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CARDIOLOGY:
VALVULAR HEART DISEASE I
REVIEW OF PE
So you start with your general data, past medical hx ob
hx etc. . in past medical you will see probable risk factors
that predisposes patients to cardiovascular diseases. for
example the patient is hypertensive, diabetic, or with
marfans syndrome, rheumatic fever, in your hpi, be
particular with for example, you have chest pain, always
be guided with your ppqrst. Always do that! Do that
always! Haha.
Lagi pag may pain always ask what provokes the pain,
what palliates the pain, quality, region, severity, timing.
Ganun lang yun, de kahon yun!
And make sure you know your terminologies also.. what
is claudication? What do you mean by syncope? Loss of
consciousness yun. Di lang fainting. Alamin nyo yan, kasi
the problem with that is sometimes you dont know
what your saying. Lagi ko nga sinasabi, How can you
make a sentence if you dont understand the word? Blah
blah memorize ni miki to..haha
What are left sided symptoms? Orthopnea, PND and
dyspnea.
Right sided failure symptoms? Edema, increased JVP and
hepatojugular reflux
palpitation, is it a sign or a symptom? Symptom
PE
When you do your pe,(NECK) what you would like to see
if you have neck vein engorgement, and then you have
to measure you jvp, at what angle? 30degrees. And then
check for your carotid pulse, but before you touch that,
you have to take note the presence or absence of bruit.
(PRECORDIUM)
Inspect, palpate and auscultate.
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DR.
BARTOLOME
INSPECTION
In your precordium what do you inspect on your
precordium? Dybamicity and your apical beat very
important. To me its more important.
So you have to define your apical beat as to:
Location what is the normal location? 5th ICS MCL
Diameter- about 2.5 cm, if more than that, there is
probably cardiomegaly. You can also put there, distance
from the left parasternal border. Normally it is 7-9 cm
away from your para sternal border.
Normally you do not appreciate any pulsations in tha
aortic, pulmonic, and tricuspid area. But mitral can be
because of the apical beat.
Cardiac auscultatory area- this is the minimum area that
you have to look at, palpate at and auscultate at.
Aortic- 2nd right ICS parasternal
Pulmonic- 2nd left ICS parasternal
Tricuspid- 4th left ICS parasternal
Mitral- 5th left ICS MCL
Question!!! Lahat kayo alam nyo 2nd ICS nyo? Lahat kayo
point at your 2nd ICS now.. hahah
PALPATION
For the apical beat which part of the hand will you use?
FINGERPADS
For murmurs you use this one.. haha di ko din alam
tawag lol
Identify the presence or absence of thrills. What is a trill
now? Its a it is a. it is a..Palpable murmur.. haha
So ang minimum grade ng murmur nay un pag may thrill
4/6 ha. And also you place this hand in the mitral area,
FRED
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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

and this on the tricuspid, pag may heave jan pwede rv - first identify S1
heave o kaya pag dito lv heave (imagining nyo nlng po
-simultaenous with the pulse
yung kamay ni doc hihi)
-basically louder at the apex.
Describe the thrills,heaves as to location, so there is a
thrill, heave or a lift on the aortic, pulmonic, tricuspid or, - due to closure of AV valves
mitral are. You can also say that it is a systolic or diastolic
thrill. - to be certain that what you are listening to
is S1, ck for the carotid artery pulsation
AUSCULTATE
- followed by S2 paulit ulit lang yan labdub
Rate in bpm labdub

