Okay guys, the next topic that we shall be studying now is by the name of murmurs. The objective would be to talk about diastolic, systolic and then obviously continuous murmurs. Turbulence in the heart is the objective of the discussion. With this, I would first like to. broach up the topic with respect to one of the commonest valvular lesion in a country that is mitral stenosis.
Look at the diagrammatic representation for it. The normal surface area mitral valve is about 4 to 6 square centimeter and if this orifice will become relatively smaller then we call it mitral stenosis. Our definition of severe mitral stenosis would be defined as mitral valve area less than 1.5 square centimeter. Do not answer as 1 square centimeter that is for critical mitral stenosis or severe mitral stenosis the cutoff is not 1 it is 1.5 or lesser.
So in this patient if you see the diastasis part where there is free flow blood into the ventricular you will notice the fact that on the left side the free flow blood will be hampered because of the narrowed mitral valve and therefore two things will happen one the amount of blood coming in the left ventricle will be lesser as you can see in the sketch because of the obstruction and second there will be turbulence or noise generated because the blood is traveling through a narrowed valve you can see here that the image shows that the mitral valve is open and once the mitral valve will open That is when the blood will start going from the left atria to the left ventricle of the patient. So the murmur will always begin once the mitral valve will open and the opening of the mitral valve is known as opening snap. Therefore, in patients who are having mitral stenosis, when you auscultate the patient, the murmur will not begin right at S2. It will begin from opening snap because opening snap is the... time when the mitral valve opens.
A patient of mitral synopsis will also be having a loud opening snap. The reason for loud is that because the pressure here is higher, so the higher pressure will result in forcible opening, much more forcible than what happens in a normal person. So there is a loud opening snap in a patient and subsequently in the patient, the blood would be traveling and would be causing turbulence. So there would be a murmur in the middle of the diastole that would be called as a mid-diastolic murmur and it will also have a small secondary spike. The murmur that is seen in matrosynosis is known as mid-diastolic murmur.
It is not called as mid-diastolic because it is beginning from S2. It is called as mid-diastolic because it is starting from the opening snap. This murmur which is starting from the opening snap will peak in the middle of diastole middle of the diastole and this murmur will also be having a small secondary spike. This small secondary spike will be called as pre-systolic. Pre-systolic because after S1 there is starting of systole.
You see this period is known as systole. So because after S1 there would be systole. So this spike would be called as pre-systolic accentuation. So matrosynosis results in MDM that is a mid-diastolic murmur with a pre-systolic accentuation. Now if we look at the diastole part again I would like to put it like this.
that period between S2 and opening snap, this period S2 and opening snap, this period is known as isovolumetric relaxation. Then from the opening snap onwards, this particular area is the free flow blood into the heart of the patient. This is the diagram that I made before you that you can notice the fact that there is free flow blood into the ventricular cavity. So this would be called as diastasis and then a small remaining part of the diastole. This particular part of the diastole that I have now marked out before you, the remaining part, this is the one which is atrial systole.
Atrial systole occurs in the terminal part of ventricle diastole. You see we all know that when ventricles are relaxing then atria are contracting vice versa. Atria are contracting, ventricles are relaxing.
So here when the ventricles are relaxing atria is contracting, atrial systole. And when atrial systole will happen, when atrial systole will happen, the blood will be again forced through the small narrow narrowed opening. So due to the forcing of blood through a narrowed opening during atrial systole there is a small secondary spike that is known as pre-systolic accentuation which is due to atrial systole. When I am saying pre-systolic it means pre-ventricular systole. So it is atrial systole contributing to this small secondary spike and in the UPSC exam that is combined medical services exam where you get recruitment into railways etc.
There they had asked that in mitral synopsis when would pre-systolic accentuation disappear? Then pre-systolic accentuation would disappear if atrial systole is not happening and atrial systole is not happening in atrial fibrillation. Atrial fibrillation is a condition where there is a twitching of the atria, so there is no power and if the atria will twitch then the spike cannot happen because there is no power generated by the atria of the patient. Pre-systolic accentuation disappears in, that was the question.
The pre-systolic accentuation of mitral stenosis murmur disappears in atrial fibrillation because the atria are twitching in a patient. That is why we say that the pre-systolic accentuation disappears. Also remember the fact that if they ask you about the severity of matriculosis, then severity of matriculosis is not decided by a loud S1, it is not decided by a loud P2, it is not decided by the intensity of the murmur.
