Squatting will decrease the murmur in mitral valve prolapse and increase

that of hypertrophic obstructive cardiomyopathy.

In First aid step2 CK , it is commented as the squatting increases the
systemic vascular resistance but deceases cardiac preload. However, in
explanation in UW, squatting increases the preload.
This makes me disszy not only because they contradict with each other
but also cause either way can give a nice explanation of the effect of
squatting on murmur.
So plz help me.
Thank you.

Dr.Angina Jan 07, 2011 - 2:16 PM #2

Forum Newbie hi njwwj,

i think ur initial statement is incorrect... b/c
Topics: 1 Squatting actually DECREASES the systolic
Posts: 22 murmur of BOTH MVP and HCM.(squatting
wont increase HCM murmurs as outflow
obstruction decreases...Read on...)
With regards to what happens in Squatting...
Yes it Increases Afterload(increases vascular
resistance)
but mainly, Yes it Increases Preload (more
venous return), [will not decrease preload!!!]

from here on, my reply is long..as it may help

those who always gets confused with such
questions...

The quick way to remember, (n this is how i do

it when faced with a timed exam question)....
For cases of MVP Murmur & its changes with
various activites...I always ask myself.."what
happens to the chordae tendinae with the
given activity" n it gives me all the answers i
want.
Read the following detailed explanation,
understand the logic, then carry the above
ques with u to any exam u face (its my version
of logic, so correct me if any mistakes
exsist..orelse ill go to the exam with the wrong
ideas!!).

First of all..the basics:

a) Decreased preload (Valsalva, standing,
hypovolemia, vasodilators etc)
b) Increased Preload (Squatting, Intravascular
volume expansion, Bradycardia, Beta
blockers ..etc)
c) Decrease in afterload (Hypovolemia,
Nitrates....etc)
d) Increased afterload ( Squatting, Alpha
stimulation, hand grip exercise, Intravascular
vol expansion..etc)

Now, in Mitral Valve prolapse:

Auscultation of a pt with mitral valve prolapse
reveals a Mid-systolic click, followed by a
Late(ie closer to S2) systolic murmur heard
best at the apex.
And in HCM:
Auscultation reveals a Systolic ejection
murmur (typically is a systolic ejection
crescendo-decrescendo murmur) with no
clicks at all. This is best heard between the
apex and left sternal border and radiates to
the suprasternal notch but not to the carotid
arteries or neck

The murmur of MVP (& HCM) is

1) ACCENTUATED(Accentuated for MVP

means=Earlier systolic click and Longer
murmur)by Decreasing Preload; eg. by
standing or valsalva maneuver

The mech by which this occurs in MVP is...both

valsalva maneuver and standing Decrease
Venous Return to the heart thereby
Decreasing Preload. This causes more laxity
on the chordae tendineae which allows the
mitral valve to prolapse earlier in systole,
leading to an earlier systolic click (i.e. closer to
S1), and a longer murmur(more time for more
blood to regurgitate).
(in HCM..decreased preload increases the
outflow tract obstruction)

2) DIMINSHED[ie.in MVP= Later systolic

click(closer to S2) and Shorter/Lesser intensity
murmur] with Increased preload (eg.
Squatting, as is the case in ur doubt), .
[Hint: For MVP....the more filled the
ventricle...the more its wall is stretched...the
more the pull/tightness on the chordae
tendinae..hence, it will be more later during
the systole that the valve will be compromised
n so the click will be heard later(nearer to S2),
& b/c the prolapse is occuring later, this allows
little blood to regurgitate into the LA thereby
decreasing the murmur intensity]
[for HCM,the murmur decreases (not increases
as u mentioned)..b/c this increased preload
causes greater decrease in outflow tract
obstruction]

So, if both MVP n HCM have same ausc

findings with changes in preload, how do we
diff them with auscultation??This is where
Afterload comes to our rescue/or may i say
worsens our lives as we have one more thing
to learn.
This afterload test actually helps to diff b/w
MVP and Hypertrophic cardiomyopathy/HCM
as BOTH of them have a systolic murmur
which Increases on
standing/valsalva/decreased preload(less
preload in HCM...more the obst to outflow) &
viceversa with increased preload.
(note: with other systolic murmurs, a decrease
in preload decreases murmur intensity, so this
issue only arises to diff b/w mvp vs hcm)

So, What happens with increase in

afterload...Murmur intensifies in MVP, but
Decreases in HCM.
How?? By increasing the afterload (eg with a
hand grip exercise)...
In MVP, the intensity of the systolic murmur
increases,(note: not the timing of the systolic
click) as also seen with increased preload.(this
is due to the increased back pressure on the
mitral valve)....
BUT in Hypertrophic cardiomyopathy, the hand
 grip or increased afterload decreases murmur
intensity b/c obstruction in outflow tract
decreases, due to greater pressure gradients
which have to be overcomed across LV outflow
tract to eject the blood,
(... of course the easy way to diff is that no
clicks r heard in HCM, if it is mentioned in
ques)

Summary...
[so, a quick summary for HCM...
if preload decreases...murmur increases
if afterload decreases...the murmur
increases....
whereas if preload increases...murmur
decreases, n
if afterload increases...the murmur will
decrease]

{quick summary for MVP...

