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Cardio Week 3 > Lecture 30: Cardiac Valve Stenosis > Flashcards

Lecture 30: Cardiac Valve Stenosis Flashcards

1
Q

What are the physiologic consequences of stenotic valves?

A

Decreased orifice size = increased flow velocity (continuity equation)
Thus higher pressure gradient necessary in order to drive flow (higher velocity = lower pressure)
The pressure gradient subjects the chamber upstream from the valve to a PRESSURE LOAD

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2
Q

What is the physiologic impact of stenotic valve on heart determined by?

A

Determined by valve position and obstruction severity

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3
Q

What is the relationship between pressure and velocity?

A

Quadratic and inversely proportional

The higher the velocity, the lower the pressure (by a square root)

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4
Q

What is the continuity equation?

A

Flow RATE = flow RATE
Flow rate in any section in a pipe is the SAME
Flow rate = mean velocity x cross sectional area
A1 * V1 = A2 * V2

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5
Q

What is the relationship between area and velocity?

A

Inversely proportional
More stenotic a valve, the greater the flow velocity
Flow velocity is INVERSELY related to cross sectional area (CSA)

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6
Q

How do we apply the Bernoulli theorem?

A

Allows us to enable calculation of valve orifice area from measurements of pressure and flow rate
First we record pressure difference and use it to correlate with velocity (quadratic and directly proportional)
Then we get flow rate and take flow rate/flow velocity = cross sectional area

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7
Q

What happens to the pressure gradient in a normal valvular orifice?

A

At physiologic flow rates, normal orifice size yields flow velocities that evoke negligible pressure gradients

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8
Q

What are the determinants of flow rate (ml/s)?

A

Cardiac output = positive linear correlation

Time available for flow = negative linear correlation

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9
Q

What are the determinants of flow velocity (cm/s)?

A

Has a positive linear correlation with flow rate

Has a negative linear correlation with valve orifice area

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10
Q

What is the determinant of pressure GRADIENT?

A

Is positively and quadratically related to flow velocity

However, remember that pressure at the point of faster velocity is slower (so inversely proportional at a point)

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11
Q

What is the Gorlin Valve area equation?

A

A = F/ [C44.3sqr(P1-P2)]

A = valve area
F = flow rate
C = constant
44.3 = dimension corrections
P1 – P2 = pressure gradient
Denominator = the flow velocity!
Holy shit this is so complicated for nothing…
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12
Q

Why is chamber upstream of the high velocity low CSA stenotic valve subjected to higher pressure?

A

Because the upstream chamber is MAINTAINED at a higher pressure (think of squeezing a balloon full of fluid through a starbucks straw

  • fluid through the starbucks straw might have high ass velocity, but it takes the balloon longer to get rid of the fluid due to the increase in resistance
  • increase in resistance (as seen by stenotic valve) leads to decrease in flow
  • therefore, your upstream balloon (LV) is subjected to higher pressures for longer
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13
Q

What are the key observations from the valve area relationship?

A

In order to Increase blood flow across stenotic aortic valve, you will require a large increase in pressure gradient (and thus more systolic pressure load on LV)

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14
Q

Why must you always calculate pressure gradient and CO to determine orifice area?

A

At low rates, even with a small valve orifice area, the valve pressure gradient may be deceptively small (flow rate and pressure relationship)
Valve area must always be calculated using the pressure gradient and cardiac output (flow) to determine what is deficient

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15
Q

What are the key characteristics of stenotic valves?

A

Cannot respond well to increased demand

CO is impaired

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16
Q

What are the consequences of increasing blood flow across stenotic valve?

A

Increases systolic pressure load on LV
Limits ability to increase CO in response to demand
Must draw predominately on HR incrase
Substantial increase in demand

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17
Q

What is the cardiac adaptation to aortic stenosis?

A

A chronic disease that does not develop acutely

Concentric LV hypertrophy to offset greater wall stress

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18
Q

What are the limitations to cardiac adaptation?

A

Limitations to hypertrophy process due to limits of

i. coronary circulation
ii. coexisting epicardial coronary disease
iii. degradation of myocardial performance 
iv. change in diastolic compliance
v. Progression of stenosis severity
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19
Q

What are the symptoms of decompensated AS?

A
  1. Angina pectoris
  2. Effort-related syncope or presyncope
  3. Congestive heart failure
20
Q

What is the mechanism that leads to angina in AS?

A

limitation of coronary circulation to keep up with demand

-increased LV wall thickness reduces perfusion to subendocardial region

21
Q

What is the mechanisms that leads to effort syncope/presyncope in AS?

A

Inadequate CO response to exercise

22
Q

What is the mechanism that leads to congestive heart failure (systolic or diastolic)?

A
  1. inadequacy of LV hypertrophy to normalize wall stress
  2. Degradation of myocardial contractile performance (because sarcomeres added are dysfunctional)
  3. Decrease in myocardial diastolic compliance
23
Q

What does decompensation mean?

A

A functional deterioration of previously working structure or system

24
Q

What are the implications of NOT having symptoms with AS?

A

Compensatory mechanisms are working

25
Q

What are the implications of having symptoms of AS?

A
  1. AS severity has progressed, compensatory mechanisms have reached their limit to adapt
  2. LV function has deteriorated
  3. Aortic valve replacement indicated
    BIG TROUBLE lol
    Do surgery right away!
26
Q

Are patients without symptoms really absent of symptoms?

