Leopard
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blueocean wrote:
physiological S2 splitting is exaggerated by inspiration which lowers intrathorasic pressure causing more blood to be drawn from the superior and inferior vena cava; the increase of venous return to the right ventricle means takes longer to empty, leading to an additional delay in closure of the pulm. valve.
So the answer is D.
Very nice
But let us extend the thread
Why there is increase in "afterload of right ventricle " during inspiration ???
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| young_doc
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I have to disagree here...I'm pretty sure it's C.
During inspiration, the pulmonary blood vessels see more O2, hence dilate...this therefore decreases the pulmonary vascular resistance, and DECREASES the Afterload of the Right ventricles. This therefore puts less pressure on Pulmonary valve to close, and so it closes slightly later than the Aortic valve.
The comment about more venous return during inspiration is true, but this would affect preload, not afterload.
Correct me if i'm wrong..
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| young_doc
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And notice how "Increase in Right Ventricle Preload" is NOT an option!!! (cuz that would also have been correct)
=)
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| Leopard
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Young Doc
You want to say the O2concentration goes on changing with each respiration which in turn causes goes on decreasing pulmonary vascular resitance during inspiration and increaseing pulmonary vascular resistance during expiration ???? Not at all dear this is not the reason .Think over it read PVR.
Best of luck
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| drpkaur
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Well guys i have to agree with young_doc ..the correct answer is C..Physiological S2 splitting: inspiration-->decreased intrathoracic pressure--->increased venous return to right heart-->increased right heart preload
therefore right ventricular output is increased,then pulmonary vessels expand and resistance toblood flow from pulmonary artery to rt ventricle decreases(afterload) so that blood flows easily to pulmonary circuit and volume of blood in pulmonary circuit increases....so rt ventricular afterload decreases
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| young_doc
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You got me all wrong Leo...
"The delayed P2 and the early A2 are due to a complex interplay between dynamic changes in pulmonary vascular impedance and changes in systemic and pulmonary venous return.The net effect of these changes is the prolongation of the right ventricular ejection and a concomitant decrease in left ventricular ejection that results in widening of the splitting interval during inspiration."
In other words, IT'S DUE TO BOTH INCREASED PRELOAD, AND DECREASED AFTERLOAD.
And guess what...only one of these is an answer option, and it ain't D!!!
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| Leopard
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Then what is the option??? ,come on young man/lady
Hurry up you are getting late
Best of luck
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| young_doc
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Now i'm just starting to get offended. Read answer C again. It's bad enough that you insult my intelligence in your previous post and tell me to read up on my Physio when i had the right answer, and now this:
"Then what is the option??? ,come on young man/lady
Hurry up you are getting late"
I don't know who you think you are but this is no way to talk to anyone.
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| Leopard
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Sorry gentleman
I was just kidding and you got offended .Again sorry sorry sorry.
But fact is I wanted to let you know the reason for the change in Pulmonary vascular resistance during respiration.Honestly speaking the reason which you told is not true.
Sorry again
GL
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| blueocean
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you are right guys; the answer is C. my explanation was right but my answer was wrong!
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| Leopard
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Let us wait for the correct answer.
But Blue ocean how can you say that during inspiration afterload of right ventricle is decreased?
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| IMMuDoc
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I am new but I totally agree with young_doc. Correct answer should be C or increased preload which is not listed.
And I personally think(may not be correct) that Leopard's explanation is actually referring to increased right Ventricle PRELOAD but not afterload, the explanatoin is PERFECT, but D is not the right summary.
Just my own opinion, No offense to anyone
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| Leopard
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DearIMMUDoc
Pulmonary vasculature is the after load for right ventricle not the pre-load for right ventricle
Correct me if I am wrong .Thanks in advance
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| blueocean
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WHAT THE VASCULATURE DOES WHEN RECEIVE MORE BLOOD?has to relax, so the afterload has to decrease.Anyway if in the possible answer are nor RV preload increases or LV preload decreases ( because the bigger is the volume of RV the bigger is pressure on the IVS and that means the LV volume decreases) the only answer remains C.
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| IMMuDoc
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Dear Leopard,
Sorry for the confusion, I agree that for RIGHT ventricle:
Afterload=pulmonary vascular resistance
Preload=end diastolic volume==system venous return
What I meant was that: During INSPIRATION. Split of S2 is due to
either DEcreased right ventricle afterload(lower pulmonary resistance)
or INcreased preload(system venous return).
