Musuq
Forum Guru
Topics: 103
Posts: 425
|
A 72 years old woman came to physician due to an episode of acute substernal chest pain that occurred while she was rushing to catch a bus. She has basilar crackles at both lung bases.S1 is nomal and S2 is decreased.A grade 3/6 systolic murmer is heared best at the upper right sternal border and radiates to the neck.the following data obtained during cardic catheterization were taken before and during excercise:
.................aortic pressure- EDV - ESV - HR
control ...........130/70 140 50 85
excercise ........160/80 165 58 120
While excersicing the woman developed shortness of breath but no chest pain.Which of the following is the most likly cause of shortness of breath?
A) decrease cardiac output during excercise
B) decrease the pulmonary blood flow
C) increase aortic pressure
D) increased end- diastolic pressure of LV during exercise
E) tachycardia
Guys, I know this has been discussed before but nobody really explained it, and I just don't get it, please somebody?
|
| ssrpk
Forum Fanatic
Topics: 154
Posts: 2,796
|
well a, b, c & d are definitely out! so it has to be E!
but i am not too convinced with E as well as to why wud tachycardia be responsible for her shortness of breath!
maybe someone can explain this dilemma!
___________________
life is guud
|
| drfax
Forum Elite
Topics: 21
Posts: 233
|
The answer is D. but why ? at the stem of the Q thy say that the patient has decreased S2 heart sound, recall that S2 is produced by CLOSURE of aortic and pulmonary valves, simply any decreased in S2 heart sound means problem in closure of one or both of these valves, and impairing closure of valves mean regurgitation of blood back into the ventricles which in this case it is obvious that it is the aortic regurgitation because the patient has pulmonary edema by saying(basilar crackles at both lung bases) which means it is accumulation of blood in the LEFT VENTRICLE and consequently leads to backward of blood into the pulmonary veins and INCREASING pressure in the alveolai which is one mechanism of Edema formation, also says at the stem of the Q that the ptn has 3/6 systolic murmur AT THE UPPER RIGHT STERNAL BORDER which is the area that u hear aortic valve problem best. By this pressure at the end of diastole will INCREASE IN LEFT VENTRICLE I hope my explanatio to be write , Enjoy studying medicine
___________________
My best friends are these Gentlemen :Why & How.
|
| neuro312
Forum Newbie
Topics: 0
Posts: 11
|
drfax,
you are missing the point that the murmur is systolic that means aortic stenosis.
If it was aortic regurgitation, the murmur would be diastolic.
it is e.
Explanation for this is, in aortic stenosis since you have decreased cardiac output you have less filling of coronary arteries during diastole. With tachycardia, you are increasing the O2 demand of heart in addition to decreasing the time for diastole by tachycardia meaning supplying less blood to heart.
Also the data from catheterization supports this.
|
| ssrpk
Forum Fanatic
Topics: 154
Posts: 2,796
|
agree, but first and the foremost where is the decrease in cardiac ouput in this case, it has actually increased by 18 % percent! secondly how wud this decrease in coronary flow due to tachycardia cause shortness of breath????
___________________
life is guud
|
| drfax
Forum Elite
Topics: 21
Posts: 233
|
neuro312 wrote:
drfax,
you are missing the point that the murmur is systolic that means aortic stenosis.
If it was aortic regurgitation, the murmur would be diastolic.
it is e.
Explanation for this is, in aortic stenosis since you have decreased cardiac output you have less filling of coronary arteries during diastole. With tachycardia, you are increasing the O2 demand of heart in addition to decreasing the time for diastole by tachycardia meaning supplying less blood to heart.
Also the data from catheterization supports this.
but can u explain why S2 heart sound is decreased ??
___________________
My best friends are these Gentlemen :Why & How.
|
| neuro312
Forum Newbie
Topics: 0
Posts: 11
|
ssrpk,
there is no decrease in CO (Cardiac output) with exercise. The point is, with tachycardia the duration of one cardiac cycle is decreased, right? Ok, and the major factor responsible for this decrease is the decrease in the duration of diastole. That means less coronary filling with tachycardia, causing angina.
Tachycardia is not responsible for the shortness of breath, those basilar crackles are due to back pooling of blood in aortic stenosis.
drfax,
it is due to probable parodoxical splitting of S2. (Although there is nothing about splitting in the question, the decreased S2 seen in aortic stenosis patients is due to this.)
More with Aortic stenosis:
-Most common valvular lesion causing angina
-Most common valvular lesion ass. with syncope with exercise
-Most common cause of microangiopathic hemolytic anemia with schistocytes
|
| ssrpk
Forum Fanatic
Topics: 154
Posts: 2,796
|
the S2 is decreased because, if the valve is stenosed it won't open completely nor wud it close tht apruptly as much as a normal valve!
paradoxical splitting occurs when there is left bundle branch block- in which A2 occurs later than P2, and also it occurs during expiration!
now, CO definitely increases with excercise however it does'nt inc. tht much with aorti stenosis which is why pts present with syncope! and the stage of pulmonary congestion is the last stage, where when pts with aortic stenosis develop symptoms of heart failure,the average survival is from 12 to 24 months and at tht stage even valve replacement surgery is useless!
however in the given question, if it aint tachycardia then none other makes any sense pertaining to the given scenario!
___________________
life is guud
|
| Addicudo
Forum Guru
Topics: 124
Posts: 608
|
It cannot be tachycardia ..
As in the Cardiac Cycle ... Heart recieves it blood supply during Diastole ... !!
And also that diastole time is decreased to a GREATER EXTENT than the Systole during Tachycardia/ Excercise...
Therefore .. IF GIVEN THE OPTION D) .. End Diastolic Pressure is increased .. which is in this case scenario ... lead to a GREATER PRESSURE OF THE VENTRICULAR DURING DIASTOLE .. which will lead to BAD PERFUSION AGAIN ..
However .. Option C) ... Increased Aortic Pressure .. is a good answer .. as .. an INCREASED AORTIC PRESSURE will mean that .. after systole .. when the AORTIC VALVE has closed ... a GREATER PRESSURE IN IT .. willl allow more / good amount of blood to go into the coronary sinus .. and perfuse the ventricular walls better .. !!!!
___________________
... Idle hands are the DeVilS play ground ...
|
| ssrpk
Forum Fanatic
Topics: 154
Posts: 2,796
|
contradictory to all my above mentioned explanations...answer has to be D
lemme try and explain!
whenever there is an increase metabolic demand, blood flow increases which will subsequently increase the cardiac output, now the variables of cardiac output are CO = SV X HR.
therefore, inorder to increase cardiac output there has to be an increase in contractility as well as increase in heart rate.
Normally preload don't increase with excercise, however in congestive heart failure where myocardial contractility is depressed ,ejection fraction decreases, stroke volume decreases while end-diastolic pressure increases [EF = SV/LVEDV], therefore to keep up with the demand of the stroke volume frank-starling mechanism comes into effect and maintain the stroke volume at the cost of increased end-diastolic pressure which will be reflected as increased pulmonary capillary wedge pressure --> dyspnea
___________________
life is guud
|
|
| |
| | | | | | | | | | |
