1-Physical examination محمد الجندي

Ramadan

technology presentation

Clinical examination

examination

heart disease

failure

congenital heart disease

heart disease.

preventive cardiology

hypertension, pulmonary hypertension,

pericarditis, aortic disease, peripheral

artery disease, venus throbo emolism,

pregnancy and the heart disease,

non-cardiac surgery and then series of

evaluation of the cardiac patient

in form of summing up different

information

preceding it including exercise testing,

nuclear cardiology, hemodynamics,

coronary angiocard CT, cardiac MRI and

new studies

advanced technology

examination. There are several important

things which makes physical examination

still fashionable in 2020. I will

mention two of them

and physical examination is a cheap

technology. It's a lot technology but

it's a cheap technology. So it can be

repeated several times without adding a

financial burden institution.

But more importantly

physical examination if done prudently

done successfully it will help you

selected appropriate investigations.

I belong to a school.

You try your best by physical

examination to reach a final diagnosis,

a semi-final diagnosis or at least a

very narrow differential diagnosis and

then you choose the appropriate

investigations and you see whether the

results of the investigation is matching

results of your clinical examination or

not. If not, this means that you need a

further work up. Let me give you an

example. You examine a patient, you come

to the conclusion that it's a tight

micro stimosis. But you do an echo and

the echo reveals that it's a mild mild

or moderate mital stimosis. then

probably you need to exercise the

patient or look at a different method by

calculating the mital valve area like

continuity equation like or you might

need a three-dimensional echo to map and

find out the mital orifice in a very

realistic way so that's the importance

of physical examination it will never be

up outdated so I will take you to the

first year of the medical school the

cardiac cycle the cardiac cycle is the

iconic diagram

of cardio and it was put in this way by

Carlo Wigger. Carl Wigger was a founding

editor of circulation research and he

was considered because of that or

essentially because he could collected

the various stages of cardiac activity

into this diagram because of that he was

considered the dean of American

physiology. So it's very important. I

know that you are very well acquainted

with the different phases of the cardic

cycle. But let me point out four

important points. First of all, this

point in the left downward corner of the

diagram. At this point you will have

elevation of the left ventricular

pressure. It exceeds the left atrial

pressure and in this way the mitral

valves gets shut. Now spectral analysis

of the heart sound revealed that the

energy produced by shutting the mital

valve is not an enough explanation for

oscultating the first sound. There must

be a higher energy. So as a result of

that experiment experimental

investigators

proposed the following theory. If you

would have the mital valve sh shut then

the base of the heart will be moving

towards the apix. The apex is usually a

fixed structure in the in the heart and

the mobility of the heart and the

contraction of the left ventricle is at

partly because of the descent of the

base. So the blood is moving from the

ventricular cavity towards the outflow

tract but it meets a surprise

surprise

meets the descent of the base of the

mital of the mital ring the mital ring

towards the the moving blood. So the

blood decelerates and this deceler this

this deceleration puts into vibration

what we call the closed cardiohemic

system. What's that? That's the heart

and the blood contained in the various

chambers and it is this of the closed

cardio

system is what is responsible for the

generation of the first sound. As a

matter of fact, this closed theory

hypothesis proposed by Rashimmer several

decades ago is the most accepted, but

it's still a theory. So you might get

some violations of this. Now after the

left ventricular isolomic contraction

period elapses and it exceeds the

diastolic aortic pressure, the aortic

valve the aortic valve opens and this is

a soft opening. You never hear it and

then ejection continues. And the second

point I wanted to call your attention to

is this point the start of the

isopolomic relaxation phase which is co

which coincides with the dicrotic notch

of the aortic box. Now at this moment

the aortic valve the aortic valve and on

the right side the pulmonary valve but

there is a market difference that we

will come to very soon. the aortic valve

closes and this generates the second

heart sound. But again, it is the

deceleration of the blood in the aorta

that's going back towards the closed

aortic valve that puts the cardioic

system into vibration and this is

responsible for the generation of A2 on

the right on the left side of the heart

and P2 on the left side of the heart

with something in between called the

hang out interval that I'm going to

explain very soon. Now as the isopolomic

relaxation phase continues it drops

below the left atrial pressure the mital

valve opens and then active relaxation

in the normal heart brings the left

ventricular pressure curve sub zero

and this is the rapid filling phase and

then we get a diastthesis corresponding

to that the left at empt its blood and

produces the wid descent and remember

this point because This point has

deserved very little attention in the

previously but we will detail many

important points about it. Now the third

point that I want I wanted to call your

attention to is the this point this

point is lead the history where the

Awave produces elevation of the left

arterial pressure and pushes the blood

into the left ventricle and this

generates the fourth heart sound. So the

first heart sound occurs at the

beginning of the isobolomic contraction

period. The second heart sound

particularly A2 will come to P2 very

soon occurs at the beginning of the

isobolomic relaxation period. The third

heart sound is produced by the fall of

the blood from the left atrium being

sucked into the actively relaxing left

ventricle and this causes resonation of

the blood inside the left ventricular

cavity and this produces S3. Now, as you

see from this diagram, I put S1 and S2

at a higher level than S4 and S3 because

the the vibrations and the intensity of

the first sound and the second sound far

exceeds the dull quality of the S4 and

S3. You hear that with the frame of the

stethoscope. You hear that by the bell

of the stethoscope. Now h having said

that I embedded usually many uh

questions in the presentations all over

the course and these questions are very

simple question. They are not intended

to to examine the the scientific

knowledge of anybody but they are

usually

embedded here to keep you engaged into

the discussion that follows the

question. So this simple question says

that classic corroted findings in severe

aortic reg is associated with pulsus or

commands pulsus ppherians pulsus

parasardus and bifid corroted pulse.

Obviously what I am looking for here for

severe aortic reg is pulsus pisperience

and this sets the stage for details

about the coroted position. Now in the

years past we used to palpate the the

the arterial pulse and talk about the

different forms of palpatory findings in

the coroted or the radial or the

brachial or the femoral or other

positions. But now we know that we see

the arterial positions. If you are in

the CCU and you have an intra arterial

canula, you see on the monitor the

arterial pulsations. If you are in the

Kath lab, you see the arterial

pulsation. And hence you need to detail

the morphology of the arterial

pulsations and you will get some benefit

of that in both palpating and inspecting

the pulse wave for. Now as you see here

the normal coroted pulsations here there

is an upstroke called the anacrotic

limb. The steep of the of this upstroke

if it is more steep it means that the

left ventricular contractivity is okay.

So if you have a shocked patients in the

CCU and you find that this is sloping

this way then you give him inotropic

agents it moves to this way then you

achieving your target and then this

moves it to the uppermost part of the

pulse wave here which is called the

tidal wave the blood gets ejected from

the heart and gets reflected from the

upper part of the body. the bifurcations

of the vessels in the upper part of the

body and the peripheral vuscular

resistance in the upper part of the body

and this will get reflected during

history. This is the percussion wave.

This is the tidal wave and then you get

in the

end of ejection you get recoil of the

aorta and this recoil of the aorta will

produce the dicrotic wave following the

dicrotic notch caused by chlor of the

aortic band. Now this dicrotic notch

this dicrotic wave is the outcome of two

things. The recoil of the aorta which

will be impaired if you get aortic

across calcification etc etc and the

reflection of blood the blood from the

lower limbs and the bifurcation of the

superficial femoral the profound and so

forth you get a reflection from this.