Severity of matriculosis is not decided by loud S1, loud P2 or intensity of the murmur. Severity is decided by the length of the murmur. Well common sense here is the opening will become smaller, it will take more time to blood to go from left atria to left ventricle. So length of the murmur, length of the murmur is the main determinant of severity of mitrosynosis. I can just redraw this again.
This is systole S1 S2, then is diastole. They have been made of unequal size because of the fact that systole and diastole do not occupy the same amount of space. Systole will take less time and diastole will take a relatively longer time. This is the opening snap. So the murmur starts from the opening snap then peaks in the middle of the diastole and then the pressure begins to fall but then this is small secondary spike due to atrial systole.
In patients who are having mitral synopsis worsening because the pressure will become higher therefore there will be a earlier opening snap. If the opening snap will become early, I have just shifted the position of the opening snap to early to left. Reason why I'm saying early is because remember the pressure of the left atria is higher. So, higher pressure of the left atria will cause a earlier opening of the mitral valve and therefore, in the patient you can notice the fact that the murmur duration if you compare the murmur and red with respect to the murmur in colour black you will notice that the length of the murmur is increasing. See if you compare the original length of the murmur, if you compare the original length of the murmur.
and the current length of the murmur then there is definitely an increase and the opening snap is coming closer to the opening snap is coming closer to the second hudson severity of material synopsis is decided by length of the murmur or in some mcqs he will write it in a different fashion it will be written as s2 opening snap gap you can notice in the diagrammatic representation that when the length of the murmur will increase then opening snap will come closer to s2 so the gap will reduce both of my statements mean the same severity of metal synopsis is length of the murmur directly gross length of murmur simple english or just to make it sound sophisticated he will say severity of the metro synopsis is decided by s2 opening snap gap in a sense that If the mitral synopsis is more severe, then the gap will become lesser. You can see that S2 will come closer, so the gap between S2 and opening snap is becoming lesser. Both of these statements mean the same.
They just, I would say the examiner is trying to make it look little more sophisticated. That is why you are having these two inputs and both of them basically mean the same. For mitral synopsis of the severe variety, since there is a physical obstruction which is causing extreme pulmonary edema.
we will have to puncture the basalic vein of the patient. From the basalic vein, I will go into the subclavian vein. From the subclavian vein, we move into the right atria. Then we puncture the inter-atrial septum. We go into the left atria.
There will always be a sensor at the tip of the guide wire. So this procedure is obviously done under fluoroscopic guidance. and my objective is to reach this narrowed stenosed valve which is at the junction of the LA and the LV. Once I reach this area that is the stenosed valve at the junction of the LA and LV, then I deploy a balloon here and when this balloon is deployed with force, it will result in dilation of the narrowed valve.
So, I went by puncturing the basalic vein and travelled retrogradely into the right atria via the interatrial septum, we punctured that actually and went into the left atrium. This would be called as percutaneous mitral balloon valvotomy. So, PMBV, percutaneous mitral balloon valvotomy, percutaneous mitral balloon valvotomy is the procedure of choice for patients of severe mitral stenosis. If you read a question that mentions the fact that there is a calcified severe mitral synostasis in a patient.
In calcified severe mitral synostasis in a patient, percutaneous mitral balloon melvatomy is contraindicated because in this particular case, when you deploy the balloon with force, it will cause the valve to break into pieces and the fragments of the valve, the fragments of the valve would go into the brain of the patient. you can mentally visualize that when the balloon will be deployed, the pressure of the valve will cause the valve to break into pieces like a biscuit will break into pieces or I would say like a cake crumbles. Similarly, here the valve will break and there would be a risk of embolic stroke developing in a patient. So, PMBV is contraindicated due to risk of embolic stroke in calcified severe mental synapses.
Similarly, in a question, if he mentions the fact that patient is having severe MS with MR, then the logic is that when you will deploy the balloon severe MS will improve but MR will worsen. Therefore because of the worsening of the MR the procedure would again be contraindicated. Similarly they've asked in the previous years if a patient is having severe metral synopsis with left atrial appendage thrombi left atrial appendage thrombi then in those circumstances when a patient is having a severe left atrial appendage thrombus then in the patient there if you if you dilate the stenosed valve then these thrombi will have higher chances of going into systemic circulation. You see the opening earlier was smaller so there would be lesser chances but now since the opening will become relatively bigger so there would be higher chances of the emboli going into the systemic circulation of the patient.
