What is stenosis?
Narrowing of valve that limits blood flow
What is insufficiency?
Leak across a valve that allows retrograde blood flow (aka regurgitation)
What are the determinants of blood flow through valves?
- Pressure difference
- Orifice geometry (valve area)
- Time of blood flow through the valve
- Fluid rheology
- Chamber stiffness
What is the pathophysiology behind valvular heart disease?
Valve injury causes overload
- Acute overload -> pulmonary edema
- Chronic pressure/volume overload -> hypertrophy
Hypertrophy-> Heart failure
Regurgitation causes what type of overload? Results in?
Regurgitation -> Volume overload -> Eccentric Hypertrophy
Stenosis causes what type of overload? Results in?
Stenosis -> Pressure overload -> Concentric hypertrophy
What are some consequences of valvular heart disease (concentric or eccentric hypertrophy)?
Congestive Heart Failure
- VT/Vfib (risk of sudden cardiac death, esp AS)
- A fib (with ALL, more with MS and MR) Infective endocarditis Embolism
What type of valvular heart disease most often causes VT/Vfib and sudden cardiac death?
What type of valvular heart disease most often causes Afib?
Mitral stensosis and mitral regurgitation (although all can)
What underlies infective endocarditis? Consequences?
A structurally abnormal valve + turbulence is at risk for bacterial growth. May damage valves further with worsening regurgitation
For who is endocarditis prophylaxis routinely recommended?
- Prior Hx of endocarditis
- Prosthetic valves
- Cardiac transplant with valvular disease
- Congenital heart disease: cyanotic CHD or repaired with a prosthetic material in under 6 mo
What conditions make an embolism (systemic/cerebral) more likely?
Systemic and cerebral most likely with:
- Large atria
- Large LV (e.g. DCM)
- Low EF
- Endocarditis (vegetations can break off)
Where are mitral valve murmurs best heard? Radiate?
- Best heard at apex (about 5th ICS)
- Radiate to axilla
Where are aortic valve murmurs best heard? Radiate?
- Best heard at base of heart over aortic area (2nd R ICS)
- Radiate to carotids/neck
In what state of the valve due stenotic and insufficient valves cause problems?
Stenosis: with normal flow across valve [systole]
Insufficiency: when valve is (supposed to be) closed [diastole]
List all the systolic murmurs
- Aortic stenosis
- Mitral insufficiency
- Tricuspid insufficiency (less common)
List all the diastolic murmurs
- Aortic insufficiency
- Mitral stenosis
- Tricuspid stenosis (less common)
Breakdown causes of aortic stenosis by age?
"Young" pts (under 70)
- Mostly bicuspid (earlier clinical onset, 50s)
- Rheumatic disease
Older pts (>70)
- Mostly degenerative
- Rheumatic disease
*Senile calcific "degenerative" later onset (70s-80s)
Average onset of bicuspid aortic valve stenosis/
Average onset of senile calcific "degenerative" aortic valve stenosis?
What is shown here?
Bicuspid aortic stenosis
- Two cusps
What is shown here?
Senile calcific aortic stenosis
- Three cusps
Explain the mechanics of aortic stenosis causing murmur. What kind of heart failure
Obstruction to LV outflow
- Pressure gradient between LV and aorta
- LV pressure overload results in concentric LVH over time -> diastolic dysfunction (earlier) -> systolic dysfunction (later)
- Acceleration of systolic flow produces a systolic crescendo-decrescendo murmur at base radiation to neck
Explain the pressure gradient across the aortic valve in aortic stenosis?
- LVP > aortic P in systole
- Pressure in LV remains higher than aorta all through systole until it finally relaxes
What are some key physical exam findings of aortic stenosis?
- Systolic, crescendo-decrescendo
- At base (R and possibly L 2nd-3rd ICS), radiating into neck
Slow, weak carotid upstroke
PMI forceful, sustained
Soft S2 (if calcified, doesn't close quickly) with delayed A2 (takes longer for LV to empty)
- Single S2 or paradoxically split S2
What is the classical clinical triad of aortic stenosis?
Think of initials: A-S-D
- Angina/chest pain
What causes the angina/chest pain in aortic stenosis?
- Demand increases (LVH)
- Subendocardial flow decreases (high LV diastolic pressures)
- +/- coronary artery stenosis
What causes heart failure in aortic stenosis?
- Hypertrophy with fibrosis
- Chamber stiffness increases
- Diastolic failure first, later systolic failure
What causes syncope/sudden death in aortic stenosis?
Exercise-induced: fixed small orifice, so unable to increase CO
- Arrhythmia: Vtach or Vfib
- AV block
Describe the natural history of aortic stenosis (length of symptoms, survival...)
Long initial asymptomatic course
Once symptoms occur, prognosis worsens
- Worst with HF
- Better with syncope
- Best with angina (ASD triad)
Treatment for aortic stenosis? When done?
- For severe, symptomatic aortic stenosis
What is acute aortic insufficiency?
Injury to aorta or leaflets -> sudden diastolic retrograde flow into LV resulting in heart failure
- No time for compensation
What is chronic aortic insufficiency?
The pathophysiology and leak evolve slowly over years
- Allows compensation by LV dilation
- Delays the onset of symptoms of heart failure
Causes of acute aortic insufficiency?
Causes of chronic aortic insufficiency?
- Marfan's (heritable)
- Inflammatory: syphilis
- Annulo-aortic ectasia
Cusp issues: (more common)
- Bicuspid valve
- Rheumatic disease
- Late sequelae of infection
What are some key features (heart sound wise) of aortic regurgitation?
- Causes LV volume overload
- Due to regurgitation of blood into the LV
- Shorter in acute than chronic b/c pressures "equalize" faster in acute AI
How to calculate % regurgitation?
= regurgitation/(regurg + forward)
Describe LVP and AoP during aortic insufficiency
- Pressure difference between LVP and AoP during diastole is pretty significant; decreases with regurgitation back through aorta
- Quicker P equalization causes shorter murmur (earler diastole) (pic h)
What is the phathophysiology/consequences of acute aortic insufficiency?
Recall: acute AI = sudden disatolic leak
- LV enlarges, but only minimally (not enough time)
- Acute increase in volume in small chamber -> significant increases in LV diastolic ps
Acute pulmonary edema results
Effective forward CO is reduced acutely
-> low BP
-> circulatory collapse (shock)
What is pathophysiology/consequences of chronic aortic insufficiency?
Recall: chronic AI = progressive leak over years
- LV eccentric hypertrophy (LV dilation): compensatory increase in SV
- Diastolic BP drops due to AI, systolic P may rise (increased SV), causing a WIDE pulse pressure (SBP-DBP)
- Systolic function declines over years (less forward, more regurgitant volume)
- Further LV dilation and untimely CHF results
Key clinical findings of acute vs. chronic AI?
- Acute: normal or low
- Chronic: wide pulse pressure, bounding pulse (large volume)
- Acute: Severe CHF signs
- Chronic: No CHF signs
- Acute: normal position
- Chronic: displaced, enlarged
- Acute: short early diastolic murmur
- Chronic: long diastolic murmur
- Acute: no LVH
- Chronic: LVH
- Acute: No LVH; Al jet
- Chronic: Eccentric LVH, Al jet
Treatment for aortic regurgitation?
- MIld/moderate: vasodilators (to decrease afterload, unload ventricle, and increase SV)
- Severe: valve and/or aortic root repair or replacement
- Acute: surgical emergency
Key Points of AI
Key points of AS