Now after that you get a descent a

smooth descent of the flow of the blood

of the pressure of the blood as the

blood moves towards the peripheral. Now

so long as you get a normal vascular

resistance this is the slope. If you get

a low peripheral vuscular resistance

like in certain forms like for example

in septic shock this will be very steep

like that. If you get a high vascular

resistance this will be almost

horizontal like that. The area between

the anacrotic limb and the dicrotic limb

corresponds to the stroke volume. So the

wider

sorry

so the wider the pulse wave form here

the the the better the stroke volume. So

these kind of information if you if you

you observe it in the CCU or in cath can

give you a lot of informations which

cannot be get which you cannot get

easily without understanding the pulse

wave for. Now the question was about the

kind of the pulses. This is a pulse of

of one of the commonest revival diseases

at least in America

the commonest devel.

And what happens here is that because of

the obstruction you get a less slope of

the ascending limb. You get pulsus parus

because the amplitude is less than

normal. So it is pulsus barbus and the

apex or the peak of the pulsation is

So it's retardus as well. How

can we find out that it is by

oscultation? So this this is a what we

call reverse timing. Usually we time the

oscar we findings by palpating the

corroted pulse or the any other central

pulse but actually in under certain

circumstances we do it in the reverse

way. So this is one of the few

circumstances in which we time the

palatory findings by Oscar. So as you

see here in normal pulse you get the

peak of the pulse in the first part of

cy first one/3 of cy three but in pulsus

paras andardas you get the peak of the

pulse in the terminal part of cy.

Now as we move as we move towards the in

answering the question which we asked

this is the pulsa specificance. The

pulserence occurs in aortic grip

upstroke or anacrotrotic limb. You get

two peaks in one one of the peaks is the

tidal volume and the other percussion

percussion wave. The second is the tidal

wave. Remember and notice that these two

waves are systolic events. And because

of the peripheral vaso dilotation, the

descending limp will be more steep. As

you see, it's more steep in comparison

to normal. And the dirotic notch will be

lower down here. Since the pulmonary

artery pressure is lower than the aortic

systemic pressure because of the

pulmonary vascular resistance is much

lower and the pulmonary compliance is

much higher. Then you will find that the

dirotic notch of the pulmonary

circulation is lower than the dicrotic

notch in the systemic circulation. If

you look this is the systolic blood

pressure. This is the diastolic blood

pressure. This is the closing pressure

and in the systemic solution the closing

pressure is one/ird down the pulse

pressure and there is something called

the proportional pulse pressure. What's

the proportional pulse pressure? It's

the pulse pressure divided by the

systolic blood pressure. And what's the

importance of that? If you get this

ratio less than 25%. If the pulse

pressure divided by the systolic blood

pressure is less than 25% it cones that

the cardiac index is low below 2.2 L per

square meter body surface area per

minute. Now this pulserience is

completely different from the bacterian

pulse or the spike and the dome pulse or

the dome and the dark parts. This is are

different descriptions for the pulse of

hypertrophic card. This is the

percussion wave and this is a second

wave. This is not a tidal wave. And in

between you get the obstruction of

hypertrophic obstructive cardiammyopathy

from the opposition of the anterior lip

to the mal against the sector. But under

this circumst circumstances there is no

peripheral vascular dilation. So as you

see here the drotic limp will come

decently down not as steep as what what

occurs here.

Now another form of pulse is pulsus

alternance. Pulsus alternance occurs in

advanced heart failure provided that you

are palpating it in a patient with

regular sinus rhythm and a at a normal

heart rate. Remember that in supra

ventricular tachicardia you got you get

process alternates but this is not a

manifestation of heartbeat. It's a

manifestation of supra ventricular

ticard. So you need to diagnose process

or lens as a manifestation of heart

failure. You need to get sinus not

atrial fibrillation and you need to get

normal heart rate. But if you find it

it's called the death the death rattle

of of the heart. So this is a terminal a

very ominous sign of a very ominous sign

of heart failure. What you feel by your

fingers is a strong alternating with a

weaker pulse. So this is a bad sign in

patients with heart failure. Now we move

to another form of pulsa abnormality

pulsus paradoxis. Now this is very

important. It's a sign of cardiac

tempon. It's not a sign of constrictive

picarditis. It is it's rarely

encountered in constrictive picarditis.

And if you find it in constrictive

pericarditis probably it's an eusive

constrictive pericarditis rather than

guarded variety normal type of

paricarditis. So what do you find? You

find a decrease in the stroke volume in

the systolic blood pressure in the pulse

wave amplitude during inspiration. And

why is that? Under normal circumstances,

you get a normal fall of the blood

pressure less than 10 mm of mercury. But

in in cardiac temponet, if it if it

reaches 15 mm of mercury, you will feel

it in the brachial p. If it reaches 20

mm of mercury, you feel it in the radial

pulse.

Previously we used to calculate the

degree of pulses paradoxis by using the

spig monometer. No longer that's

required. If you feel it in the brachial

you know that it's the pul the degree of

pulses paradoxis is 15. If you feel it

in the radial you know you are above 20.

What's the cause of that?

This is what we call dissociation

between the intrathoracic pressure and

the intracapetary pressure. The intra

left side of the heart capillary

pressure. So if you have pericardial

eusion that's a protection that's a

shield between what happens in the

pulmonary circulation and what happens

in the left side of the heart. You take

a deep breath the intrathoracic pressure

gets more negative. This is freely

transmitted to the pulmonary

circulation. Essentially the pulmonary

veins the flow into the left side of the

heart decreases and the stroke volume

decreases. Now if you don't have a

dissociation between what happens in the

intrathoracic cavity and in the intra

ventricular cavity you don't get pulses

or alternates although you might be

having a strictive phys

right ventricle infuction and right

ventricle inction the right ventricle

suddenly dilates gets restricted by the

paricardium as a result of that you get

a constrictive or a restrictive

physiology but no pulsus paradoxes and

this pulsus paradox toxics does not

occur. Why? Because there is nothing to

dissociate the intrathoracic negativity

from the intra capabilary pressure. Now

this is it's it's important to realize

that this is not a sign of of conricted

pericarditis. It occurs only in 15% of

patients with constricted precarditis

but occurs in the majority of cases of

cardiac template.

Now in 2020 probably inspection of the

jugular venus proxation is at is is is

one of the most important findings in

cardio cardiovascular physical

examination if not the most important.

Now I wanted to call now this is again

wiggers diagram but on the right side of

the heart this is the right antrial

pressure this is the right ventricular

pressure you get two positive waves and

you get two negative waves. Now I know

that you know a lot of information about

that but I wanted to call your attention

to two points. Number one the X descent

and number one the needle of the Y

descent. Now the X descent what happens

here the right ventricity contracts. It

shortens it pulls the base of the

tricusp the tricuspid ring or the base

of the right atrium downward. So the X

descent the depth of the X descent is a

test of right ventricular function. We

are always wondering about how can we

measure the right ventricular function

in the appropriate way. This is one

physical sign that's really helpful in

this context. You get a deep extent.