So there are three contraindications for percutaneous mitral balloon valvotomy and I can just write them again so that we can get the perspective right. PMBV is contraindicated in. The first time it is contraindicated is for a patient who is having a calcified valve because in a calcified valve the fragments can go towards the brain of the patient so calcified mitral synopsis which is severe we are not going to do a balloon dilatation then he says severe mitral synopsis with MR because MR will worsen MS will obviously improve. and then would be severe metral stenosis with left atrial appendage thrombus is again a contraindication for percutaneous metal balloon velvotomy. So metral stenosis is the most common valvular lesion in the country.
That's why I spoke about the treatment part of this also. And remember the fact that the murmur of metral stenosis is heard better in left lateral decubitus position. Why left lateral decubitus? Because when patient will turn to left, heart will come closer to the chest wall. So, therefore the murmur will be heard better in left retinal decubitus.
The diagram I made by Mitral synopsis, this has to be compared with the subsequent set of diagrams and this time I will be describing a different murmur. I will write down the name in few minutes from now, but first listen to the inputs here. The first diagram here shows ventricular systole where the ventricles are generating force and this is causing opening of aortic and the pulmonic valves. So, ATML blood is racing into the aorta and ATML blood is racing into the pulmonary artery of the patient.
But then after few milliseconds later when the ventricles have done their responsibility, the ventricles will relax and aortic and pulmonic valve will close. That's where the problem starts. I am here signifying or showing that aortic valve is closing but is not closing properly unlike pulmonic valve which is closing rock solid. You see the pulmonic valve is closing. efficiently so that there is no leakage of blood back into the heart of the patient.
But in my patient, there is a defective closure of aortic valve which is causing blood to leak back into the ventricular cavity of the patient. So in patients who are suffering from severe aortic regurgitation, the words are severe, where as much as 50% of the blood could be leaking back into the heart of the patient out of 80 ml, 40 ml is coming back. So in severe aortic regurgitation, there is a substantially large volume of blood that is going to come into the heart of the patient.
And some of this blood you can see, like, you know, it's going to hit the mitral valve leaflets also. This is where the mitral valve leaflets are, triglyceride valve mitral valve. So the blood is going to raise back into the heart of the patient with so much of aggression that even it is going to hit mitral valve leaflets. Though there is no disease of the mitral valve, but even mitral valve here is getting accidentally involved in a sense that the blood is racing back into the heart and it is creating turbulence.
It is creating noise. This noise is due to defective A2. That is defective aortic valve closure. So, this is how it is when you will auscultate this patient. You will notice the fact that in this patient, the murmur will not begin from opening snap because opening snap is the time when mitral and tracheosporid valve will open.
So, the murmur will not begin from opening snap. Problem is not in the mitral valve. It will begin from S2. It will peak in the middle of the diastole and then gradually the pressure will come down.
So, this would once again be called as a mid-diastolic murmur. It is called as mid diastolic because the max intensity is in the middle of the diastole. Do remember the fact that mitral synapses murmur starts from the opening snap peaks around this time and then it has a small secondary spike. So this mitral synapses murmur that was discussed earlier has a configuration different from that that I have described at the moment to you. At the moment what I have described to you is. that if a patient is having severe variety of aortic regurgitation, the volume of blood leaking back into the heart of the patient is substantial and this can cause a development of a mid-diastolic murmur in the patient.
This is technically known as Austin-Flint murmur. Austin-Flint murmur is a classical term to describe mid-diastolic murmur or severe aortic regurgitation and the starting point of this particular murmur is from S2, that is second heart sound and not from the opening snap. which is shown in color red belongs to mitral stenosis now just to see whether you and me are on the same frequency uh look at the diagram again and compare with the previous one in this sketch i will be showing mild aortic regurgitation so this is the representation of diastole just be patient give me a few seconds harmonic valve is closing rock solid but aortic valve is not closing properly. So there is leakage of blood back into the heart of the patient, but the amount of blood leaking is very less, very limited amount of blood.