Rhythm is regular or irrelgular. - anything b/w S1 and S2 are ALL SYSTOLIC

events systolic murmur
And then the heart sounds, S1, S2, S3,S4, physiologic
splitting of S2. - anything b/w S2 and S1 are ALL DIASTOLIC
events diastolic murmur
You should know how to use your stethoscope. You have
the diaphragm, to appreciate the high pitched sounds (s1 -S3 and S4 are basically diastolic events S3 occurs
and s2) how do you apply it? It should be applied, just after S2 and S4 occurs just before your S1
madiin. Hanggang marka pwede.. haha it should be -S1 and S2 are high pitched sound, so you use your
applied firmly. diaphragm, then to hear S3 and S4 (low otched) you
use the bell. So pag malakas sya sa bell most
use the bell to appreciate low pitched sounds (s3,s4) you
probably that is S3 and S4
apply the bell lightly.
- this is why one should know the
Pero what is the most important part of your auscultatory areas
stethoscope is what is in between the otwo eartips.. and
that is your BRAIN!!! Even if you use a hi-tech steth, hindi
mo naman alam pinapakinggan mo
- also describe S1 and S2
Nageemphasize tlga ako class sa hx and pe. Kasi pag
- are they:
tama ang hx at pe nyo 60% tama ang diagnosis nyo kahit
walang laboratory test soft
loud

Auscultate - check fot you physiologic splitting. Normally, lagi

kayong may physiologic splitting. Kaya pag sinabing
- see if there is presence of a diastolic or systolic not appreciated, probably you cannot hear it very
murmur well.

FRED
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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

- what is physiologic splitting? - its location

- normally when you inspire, there is A2 P2 - where is it radiating?

coupling which widens b/c of delayed closure of the
P2 Insert table ng murmur

- then when expire, the A2 P2 narrows
- also report the presence or absence of S3
- also report the presence or absence of S4
- report also murmurs and friction rubs
S3 S4
During systole (ventricular contraction) the
semilunar valves should be open to allow bld
coming from the ventricles to go to the
arteries. The AV valve should be closed to
prevent regurgitation of bld coming from the
atria
If there is an obstruction or production of
turbulent bld, would be called aortic stenosis
and pulmonic stenosis
So, as said before, the AV valves prevent
regurgitation of bld. So if there is production
of turbulent murmur, then it is called tricuspid
regurgitation and mitral regurgitation.

- extra sound - extra sound

heard during diastole heard during diastole
- heard just after - hear just before
S2 S1
Significance of S3 - thats why it is
called a gallop rhythm
- tells you that there is
ventricular dysfunction - S4 may be
present due to a forceful
atrial contraction
- There would be
a forceful atrial
contraction if there is a
ventricular dysfunction
How do you describe murmurs?
- one of the impt things in describing
murmurs is to #1: appreciate it
- systolic or diastolic?
On the other hand, during diastole, this is the
time for ventricular filling
bld is coming from the atria to the ventricle
if there is obstruction to ventricular filling,
then it is called mitral stenosis and tricuspid
stenosis
Also, during diastole, the semilunar valves
should be closed to prevent regurgitation of
bld coming from the great arteries (aorta and
pulmo arteries)
If there is a regurgitant bld flow coming from
the aorta and pulmo arteries, then it is called
aortic regurgitation and pulmonic
regurgitation.
So a turbulent bld flow b/w S1 and
S2, is called a systolic murmur and
b/w S2 and S1 is called a diastolic
murmur
And it also depends on its location: is
it in the pulmonic, aortic, tricuspid or
mitral
Check fotr neck vein engorgement, Then you
palpate for your peripheral and carotid pulsations,
again before you palpate you auscultate and check

