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Mitral
Stenosis:
Hemodynamics
Anatomy of the normal mitral valve
The whole valve is like an apparatus, made up
of two leaflets suspended by about 120 chordae
tendinae to two papillary muscles.
The valve is located between the LA and LV and
projects into the LV.
It is essential to note that the whole apparatus
should function properly in order that the valve
functions properly.
It is a bicuspid valve.
There are two leaflets- anterior mitral
leaflet(AML) and posterior mitral leaflet(PML).
The PML has 3 scallops and are named P1,P2,
and P3.
The corresponding areas of the AML are known
as A1,A2 and A3, though they do not have any
scallops.
Mitral valve as seen from above.
The normal valve has an orifice of 4-6 square
cms.
The valve functions as a door, allowing the entry
of blood into the left ventricle during diastole and
closing appropriately during systole to prevent the
back flow of blood.
In mitral stenosis, the valve orifice becomes less
than the normal size.
Minimal mitral stenosis is valve orifice>2.5 sq cm
Mild- 1.4-2.5sq cm
Moderate- 1.0-1.4 sq cm
Severe- <1.0 sq cm
when the valve orifice is stenosed,there is
obstruction to flow of blood from the LA to LV.
Whenever there is stenosis in the valves, there
is development of a hemodynamic entity called
pressure gradient.
What is pressure gradient?
In stenosis the pressure in the upstream
chamber(LA) is really higher than the pressure in
the downstream chamber(LV) during flow of
blood from LA to LV because the LA tries very
hard to empty its blood into the LV.
This is called a pressure gradient.
The mitral valve orifice area and the pressure
gradient are inversely related to each other.
So if valve area decreases, the pressure
gradient increases and if valve area increases,
the pressure gradient decreases.
The pressure gradient also depends on the flow
rate of blood through the chamber.
For a normal valve, as the flow rate increases(as
in tachycardia due to exercise) the pressure
gradient also increases, but only to a little extent.
However in a stenosed valve, the pressure
gradient increases to a greater degree with the
increase in the flow rate, and in severe stenosis,
a pressure gradient may be present even at rest.
Diastolic pressure gradient(mm hg)
Flow rate
ml/sec
The
numbers
0.5,1,2,3,4
and 6
indicate
the area of
the mitral
valve
orifice in sq
cm.
Hashed
area
shows
normal
flow rate.
Now due to the development of a pressure
gradient, the LA has to work really hard to keep
on pumping the blood and hence the LA pressure
gradually increases.
In the initial stages it might be only on exertion,
but later it might be elevated even at rest.
The elevated left atrial pressure is reflected on the
pulmonary veins resulting in pulmonary venous
hypertension and later pulmonary artery
hypertension.
Pulmonary artery hypertension can be of two
types, passive pulmonary hypertension(passive
backward transmission of the LA pressure) or it
can be of the reactive type, in which there is
reflex constriction of the pulmonary arterioles in
response to the elevated pulmonary vein pressure
and the LA pressure.
What are the consequences of this pulmonary
hypertension?
The main result is that it poses a great load to the
RV because it has to now, pump blood against
tremendous pressure continously, and hence after
some time the RV undergoes hypertrophy and
finally dilation.
What will happen if dilation occurs?
Normally the heart is elliptical in shape with a well
defined apex. This shape contributes a lot to the
contractile ability of the heart.
When dilation occurs, the shape of the heart
becomes more spherical and the apex is lost.
The apical shape of heart allows maximum
shortening and lengthening of the muscle fibres
and allows maximum contraction. So if this shape
is lost contractile efficacy will be lost.
It is usually the spiral arrangement of the muscle
fibres that gives the blood a real push towards the
opposite side.
However when the original shape is lost, the
muscle fibres become more transverse and hence
the spiral shape is lost and so the ability of the
heart to push blood in a specific direction is
further decreased.
sometimes due to RV dilation, the tricuspid ring
also gets dilated, due to the movement of the
papillary muscle towards the lateral wall of the
heart.