So in this sketch, you can see the fact that I have tried to show mild variety of aortic regurgitation where little bit of blood is leaking back in the heart, let me say 5 ml and not a substantially large volume. Even this patient will be having a defective A2. but you would agree to the fact that in this patient because less amount of blood is coming back therefore the noise in the heart will be lesser previously more blood was coming in so the noise will be relatively more here less blood is coming coming in so the noise would be lesser and secondly the murmur will also last for a shorter duration less blood shorter duration and more blood longer duration so mild aortic regurgitation the murmur can be represented in the following fashion you will you will definitely hear turbulence in the phasor diastole.
But this turbulence which I am now showing before you will begin from the A2 part. A2 is defective. So the turbulence will begin from here and would die down very soon.
This kind of a triangular configuration that I have given before you is known as early diastolic murmur. So in mild aortic regurgitation, because there is little bit of blood going in the heart, the duration of murmur will also be shorter. We are going to call it early diastolic murmur. And in case you just missed it out, I can just do this again on the continental side.
Follow the words. If a patient is having a mild pulmonic regurgitation, there is a defective P2, for example. then in defective P2, little bit of blood will leak back in the heart of the patient and will produce noise. So, I am going to show another murmur here in a different fashion, but with a different color, to highlight the fact that if there is a defective P2 in the patient, then the murmur will definitely occur in a patient.
That would also be called as early diastolic murmur. But, aortic and pulmonic valves do not close together. Remember, yesterday we discussed splitting of second heart sound is best heard at the air spine.
this time lag is about 30 milliseconds. So in case both aortic and pulmonic regurgitation of the mild variety are present in a patient, then mild aortic regurgitation murmur will occur first and then pulmonic regurgitation murmur because there is a time lag of 30 milliseconds between the two. So this would be called as early diastolic murmur.
Time lag of 30 milliseconds is present between the two closure of the aortic and the pulmonic wells. In contrast, the previous murmurs were mid-diastolic. Moving on, if a patient is suffering from pulmonary artery hypertension, then pulmonary artery hypertension in a patient can result in development of mild pulmonic regurgitation. And when pulmonary artery hypertension will cause a mild pulmonic regurgitation, it will result in early diastolic murmur in a patient. I just explained to you the fact that if it is mild pulmonic regurgitation, less volume blood is coming in so the noise will last for lesser duration, so early diastolic murmur.
This information that I have now marked out before you, pulmonary artery hypertension causing mild PR and early diastolic murmur. This representation or this information that I mentioned before you at the moment, this is technically known as Graham steel murmur. So one more classical name, Graham steel murmur.
It is a murmur of pulmonary artery hypertension where there is a mild PR. The pressure in the pulmonary artery is so high that it is causing input incompetence of the pulmonic valve. And because little bit of blood is leaking, so there would be early diastolic murmur.
Now since I squeezed in substantial amount of data in the previous 5 to 7 minutes, I would like to say the fact that I have described to you the topic of diastolic murmurs. This can be artificially divided into 1. early diastolic murmur, a mid diastolic murmur and a late diastolic murmur. For early diastolic murmur, you can remember a small mnemonic by the name of GAP. Here G would stand for Graham steel murmur, A would stand for aortic regurgitation of the mild variety and PR would stand for pulmonic regurgitation of the mild variety. So, gap is Graham steel murmur, aortic regurgitation, pulmonic regurgitation of the mild varieties.
Mid-astrolithic murmur, I would like you to remember two names that we discussed today. Mid-astrolithic murmur is a feature of mitral stenosis, where I had mentioned regarding a small secondary spike of pre-systolic accentuation. And then I described before you a murmur of severe aortic regurgitation that is known as austen-fed murmur.
So, murmur of severe aortic regurgitation is Austin-Fried murmur. Then is late diastolic murmur. Late diastolic murmur is I would say more of a pediatric part because this is a characteristic murmur of rheumatic etiology and this would be called as a Kerry-Cooks murmur.
So, this is a summary table that is to be remembered by you for the topic that we have just taken care of that is diastolic murmurs. Most of the time in the exam, they ask you classical names. So, the classical names to be remembered by you are Graham steel murmur that is early diastolic, Austin flint that is severe aortic regurgitation, this is mid diastolic and then Kerrycombs murmur which is a characteristic murmur of the rheumatic process. Rheumatic chorditis, the characteristic process results in Kerrycombs murmur.
So, these classical names are to be remembered by you. In fact, I can add one more entry in this summary table. I will provide explanation for this in the when I finish this table that is known as a flow murmur and flow murmur I will provide explanation below this, but this can be added to the discussion of mid diastolic murmurs.