This is corresponding to the Pepsi in

the echo cardiogram. So this is the

physical sign which tells you about how

there is longitudinal strain or

shortening of the right ventricle. The

deeper the X, the more appropriate the

right ventricular function. Now then you

get the filling of the right atrium

during the vent during

isometric relaxation period of the right

ventricle the triricuspid valve opens

the white center occurs and then you get

this period of diastasis. This is

important because of what because you

many patients with heart failure get

elevation of the general ravenous

pressure.

Now at the end of the Y wave this is

corresponds to the filling a pressure of

the right ventricle. As a matter of fact

cardiologists are very obsessed by

finding the filling pressure of either

ventricle because filling a pressure

will tell you about the function of the

corresponding ventricle and is also

responsible for the symptomatology. If

you get elevated left ventricular

feeling pressure, you get dysmia and

this is symptomatology or you get

manifestations of rightsided heart

failure if you are talking about the

right side of the heart. But what's the

filling pressure? People have divergent

opinion. Is it the end the the post

awave pressure? Is it the pre-awwave

pressure? Is it the early diastolic

pressure? Is it the mean pressure? The

majority of people are proponents that

it is the mean pressure. Now the main

pressure is this segment actually. So

when you never whenever you have a

patient with heart failure and you

diarase him you need a jugular venus

pressure to drop to drop to which level

to to drop to a level of 6 to 7 cm of

the neater of the Yave. You don't look

for the mean jugular venus pressure. You

look for the nater of the Y wave because

that's the failing pressure of the right

ventricle in most authorities opinion.

So as you see on the in the veins you

can get awave you know the various

causes of elevation of the Awave you

know the various causes of elevation of

the Bwave but I like to draw your

attention of the to the importance of

the x descent and the importance of the

wide descent and the importance of the n

of the wide descent. Now let's use this

u information and looking at these

different diagrams. Sorry for the

quality of the diagrams but it will make

the points that I wanted. It will

illustrate the points that I wanted to

make. Now this is the jabular venus

special in patients with constructive

per x descent is deep why it's deep

because the mioardium is healthy. So if

you have a healthy mioardium you get a

good descent of the base of the right

atrium or the tricuspid ring and then

you get a good exent. The fourth common

cause of constructive pericardis

nowadays is radiation following other

causes like idiopathic pericarditis

tuberclois the common cause worldwide

and viral pericarditis. Number four is

radiation periods particularly in

patients being iterated by radiotherapy

for cancer breast and particularly for

leftsided cancer breast where the heart

is immediately below the the radiation

beam

in radiation pericarditis radiation

affects almost every structure of the

heart affects the paricardium the

mioardium the endocardium the valves the

conduction system and the per and

coronas

so under this circumstance senses you

get pericardial constriction but you get

macardial affection. Under these

circumstances the descent will not be

that deep and during the rapid filling

period the heart empties the left atrium

empties into the left ventricle

unimpeded because the shell of the

paricardium at that time is not

constricting the heart the area the area

of rapid period is intact. So you get a

deep Y descent. So a deep X and deep Y

not known to every one of you it's a

sign of constriction but this white

descent is not as free as this as you

can see here in patients who stamp on it

in pericardial eusion you can imagine

the situation as if there is a rubber

band around the left ventricle

preventing it from relaxing effectively

right from the beginning you don't get

emptying of the left atrium into the

left ventricle freely as an obstriction

And as a result of that the Y descent

will not be as deep as in it's going to

be a shallow Y descent. But the X is

deep. Why the X is deep? Because this is

again is a pedicardial disease is not a

micardial disease. Right ventricular

function is intact. So get a deep Xcent

and a shallow center. Now if you get a

restrictive cardiammyopathy the X is

shallow because a longitudinal

shortening of the right ventricle is

impaired here in contrast with

constructive pericotitis and you get a

prominent Vwave with triricuspid this is

very well known to every one of you but

I wanted to call attention to most of

the young doctors to the follow most

most most cases of tricuspid regation

particularly in absence of permanent are

silent you don't hear a murmur or you

hear a very soft murmur on which too

many specialist divergence of opinion.

So how can we detect it by looking at

the neg. So the main side the main sign

of tricuspid the gauge is a prominent

Bwave and the intensity of the tricuspid

regge is judged by the elevation of the

Bwave and it's important to realize that

the absence of murmur on the tricuspid f

doesn't mean anything doesn't exclude

tricuspid regularly

if pulmonary hypertension is not

existing but even if it is existing and

even if pulary hypertension is is severe

you get absence of the Awave and at the

fibrillation and you get canon

awesiation.

I give him an example here ventric card

but heart block is another example but

let me add to one important point

remember the QT interval from the

beginning of the Q wave to the end of

the T-wave and we'll come to that when

we discuss

during this interval the tricuspid valve

is closed so if the atrial activity

occurs it will generate an e so every

nar re-entry ticardia and every re-entry

ticardia in other ways

Short RP ticardia. There is atrial

activity occurring during the closure of

the tricuspid valve. Closure of the

tricuspid valve during the canon the QT

interval. This is called the canon zone.

So they produces irregular canon waves

but at a pos. So this is important

points my messages. We go to the second

question.

Splitting of the similunar valves is

associated with the following

statements. It occurs normally in

expiration. In left bundle branch block

it occurs during inspiration. In right

bundle branch block it occurs during

inspiration and expiration and is

greatest or loudest in severe stenosis.

The appropriate answer I'm looking for

is number C. Right bundle branch block.

The splitting of the second sound occurs

in inspiration and expiration. And that

leads me to discussion of the heart

sounds.

The heart sounds, the first heart sound

is composed of a mital component and

recuspic component. The second heart

sound is composed of aortic component

and pulmonary component. We know that

right sided val

earlier and they close last. And what

happens in inspiration? Increased Venus

return increased the preload the mital

and the tricuspidal valve gets widely

separated but this degree of separation

is just 20 to 25 millisecond for the

average ear and average temporal lo you

cannot distinguish this splitting some

people try to convince us they hear the

split second first sound that's okay but

that's not the common thing but this is

in contra distinction to to the second

heart sound the second heart sound

occurs a2 occurs before P2. And why is

that? Remember when we talked about the

second point on the WERs diagram, we

talked about when we started the

isopolomic relaxation period on the left

side of the heart, the aortic grad

closes and that produces whatever it

produces to to result in A2.

But what happens on the right side of

the heart is completely different. At

the beginning of the isovolomic

relaxation period,

the pulmonary valve doesn't close. The

blood flow from the right ventricle

continues to flow into the pulmonary

circulation despite the start of the

isoblomic relaxation. And why is that?

That this is because the compliance of

the lung prevent the the the

closure of the pulmonary ve the

compliance is in is why is increased. So

the blood continues to flow and as a

result of that P2 occurs a certain

interval after E2. This per period, this

time period between the closure of the

pulmonary valve and the closure of the

aortic valve is called the hang out

interval and the reason is the

continuing flow of the pulmonary blood

of the pulmonary blood despite the fall

of the right ventricular diastolic

pressure below the pulmonary pressure.

Now if you take a deep breath the penis

return will increase the blood flow

across the pulmonary circulation will

increase and A2 and B2 will widen. So

the hang out interval will increase it

can reach to 60 milliseconds that's all

and vice versa during expiration.

