Physiological responses to valvular disease Flashcards

1
Q

The heart valves open and close because of

A

changes in pressure on either side of the valve

(they are not pulled by muscles)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

The heart sounds are due to

A

the turbulence that occurs as the valves close

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Systole occurs between which heart sounds?

A

S1 and S2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the normal volume of the LV?

A

140mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the normal stroke volume?

A

70mL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is ejection fraction?

A

SV/EDV

~50% (lower in heart failure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is valve stenosis?

A
  • narrowing of valve
    • does not open fully
    • flow is restricted
    • creates a pressure gradient across the valve
      • need a higher pressure to overcome (see below)
    • creates higher pressure in chamber behind valve
      • LV in aortic stenosis
      • LA in mitral stenosis
    • leads to pressure overload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is valve incompetence?

A
  • regurgitation or leaking back of blood
    • valve does not close fully
    • blood leaks back into previous chamber
    • heart required to pump greater SV to maintain SV and CO because part of the flow goes backwards
    • greater volume in the ventricule
      • increased EDV so SV can be larger
    • increased ejection fraction
    • leads to volume overload
      • problem is in the ventricle​ that contributes to heart failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Diastole occurs between

A

the second and first heart sounds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What situations cause innocent flow murmurs?

A
  • high flow
    • children, fever, anaemia, pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Which part of the cardiac cycle is shortest?

A

systole (1/3rd)

diastole (2/3rds)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Aortic stenosis murmur is heard

A

systole, between S1 and S2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Mitral regurge murmur is heard

A

in systole between S1 and S2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Aortic regurge murmur is heard during

A

diastole, between S2 and S1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Mitral stenosis murmur is heard during

A

diastole, between S2 and S1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Patent ductus arteriosus murmur is heard

A

continuously through diastole and systole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Which murmurs are heard during systole?

A

aortic stenosis and mitral regurge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which murmurs are heard during diastole?

A

Aortic regurge and mitral stenosis

19
Q

What are the symptoms of mild and moderate valvular disease?

A

none - cardiac compensation is effective such that even severe lesions can be asymptomatic for many years, until the heart fails

20
Q

What is critical in the treatment of regurgitation?

A
  • irreversible LV changes occur at the same time symptoms present
    • tf valves are operated on before symptoms appear
21
Q

What is the timing of treatment of aortic stenosis?

A
  • LVH changes (concentric hypertrophy) are usually reversible even when symptomatic
  • tf tend to wait until symtpoms appear before operating in stenosis
22
Q

What is the assessment of valvular disease?

A
  • history (SOB)
  • examination - murmur, pulse
  • ECG
  • echo
    • diagnosis, severity, ventricular size & function, atrial size, pulmonary artery pressure
    • can show LV changes before they are irreversible (trigger for intervention in regurge)
23
Q

What is aortic stenosis?

A
  • progressive narrowing of the aortic valve
    • fibrosis, then calcification
  • reduces valve area
    • normal > 2.5cm2
    • severe < 0.7cm2
  • generates a pressure gradient across the valve (normally 0)
    • severe can be > 50mmHg
    • tf LVP can be 170mmHg if SBP is 120mmHg
24
Q

What is the left ventricular response to aortic stenosis?

A
  • pressure overload
    • leads to concentric hypertrophy
  • thicker, stiffer walls lead to decreased compliance
    • diastolic dysfunction bc harder to fill
    • need higher LA pressure and EDV
  • incresed LVEDP to fill LV
  • atrial contraction becomes crucial to LV filling (not normal)
  • LV changes usually reversed after surgery
    • removes the pressure gradient
  • LV can blow out and fail
    • tamponade, death
25
Q

What is the most common valve lesion?

A

Aortic stenosis

26
Q

What are the symptoms of aortic stenosis?

A

SOB, chest pain, blackouts

27
Q

Systolic murmurs are (sound)

A

systolic tf crescendo-decrescendo murmurs

murmur gets louder as the gradient increases throughout the cardiac cycle

28
Q

Where are systolic murmurs best heard?

A

over the upper R sternal edge

(crescendo-decrescendo)

29
Q

What causes aortic regurgitation?