I will provide information for flow murmur in the following sense that this can be taken as representation of ASD atrial septal defect in patients who are having a atrial septal defect. as you can see in the representation there would be shunting of blood from left atria to the right atrium this will cause volume overloading of the right atria and of the right ventricle of the patient in patients who are having a asd a atrial septal defect there is a gradient between the left and the right atria which is causing shunting of blood this gradient is only only 4 millimeter mercury so the movement of blood will definitely occur but there will be no murmur because the pressure is very less. So, AST does not have a shunt murmur. Shunt murmur is absent in AST.
Why? Because of the fact that there is a pressure difference of only 4 mm mercury. But in the same patient, because there would be venous return happening during the phase of diastasis, as you can see in the figure, the amount of blood going in the right ventricle, left ventricle will not be equal.
On the right ventricle, there will be more blood going from right atria to right ventricle because some blood in the LA is also coming to the right side and venous return is also coming. So in this patient, this more blood flow across the tricuspid valve, this more blood flow across the tricuspid valve is the one which is responsible for flow murmur. The diagram is that of diastole diastasis.
So the flow murmur will be a diastolic murmur. and diastasis occurs in middle part of the diastole. So therefore flow murmur is a mid diastolic murmur. I have tried to give you explanation for why flow murmur of ASD is called as a mid diastolic murmur simply because diastasis is the middle part of the diastole where the maximum flow will occur across the triglyceride valve of the patient.
In ASD we do not hear a shunt murmur. Why? Because pressure difference is very less and we tend to hear rather a development of a flow murmur which is known as a MDM which will be added to this list and therefore there are three causes for mid-diastolic murmur mitral stenosis, austen flint murmur and a flow murmur. Austen flint remember is a murmur of severe aortic regurgitation.
Mild aortic regurgitation, mild aortic regurgitation will result in development of a early diastolic murmur. Once we're done with these lists we'll take up another disease In this particular topic, I will be explaining to you regarding coarctation of aorta and the murmur that can be seen in the patient. The most common site of coarctation of aorta would be at the aortic isthmus.
The diagrammatic representation for this topic would be in the following sense, that if you look at this particular recording, you will notice the fact that the location of coctation of iota is distal to the subclavian arteries. This is the narrowing. So, if they ask you what is the most common site of coctation of iota, it is present distal to the origin of the left subclavian artery. In these patients, there would always be a development of collateral circulation. From anatomy, you would have studied that these collateral circulation that is represented here will be the intercostal arteries.
So the intercostal arteries of these patients are dilated. The intercostal arteries of these have become tortuous. And these intercostal arteries are the ones which are allowing the transit of blood. from the proximal part of the aorta to the distal part. Now because there is high pressure blood from the aorta traveling via these narrow blood vessels that is collaterals, there will be a noise or turbulence created in auscultation of this patient.
When you listen to this patients, when you do a cardiovascular evaluation of the patient, you will hear a noise which will be present in this patient both in the phase of systole as well as diastole. Since the pressure in the proximal part of the aorta is more than the pressure in the distal part, so there would be a continuous movement of blood from the proximal to the distal part. And therefore in this patient, you will hear a murmur which is heard both in systole and diastole.
And at the same time, the murmur will also peak at S2. So, whenever you get this situation that murmur is heard both in systole diastole and it is peaking at S2 then it is referred to as a continuous murmur. So, remember coarctation of ulta has a continuous murmur and the diagnostic criteria for continuous murmur is heard both in systole diastole and peaks at S2. Hence the causes of continuous murmurs to be remembered by UR as follows.
One of the important causes of continuous murmur I just discussed with you that was coarctation of ulta. which is going to be associated with Turner syndrome. Well this does not mean that the commonest cardiac lesion in Turner syndrome is coarctation of aorta. The commonest cardiac lesion in Turner syndrome should be remembered as bicuspid aortic valve and after bicuspid aortic valve the next one that is seen is coarctation of aorta. The language of the question is most common cardiac lesion in Turner syndrome.
that would be bigas produtigum. Second is coarctation of ureter. Continuous murmur is also read by you in literature of patent ductus ulcerioresis.