So paradoxical splitting is a situation

is always pathological and is a

situation in which P2 occurs first. A2

is delayed. Why it's delayed? Because

there is delayed activation of the left

ventricle like in patients with left

branch block like in right ventricular

pacing like for example if you have um

uh an aortic stenosis. So as a result of

that type BW WBW also there is a delayed

activation of the lift vent or you have

a prolonged ejection actually prolonged

pre-jection period if you have an aortic

stenosis the ejection period will be

elevated if you have patient patients

with heart failure the pre-jection

period will be increased the ejection

period will be shortened but the time

from the start of contraction and the

closure of the second will be prolonged

So always when you get paradoxical

splitting you are going to have an

unfysiological situation persistent

splitting occurs in right border branch

block and the pulmonary hypertension and

we will detail that very soon and you

get fixed splitting in atrial sector

defect because it's well known that

increased Venus return will be balanced

by reciprocal diminion of the sh across

the atrial circle.

Now let us detail about what happens in

the stoolic periods. In the astrology we

have the third heart sound and the

fourth heart sound. And since the the

both of them both of them are diastolic

events they do not correlate with the

ejection fraction. The ejection fraction

is a systolic event. Hearing a third

heart sound or hearing a fourth heart

sound does not let you guess what's the

ejection fraction. It gives information

which we are going to detail now but it

doesn't tell you about the uh the

ejection fraction. Now let's see what's

happening during third sound. Tell our

son if the patient is below the age of

30 and he does not he does not he does

not have any manifestations of cardiac

disease no cardiac enlargement no

ejection click no diastolic mm no

paradoxical splitting then it's

physological with the age of 30 and

there is no company that it keeps with

it no evidence of other disease it's

it's physiological now the genesis of

the of the third found under

physiological circumstances is different

from LCGenesis under pathological

circumstances. Here the active

relaxation of the left ventricle brings

the left ventricular pressure curve to

sub zero and then there is an area

between the left atrial pressure and the

left ventricular pressure. The left

ventricle being actively relaxing so to

speak sucks the blood from the left

atrium and produces the resonation into

the left ventricular cavity responsible

for the generation of the third heart

cell. But if we have heart failure with

systolic dysfunction or preserve it

systolic dysfunction or preserve its

systolic function then we will find that

there is elevation of the left

ventricular thetoric pressure. The left

atrial pressure is even higher and the

left atrial pressure has to push the

blood rather than to suck the blood in

this under this circumstance. But both

of them both of them are related to this

period of the cardiac cycle. Both of

them are manifestations of filling of

the left ventil whether it's being

sucked or whether it is pushed. Actually

what differentiates between whether it's

a physiological third sound or

pathological third sound is two things

age below 30 age above 40 but more

importantly the company it keeps here we

get manifestations of heart disease

cardiac enlargement symptomatology

patient is having either stoic murmur is

having pathological clicks and so forth.

The fourth heart sound corresponds to

the late diastolic event. This is the

occurrence of atrial activity pushing

the blood into the vent. Remember it's a

ventricular phenomena. It's not an

atrial phenomena. It's related to the

atrial contraction but is not caused by

the atrial contraction. If you have a

stiff ventricle like in patients with

hypertension like in patients with left

ventricular hypertrophy then you get

stiff ventricle atrial pressure rises

pushes the blood but resolution occurs

in the left ventricle and as a result of

that you get an S4. So S4

previously we saw that S4 in old age is

a physiological phenomena. This is

extremely doubted. You can safely say

that S4 is always pathological. S3 can

be physiological and can be pathologic.

Remember S4 disappears in atrial

fibrillation. But there are other

situation in which you can never get an

S4. Micro stenosis is one of them. You

cannot get transmission of the left

atrial high pressure to the left

ventricle being protected by the

stenotic mal. Another situation is

constructive paraglides. Impossible.

Why? Because most of the blood filling

the left ventricle occurs in early area

in the rapid filling period and there is

small remaining amount of blood in late

diast. So there is no need for the atria

to contract strongly. So atrial

fibrillation consecutive pericarditis

per menosis are these are the important

three conditions in which you don't get

an S4 impossible.

Now is S3 the only early diastolic

sound? No. You can get an opening snap.

You can get a tumor plot. You can get a

pericardial knock. Previously, we can

get the the opening sound of uh the old

kinds of prosthetic valves. All of these

are early diastolic feelings. What about

pulmonary P2? P2 gets accentuated in

pulmonary hypertension. But remember

from the start that the degree of

loudness of the pulmonary component of

the second heart sound doesn't have

anything to do with the degree of

elevation of the pulmonary arterial.

Number two, what about the splitting of

the second heart sound? The important

feature of pulma hypertension is

accentuated P2. If it is held on the

apex, it's accentuated because normally

it is not heard except on the pulmonary

area. If it can travel to the apex, it's

accentuated. Whether the second art

sound is closely split, is single, is

widely split or normally split. The four

conditions occur in perman hypertension.

Let me give you examples. In the garden

variety, common type of perman

hypertension particularly the early

stages, it's closely split. the hang out

interval gets

shrunk because of the increased

stiffness of the lung and the pulmonary

circulation. But in another condition

like for example as a minger VCD it's

single

if you get pulary hypertension with

pulmonary artery dilation

then under this circumstances you get

normally splitting the hang out interval

gets normal because of the increased

compliance of the pulmonary circulation

and you sometimes you get wide splitting

pulmonary embolism is an is an example

in pulmonary embolism the right vertical

fields pre-jection period of the right

until it gets prolonged. P2 gets

delayed, pulary hypertension is there,

but the second out sound is why it is

split. So the degree of splitting is not

that important in diagnosing pulary

hypertension. It is the accentuation of

P2. If it's heard over the apex, then

you know it's loud. If it's loud, you

cannot predicted the degree of elevation

of the pulmonary artery pressure under

this circumstance.

Now let's question. A 60-year-old female

presents with vague non-exertional chest

pain. She has a history of long murmur

but has been asymptomatic until

recently. S1 and S2 is normal

physiological splitting of the second

sound. There is a midstoric click heard

over the apex and preceded and preceded

onetoric me and the important thing is

is coming here. Now upon rising promptly

from the sitting to the standing

position the systolic leaks moves early

in history and the memor gets longer

and longer and more longer. So everyone

knows that this is mital valve prolapse.

The clinical findings are most

consistent with hypertrophic cardopathy

cannot be because there is a click

innocent cannot be because there is a

click mitral valve prolapse with mild

malage that's the appropriate answer by

cusp aortic valve and severe aortic

stenosis this is an injection click and

not an injection click so that

introduces us to the historic mas now

the most important is to find out

whether this historic murmur is innocent

or functional m is a pathological memor

The American Society of Echo

cardiography in insists that you

investigate by echo systolic mm that are

pathological. And the class three

recommendation is to put the patient for

echo study when he has an innocent

murmur. The innocent murmur is usually a

short murmur. It's usually grade one to

two in intensity. It's held at right

sternal border. It's systolic ejection.

If you decrease the payload, for

example, by letting the patient stand

up, then usually it decreases in

intensity, it has no other pathological

features associated with it. No

diastolic murmurss, no abnormal sounds,

no gallops, no clicks and so forth. No

cardiac enlargement. Now

there are very important functional

mess. Aortic sclerosis for example in

old age this is a functional systolic m.