You also asked that "Why there is increase in "afterload of right ventricle " during inspiration ??? "
Actually during INSPIRATION, there CANNOT be increase of right ventrile afterload(pulmonary resistance), because lowered intrathorasic pressure and expansion of lung during inspiration cause the dialation of compliant pulmonary vascular system, which furthur leads to the decreased pulmonary resistance(afterload).
Hope I did not confuse you again.
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| Leopard
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Here what I think ,if right ventricular afterload is increased then naturally ejection time of the right ventricle is increased which means delaying of P2.The normal composition of S2 is A2-P2.
Splitting can occur if A2 is earlier or P2 is delayed.
If we increase the afterload of any ventricle then stroke volume is reduced (pleasse refer to Pressure volume curves of the ventricles), ejection time is increased .If this happens to right ventricle then naturally right ventricular emptying is delayed leading in delaying of P2 and cauing splitting.
As far as Pulmonary vaculature resistance (total) is concerned during inspiration and expiration it is increased .It is minimum only at FRC level.Because pulmonarly vascular resistance is related to lung volume (putting aside chemical control).Any deviation of volume from FRC (inspiration or expiration) will increase pulmonary vacular resitance .Please refer to "pulmonary physiology and pathophysiology by John B West page 88 diagram No 6-5
That is why I requested young doc to refer to Pulmonary vascular resistance diagram ,the things will be clear.But he got annoyed.Any productive input will be appreciated.
GL
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| IMMuDoc
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A. "if right ventricular afterload is increased then naturally ejection time of the right ventricle is increased"-------NOT true(ejection time is determined by total stroke volume and flow rate)
B. "If we increase the afterload of any ventricle then stroke volume is reduced (pleasse refer to Pressure volume curves of the ventricles)"--------TRUE(IF preload is the same)
" then ejection time is increased"------------------NOT TRUE (less volume to be ejected, less time needed for ejection, flow rate same or similar under normal physioloyical situation)
C. INspiration-----Decreased intrathorasic pressure----decreased pulmonary artery resistance(dilation)------and increased systemic venous return-------INCREASED right ventricular stroke volume--------longer ejection time-----Delayed P2
(AT the same time)Decreased intrathoracic pressure------increased pulmonary venous capacitance(dilation)------decreased left ventricular filling(decreased left preload, not listed in the answers)-------decreased left ventricular stroke volume-------shorter ejection time----------------Earlier A2
C is what happens in normal physiological situation during inspiration.
Please give it a good thought before you decide not to believe it.
"As far as Pulmonary vaculature resistance (total) is concerned during inspiration and expiration it is increased .It is minimum only at FRC level.Because pulmonarly vascular resistance is related to lung volume (putting aside chemical control).Any deviation of volume from FRC (inspiration or expiration) will increase pulmonary vacular resitance .Please refer to "pulmonary physiology and pathophysiology by John B West page 88 diagram No 6-5"-----------------DO YOU even believe what they said, if so, explain WHY?
Thanks for your helpful discussion.
YL
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| Leopard
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Well this you can appreciate we you look at the diagram.The pulmonary vascualr resistance Curve is U shaped.
FRC = minimum resistance
Decreased lung volume = more resistance
increased lung volume = more resistance
Resistance during increased lung volume >>> resistance during decreased lung volume.
If you get hold of any book on pulmonary physiology have a look on this graph ,then probably it will be easy for us to discuss something further.
Any way I appreciate your time and interest.
Best of luck
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| MRMAVERICK
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| Luckyall
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Totally agree with young_doc...is either an incr in RV preload ( not listed among options) or decr RV afterload !
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| ManuNastai
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You got it all wrong..
the answer is D. The splitting is because the closure of the pulmonic valve is delayed!!! If you tryed auscultating to your hearts while taking a big brath you will notice that the splitting occurs in the 2nd or third heart beat (cycle) after inspiration. (we all know that there is about a 3:1 ratio of heart cycle : inspiration). That is because a increase in right heart preload (which occurs in inspiration) will produce an increased length of the cardiac muscle cells. Frank and his friend Starling say that increased length of fibres generate increased force of contraction, but not from the first contracting following that event. There is about 4 heart cycles before the heart fully copes w/ the increased preload. Following the 4th cycle, the splitting will disappear!
young_doc, try not to get so offended by leopard. this kind of attitude causes atherosclerosis (not that you would be in the age interval at risk  ). try to get some ginko (I heard it helps)
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