Decreased preload...murmur increases
Increased preload...murmur decreases
Decreased afterload...murmur decreases
Increased afterload..murmur increases}

[Also, as said earlier Aortic stenosis has a

systolic murmur, but its intensity decreases
when preload decreases n viceversa, unlike
MVP and HCM].

i hope this helps u..Sorry, for making this too

long.

Edited by Dr.Angina on Jan 07, 2011 - 2:23 PM

njwwj Jan 10, 2011 - 5:20 AM #3

Forum Newbie Hi Dr.Angina,

Thanks a lot for the detailed explanation.
Topics: 5 Yes, I made a mistake at first. Squating
Posts: 12 decrecases the murmur of HCM and MVP
both.
The point of focusing at the effect on chordae
 tendiae is impressive and it helps a lot.
Increased afterload accentuates the murmur
of MVP and increased preload diminishes it,
correct? Then squating, which increases both
pre and after load , accentuates the murmur in
MVP. Does this mean that squating has more
effect on preload?
btw, the nitrates has more effect on
decreasing the preload as long as I can recall :
)

Dr.Angina Jan 11, 2011 - 10:31 AM #4

Forum Newbie hi njwwj... ur welcome!!

Topics: 1 A helpful reminder with regards to focusing on

Posts: 22 the chordae tendinae rule...
REMEMBER..Use it ONLY to solve questions "in
the exam" on Mitral valve prolapse murmurs...
(it saves us a lot of time..)..be careful not to
apply it with MR, u'll get the ans wrong!!

Another quick way to remember effect on

Murmur with preload changing activities is
"whenever preload Increases..ALL MURMURS
(AS,AR,MS,MR and their Pulmonary n Tricuspid
Equivalents) become LOUDER....
EXCEPT....murmurs of MVP and HCM which
become SOFTER ....n viceversa."

Now,
ur RIGHT with these 3 facts....
1) Increasing afterload ( eg. asking the pt to
grip ur finger with both his palms as tightly as
possible while breathing deeply n then
Auscultating) ACCENTUATES MVP murmur ..
( a small point i mentioned in the previous
post about the timing of sys. click not
changing is true, but i dont think it is exam
worthy...)
2) Increased preload DIMINSHES MVP Murmur.
3) Squatting initially Increases preload, AND
eventually/later Increases afterload &
decreases preload

BUT...
"Squatting will DIMINSH/ make SOFTER the
murmur of MVP".( not accentuate it as u
said...why ??...read on.)

im not sure, but I think i know where ur getting

confused...
u seem to know that squatting increases
preload and afterload,
but u cant decide whether to use the preload
effect or afterload effect for determining
murmur changes.

Let me solve this problem for u!! ..its simple

once u understand whats said in next few
lines...

There r 2 scenarios where squatting comes in

usmle step 2...

1) Squatting (or its equivalent Knee-chest

flexion in a supine/old pt) is done as a
maneuver during "physical examination" of a
pt with a murmur/or suspected MVP who is
Asxtic, to test whether we know what happens
to various murmurs with changes in
hemodynamics brought about by squatting...

Here, remember..we(physicians) r actually

sitting n then asking a standing pt to "squat
suddenly"...n all the while we r continuously
auscultating..
now..immediately when the pt squats, he
squeezes blood back to the
heart...INCREASING PRELOAD...it is THIS early
increase in preload that we r trying to take
advantage of during auscultation to determine
what happens to our old murmur... then (in a
minute) we ask him to stand again while still
continuously auscultating..n hear what
changes occur with the now decreased
preload.
2) Children with Tetrology Of Fallot Squat
during dyspneic episodes/Tet spells/After
playing n getting blue lips...etc (because
experience tells them that doing this makes
them feel better, althou some of them say
they do it b/c they know cardiology better than
us ;->)

Note that here, the child "remains" squatted

till he feels better (unlike the earlier scenario)..
what happens here is that..."prolonged"
squatting compresses the femoral
arteries..increases systemic vascular
resistance ..INCREASES
AFTERLOAD..eventually increasing LV
Pressure...making it more difficult for the
deoxy blood to shunt from RV to a higher
pressure LV throu the VSD, instead forcing
blood to go to Pulm Art...lung...gets
oxygenated..improves hypoxia...blah.blah...