But remember

10 to 25% of patients with aortic

stenosis will end up having aortic

stenosis and many of them will undergo

surgery or that's one thing this is in

contra distinction to the situation with

bicuspid aortic valve bypid valve the

murmur is not a an innocent m but

remember as a corerary that this

bicuspid aortic valve if you have a

bicuspid or valve and you reach the age

of 60 or

then sure you will be having either a

severe aortic stenosis or severe aortic

regation that needs intervention. So the

situation is different between our

screws and our andobic our now we have

other conditions in which there is a

function historic murmur in infants on

the other hand and in children you have

a steel's m still murmur is a vibratory

murmur sometimes it has a musical

character heard along the right sternal

border we don't know whe what is the

origin of it the proposal is that it's a

vibration of the event or a false tendon

in the left ventricle.

Sometimes we hear a cervical venus hum

in my professional life I didn't hear a

cervical venus sound I read about it now

the cervical venus hum is a continuous

me with a more prominent story component

and is heard in the supraclavicular

fossa and to the right of the sternum

and gets louder when the patient moves

his neck to the left side of the heart

it's due to acceleration of the blood in

the venus system but it's extremely

so That's enough about systo functional

systolic memor. Now we go into the

clicks. The we have two types of clicks.

Ejection clicks and non- ejection click.

You should be able and find out the

difference by palpating the corroted

pulse. If it occurs at the rise of the

corroted pulse in the anacrotic

anacrotic limb then you ought to think

of bicuspid aotic valve or bicuspid

pulmonary valve and I detailed the

importance of bicuspid aortic pad

autotoal dominant disease with low

penetrance 9% inherence our non-

injection click the common by far my

drug prolapse differential diagnosis

will be ventricular analysis at

receeptal analysis cardiac tumors pulary

hypertension and systemic hypertension

and important to notice all rights sided

phenomena increase with inspiration

except one thing the systolic ejection

click of permanent origin. Why is that?

Because if you take a deep breath then

the atrial complexion at that time with

the deep breath will increase the

ventricular pressure and opens the

pulmonary valve partially. Now systolic

ejection starts now. So it opens it from

the partial open position to the

complete open position. So that doesn't

produce sound or produces a faint sound.

So the only right-sided phenomena which

decreases with inspiration or the with

increase the preload is the pulmonary

ejection click otherwise everything on

the right side increases with

inspiration particularly tricaspid

what's called carval side.

Now we go into the systolic murmurss.

Most prominent among these is mitral

regurgitation which comes in two flavors

acute and the chronic and they are

completely different. Now the acute

mitral reg you get a very short systolic

m as a matter of fact most of the time

we don't hear it. Why is that? Because

the left ventricular

the stoic pressure will be high and

during ejection it will eject the blood

into the left atrium which is not

dilated and as a result of that the

pressure in the left atrium is high. So

the gradient builds up into the left

atrium very quickly and the merma is

short and determinates here in midtory

or but more importantly these patients

are usually in pulmonary edema. So you

have a lot of crackers, a lot of

bubbles,

wheezes over the chest which should

prevent you from hearing this up. Now

how how can we detected this condition?

If you find a patient with myocardial

infarture or an acute event including

the trauma and the calf ventricle

despite that is hypercinetic.

Be careful to look for a short systolic

murmur and investigate for that because

that might be an acute m regurgitation.

In acute micro regurgitation like in any

micro regurgitation we get third heart

sound but a specific entity here is a

fourth heart sound. Previously we

explained this for heart sound that the

left atrium gets angry indignant and its

contraction produce this sound. But

probably this sound is secondary to

eskeia which is underlying it of the

acute malage. Now the situation is

different from chronic malage where you

get a panctoric me. Everyone knows about

that. But why I want to make a point

here you know everyone knows that this

historic advanced historic memor starts

early here in history. So there is no

isolomic contraction period but it's not

very well known to many of you that it

overlaps the aortic component. Another

feature of the pancistolic memor is that

if this is A2 it ends after A2. Why is

that? Because at the time of closure of

the aortic valve there is still a

gradient between the left ventricle and

left atrium and the blood continues to

flow. So as a result of that it starts

very early and it terminates after a2.

So these are the same quanton features

of a panctoic me in compar distinction

to the short systolic m of acute mage.

And here is the the key differences

between acute and and chronic microage.

These patients are sitting upright

because of the pulmonary edema. They

have rolls all over. They have a short

or a subtle murmur in contra distinction

which happens in chronic mary. You get

left ventricular enlargement. You get

pulmonary hypertension or very minimal

pulmonary findings due to congest

chronic congestion. Not the pulmonary

edema findings here. and you get a third

heart sound that might be palp remember

if you palpate a gallop it's

pathological situation now it's very

well known that you can identify which

leaflet is pathological if the if the

mermma is radiating to the sternal

border it's the the the

posterior leaflet if it's radiating to

the axilla and to the back the anterior

leaflet other causes of holy systolic

murmur including the tricuspation and

vvelic defect remember that mitro reg

the systolic mammar gets accentuated by

increasing the afterload you elevate the

blood pressure by kinking femoral artery

or by squeezing your fists hand grip

they increase but truspid

increases by increasing the preload you

take a deep breath and it increases

now this tells us the physical findings

that are diagnostic of mital verd prolap

It's a confusing situation but if you

find this physical signs which might not

be present in every case but they are

present it clenches the diagnosis

irrespective of what. Now if you squat

actually what you do is increasing the

preload and the after load. You kink the

femoral artery and that increases the

afterload or the pressure and you

squeeze this planking circulation. In

this conditions you increase the penis

return or the preload. As a result of

these two events, you increase the left

ventricular size. The prolapse will

occur later. The liquid moves later and

then the mmer will become shorter and

usually fainter.

If you stand then the opposite occur.

The preload will decrease the after load

will decrease. Left ventricular size

will decrease the click comes earlier

the murmur will become longer and will

become louder. And that's important. Now

the same changes occurs in hypertrophic

but there is no click in hypertrophic.

So finding the click sculptating the

click making sure it's existing can

differentiate between these two

situations which can be confused with

each other. This leads us the commonest

murmur abroad is aortic stenosis murmur

historic ejection murmur classic

teaching is that if you have the peak

delayed then you have a severe aortic

stenosis but at that time we didn't know

much about stage D2 and D3 aortic

stenosis aortic stenosis with low flow

low gradient types of aortic stenosis

under this circumstances you might get

severe aortic stenosis is a faint murmur

with an early peak. So this murmur is

classic for the unusual types of aortic

stenosis but not classic for the unusual

forms what we call stage D2 and D3 or

the low flow low gradient aortic

stenosis. But a constant feature of

aortic stenosis is the weak faint or

absent A2. You get the val sclerotic.

You get the val fibrotic get the

valified A2 disappears. But generally

classically you get here an delay

ejection m delay and ejection systolic

mm great peak weak A2 means the presence

of severe aortic stenos. But what about

S4? S4 cannot be used to identify the

severity of the aortic stenos. These

patients very commonly have eskeemic

heart disease have associated chronic

heart disease. S4 might be a reflection

of that rather than the severity of the

aortic stenosis. Now here she shows us a

conditions of severe aortic stenosis

where the murmur goes all the way and

even it drowns the P2. A2 is delayed. So

if P2 occurs earlier and there's a

paradoxical splitting. How can we know

that? Take a deep breath. P2 moves

towards A2 and the ner splitting gets

narrow. Usually we don't give attention

to paradoxical splitting but sometimes

they are very helpful signs in clenching

the diagnosis. You might say that let's

do an echo for the patient but you can

do an echo and you get confusion. You

can do an echo and your clinical science

say that this is severe.

