation and failure from pulmonary HTN
7. Large LA results in Arrhythmias
8. Symptoms: none for years, dyspnea on exertion/fatigue. We tend to see more symptoms with the onset of Afib. Later we see RHF with edema and venous congestion’s. There is also increased risked for emboli in the periphery and cerebral.
9. Physical exam: (1) Loud S1, opening snap (2) low diastolic rumble (3) RV enlargement (4) severity of MS can be estimated by P.E.
10. long latent period after the initial rheum. Fever. We start seeing symptoms at 1.2 cm and there is a steady progressions afterwards
11. Early medications include diuretics to decrease LAP, Beta blockers to decrease Heart rate and allow for LA decompression. Future therapy could include MVR or Balloon MVP

Question 17

Mitral regurgitation:

1. What is it?
2. What does it create?
3. Etiology?
4. Pathophysiology and impact on chambers
5. Symptoms
6. Physical exam: (1) murmur (2) S1 (3) S3 (4) LV (5) later findings
7. As LAP increases
8. As LV dilates and EF decreases
9. treatment
10. MV repair vs MV replacement

Answer 17

1. Ejection of portion of the SV into the low-pressure LA
2. Created chronic volume overload of the LV
3. Etiology: rheumatic, non-rheum.: MVP, papillary, endocarditis, LV dilatation, Mafan’s
4. (1) LV dilatation and hypertrophy from volume overload (2) LA dilatation and increased LAP from regurgitant volume (3) Later: pulmonary HTN and RV failure
5. None for many years until high LA pressures leads to SOB and fatigue due to decreased SV and LA dilatation leading to Afib
6. (1) loud holosystolic murmur, apex to axilla (2) decreased S1 (3) S2 rumble complex (4) Large LV (5) later: increase P2 and RV
7. As LAP increases, symptoms of SOB begin
8. As LV dilates and EF decreases, HF sx worsens
9. Treatment: (1) medical: afterload reduction and diuretics (2) surgery: sooner than later to avoid irreversible damage
10. MV repair is recommended over MV replacement in the majority of pts.

Question 18

Tricuspid and pulmonic stenosis:

1. Usually ________ with early symptoms
2. Sx and signs due to ________ on chamber proximal to valve
3. In adults—>
4. Treatment for adults

Answer 18

1. Congenital
2. Pressure overload
3. Carcinoid syndrome
4. Balloon valvuloplasty

Question 19

Tricuspid regurgitation:

1. Etiology: (1) secondary to \_\_\_ and thus \_\_\_\_\_ (2) 
Endocarditis in \_\_\_\_\_\_
2. Results in \_\_\_ and \_\_\_\_ dilatation
3. Large \_\_\_\_\_ waves on PE
4. Systemic complication
5. Treatment: (3)

Answer 19

1. (1) usually secondary to RV and thus annular dilation (2) endocarditis in IVDA
2. Results in RV and RA dilatation
3. Large V waves on PE
4. Systemic venous congestion
5. treatment: (1) address primary process (2) diuretics (3) surgical repair such as tricuspid annuloplasty