So, the point im trying to convey is that

squatting increases preload "initially" n this is
what we use during auscultation of murmurs,
whereas "eventually" the inc. afterload effect
of squatting dominates n this is what brings
benefit to the TOF child, we dont wait for this
effect of squatting to use it in auscultation.
[ if we want to check the effect of afterload on
murmurs, we usually wont ask the patient to
squat for several minutes (althou it works),
instead we ask him to do a hand grip
maneuver n auscultate for murmur changes in
the next few cardiac cycles].

lastly...thanks for pointing it out.. yes...nitrates

MAINLY causes a decrease in venous
capacitance, ie the main action of nitrates is to
decrease preload, this is the mechanism of
pain relief by nitrates in angina. They also
decrease afterload, but we use it in angina b/c
of its preload effect.

( sorry, i forgot to type this obvious fact along

 with the other factors decreasing preload
althou it was running throu my mind at that
very moment...
gosh!! im having flight of ideas....thats why
my posts dont seem to end!! , i hope im not
showing any of the other bipolar sx ).

Bye!!

Edited by Dr.Angina on Jan 12, 2011 - 6:57 AM

Misrati Jan 11, 2011 - 3:38 PM #5

Forum Junior Please be careful guys, the effect of squating

in TOF always like this

both afterload and systemic vascular

resistance will increase

Topics: 43 Preload decreases

Posts: 610
for more clarification please review
this http://www.prep4usmle.com/forum/thread/
104361/

anatomie Jan 11, 2011 - 4:29 PM #6

Forum Newbie well guys i have a different approach that

might help you....this is what i know:
Topics: 14
Posts: 47 murmurs could sound louder or not with
different maneuvers...the question is why?
some say because of preload, some say
because of afterload, etc; here is what i know:
no matter what you do, that murmur will
increase or decrease in intensity only if the
quantity of blood passing through that
'pathology' is different from baseline...more
specific: murmur will increase in intensity if
blood flow will increase and murmur will
decrease if blood flow will decrease! this is the
rule but has only few exceptions(later on)

now.....if we modify preload, the blood flow

towards the heart will be changed; this is the
easiast part and very easy to remember:

increase preload=increase blood flow to the

heart which means ALL type of murmurs will
increase in intensity(or get worse)

decrease preload=decrease blood flow to the

heart which mean ALL murmurs will decrease
in intensity(or will improve)

the only exceptions from this rule is mitral

valve prolapse(MVP) and hyperthrophic
obstructive cardiomyopathy(HOCM) which
does not respect this rule and goes in opposite
direction(increase blood flow will decrease in
intensity and decrease in blood flow will
increase in intensity);

now if we modify afterload....this gets a little

tricky but always remember the rule: increase
blood flow through that pathology makes the
murmur increasing it's intensity and
decreasing blood flow will make that murmur
decreasing intensity; with this in mind, we can
do 2 thinks:

increase afterload(hand shake, alpha agonist,

beta 2 blocker, etc) means
vasoconstriction.....problem here is what type
of murmur you have: forward flow(aortic
stenosis, mitral stenosis, MVP, HOCM) or
backward flow(aortic and mitral regurgitation,
VSD)....this is critical to understand because
murmur will be totally different.

increase afterload for forward flow

murmur=we do a vasoconstriction and,
pressuming that heart does not do extrawork,
less blood will be able to go into vessels which
means less blood will flow through a stenosis
for example; less flow means less
intensity(again, remember the rule) which
mean a hand shake in a patient with aortic
stenosis will make the murmur less intens(or
improve)
increase the afterload for backward flow
murmur (let's say aortic regurgitation)-
pressuming that heart did not do extra work
for pushing more blood in vessels, less blood
will go into systemic circulation....this
difference of blood which should go normally
into circulation will flow back through that
incompetent valve....this means increasing
blood flow through that pathology(aortic
insufficiency)....look at the rule: increase blood
flow=makes murmur more louder which mean
an increase afterload(hand shake/grip) will
make an aortic regurgitation to sound louder

decrese afterload=more blood will flow into

systemic circulation which mean that more
flow will pass through a stenotic aortic
valve=will increase intensity but on a aortic
regurgitation less flow will be able to
regurgitate which mean less blood flow
through that incompetent valve=will decrease
in intensity; for the exam most likely they will
tell us about amyl nitrate or hydralazyne(both
dilate arteries)

i saw a problem with squatting: squatting does

one thing=compress vessels; in TOF we have
a VSD plus a hyperthrophic RV.....normally
some deoxygenated blood gets into systemic
circulation; in tet spells this quantity is higher
than normal.....the kid has to do something to
decrease it.....so the kid will squatt which give
vasoconstriction=increase afterload; this
means less blood will flow into systemic
circulation but the difference of blood which
should go into systemic circulation will flow
into pulmonary circulation through VSD; in this
 way the kid will be less cyanotic in seconds;

hopefully it helps.....