The echo says no. Now under these

circumstances you can go back and do an

echo with another windows from the right

sup right parna from the supraclav by

the ped

probe from the subternal angle you might

like to do a transopial you might do a

palmmetry by 3D and do different things

and can you can check your physical

signs as well so on either way you don't

use them physical signs against

investigation as competitors but as

complimentary and as a checker of each

one against the other.

Now in hypertrophic cardiammyopathy

which is a very common condition the

apex beat is either pifid or triple and

the triple it's called it the triple

ripple the triple pulsations is due

prehistoric gallop and then two

pulsations one before the injection

before the obstruction in the outflow

tract and the second after the

obstruction of the outflow tract. Now

this is important. Why? Because every

now and then we examine athletes and

there's a confusion between the physical

findings, electroc cardioraphic

findings, investigation findings between

hypertrophic cardmopathy and the athlete

arm. Simple physical examination if you

find triple ripple it clenches the

diagnosis cannot be present in the

athlete.

An important thing

in in hypertropical neopathy is a

presence of a loud murmur. Usually the

murmur is loud and anything which

shrinks the left ventricular volume

accentuates the murmur. This murmur is

commonly heard in the sternum but the

associated mal regurg because of

movement of the anterior leaflet of the

mital valve generates another murmur

goes to the axilla and even to the back.

But the important thing here is the

effect of the strain phase of our salva

maneuver. By the way, Balva was an ENG

specialist has nothing to do with

cardology and he was you used the

maneuver of straining it to discharge

bus from the middle ear but somehow how

it found its way to cardiology and is

being used frequently for

differentiating the types of Mer. Now

during the strain phase venus return is

hampered preload is diminished. This

diminishes the murmur of valvular

stenosis because the flow will diminish

but will shrink the ventricular size

increase obstruction and decreases the

murmur. A my nitrite is no longer used

or PVC does not differentiate. So the

differentiation between a stenosis and

hypotropical neuropathy is essentially

by realva maneuver during the strain not

the release phase. And this brings us to

dynamication. We have a variety of

things am I tried we don't use them hand

grip hand grip we usually do it by

making a hand grip of both arms and try

not to use the the the diaphragm of the

stethoscope because it might make a

friction against the contracting

pectoralis major use the belt and make

sure that you are not hearing the

contraction of the pectoralis major if

you do a handicap it increases the blood

pressure increases the afterload as a

result of that mig increases aortic gage

diminishes and under these circumstances

the left ventricular cavity increases.

So the obstruction will diminish and

hypertrophic cardopathy will decrease

and as we said vulva will diminish the

preload during the strain phase and

differentiates between our stenosis and

hypertrophic cardia but the square to 10

is is the most important findings to

differentiate these three uh

pathological conditions. is not sitting

to stem. It's squat to stem. You cannot

get much differentiation between sitting

to stem. Now if you squat, you kink the

femoral artery and so you increase the

afterload. You compress the splanking

circulation you increase the preload and

these two conditions will increase the

mm of my will decrease the m of stenos

and hypertrophical.

So when hypertrophic nemopathy if you

squat you increase the left ventricular

size the dimensional obstruction you

diminish the murmur now you stand up the

reverse occurs the murmur increases

while the other two there is no change

postVC is important if you find a long

cycle whether it's an atrial

fibrillation long cycle or the whether

it's a PVC after it there is a post PVC

compensatory period in which you during

this condition you get increase in the

afterlow Because of the reparation of

calcium during the PVC you increase

contractility and this conditions this

PVC with a long cycle operate you will

find under this circumstances in this

contractility. So the murmur of

hypertrophic cardopathy increases

because of increased contractivity but

it doesn't affect the murmur of mital

gage always the gradient is very high

between the left ventricle and the left

atrium. So this minimal changes doesn't

affect it. So remember post pregnancy or

long cycle lateral fibrillation

differentiates between the murmur of

mital reg and hypertrophic myopathy but

unfortunately you might get the two

situations.

Now this leads us to diastolic mmmers

aortic regurgitation remember in aortic

regurgitation it's not early diastolic

murmur only it's an early diastolic

murmur and historic murmur. So this is

the two and through murmur of aortic

regation and again we get aortic

regation in two levels chronic aortic

regic murmur the length of the murmur

rather than the intensity of the mar is

what determines the severity of aortic

reg but the most important findings in

aortic in pre-awortical gage is a white

passion you can never get a severe

aortical gauge uncomplicated

not complicated but failure not

complicated by aortic stenosis, not

complicated by mitroenosis. You cannot

get a free uncomplicated oric gage

without a white pulse pressure. Remember

this.

Now the the regurgitation of the blood

from the aorta the left ventricle will

push the anterior lift of the mital

valve to the semi-closed position

creating something like mital stenosis

and therefore you get a midtoic murmur

known as the oip.

In patients with acute aortic reg for

example the if you get an aortic

dissection under this circumstances the

blood flowing from the aorta to the left

ventil marketly elevate the left

ventricular endos pressure and stops the

murmur right here. So the mer is shown

and you may not be able to detect it at

all.

Now mitro stenosis very well known to

everyone but I wanted to make certain

points here. In early mital stenosis

there are two members. It's not one

single murmur. Now these two mmas is an

early diastolic murmur here following

the opening snaps. Not actually early in

terms of being after E2, but there is a

space after the opening step. You get an

early due to the flow of the blood from

the left atrium to the left ventricle

during the rapid filling period and then

you get an area of silence and then as a

result of atrial contraction you get

another M. Remember that this piece of

the murmur is actually not a diastolic

phenomena. This is the first heart

sound. This is the beginning of clinical

history. But it's not the beginning of

physiological history. Why is that?

Because the left ventricle contracts

before the first heart sound has to move

the blood which gets deceleration behind

it. So actually the left ventricle

starts contracting here. So this part of

the murmur is in actual physiological

system and that's the reason if you have

atrial fibrillation no atrial kick the

prehistoric accentuation might and might

not disappear.

Now if m stenosis becomes severe then

the gradient will not be not early and

not late only that but will be all

through. So you get the long rumbling

the stoic murmur which ends with an

accent sound. Now everyone is acquainted

between the significance between A2 and

the opening snap. The tighter the

stenosis, the closer interval. But mind

that there are two exceptions of this.

Hypertension

as well as atrial fibrillation. In

hypertension the isovalometric

relaxation period is prolonged because

you have to drop down from the high

aortic pressure down to below the left

atrial pressure in order to for the

mital valve to open. So you get widening

of this interval even if mistenosis is

is tight and in long in atrial

fibrillation long cycle is inversely

proportional to the left atrial

pressure. So sometimes opening the

aortic valve the mital valve prematurely

despite the micro stenosis is not that

severe. So taking these precautions in

consideration is important. An important

thing which not known to everybody if

you get a loud first sound. If you get a

crisp opening snap you have mital valve

you expect that the mital valve score

will be less than eight and the patient

is fit for mital val.

Now

uh going to the stoic murmurs other

diastolic mmmers pulmonary regurgitation

is very important nowadays. Why is it?

We know that in severe pulmonary

hypertension, pulmonary regurgitation

can occur under the circumstances

P2. But sometimes you get a pulmonary

gurge and the pulmonary second sound is

not that loud. For example, in patients

with carcinoid syndrome, pulmonary valve

is is fixed in the semi-open position

cannot close, cannot produce a loud P2.