This type of regurgitation is called functional
regurgitation.
LA undergoes dilation, and that is why it is more
prone to, atrial fibrillation and due to blood stasis,
it is prone to develop thrombi.
The ejection fraction will reduce because there is
less amount of blood coming into the LV( there is
a decrease in the preload).
Pathophysiology: MS
Fatigue/Dyspnea/
↓Functional capacity
↓ MVA
Pul congestionAFib
↑ LAP
↑ LAP transmitted to pulmonary venous system
LA enlargement (compensation to attempt to lower
LAP)
↑ LAP, LAE LA remodelling
LA clot
Exertional Dyspnea
/Pul edema
↑PVR ,PHTN RV pressure overload RVH
RV dilates & fails
With significant obstruction to
flow from PVR & MS
CO ↓ (first with
exercise then at
rest)
Pulmonary Hypertension
Backward transmission of the elevated left atrial pressure
↑ Pulmonary artery pressure
↑RAP & development of right sided heart failure
RV hypertrophy & enlargement
Hepatomegaly &
Pulsatile liver
Tricuspid regurgitation
JVD
Parasternal heave
Prominent v wave
Prominent a wave
TR
Peripheral edema
Loud P2, later
becomes palpable
Pathophysiology
LAE
Atrial Fibrillation
↑LAP precipitate pul edema
 Acute dyspnea
↓Ventricular fillingThromboembolism Palpitation
Stroke
Hoarseness :due to compression of the LRLN by a dilated LA or pulmonary artery (Ortner
syndrome)
High pressure ruptures Pulmonary
vessels :hemoptysis
Thank You!

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Mitral Stenosis

  • 2.
  • 3. Anatomy of the normal mitral valve The whole valve is like an apparatus, made up of two leaflets suspended by about 120 chordae tendinae to two papillary muscles. The valve is located between the LA and LV and projects into the LV. It is essential to note that the whole apparatus should function properly in order that the valve functions properly.
  • 4. It is a bicuspid valve. There are two leaflets- anterior mitral leaflet(AML) and posterior mitral leaflet(PML). The PML has 3 scallops and are named P1,P2, and P3. The corresponding areas of the AML are known as A1,A2 and A3, though they do not have any scallops.
  • 5. Mitral valve as seen from above.
  • 6. The normal valve has an orifice of 4-6 square cms. The valve functions as a door, allowing the entry of blood into the left ventricle during diastole and closing appropriately during systole to prevent the back flow of blood.
  • 7. In mitral stenosis, the valve orifice becomes less than the normal size. Minimal mitral stenosis is valve orifice>2.5 sq cm Mild- 1.4-2.5sq cm Moderate- 1.0-1.4 sq cm Severe- <1.0 sq cm
  • 8. when the valve orifice is stenosed,there is obstruction to flow of blood from the LA to LV. Whenever there is stenosis in the valves, there is development of a hemodynamic entity called pressure gradient. What is pressure gradient?
  • 9. In stenosis the pressure in the upstream chamber(LA) is really higher than the pressure in the downstream chamber(LV) during flow of blood from LA to LV because the LA tries very hard to empty its blood into the LV. This is called a pressure gradient. The mitral valve orifice area and the pressure gradient are inversely related to each other. So if valve area decreases, the pressure gradient increases and if valve area increases, the pressure gradient decreases.
  • 10. The pressure gradient also depends on the flow rate of blood through the chamber. For a normal valve, as the flow rate increases(as in tachycardia due to exercise) the pressure gradient also increases, but only to a little extent. However in a stenosed valve, the pressure gradient increases to a greater degree with the increase in the flow rate, and in severe stenosis, a pressure gradient may be present even at rest.
  • 11. Diastolic pressure gradient(mm hg) Flow rate ml/sec The numbers 0.5,1,2,3,4 and 6 indicate the area of the mitral valve orifice in sq cm. Hashed area shows normal flow rate.