FRED
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CARDIOLOGY:
VALVULAR HEART DISEASE I
for presence or absence of bruit, specially for stroke
patients. You also auscultate for you aorta, renal
arteries. Report for the presence or absence of
friction rub
All of you know your brachial pulses? Radial,
femoral, popliteal, dorsalis pedis, posterior tibialis.
Oh touch her..palpate her pala(cheska touch her
hahaha) check the rate and rhythm and the stregth
of the pulse . palpate nyo yan kasi uso ngayon ang
parot (parrot dinid ko eh haha) ngayo sa mga
diabetic. Peripheral arterial occlusive disease
0- Not appreciated
1- Weak
2- Normal
3- Bounding
Bakit kelngan nyo ipalpate ang pulses nyo? Youve
been to hypertension already? There is primary and
secondary hpn
Is coarctation of the aorta primary or secondary?
SECONDARY there is hypertensive upper
extremities and hypotensive lower extremities
because there is occlusion just below the
subclavian. So when you palpate for the pulse,
bounding pulse sa upper extremities, tapos mahina
sa baba. Then you can already say that this patient
might be suffering from coartation just by PE alone.
For example you have a patient with chest pain and
assymetriacal pulse, that patient probably has aortic
dissection. It is a medical emergency. That is what
happened to mike arroyo.. he was lucky that he
went to a hospital where the doctor did the PE..
requested for x-ray. There is a widened
mediastinum and requested for ct-scan, and
revealed dissected aneurysm
So make sure you try to appreciate your pe..kahit
yan lang matutunan nyo ok na sakin.pampalubag
loob haha
Alam mo bang mas mahal pa tong slide ko jan sa
lecture mo? Kelangan, bago magawa yan susuhulan
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DR.
BARTOLOME
ko pa si dra bartolome..hahaha --- eto na start nan g
totoong lecture nya lol
Actually tapos na.. haha
If you have mitral stenosis, there is pressure
in the left atrium
When we say you have stenosis, it does not
allow a normal blood flow becauase of the
narrowing or constriction of the paasage or
orifice.
With that I produces pressure on the
chamber PRIOR to the stenotic area. Take
note!!!
There is pressure on the chamber PRIOR to
the stenotic area. So it means that if you
havemitral stenosis, there is pressure in the
left atrium.
So you have to imagine that (your circulation), so
if you have a chamber, prior to that stenotic
area, that chamber will be the one to have
problems later on.
And then if you have a regurgitant or backward
flow through a defective valve, regurgintan flow
priduces volume overload on the chamber below
and after that defective valve. So can you
imagine that? For example if you have MR what
happens now to the left atrium and left ventricle?
You will have volume overload on both
chambers and then probably later both of this
chambers will end up up being large. So you
would end up having left atrial enlargement and
left ventricular enlargement.
In systole, the AV valves are closed whereas the
semilunar valves are open
In diastole, the AV valves are open and the
semilunar valves are closed.
ETO TOTOO NA TALAGA.. MITRAL
STENOSIS NA HAHA
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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

MITRAL STENOSIS Increased heart rate shortens diastole proportionately

EPIDEMIOLOGY more than systole + diminishes time available for flow
across the MV further elevation of LA pressure
More common in females Isolated MS normal LV diastolic pressure and ejection
Congenital MS rare fraction
MS + MR generally rheumatic in origin MS with sinus rhythm prominent a wave and gradual
Pure MS 40% of patients with RHD pressure decline after MV opening (y descent)
Severe MS pulmonary arterial pressure (PAP) elevated at
PATHOLOGY rest and increases during exercise cause secondary
increase of RV end-diastolic pressure and volume
Valve leaflets diffusely thickened by fibrous tissue and/or
calcific deposits
Fusion of mitral commissures
Fusion and shortening of chordae tendinae

Rigid valvular cusps narrowing at apex of funnel-shaped

valve (fish mouth)

-if you have stenosis (orifice less than 4cm) then you
have increased blood gradient from the LA gong to the
LV

- an abnormally elevated atrioventricular pressure is

present in this condition which is the hemodynamic
hallmark of mitral stenosis.

- you will end up having left atrial hypertension, and if

you have left atrial hpn, where will will the blbood go
now? To a chamber with lesser pressure, and that is
your pulmonary vein
PATHOPHYSIOLOGY
2
Normal MV orifice = 4 6 cm
2
If orifice < 2 cm Hemodynamic profile of mitral stenosis. The left atrial (LA) pressure is
Blood can flow from LA to LV only if propelled by an elevated, and there is a pressure gradient (shaded area) between the
abnormally elevated left atrioventricular pressure LA and left ventricle (LV) during diastole. Abnormal heart sounds are
gradient - hemodynamic hallmark of mitral stenosis present: there is a diastolic opening snap (OS) that corresponds to
2
If orifice < 1 cm opening of the mitral valve, followed by a decrescendo murmur.
Referred to as critical MS There is accentuation of the murmur just before S1, due to the
LA pressure of approximately 25 mmHg required to increased pressure gradient when the LA contracts. EKG,
maintain normal cardiac output electrocardiogram.
Elevated pulmonary venous and pulmonary arterial wedge
pressure reduced pulmonary compliance exertional Cardiac Output
dyspnea Moderately severe MS
2 2
MV orifice 1.2 cm to 1.7 cm )