A

Probably not truly asymptomatic

Would have reduced exercise capacity if rigorously tested

27
Q

When is the optimal time to replace the aortic valve?

A

ASAP

28
Q

What are the characteristics of severely decompensated AS?

A

The sinking aortic

People have symptoms of cardiogenic shock (Low ass cardiac output)

29
Q

What do you do for sinking aortic stenosis (severely decompensated AS)?

A

Aortic valve replacement

Because you’ve corrected the afterload excess and saved the remaining myocardial performance

30
Q

What are the gross features of mitral stenosis?

A 
Calcified valve (is stuck together)
Very small hole with which to get flow across
31
Q

What is the geometry of the heart in MStenosis?

A

Normal to small LV
Enlarged LA (upstream)
Variably enlarged RV
Thickened mitral valve leaflets
i. anterior and posterior leaflets stuck together
ii. limited leaflet motion
iii. valve stays open throughout LA diastole
“Smoke” in LA moving sluggishly inot the LV (slow and stagnant flow)

32
Q

What are the key characteristics of mitral stenosis?

A

MStenosis is adversely affected by increases in heart rate
The less filling time = the less time LA and LV can equilibrate
Therefore, for a patient with MStenosis, you want to reduce HR
Degree of decay of inflow velocity decreases as duration of diastole decreases (slide 41)

33
Q

Why is increasing heart rate contraindicated in Mstenosis?

A

Because there is less filling time to allow LA and LV to equilibrate
This does not affect LV in AS because the diastolic filling is normal (since mitral valve works)

34
Q

What are the mild, moderate and critical sizes for Mstenosis?

A

2.0 cm^2
1.5^2
1.0^2
Smaller CSA is not as well tolerated in Mstenosis in comparison to AStenosis

35
Q

What does the heart do to adapt to mitral stenosis?

A

NOTHING

There are no compensatory mechanisms lol (slide 46 is intentionally blank)

36
Q

What are the consequences of no heart compensatory mechanism in severe MS?

A
  1. Disorder in which Left ventricle is UNDERFILLED
  2. LA pressure greater than 30 mmHg is poorly tolerated by pulmonary capillaries
    • Limits the maximum diastolic pressure gradient to 20 mmHg
    • that means you cant hypertrophy your LA to fill adequately fill the LV (for fear of creating too much pulmonary edema
  3. Chronic LA hypertension causes dilation which impairs atrial transport function
  4. Normal circulatory reflexes in response to a demand for increased CO are detrimental (because increased HR = contraindicated in Mstenosis = less diastolic filling time)
  5. Progressive LA dilation can lead to chronic atrial fibrillation due to loss of normal reflexes for HR regulations
37
Q

What are the long-term consequences of MS?

A
  1. LA HTN and atrial myocardial degeneration
  2. LA enlargement
  3. Atrial fibrillation
  4. Sluggish flow (“smoke”)
    • Leads to Atrial thrombosis and systemic embolization
  5. Pulmonary venous HTN
  6. Pulmonary arterial HTN
38
Q

Why do you get pulmonary venous HTN in Mstenosis?

A
  1. elevation in pulmonary capillary pressure due to LA increase
  2. elevated pressure impairs alveolar gas exchange
  3. Dypsnea, particularly due to exercise
39
Q

Why do you get pulmonary arterial HTN? What are the consequences?

A
  1. increase LA pressure leads to increased pulm artery pressure
  2. Increased LA pressure leads to increased pulmonary arteriolar constriction
    • can lead to obliterative PA destruction of PA pressure elevated for too long (which would then lead to irreversible PVR increase and decreased PBF
  3. Severe right ventricular afterload excess
    • may eventually lead to RV dilation, tricuspid regurg and systemic venous HTN
  4. The back up from right side of the heart may lead to hepatic dysfunction, edema and ascites
40
Q

What is the clinical course of mitral stenosis?

A

Lack of cardiac adaptation = patients become symptomatic much faster

41
Q

What are the predominant symptoms of MS?

A
  1. dyspnea on exertion due to LA pressure elevation

2. fatigue due to sustained low CO

42
Q

What is the difference between MStenosis and AS?

A

Patients with symptoms for MS do not deteriorate rapidly like AS patients due
-gradual progression over many years as severity of valve obstruction slowly increases
Due to lack of adaptive mechanisms in MS as opposed to AS, you become symptomatic with mild/moderate severities

43
Q

What are the variants in the evolution of mitral stenosis?

A
  1. severe PA hypertension secondary to obliterative pulm arteriolar disease
  2. RV failure secondary to tricuspid regurgitation
44
Q

What are the key characteristics of the severe PA HTN 2ndary to obliterative Pa disease?

A

One variant of Mstenosis
As was outlined before
Sustained PA pressure leads to obliterative disease
Obliteration of arterioles leads to severely increased PVR (8 wood units)
Increased PVR leads to decreased PBF

45
Q

What are the key characteristics of RV failure secondary to Tricuspid Regurg?

A

When you have too much pulm vascular resistance (perhaps from obliterative disease), your tricuspid valve leaks fluid back
Severely increases RV and thus RA pressure
Thus you get ascites, edema and hepatic dysfunction as a result
Another variant of MStenosis

46
Q

What are the patients symptoms correlated with?

A

Progression of stenosis severity in Mstenosis

Cardio Week 3 (10 decks)

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