A
  • damage to the aortic leaflets or dilated aortic root
  • damage by:
    • endocarditis (staph or strep viridans on valve leaflets), rheumatic fever (strep pyrogenes outside heart)
    • leaflets cannot seal
  • dilation by:
    • Marfan’s syndrome (mutation in fibrillin, a CT protein), aortic dissection (media, can split to aortic valve and root or dissect completely), collagen vascular disorders (ankylosing spondulitis), syphilis
    • leaflets do not close
30
Q

How does the heart adapt to aortic regurgitation?

A
  • portion of SV leaks back into the LV during diastole
  • tf to maintain CO, LV pressure increases to pump greater SV
    • leads to volume overload
    • there is no pressure gradient generated
  • maintenance of CO achieved by:
    • increased EDV
    • increased EF
    • normal ESV
  • can be effective in mild to severe AR for some time
  • diastolic BP drops (~30mmHg) as blood flows back into ventricle from aorta through the leaky valve
    • crashing/collapsing pulse
    • tf pulse pressure is increased (e.g. 150/30mmHg)
      • ​generates ‘bounding’ pulse
31
Q

What determines diastolic pressure?

A
  • systolic pressure
  • peripheral run-off
    • where the blood goes out of the aorta
    • how stretchy/stiff the aorta is
  • if aortic valve does not shut, get backflow into the LV
    • decreases DBP
    • increases pulse pressure
32
Q

What is the sound of the aortic regurgitation murmur?

A
  • lub-woosh instead of lub dub
    • don’t hear S2 because the aortic valve is not closing
33
Q

What are the effects of prolonged severe aortic regurgitation?

A
  • decompensation (irreversible) of eccentric/dilated LV hypertrophy
  • ++LV diastolic volume
  • -LV function
  • +LV systolic volume
  • when symptoms appear, these changes are irreversible
34
Q

What causes mitral regurgitation?

A
  • myxomatous degeneration (mitral prolapse, doesn’t close)
  • ruptured chordae tendinae (flail leaflet, severe)
  • infective endocarditis (strep or staph viridans)
  • MI –> ruptured papillary muscle (acute, surgical emerge)
  • rheumatic fever (strep pyrogenes)
  • collagen vascular disease (Marfan’s)
  • cardiomyopathy (change in ventricular shape)
35
Q

What are the consequences of mitral regurgitation?

A
  • portion of SV ejected into LA
  • to maintain CO, LV must pump greater SV per beat
    • leads to volume overload
    • increased EDV
    • increased EF
    • normal ESV
    • increased LA volume and pressure due to LA dilation
      • ​affecting ventricle and atrium; in aortic just ventricle
36
Q

What are the consequences of prolonged severe mitral regurge?

A
  • eventual decomponsation
  • ++LV diastolic volume
  • -EF
  • +LV systolic volume
  • changes coincide with symptoms, irreversible
    • tf operate earlier to repair valve instead of replacing it
37
Q

What are the additional risks associated with mitral regurgitation?

A
  • due to increased LA pressure and volume (dilation):
    • atrial fibrillation due to electrical instability
    • thrombus formation, embolism to brain, heart kindey, limbs
    • increased pulmonary venous pressure (due to +LAP)
      • pulmonary congestion and oedema, causing hypoxia
      • hypoxia stimulates pulmonary arteriole vasoconstriction
        • PA hypertension, can cause failure of RV
38
Q

What is the sound of the mitral regurge murmur?

A

pansystolic ‘woosh-woosh’ constant throughout systole

due to the pressure gradient between LV and LA

39
Q

What causes mitral stenosis?

A
  • almost always previous rheumatic fever, esp. in women
40
Q

What is mitral stenosis?

A
  • fibrotic, narrowed mitral valve
  • generates pressure gradient across mitral valve
  • reduces LV filling
  • LV atrial contraction becomes imporant to filling, CO
  • LV systolic function unaffected
41
Q

What are the consequences of mitral stenosis?

A
  • increased LA pressure and volume
  • atrial fibrillation due to electrical instability
  • risk of thrombus formation in LA, can embolise
    • cause of thromboembolism and stroke
  • increased pulmonary venous pressure
    • pulm congestoion (interstitium) and oedema (alveoli) causing hypoxia
    • leads to PA hypertension through PA vasoconstriction response
  • normal LV pressure, normal aortic pressure
42
Q

What is the trigger for intervention in mitral stenosis?

A
  • well tolerated if mild to moderate
  • development of symtoms or PA hypertension is trigger for tx
43
Q

What are the interventions for mitral stenosis?

A
  • valvotomy - surgical or balloon dilation
  • valve replacement