This is seen with respect to congenital rubella syndrome. Rubella is a teratogenic virus that can contribute to patent ductus ulcerioresis. Continuous murmur can also be heard in a pregnant lady. now in a pregnant lady if you are hearing a continuous murmur that is basically a memory suffle this is because of increased blood flow which is occurring by the internal memory artery Increased flow of blood through internal memory artery is a physiological finding with respect to pregnancy. So there is nothing abnormal about it.
This is just being discussed because this would be not an answer to a question but would be like maybe one of the pillar choices in the MCQ. Then venous hum. You see dilated veins in the chest can contribute to a sound which will be identical to that of a continuous murmur. So, this does not qualify as a MCQ, but it can be filler choice in one of the MCQs.
Then would be rupture of sinus of valsalva. Well sinus of valsalva rupture will result in communication developing between the aorta and the right atrium of the patient. And due to this communication between the aorta and the right atrium, you can see aorta is positive pressure, high pressure and right atrium is lower pressure.
So, there would be a. continuous flow of blood from high pressure to low pressure radial. Then remember the fact that continuous murmur is heard in peripheral pulmonic stenosis.
I am not saying pulmonic stenosis, valvular pulmonic stenosis will be causing a ejection systolic murmur. I am talking about peripheral pulmonic stenosis. In peripheral pulmonic stenosis, there is narrowing in the pulmonary artery and its branches.
Now the concept is that blood will continuously flow through. the pulmonary arteries of the patient. So, when the blood is flowing continuously from the pulmonary arteries of the patient, if there is a stenosis, it will result in a continuous murmur. So, these are examples of conditions where continuous murmur is to be remembered. I would especially like you to remember 1, 2 and 6 that is coarctation, PDA and then a peripheral pulmonic stenosis in a patient.
Now, remember the fact that suppose a patient is having metral stenosis and metral regurgitation together. Then the murmur in the patient will have the following configuration. In mitral regurgitation, we have is a pansystolic murmur. In pansystolic murmur, the intensity of the murmur remains almost the same all through the duration of the murmur.
So, mitral regurgitation murmur is called as a pansystolic murmur. Whereas, in mitral synopsis, the murmur will begin from opening snap. It will gradually peak. in the middle of the diastole and will have a small secondary spike. You will notice the fact that even in MS with MR, murmur is both in systole as well as in diastole, but we are not calling it a continuous murmur because there are two criteria for continuous murmur.
Criteria number 1, heard in systole plus diastole, criteria number 2, peaks at S2, this is not peaking at S2. So, therefore, MS with MR cannot be called as a continuous murmur. So, is the case for AS with AR. Suppose a patient is having valvular aortic stenosis with aortic regurgitation. Then in aortic stenosis, there will be a ejection systolic murmur.
In ejection systolic murmur, the intensity will rise initially and then would come down, ejection systolic murmur. In aortic regurgitation, let me say it is of the moderate to severe variety, then there will be a mid-diastolic murmur in a patient. that will begin from S2.
So even in this case you will notice the fact that there is a murmur heard both in the phase of systole and diastole but we are still not going to call it a continuous murmur because the criteria number 2 is not getting satisfied that the murmur peaks at S2. On basis of this I want you to remember that combo lesions of AS with AR, MS with MR, PS with PR or TS with TR any valvular combo lesion if given in MCQ you can look at the two diagrams simultaneously yeah. So, ah none of the combination lesions MS with MR, AS with AR, TS with TR or PS with PR, none of the combination lesions will satisfy the definition of a continuous murmur.
And you can also notice that I have just make you revise ah the common murmurs that we have discussed and combination lesions do not satisfy the definition of a continuous murmur. Based on this ah we next look at ah systolic murmurs in a patient. When it comes to systolic vermers, one would be a ejection systolic vermer. The speciality of ejection systolic vermer will be that it will peak in the middle of systole and gradually die down.
Ejection systolic murmur is seen in valvular aortic stenosis. It is seen in pulmonic stenosis. Both aortic and pulmonic stenosis will have turbulence in ejection of blood out of the heart of the patient. The same thing is valid for hypertrophic obstructive cardiomyopathy, which is an example of a subvalvular aortic stenosis or I can mention regarding tetralogy of allot where there will be a subvalvular pulmonic stenosis in a patient. So, all these are examples of conditions where there would be there would be a ejection systolic murmur.
Then is pansystolic murmur. The speciality of pansystolic murmur is that the intensity remains almost the same all through the phase of systole. This would be metal regurgitation and triglyceride regurgitation. And then would be a late systolic murmur.
