this is one of the questions of uw...but i cudnt understand the explanation..so plz guys help me wid dis one-

A 46 yr old Caucasian female presents to ur office becoz of easy fatiguability n exertional dyspnea. Auscultation of heart reveals a diminished first heart sound and an apical holosystolic murmur radiating to d axilla. Lungs have bibasilar crackles. There is no elevation of JVP or peripheral edema. Which of d following wud most likely increase forward to regurgitant volume ratio in this patient?

A. Decreasing LV preload
B. Increasing LV contractility
C. Decreasing LV afterload
D. Decreasing heart rate
E. Increasing left ventricular volume

The patient has MR. The question simply asks: what would increase the amount of blood pumped forward through the aortic orifice more than that pumped back into the left atrium.

Answer is C. Decreasing LV afterload.

Because simply when you decrease the afterload (i.e. systemic pressure), there's less resistance to outflow, and so in theory, more blood will likely be pumped forward to the aorta.

A. Decreasing LV preload: decreasing the VR to the LV means a lower left atrial pressure, and so there will be more tendency for regurgitant flow back to the left atrium.

B. Increasing LV contractility: does not necessarily mean that there will be more forward flow, because it would equally lead to increased regurgitant flow, if all other criteria remain unchanged.

D. Decreasing heart rate: would not have a perceivable effect on this ratio. In fact, it may lead to increased VR, increasing LV volume, and more blood going back to the left atrium.

E. Increasing left ventricular volume: see explanation for D.

Yup, or, otherwise, you can look at it like it is in First Aid...

On p. 255 on the 2010 FA, we find that a "Holosystolic, high pitched "blowing murmur" is either Mitral or Tricuspid regurg. It's not in the tricuspid area, so this is mitral regurg.

Okay - Since we've established that, in the description, it says "Enhanced by maneuvers that increase TPR (squatting, hand grip) or LA return (expiration)

So, since this is a regurg, then we know that anything which increases the murmur must increase the BACKWARD flow and therefore the opposite is true for increasing the FORWARD flow.

So, anything which decreases TPR or LA return would decrease the backward flow and therefore the murmur. Decreasing LV afterload would decrease TPR. Tadaa...

I'm not that great with cardiology, but I'll try this out.

So you're told the patient has a holosystolic murmur loudest at the apex that radiates to the axilla = Mitral Regurgitation.
By the way the decreased S1 is because your mitral and tricuspid valves close to produce S1 and your mitral valve is not closing that well because of the regurgitation.
You're also told the patient doesn't have a raised JVP or peripheral edema = NOT in heart failure
What are you being asked? You want to increase forward to regurgitant volume = you want the blood to move forwards to the LV instead of backwards to the LA like it normally does in MR.

What happens in MR?
The mitral valve (between the LA and LV) doesn't close properly. If it doesn't close properly then blood is leaking back into the LA during ventricular diastole (relaxation/filling). This means your LVEDV (preload) is lower than normal because blood that would've gone to the LV is able to go back to the LA. This also means you can't generate as high of a pressure as you would want to in the LV during ventricular systole (contraction) because blood is continually leaking back. If your LV systolic pressure is lower than normal then you have to use more effort to get the blood from the LV to the aorta and you're not able to send as much blood to the aorta during ventricular systole. (This is because blood always moves from high pressure to low pressure in the heart so blood can only move from the LV to the aorta when the pressure in the LV is higher than the pressure in the aorta.)
You want to increase the forward movement of blood (LA -> LV -> aorta) right? So either you have to increase your preload (LVEDV) because it's lower than normal in this case or you have to decrease your afterload (Aortic Diastolic Pressure or TPR). You want to decrease your afterload so that the pressure difference between the LV and Aorta becomes higher which allows you to move more blood from the LV to the Aorta.

Someone please check and make sure what I said is correct. Hope this helps you.

now i get it....i knew d answer just wasnt sure about decreasing d preload thing...but u made it clear....thank u...

i get wat u r hinting n it makes sense...so if dere was an option of increasing d preload n decreasing d afterload of LV,both wud be correct???
but how can we increase d preload????
sorry but i m still confused about dis preload concept....
so now my question is if both these choices come....wich 1 shud we choose???

I would think that decreasing the afterload is better than increasing the preload because if you increase the preload for a long time you may end up with eccentric hypertrophy (dilatation and hypertrophy) and eventually systolic heart failure. I'm not sure how you would just increase the preload without affecting the afterload or any other parameters.

yeah...dats wat i thot too.....
afterload decreasing wud be d better option....thanx

nice!
thanks

I would just like to make a small comment here. Please note that peripheral edema and a raised JVP are signs of right-sided heart failure. In the patient in question, we are dealing with mitral regurgitation, which (though rarely in isolation) can lead to left-sided heart failure. The mechanism is that regurgitation of blood flow from the left ventricle to the left atrium, will firstly cause left atrial enlargement due to increased left atrial pressure, and then, lead to pulmonary edema. This pulmonary edema can manifest itself on a plain chest film, or be revealed as crackles on auscultation, or, in the extreme case, may lead to paroxysmal nocturnal dyspnea and orthopnea.
In the question mentioned above, the patient is noted to have bibasilar crackles in the lung, which may be an early indication of pulmonary edema and hence, left-sided heart failure.

I have a question to you guys. After reading some of the responses, I was just a little curious, because I dont remember the physio too well.


If you slow down heart rate, are you also increasing preload, because you are giving the ventricles more time to fill?

If you are doing that, you are keeping cardiac output roughly the same as it was at a higher HR. Because CO = SV X HR


Just a little confused.

Also, if you give a selective beta blocker, it is slowing HR, but how is BP decreasing?