Goljan and Mitral Prolapse

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Ihateverbal

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Goljan talks about how decreased preload would cause the murmur (the click) in mitral prolapse to be closer to S1 (when the mitral/tricuspid valves close). Closer to S1 means closer to the beginning of systole.

Wouldn't an INCREASE in preload cause the click to be earlier in systole because of more volume? I don't see the correlation of how decreased preload would cause the click to be closer to S1, and an increase in preload causes the click to be closer to S2.

I would think its the opposite. Anyone have any thoughts on this?

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Goljan talks about how decreased preload would cause the murmur (the click) in mitral prolapse to be closer to S1 (when the mitral/tricuspid valves close). Closer to S1 means closer to the beginning of systole.

Wouldn't an INCREASE in preload cause the click to be earlier in systole because of more volume? I don't see the correlation of how decreased preload would cause the click to be closer to S1, and an increase in preload causes the click to be closer to S2.

I would think its the opposite. Anyone have any thoughts on this?
In mitral prolapse there is a normal preload w/ regurg. It causes a midsystolic click (the presure/backwash causing prolaspe into atria until chordae tendonae are taught), Followed by a crescendo murmur with loudest being at the S2!
 
Goljan talks about how decreased preload would cause the murmur (the click) in mitral prolapse to be closer to S1 (when the mitral/tricuspid valves close). Closer to S1 means closer to the beginning of systole.

Wouldn't an INCREASE in preload cause the click to be earlier in systole because of more volume? I don't see the correlation of how decreased preload would cause the click to be closer to S1, and an increase in preload causes the click to be closer to S2.

I would think its the opposite. Anyone have any thoughts on this?

The best way I've ever heard it explained is that the click always occurs at the same ventricular circumference. Therefore, decreased preload means you get to "click circumference" sooner, putting it earlier in systole/closer to S1, whereas an increased preload means it takes longer to get to "click circumference" and therefore later in systole.
 
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that was pretty sweet, I'm not even sure how i ended up looking at this thread... but that's an awesome way to remember it
 
You know when you've been studying too much when I saw your member name and thought it said MPTP and immediately though of Parkinsons.
 
Goljan talks about how decreased preload would cause the murmur (the click) in mitral prolapse to be closer to S1 (when the mitral/tricuspid valves close). Closer to S1 means closer to the beginning of systole.

Wouldn't an INCREASE in preload cause the click to be earlier in systole because of more volume? I don't see the correlation of how decreased preload would cause the click to be closer to S1, and an increase in preload causes the click to be closer to S2.

I would think its the opposite. Anyone have any thoughts on this?

One of the orevious posters had a good explanation, but here is the way I always thought of it just in case it helps... When you have increased preload you've got more volume in the ventricle that is holding the chordae tendineae/papillary muscles tighter for longer and is thus holding the valve closed longe. Therefore the click and murmur will come closer to S2. Then its just the opposite with less preload
 
The best way I've ever heard it explained is that the click always occurs at the same ventricular circumference. Therefore, decreased preload means you get to "click circumference" sooner, putting it earlier in systole/closer to S1, whereas an increased preload means it takes longer to get to "click circumference" and therefore later in systole.

Along the same line, another way of thinking about this is to remember that in many cases, MVP is associated with myxomatous degeneration (usually excess deposition of dermatan sulfate). This leads to the mitral valves growing and flopping over on each other, which compromises the seal that a normal mitral valve would make to prevent backflow. However, when preload increases, the mitral valve ring stretches (the "circumference" that an earlier poster mentioned) leading to a better seal formation, thus preventing regurgitation until enough blood has been ejected during systole. On physical exam, this phenomenon is observed as the midsystolic click and murmur being closer to S2.

As a side note, stretching of the mitral valve ring in left sided heart failure, for example, leads to functional mitral valve regurgitation.

I hope that's a clearer explanation.
 
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