Like I mentioned a late diastolic murmur before you that is a Kerry-Coombs murmur, I am not describing a late systolic murmur that would be for mitral valve prolapse. So, remember the summary table for continuous murmurs also, where we have artificially subdivided the discussion with respect to ejection systolic, pan-systolic and late systolic murmurs. For late systolic murmur being mitral valve prolapse, the explanation for that I will just provide inferiorly for MVP that is mitral valve prolapse.
To understand matter valve prolapse, I can once say the fact that our aortic valve deflates, they close rock solid. Not a single drop of blood is ever allowed to leak between the valve deflates. The undersurface of our valve deflates will be having anatomical structures by the name of caudate and dinae. And this caudate and dinae is powered by muscles that is papillary muscles.
So, this is caudate and dinae superiorly and this that I am shading black is papillary muscles. the papillary muscles are attached to caudate tendineae on the under surface of the heart valve and the valves are closed very effectively. If this is the ventricular side and this is the atrial side, the pressure on the ventricular side is substantially high on the atrial side is substantially low.
So, ah there is no leakage of blood because the valve leaflets are properly approximated. But if following let me say MI if papillary muscle is damaged. a papillary muscles are damaged then these papillary muscles will not be able to support these anatomical structures which are mentioned here by the name of caudate and dna and therefore if there is damage to papillary muscles then the caudate and dna are not able to support the valvular flats and the pressure that is generated in the ventricles can cause these valvular flats to go up higher than normal this is what i am saying in a normal person you whenever the ventricles will contract with force the force of the ventricles will always cause bulge of the tricuspid well and bulge of the motor valve in upper direction and this happens in all of us that the pressure which is generated in the ventricular cavity will cause opening of the aortic and the pulmonic wells causing a team will go to russian toyota and palmery a tree but there will always be some minimalistic bulge of the aortic and mitral and tragus fluid valve in upward direction due to the pressure generated by the left and the right ventricle now if the valve is going up much much higher than normal if the valve is going up much much higher than normal then i will call it mitral valve prolapse so in mitral valve prolapse there is no leakage of blood initially in mitral valve prolapse there is no leakage of blood The valve deflate will simply be displaced much much higher than normal because the under surface of the valve where caudate and DNA are attached to papillary muscles, the papillary muscles will damage due to any reason.
Papillary muscles why are they damaged or I can just put it here I mean why would you have mitral valve prolapse in a patient? One of the reasons for mitral valve prolapse can be a maxomatous degeneration of the of the of the papillary muscles. After the maxillomatous degeneration of the papillary muscle another cause can be Ashkoff nodules of rheumatic fever. They could be damaging this papillary muscle and caudate tendine complex or it could be ischemia, it could be myocardial infarction or it could be infection like sub-acute bacterial endocarditis.
So, though they can be multiple causes for materval prolapse including defect of fibrillin 1 protein that is Marfan syndrome. So, these are the causes for materval prolapse, maxillomatous degeneration happens to be the leading cause. then could be ash cough nodules ischemia infection fibrillate one defect that is morfant syndrome but all of these are causes for mvp and in mvp what will happen is the valve will go much much higher than normal now let me modify the diagram and remove the normal valprals you can see the valve is going much much higher than normal and future what can happen is that when the valve is going higher higher the value floods will go higher and then they might get separated when the value floods get separated what can happen is that in these patients there could also be leakage of blood across these valve reflux. The leakage of blood will result in this lesion getting translated into mitral regurgitation in the longer run.
So mitral valve prolapse patients, let us see what happens. In mitral valve prolapse, there is development of extra tension in the valve reflux. There is extra tension in caudate and DNA. Since the support mechanism of quadratendina has been damaged, due to this extra tension in the quadratendina when they will be stretched one by one, there will be a development of auscultatory finding of mid-systolic.
The diagram is of systole as you can see above. There would be mid-systolic click or clicks in the patient. The reason for this click or clicks picked up by a stethoscope is that the quadratendina are getting stretched like a rubber band much more than normal. So due to the stretching of the caudate tendineae in the undersurface of the valve which is stretched like a rubber band, there is mid-systolic clicks. In the later part of the illness, you will notice the fact that in these patients, you will not only hear mid-systolic clicks, but there can also be leakage of blood across the valve deflates as shown superiorly.