FRED
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CARDIOLOGY:
VALVULAR HEART DISEASE I
CO normal or almost normal at rest but rises
subnormally during exertion
Critical MS with elevated pulmonary vascular
resistance
CO subnormal at rest and may fail to rise or may
decline during activity
Pulmonary Hypertension
Clinical and hemodynamic features of MS are influenced
importantly by the level of PAP
Pulmonary hypertension due to:
1. Passive backward transmission of elevated LA
pressure
2. Pulmonary arteriolar constriction triggered by LA
& pulmonary venous hypertension (reactive
pulmonary hypertension)
3. Interstitial edema in walls of small pulmonary
vessels
4. Organic obliterative changes in pulmonary
vascular bed
magkakaron ka na ngaun ng pulmonary venous
HPN. Ano ba mas mataas na pressure?
Pulmonary vein o pulmonary capillaries? Mas
mataas sa pulmonary vein.. so san na pupunta
yung blood? Sa pulmonary capillaries and then
youll end up having pulmory hypertension
-eh kung mataas pressure mo sa pulmonary
capillaries, anong mangyayari? Pwede mang
transudate ng fluid ngayon don
-so, mgkakaron ka nmn ng pulmonary edema.
-now that pressure can also be transmitted to
your pulmonary artery, and youll end up having
what you call as pulmonary arterial hpn.
And if you have pulmonary arterial hpn, the
physical examination finding would be, Loud
second heart sound loud P2 to be
exact..(pakicheck kung p2 nga hehe)
And then the pressure will now go to your right
ventricle. So what will happen now to your right
ventricle? Youll end up having right ventricular
hpn and later right atrial hpn and then later
venous hpn. You will also have enlargement of
the right ventricle, and when you have
enlargement, you will have right ventricular
heave on physical examination.
Page 6 of 18
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DR.
BARTOLOME
And when you have enlarged righth ventricle, the
AV orifice or tricuspid is also dilated and youll
end up having tricuspid regurgitation with this
patient with pulmonary arterial hpn and mitral
stenosis.
Blood pressure will now be transmitted to your
right atrium, you will have right atrial hpn, then
right atrial enlargement
Bloodpressure will now be transmitted to your
veins and youll end up with what we call venous
hpn. So ano ba yung mga signs ng venous hpn?
Neck vein engorgement, inferior venacava hpn,
chronic passive cingestion of the liver thus you
end up having inadequate secretion of your
albumin and then youll end up having acites
And then later because of venous hpn, youll
have bipedal edema.
Basta pauit ulit lang yan class. Kahit sa MI
ganun lang din halos yan. But the pressure
changes are much higher in mitral stenosis
compared to your MI.
So this is why thiiis lesion produces left sided
manifestation as well as right sided
manifestations.
Because you have elevated venous and arterial
pulmonary hpn, thus you will have what we call
exertional dyspnea
Now once you increase the heart rate of the
patient with mitral stenosis, you shorten the
diastolic filling time, so it diminishes time
available for blood to flow across the mitral valve
orifice and thus you further increase the left atrial
pressure
So ano ibig sabhn nyan? People with mitral
stenosis, they dont want ot develop tachycardia.
Kasi pag binilisan mo yung opening and closure
of the mitral valve, there is less time for the
ventricles to fill.
So if you have patient with mitral stenosis, you
always try to put them in a rate which is a little bit
low. Lower than normal.. 50s or 40s ok nay an.
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CARDIOLOGY:
VALVULAR HEART DISEASE I
Tapos demo nnaman si doc sa kamay nya
hahahah
The cardiac output in mitral stenosis maybe
normal initially but usually it is abnormal during
EXECERTION
If you have clinical mitral stenosis you can have
elevated pulmonary vascular resistance and
thus your cardiac output becomes suboptimal
and the patient develops hypotension and then
develops increased heart rate