  • 12. Now due to the development of a pressure gradient, the LA has to work really hard to keep on pumping the blood and hence the LA pressure gradually increases. In the initial stages it might be only on exertion, but later it might be elevated even at rest.
  • 13. The elevated left atrial pressure is reflected on the pulmonary veins resulting in pulmonary venous hypertension and later pulmonary artery hypertension. Pulmonary artery hypertension can be of two types, passive pulmonary hypertension(passive backward transmission of the LA pressure) or it can be of the reactive type, in which there is reflex constriction of the pulmonary arterioles in response to the elevated pulmonary vein pressure and the LA pressure.
  • 14. What are the consequences of this pulmonary hypertension? The main result is that it poses a great load to the RV because it has to now, pump blood against tremendous pressure continously, and hence after some time the RV undergoes hypertrophy and finally dilation.
  • 15. What will happen if dilation occurs? Normally the heart is elliptical in shape with a well defined apex. This shape contributes a lot to the contractile ability of the heart. When dilation occurs, the shape of the heart becomes more spherical and the apex is lost. The apical shape of heart allows maximum shortening and lengthening of the muscle fibres and allows maximum contraction. So if this shape is lost contractile efficacy will be lost.
  • 16. It is usually the spiral arrangement of the muscle fibres that gives the blood a real push towards the opposite side. However when the original shape is lost, the muscle fibres become more transverse and hence the spiral shape is lost and so the ability of the heart to push blood in a specific direction is further decreased.
  • 17. sometimes due to RV dilation, the tricuspid ring also gets dilated, due to the movement of the papillary muscle towards the lateral wall of the heart. This type of regurgitation is called functional regurgitation.
  • 18. LA undergoes dilation, and that is why it is more prone to, atrial fibrillation and due to blood stasis, it is prone to develop thrombi.
  • 19. The ejection fraction will reduce because there is less amount of blood coming into the LV( there is a decrease in the preload).
  • 20.
  • 21. Pathophysiology: MS Fatigue/Dyspnea/ ↓Functional capacity ↓ MVA Pul congestionAFib ↑ LAP ↑ LAP transmitted to pulmonary venous system LA enlargement (compensation to attempt to lower LAP) ↑ LAP, LAE LA remodelling LA clot Exertional Dyspnea /Pul edema ↑PVR ,PHTN RV pressure overload RVH RV dilates & fails With significant obstruction to flow from PVR & MS CO ↓ (first with exercise then at rest)
  • 22. Pulmonary Hypertension Backward transmission of the elevated left atrial pressure ↑ Pulmonary artery pressure ↑RAP & development of right sided heart failure RV hypertrophy & enlargement Hepatomegaly & Pulsatile liver Tricuspid regurgitation JVD Parasternal heave Prominent v wave Prominent a wave TR Peripheral edema Loud P2, later becomes palpable
  • 23. Pathophysiology LAE Atrial Fibrillation ↑LAP precipitate pul edema  Acute dyspnea ↓Ventricular fillingThromboembolism Palpitation Stroke Hoarseness :due to compression of the LRLN by a dilated LA or pulmonary artery (Ortner syndrome) High pressure ruptures Pulmonary vessels :hemoptysis

Editor's Notes

  1. Pulmonary hypertension eventually leads to right ventricular hypertrophy and enlargement, tricuspid regurgitation, increased right atrial pressure, and the development of right-sided heart failure. A parasternal heave is detected by placing the heel of the hand over the left parasternal region. In the presence of a heave the heel of the hand is lifted off the chest wall with each systole.A parasternal heave is caused by: right ventricular enlargement, or rarely, severe left atrial enlargement which pushes the right ventricle forwards
  2. left atrial dilatation :increases the risk for atrial fibrillation and subsequent thromboembolism. Paroxysmal or chronic AF :further reduces blood flow into the LV &amp; precipitating pulmonary edema and acute dyspnea. AF may also cause palpitations it causes systemic embolism with symptoms of stroke or other organ ischemia.