And this leakage of blood will always occur after the mid-systolic clicks. You see the point is first the valve will go up higher and higher. That is when mid-systolic click is happening.
and then the leaflets will separate that's when the blood will start leaking so you will be having is a generation of a late systolic murmur so mvp in early part of the illness will only cause mid systolic clicks but in the later part of the illness will be causing a late systolic murmur developing in a patient this is explanation for why do you have mid systolic clicks and why do you have a late systolic murmur in any patient of mvp If asymptomatic patient then it is only propranolol but subsequently if there are pulmonary edema features because of leakage of blood across the valvular flats, valvuloplasty would be required for the patient. Propranolol was discussed two times, hypertrophic obstructive cardiomyopathy and propranolol is also useful for mitral valve prolapse. Not that it will treat mitral valve prolapse, it will just reduce the heart rate and increase the longevity of the heart valves.
So to enhance the longevity of the heart valve that is the reason why we are advising a patient for the patient and if the valves are damaged much more than normal because it did not take this medication then valvuloplasty will be useful for these patients. I have today explained to you systolic murmurs, diastolic murmurs and continuous murmurs. Salient names that I would like you to remember are like this.
For diastolic murmurs, continuous murmurs and systolic murmurs. For diastolic murmur, I want you to remember especially for the early one, I want you to remember this name that is Graham steel murmur. This murmur develops in pulmonary artery hypotension where there is a mild pier.
Then I want you to remember amid diastolic murmur classical name that is Austin flint murmur. Austin flint murmur is a murmur of severe aortic regurgitation. Then is Late diastolic murmur, this is going to be encountered with respect to rheumatic valvulitis.
This would be a kerikoums murmur. So, three classical names. For continuous murmur, I think the data is even more simpler. Coarctation of aorta, patent ductus ulterioris and peripheral, the word is peripheral pulmonic stenosis.
This is because when it comes to a systolic murmur, in systolic murmur there can be three possibilities. One can be ejection systolic murmur, pan-systolic murmur and a late systolic murmur. For ejection systolic murmur, it is pulmonic stenosis, aortic stenosis, hypertrophic cardiomyopathy.
Pan-systolic murmur is MRTR and a pediatric heart disease that is VSD, ventricular septal defect. and late systolic murmur i just explained to you that would be metal well prolapse in a patient so i have not made you cram the data like i have not mentioned any i would say a silly way to remember it i have tried to actually explain to you how it is happening so that you can remember this table And, once you remember this table for the types of murmurs, then I also want you to remember that all murmurs decrease in intensity. All murmurs decrease in intensity with Valsava standing and amyl nitrite inhalation. The reason for that is that Valsava standing in amyl nitrate inhalation in a patient, they will decrease the venous return.
So all murmurs will decrease except hypertrophic obstructive cardiomyopathy murmur that will become longer, that will become louder. The word is louder and materval prolapse murmur that will become relatively longer. You can also remember this vice versa. All murmurs will increase in intensity with let me say patient is being made to do sit-ups. If you making the patient do sit-ups, then femoral artery will be compressed and femoral artery compression will result in upgrade of peripheral resistance.
Or there would be a hand grip. If you are shaking. hands with the patient and you are asking him to squeeze your hand with as much as power. So when he is going to squeeze your hand, the muscles of his are contracted.
That will again result in increase in peripheral resistance in the body. So if you increase the peripheral resistance, there is an increase of gradient between the heart and the periphery. If you increase the gradient between the heart and periphery, murmurs will increase in intensity.
Except HOCM and MVP, these two guys are always going to be behaving opposite of what other people do. So, in hypertrophic obstructive cardiomyopathy, the murmur will become softer and in mitral valve prolapse, the murmur will become shorter. So, remember the English words because you see these are very closely rhyming words, louder and longer and softer and shorter. So, they can be errors of judgment. So, I definitely want you to pay attention to the data.
Try to write it down and try to remember this information, either of the two because this will help you in questions where they ask you. impact or dynamic maneuvers on the intensity of the murmur. First remember that the odd men are HOCM MVP.
They always behave opposite of a normal situation. And once you remember that information, then subsequently you can remember the louder and the longer perspectives. HOCM is intensity basically, intensity.
And in MVP, it is rather the duration, which is based on the fact that the mid-systolic click will occur earlier or later. on the pressure that is present in the ventricular cavity. So, this is description for murmurs guys.