But more importantly this situation in

focusology required a surgeon opens the

outflow tract of the right vent. He

splits open the pulmonary valve the

pulmonary artery out of the pulmonary

artery and the outflow tractor of the

right ventricle. Under this

circumstances he creates pulmonary

leage. Now this pulmonary gauge is awful

and is hardly to detect. Why hardly to

detect? We know that the pulmonary

artery pressure is low in ferocythology

and if you open the pulmonary the

outflow plaque of the right ventricle

the right ventricle pressure is going to

drop the gradient will be minimum. So

despite free flowing perman the murmur

will be very soft because the gradient

is not that great but moreover the flow

will be laminar because the the

permonary cusps will be will be gone

almost disappeared completely after

surgery. So as a result of that if you

put the echo and you are not very

attentive you will not find elasin and

as a result of that you can miss you can

miss the situation all together. How can

you find it? You find that the right

ventricle after operation is getting

dilated white complex reaching point 18

ventricular ticardial occur. A role of

thumb in arismia complicating the

congenital heart disease. If you get

arythmia look for underlying hemodynamic

disturbance. If you corrected the

hemodynamic disturbance most likely the

arythmia is going to disappear. If the

ventricular arisma doesn't disappear you

think of an ICD. Don't think in ICD at

the beginning. Corrected hemodynamic

abnormality and that's a rule of thumb

which applies to the majority of

situations of congenital heart disease.

This is this situation is no exception.

So here you get pocosology. You get a

low pitched early diastolic murmur. Your

pulmonary regurgitation. Make sure that

your right ventricle is not dilated.

Don't miss this situation because it's

an ominous situation. Now continuous

murmur. The definition of a continuous

murmur is a murmur which starts in

incestually anywhere in cy not

necessarily at the beginning of system

and continues across the second cell to

diasty anywhere in the not necessarily

at the end of the prominent among the

causes is rupture silence of UB cervical

venus which we talked about just a while

ago remember coactation coactation the

collateral can create a lot of problems

can create a continuous murmur and can

create a falsely low gradient across the

coation. Remember the significant

gradient across the cartition is just 20

mm of mercury. Astonishingly low. Don't

forget the examination of the vascular

part of the cardiovascular examination.

And in this regard, I want to point out

the following. Number one, the majority

of peripheral art disease are

asytomatic. At least half of the

patients with peripheral artery disease

they don't have any symptoms and this

means that you have be on the lookout

for this and that's why guidelines is

recommending doing the ankle break index

in patients above the age of 65 or 70 as

a routine too much but that's a

guideline

or patients above the age of 50 or 55 if

they have diabetes or they are smokers

but remember peripheral artery disease

commonly asytomatic and if even if they

have symptoms. Intermittent clication.

Intermittent chordication is usually a

typical is not the pain which occurs on

exercise stops at least within 10

minutes and doesn't occur at rest. These

are the three classic criteria of

intermittent collication. They are not

present in the majority of cases. If the

asymptomatic is 50, a typical

collication is 35, typical collication

is 15%.

Clical limb eskeemia is a term which

conotes presence of rest pain

incapacitating

or rest pain or the presence of t loss

in the form of ulcer or in the form of

gender.

One simple test is the burgers test.

Revate the leg of the patient. And if

you reate the leg of the patient to a

degree like to 45 degrees, you get color

because the venus blood is went away and

the partial blood cannot replace it. And

if you drop the leg at the bedside you

get rer. This roer is delayed because

filling filling is filling from

collaterals. And the reason why there is

ruper is the capillary dilation the

eskeemia is producing accumulation of

metabolites and this accumulation of

metabolites will result in plaso

dilotation and ruper in this this is

burgers test now this is very important

the ankle brachial index it's not only

important because it detects peripheral

vascular disease it's important because

it detects peripheral artery disease

particularly we know that peripheral art

peripheral arterial disease is commonly

signed

But its importance is a risk factor for

coronary artery disease and for strokes.

So it's an important. So everyone should

be acquainted how it's being done. Not

necess not necessarily to be how to do

the technique exactly. But remember the

technique should be done preferably with

the Doppler ultrasound. And here it's

the monometer no longer is used to do

that. What we do here this ratio here

it's it's a systolic ankle pressure over

the systolic arm pressure. What we do is

that we measure the uh arm pressure by

the Doppler in the brachial artery and

we choose the higher of the two

pressures right and left leg limb and we

measure the two ankle pressures right

and left and in each ankle dorsal pedis

and posterior tibial and we choose the

posterior tibial or the dorsal pedis

whichever is higher. So it's the higher

of the two angle pressures over the

higher of the two arm pressures for the

right side and left side. Now this is

important

and this is an example although there is

also a mistake here. This is the right

side and left side 160 150. Here is the

posterior tier is 120. The cell speed

this is 180. So we choose here the

higher of the two 120 divide it by the

higher of these two. So 120 over 160.

This figure here is 80. So we choose the

the higher here which is 80 over 160 not

150 because we we we use the higher of

the two arm pressures in the denominator

and the higher of the uh two pressures

in each leg which is a normal. Now the

normal is is one between one and.9 is

borderline abnormality. you need to

exercise a patient and find whether it's

increasing or not the ankle break index.

Now if it is below than 0.9 then it's

diagnostic of peripheral vascular

disease. The nice thing about the test

is that it is reproducible. It's not

it's it imparts objectivity to the

diagnosis of peripheral vascular

disease. You don't rely on the symptoms.

Remember the symptoms is either absent

or they are atypical. you get some

nagging pain in the leg, not necessarily

related to effort, not necessarily

related by rest. So this kind of

subjectivity is nullified by the

measurement of the ankle brachial end.

If it's below 04 or 0.5, it's 4.4 or

less, then it means it's peripheral

vuscular disease. Now if it is above

1.4, Four, it means that the vessels are

abnormal, non-compressible because of

severe rigidity and or calcification

like in diabetics and patients with

renal failure. So under these

circumstances, you need to measure not

the ankle brachial index but the toe

brachial index. There is a special cup

for the toe and you measure the to the

toe pressure by the dock by Doppler

putting the Doppler probe on the pulp of

the toe and under these circumstances

you can measure the two pressure and

divide it by the higher of the two

brachial pressures and the cut off point

is 7 anything below 7 is is indicated of

now I tell you something a trick if you

are not interested in doing the ankle

brachial index and you are in and the

CCU you can put the finger oxymmetry on

the finger and on the big toe and a

difference of 2%

is as equal as an braal index which is

indicative of preferable coordin so this

is another method well documented well

validated not widely used but you can

use it if you like

now venus diseases you can get venus

insufficiency because of abnormality of

the valves You get swelling of the leg,

you get varicose veins and sometimes you

get hemocetin liberation. This hemoserin

will stain the lower limbs producing

lipo dermatosis

ulcerations may occur and you get the

blanche ulcer heal ulcer. In these

conditions sometimes the fibrosis which

occurs as a result of him of him

reposition results in contraction of the

limb giving an inverted sharp pain but

appearance something similar to paranal

muscular atrophy but in an eskeemic limb

as evidenced by eskeia and alserations

here. Now tissue loss can occur in the

form of the green as you can see here.

