HRR: physiology of valve disease Flashcards

1
Q

What is diastole?

A

AV valves are open and there is little resistance to flow, while SL valves are closed with no leakage.

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2
Q

What is systole?

A

AV valves are closed with no leakage and SL valves are open with little resistance to flow.

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3
Q

What is stenosis?

A

Obstruction to valve flow at a phase when the valve should be open; the pressure gradient serves as the hallmark.

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4
Q

What is regurgitation?

A

Inadequate valve closure leads to back flow.

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5
Q

Can a valve be both stenosis and regurgitant?

A

Yes.

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6
Q

What are the basic anatomical elements of the mitral valve?

A

Chordae tendinae, papillary muscles, anterior and posterior leaflets.

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7
Q

What is the main cause of mitral stenosis?

A

Rheumatic.

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8
Q

What are some signs of mitral stenosis?

A

SOB with exertion or laying down, fatigue, swollen feet or legs, palpitations, coughing up blood, chest pain, dizziness.

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9
Q

Describe some issues with mitral stenosis.

A

Increased LA pressure leads to pulmonary hypertension, and RV pressure overload can lead to RV hypertrophy, RV failure, tricuspid regurgitation, and systemic congestion.

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10
Q

What are some paradoxes of mitral stenosis?

A

The LV can be unaffected and pulmonary symptoms can diminish as the RV fails.

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11
Q

How does mitral stenosis impact preload?

A

It decreases it.

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12
Q

How will the pressure of the LA be impacted in mitral stenosis?

A

The pressure will be higher.

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13
Q

Mitral stenosis is a substrate for…

A

A fib.

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14
Q

What happens to a PV loop for the LV in mitral stenosis?

A

It shifts left due to lower volumes and has a slightly lower peak pressure. The curve will also narrow due to SV being decreased. The LVEDV is also decreased.

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15
Q

What are signs of mitral regurgitation?

A

Murmur, SOB with exertion or laying down, fatigue, swollen feet or ankles, excessive urination, cough.

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16
Q

What is the pathophysiology of mitral regurgitation?

A

The LA pressure is increased, and it is also dilated. The LV can also experience volume overload and dilate and experience eccentric hypertrophy. The process can lead to pulmonary hypertension, A fib, and low CO.

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17
Q

What happens to SV in mitral regurgitation?

A

It increases; there is a forward and a reverse SV.

18
Q

A tall V wave is seen in…

A

Mitral regurgitation.

19
Q

Mitral regurgitation is a substrate for…

A

A fib.

20
Q

What happens to the PV loop in mitral regurgitation?

A

It’s huge. The isovolumetric relaxation and contraction are gone, giving it a blob appearance. SV increases due to an increase in LVEDV from excess being pumped in as regurgitation from the previous cycle. The peak pressure decreases as well.

21
Q

What is the difference between compensated and decompensated mitral regurgitation?

A

In compensated, the body’s reflexes can account for the changes in the system. HR and systemic resistance will increase, creating bigger EDV and ESV than normal. This makes a large SV and EF. In decompensated, the body cannot overcome the issue. EDV is huge, but so is ESV and EF is low.

22
Q

Describe left ventricle events in chronic decompensated mitral regurgitation.

A
  1. Increase in EDV and ESV 2. Increase in wall stress and LV dilation 3. LV dysfunction 4. Decreased LV SV 5. Lower EF.
23
Q

Describe left atria events in chronic decompensated mitral regurgitation.

A
  1. Volume overload 2. L dilation 3. Increased pressure 4. Pulmonary congestion 5. Pulmonary HTN and dyspnea 6. Congestive heart failure symptoms.
24
Q

What are the cusps of the aortic valve?

A

Left, right, and posterior.

25
Q

What will a congenital bicuspid aortic valve cause?

A

Aortic stenosis.

26
Q

What are the main etiologies of aortic stenosis?

A

Degenerative calcification, congenital, and rheumatic.

27
Q

What are some signs of aortic stenosis?

A

Murmur, chest pain, fatigue, palpitation, SOB, pulsus tardus.

28
Q

Describe the pathophysiology of aortic stenosis.

A

LA pressure increases and it dilates. The LV has a volume overload, dilates, and undergoes eccentric hypertrophy. The LV can also experience concentric hypertrophy. Issues can include pulmonary hypertension, LA arrhythmia, and low CO.

29
Q

What happens to LEDP in aortic stenosis?

A

It increases.

30
Q

What happens to SV in aortic stenosis?

A

Reduced.

31
Q

What happens to pulse pressure in aortic stenosis?

A

Reduced.

32
Q

What happens to the PV loop in aortic stenosis?

A

It looks like a skyscraper. The afterload really increases, making the loop tall. EDV is slightly larger, ESV is much larger, and SV is much smaller.

33
Q

Can the body overcome aortic stenosis?

A

Yes; the body will increase HR and systemic resistance to increase output. Frank-Starling mechanisms invoke to try to make an okay SV.

34
Q

What causes angina with aortic stenosis?

A

The thickened wall means blood has farther to travel from epicardium to endocardium during diastole, which can create subendocardial ischemia and cause angina.

35
Q

How can aortic stenosis cause sudden death?

A

Subendocardial ischemia can lead to lack of oxygen in the heart tissue and cause ventricular arrhythmia and death.

36
Q

Describe the pathophysiology of aortic regurgitation.

A

LV volume overload leads to dilation and increased L pressure. The LA also dilates and there is increased optic use pressure.

37
Q

What are the compensatory mechanisms for aortic regurgitation?

A

Eccentric LV hypertrophy, increased LV compliance, peripheral vasodilation.

38
Q

What happens to aortic systolic and diastolic pressures in aortic regurgitation?

A

Systolic increases, diastolic decreases.

39
Q

What does aortic regurgitation do to afterload?

A

Increase it.

40
Q

Describe the PV loop in aortic regurgitation.

A

Another blob, but shifted right. LVEDV increases, SV increases (a lot is regurgitated) and peak pressure increases. The isovolumetric periods aren’t true ones.