Physiological responses to valvular disease Flashcards
The heart valves open and close because of
changes in pressure on either side of the valve
(they are not pulled by muscles)
The heart sounds are due to
the turbulence that occurs as the valves close
Systole occurs between which heart sounds?
S1 and S2

What is the normal volume of the LV?
140mL

What is the normal stroke volume?
70mL

What is ejection fraction?
SV/EDV
~50% (lower in heart failure)

What is valve stenosis?
- 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
What is valve incompetence?
- 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
Diastole occurs between
the second and first heart sounds
What situations cause innocent flow murmurs?
- high flow
- children, fever, anaemia, pregnancy
Which part of the cardiac cycle is shortest?
systole (1/3rd)
diastole (2/3rds)
Aortic stenosis murmur is heard
systole, between S1 and S2

Mitral regurge murmur is heard
in systole between S1 and S2

Aortic regurge murmur is heard during
diastole, between S2 and S1

Mitral stenosis murmur is heard during
diastole, between S2 and S1

Patent ductus arteriosus murmur is heard
continuously through diastole and systole

Which murmurs are heard during systole?
aortic stenosis and mitral regurge

Which murmurs are heard during diastole?
Aortic regurge and mitral stenosis

What are the symptoms of mild and moderate valvular disease?
none - cardiac compensation is effective such that even severe lesions can be asymptomatic for many years, until the heart fails
What is critical in the treatment of regurgitation?
- irreversible LV changes occur at the same time symptoms present
- tf valves are operated on before symptoms appear
What is the timing of treatment of aortic stenosis?
- LVH changes (concentric hypertrophy) are usually reversible even when symptomatic
- tf tend to wait until symtpoms appear before operating in stenosis
What is the assessment of valvular disease?
- 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)
What is aortic stenosis?
- 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

What is the left ventricular response to aortic stenosis?
- 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
What is the most common valve lesion?
Aortic stenosis
What are the symptoms of aortic stenosis?
SOB, chest pain, blackouts
Systolic murmurs are (sound)
systolic tf crescendo-decrescendo murmurs
murmur gets louder as the gradient increases throughout the cardiac cycle
Where are systolic murmurs best heard?
over the upper R sternal edge
(crescendo-decrescendo)
What causes aortic regurgitation?
- 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
How does the heart adapt to aortic regurgitation?
- 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

What determines diastolic pressure?
- 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
What is the sound of the aortic regurgitation murmur?
- lub-woosh instead of lub dub
- don’t hear S2 because the aortic valve is not closing
What are the effects of prolonged severe aortic regurgitation?
- decompensation (irreversible) of eccentric/dilated LV hypertrophy
- ++LV diastolic volume
- -LV function
- +LV systolic volume
- when symptoms appear, these changes are irreversible
What causes mitral regurgitation?
- 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)
What are the consequences of mitral regurgitation?
- 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
What are the consequences of prolonged severe mitral regurge?
- eventual decomponsation
- ++LV diastolic volume
- -EF
- +LV systolic volume
- changes coincide with symptoms, irreversible
- tf operate earlier to repair valve instead of replacing it
What are the additional risks associated with mitral regurgitation?
- 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
What is the sound of the mitral regurge murmur?
pansystolic ‘woosh-woosh’ constant throughout systole
due to the pressure gradient between LV and LA
What causes mitral stenosis?
- almost always previous rheumatic fever, esp. in women
What is mitral stenosis?
- 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
What are the consequences of mitral stenosis?
- 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

What is the trigger for intervention in mitral stenosis?
- well tolerated if mild to moderate
- development of symtoms or PA hypertension is trigger for tx
What are the interventions for mitral stenosis?
- valvotomy - surgical or balloon dilation
- valve replacement