njwwj Jan 11, 2011 - 8:46 PM #7

Forum Newbie Thanks guys!

Both Dr.Angina and anatomie mention the
Topics: 5 difference between MVP and MR.
Posts: 12 It is OK for me that MR has a backward flow
thru the valve but I do not get the point why in
MVP, the flow is forward. Actually, I think MVP
is a kind of MR where the valve is pushed back
into the atrium.
The explanation on different phases of effect
of squatting is very impressive and correlates
very well with the clinical practice. Thank you
Dr. Angina.( I like ur flight of ideas and plzz do
not curb it with lithium)
The algorithm on murmur change by anatomie
is very tightly togical and easy to remember
except the part that MVP has a forward flow.
Plzz explain it.
Also, Misrati ,thank you for bringing out the
discrepancy on whether squatting increase or
decrease preload. I viewed the thread you
gave but cannot find concrete explanation of
this. Would you please give more details?

Dr.Angina Jan 12, 2011 - 7:51 AM #8

Forum Newbie anatomie wrote:

well guys i have a different approach that
Topics: 1 might help you....this is what i know:
Posts: 22
now if we modify afterload....this gets a little
tricky but always remember the rule: increase
blood flow through that pathology makes the
murmur increasing it's intensity and
decreasing blood flow will make that murmur
decreasing intensity; with this in mind, we can
do 2 thinks:

increase afterload(hand shake, alpha agonist,

beta 2 blocker, etc) means
vasoconstriction.....problem here is what type
of murmur you have: forward flow(aortic
stenosis, mitral stenosis, MVP, HOCM) or
backward flow(aortic and mitral regurgitation,
VSD)....this is critical to understand because
murmur will be totally different.

increase afterload for forward flow

murmur=we do a vasoconstriction and,
pressuming that heart does not do extrawork,
less blood will be able to go into vessels which
means less blood will flow through a stenosis
for example; less flow means less
intensity(again, remember the rule) which
mean a hand shake in a patient with aortic
stenosis will make the murmur less intens(or
improve)

hopefully it helps.....

Hi anatomie....thanks 4 ur approach to
murmurs...

according to ur explanation.. both MVP n HCM

shud have a decreased murmur with increased
afterload...
i still have a doubt...shouldnt increased
afterload differentiate murmurs of MVP (where
intensity increases) v/s murmurs of HCM
(where intensity decreases)??...

ill have go back to my books to check upon

this fact...as i thought i learned it this
way..thanks for bringing this to my notice!!
emaadbasith Oct 31, 2012 - 5:49 PM #9

Forum Newbie I came here because I had the exact same

problem as the first person... and after reading
Topics: 0 this forum A lot made sense but there was still
Posts: 4 some controversy with some peoples posts.

After doing some research and talking to a

friend about this, we found a simple answer
that helps with why uworld and First Aid were
contradicting each other.

Squatting INCREASES PRELOAD and

INCREASES AFTERLOAD.

Think about it, if you squat, the FIRST thing to

happen is you squeeze venous blood away
from legs and up into the heart (Increased
Preload)--> Increased Preload means you have
more blood at the end of diastole in the
ventricles --> this means that the heart
musculature must stretch to contain the blood
--> which means chordea tendinea are taught
(stretched) --> and therefore are not as floppy
so the prolapse (floppiness of the valve)
occurs later therefore DIMINISHED MURMUR.

Then after a short while Squatting will cause

the sympathetic nervous system to kick in and
cause Vasocontriction (Increase TPR) -->
Increase AfterLoad (Increase the pressure in
the aorta the ventricles have to surpass) -->
less blood being pushed into the systemic
circulation --> to make up for that, blood will
flow back right away into atrium through the
Prolapse -->ENHANCED MURMUR and earlier
CLICK.

Hope this helps. I apologize for the lengthy

message.

njwwj Oct 31, 2012 - 6:26 PM #10

Forum Newbie Glad to see this thread still interest people
after 2 years!
Topics: 5 Thanks emaadbasith
Posts: 12

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