Posts Tagged ‘lv la pressure cross over’

I  wonder  this  question is being  asked  over many  generations in medical schools ,  yet to be answered clearly. The traditional explanation  given is   ”  mitral valve is  kept  open wide till onset of systole and it closes with a bang due to a long excursion it has to make ”   This concept is no longer tenable and acceptable ( For the simple reason  if the valve is wide open  . . .  hemodynamically significant  mitral stenosis  cease to exist !)

There are  two major factors that determine the loudness of S1 in mitral stenosis

  1. Hemodynamic
  2. Valve structure and morphology

Mitral valve closes whenever the ventricular pressure  curve crosses above the LA mean pressure . This is the pressure crossover point (LV/LA) .

In normal persons it happens very early after the onset of  ventricular contraction  .(ie  the LV pressure has to raise only to  about 8-12mmhg . At this point the LV pressure curve has  certain  force of contraction (Dp/Dt) .Since in mitral stenosis the mean pressure is raised well above normal  (Often 20-30mmhg)  the LV pressure cross over point is slightly delayed  and more importantly occur at a higher  slope  of LV pressure curve  . Even this slight delay adds a punch in the ventricular contractility .The impact of LV contractility on mitral valve closure especially the  AML is forceful .

(Imagine the force of  impact of a  stone hitting you  from a distance of 1 meter from above ,   is different from a stone hitting you from 10 meter above   as it gains the momentum )

The second phenomenon is  probably  more important as it involves acoustics the final step in the genesis of loud  S1  .

The mitral valve need to be  not only pliable  but also the conduction properties should be intact.

Acoustic principles state that even a speck of calcium in the AML  can dampen the sound that is generated  by leaflet motion.

(Try touching a speaker cone while it is playing  .The sound immediately drops and dampens.)

Similarly for S1 to be loud  the valve should pliable without any significant calcification or extreme rigidity or subvalvular  fusion .)

It is important to realize the PML  contributes less to the intensity of S1 . Hence even if some calcium present in PML it won’t  affect the intensity of S1

Other important factors that affect the intensity of S1 include

  • LV function ( Onset of LV dysfunction elevates LVEDP reduces the net gradient across mitral valve )
  • Presence of  mitral regurgitation .
  • Aortic valve disease (Especially AR )
  • Heart rate
  • Rarely associated Tricuspid stenosis make T 1 component of S 1 louder

Final message

The loud S 1 is due to both physiological and anatomical factors  of mitral valve   .The condition of valve may be  more important  for the simple reason , whatever be the hemodynamic  predispoistion  for loud S1 ,  the  prevailing  valve morphology  has a potential to nullify it !


The image modified from  http://www.texasheart.org

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