Now another question. This is the one

before the last. A 46 year old patient

of your partner arrives for an urgent

visit. He has recently been placed on a

new medication for congestive heart

failure management.

Which of the following is the most

likely new medication? Metropolin.

This is NGO edem and we we see it

infrequently but we see it particularly

with the widespread use of ACE inhibitor

and arbs. Now the guidelines is clear.

If you have it with ACE inhibitor you

stop the AC inhibitor you replace it by

ARBs. Does ARB produce anic edema? The

answer is yes but less frequently. And

if you have angitic edema you cannot use

arn. So you have to angotic edema occurs

in the soft tissues here. It's an

extension of articaria and it's

sometimes itchy because in the soft

tissues like the eyelids, the mouth in

the mouth, in the lips and in the

tongue. Sometimes it's life-threatening.

You don't need to treat it in the larger

majority of cases but it affects the

tongue and the larynx. You need to give

corticosteroids and anti-histics.

Now skin manifestations of

cardiovascular disease are protein but

let me concentrate on some of them.

Osgar Weber window syndrome

hemorrhagicia in the mouth it's not very

rare remember that this is frequently

associated with pulmonary arteriovenous

fistula. So this is associated central

blood cyanosis then you ought to think

of pulmonary arterian fist

this is not amoid this is amudarone this

is the skin of chronic amudarone the

therapies ley color the purple skin

affecting the face affecting the hands

affecting the chest wall osteiogenesis

imperfecta the the scalera is thinned

out so the vitrius appears behind it and

this is commonly associated with

connective tissue diseases named The

mitro valve prolapse, aortic dilation,

pulmonary artery dilation and aortic

dissection. Temporal arthritis you treat

first, you biopsy second. Although

nowadays biopsy is not invoked, biopsy

will result sometimes in false positive

or false negative results because of the

segmental effects of the disease. Ultra

sonography can be very helpful. We chose

the halo sign of edema around the vessel

and a segmental narrowing with diffuse

affection of the temporal artery and

that might be diagnostic. You don't need

biopsy in the large majority of cases.

Carcinoid purple huge discoloration

affecting of the right sided of the head

the right side of the right sided of the

right sided valves occasionally the left

side because of patent for and then this

picture is very important. This is a

myoid. You get pera in the eyelids. You

get raccoon eye.

You get a large tongue. You get

indentations of the tongue being from

the mouth. We know that this patient is

having amyrosis. We know now that there

is definitive treatment for transit

amidosis as well as for a amidosis.

Zanthasmus in the young think of

hypocria. Look for tubular zeneroma,

plenaros xenthoma, palmer zenthoma and

tubular xenoma. So these are important

things to look at.

The stigmata of infective endocarditis.

I know that the the cardiac department

of tyro university is very active in

endocarditis. You don't see that because

you are treating these patients in the

appropriate way. But when whenever these

cases are neglected or whether when they

are recurrent like in in injection

used patients you get splinter

hemorrhages. But an important point here

the splinter hemorrhage of the of

infective induces does not reach the

edge of the nail. I will show you

splinter hemorrhages common cause of

splinter commonest cause of splinter

hemor is actually trauma. And the way

you differentiate them is that in trauma

it reaches the age of eight. I will show

you a picture now and in bacteria and

ducatis it's usually proximal to the

edge of the knee you get mucosal pera

you get osar's node you get jane waist

node use which are painless in contrast

to osner nodes which are painful now

this is the traumatic the common type of

splinter hemoris is traumatic and

reaches almost the age of the knee and

this is not bacterial inocarditis

now this is the last question and I'll

be you finishing up that unless

professor

yesterday he has some question I'll be

happy to answer them it's now one and a

half hour I was very fast I apologize

for that but anyhow I think you will be

having the fun of criticizing what I did

I hope you I satisfied your ambition a

26 year old patient referred after

presenting to his orthalmologist by the

following look at the picture he the

question is about what is the next best

imaging method for assessment of this

patient MRI echo CT or the plex real

this is a suboxitated islands now I

think in kai university they are fond

with mafan syndrome and I don't know

where they are bringing these patients

in every examination we find mafan

syndrome but that's competence no doubt

about it now the diagnosis of maran

syndrome is resting now on the revised

Gent criteria. Gent is a is a city in

Belgium.

Very wise people collected there and put

criteria which has been revised several

times. The revision results in

subdivision

by forating patients with Maran syndrome

into two categories. Those with positive

family history and those with negative

family history. And those with positive

family history need to have aortic

radication or

ectopia lentis or a score of seven. The

score of seven or more we are talking

about the various manifestations of

maran syndrome. Increase the span,

increase the height, high arched pallet,

high foot deformity, dural easia, uh the

finger

wrist sign and so forth. If you get

seven or more of that or if you get

aortic root dilation or if you get

ectopia that's enough with a positive

family history but the majority of

patients you don't have a family

history. So these are the criteria in

the absence of a family history. You

need to get aortic dilotation plus

ectopentis or aortic dilutation plus

fibbrin mutation or aortic dilotation

plus score equal or above seven or you

get ectopia and fibbrin mutation. What's

fibbrin? Fibbrarian is a protein which

protects the connective tissue matrix.

But more importantly

it inhibits the transforming factor

which is transforming

growth factor beta and if you get

mutation of the fabrielin gene then the

signal from the transforming growth

factor beta will very active and that's

the reason behind digesting the

connective tissue elastic and color

tissue of the aorta and other large

vessels and resulting in aortic ization

and or the section. So I apologize for

being too long but I think I had give

you some pearls. There are other pearls

of course but that will be unfolded in

the coming lectures in cardiology. Thank

you very much. Have a good night and uh

I will be happy to answer any responses

any criticism any questions and so

forth. So the microphone now is for

professor

and us Dr. Muhammad, thank you very much

for this uh very informative uh

let me repeat it

just a few seconds

with a slight modification.

like we are going to have in addition to

the this is the first lecture physical

examination then we will have five

lectures coming inshallah

about eskeemic heart disease they will

involve ST elevation meard infection non

ST elevation meard infection stable

angina particularly in the light of the

newly published eskeemia trial and two

lectures for preventive cardiology

because that's the fashion nowadays. And

then we'll have three lectures for heart

failure, six lectures or seven lecture

for arismia, two lectures for congenital

heart disease. We will have uh three

lectures for valvular heart disease and

then one lecture for each of the

following systemic hypertension

pulmonary hypertension pericarditis

aortic disease peripheral arterial

disease venus throbo emolism pregnancy

and the heart non-cardiac surgery and

then we will have a series of lectures

for evaluation of the patient exercise

testing in nuclear cardiology

hemodynamics and then I will ask Dr.

Ahmed shahhata he's now very expert in

CT to talk about CT and then professor

Muhammad Ardani will choose one of our

colleagues who are very acquainted with

cardcar MRI to talk about cardiac MRI

and if we have time we will talk about

the new major studies that have been

delivered during this period of Ramadan

and the coming four months hopefully

this era ends

Ahmed is very energetic. He's very

disciplined. He has been very of extreme

help to me in the past several years and

I have been giving lectures since 1994

with modification every year

>> and you'll have some modification during

this interval as well.

>> Any question?

meetingham

Gandhi Muhammad.

I hope useful and entertaining. We are

in Ramadan.

If you have some fun in this lecture,

then it achieved at least part of its

object. Thank you very much.