-can you imagine that passive backward
transmission of elevated LA pressure
-so you have elevated LA pressure, and it
goes down to the chamber with lesser pressure,
the PV then you end up having PV HPN.
-the blood now goes to PC then yu end
up having PC HPN and will now be transmiited to
PA thus you will end up having PA HPN
-another thing that produces PHPN in MS is what
you call as reactive PHPN. You can remember
that you have capillaries that can dilate and
constrict.
so for ex. You have hypoxemia, it can constrict
further. Thus you end up having what? Increased
pulmonary pressure
another is interstitial edema which is basically an
anatomic problem and also an oragnic
obliterative changes within the PC bed
if you have fibrotic changes now in your
capillaries and also at the same time ypu have
edema of the small pulmonary vessels what will
happen now? You have edema of the vessels so
it is edematous, so it has a lesser caliber now.
thus you end up having PA HPN
meaning to say you will not be allowing blood
flow from tha PA to the PC and thus yu end up
with PA HPN
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DR.
BARTOLOME
SYMPTOMS
th
Most patients begin to experience disability in the 4 decade of
life
Once seriously symptomatic, disease progresses
continuously to death within 2 5 years
1. If valvular obstruction mild physical signs may be
present but without symptoms
If with marked elevation of LA pressure dyspnea
and cough precipitated by severe exertion,
excitement, fever, severe anemia, tachycardia,
sexual intercourse, pregnancy and thyrotoxicosis
diastolic murmur of mitral stenosis
They may be asymptomatic initially but
when they develop tachycardia and they
end up havinh LA HPN
so basically ang kalaban nyan dito is
increase in heart rate.
So what will you do now? How
would you slowdown the heart rate
of the patient with MS?
You give a drug that has a NEGATIVE
CHRONOTROPIC EFFECT
CHRONO is a watch so it has
something to do with rate
So will you allow your patient to
have sex? Yes but tell the patient to
have sex with caution haha
So how do you manipulate now
knowing your drugs? Excitement
tachycardia is basically what? A
sympathetic in origin. So you give
anti sympathetic drugs.
2. Severe MS lesser stresses precipitate dyspnea
limitation in daily activities
3. Assumption of recumbent position (+) redistribution
of blood from dependent portions of the body to the
lungs orthopnea & paroxysmal nocturnal dyspnea
4. Sudden surge in flow across narrowed MV orifice
pulmonary edema
5. If moderately severe MS for several years atrial
arrhythmias (AF) -
6. Pulmonary venous hypertension rupture of
pulmonary-bronchial venous connection (+)
hemoptysis
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CARDIOLOGY:
VALVULAR HEART DISEASE I
7. Recurrent pulmonary emboli, sometimes with
infarction
8. Pulmonary infections - bronchitis, broncho-
pneumonia, lobar pneumonia
9. Infective endocarditis - rare in isolated MS
Atrial arrhythmia have you seen atrial fib on
ECG? Why is it that you dont have Pwave?
because there is no atrial contraction.
tapos may dinedemo nnman sya sa kamay nya
imaginin nyo nalang haha
These heart condition can lead to stasis and
develop THROMBUS and later develop EMBOLI
patient can also complain of HEMOPTYSIS. Sabi
hemptysis is associated with tb db? PWEDE! But
dont forget to auscultate your patient.
take note that it is not only due to P HPN that
you end up having hemoptysis.
Other things that can cause hemoptysis:
Bronchitis
Bronchopneumonia
Pulmonary infarction
-Patients with MS are prone to have infective
endocarditis so later you have to give infective
pericarditis prophylaxis to patients with MS
Pulmonary Changes
Due to increased transudation of fluid from pulmonary
capillaries into interstitial and alveolar spaces
Fibrous thickening in walls of alveoli and pulmonary capillaries
Reduced vital capacity, total lung capacity, maximal breathing
capacity, and oxygen uptake per unit of ventilation
Increased pulmonary capillary pressure during exercise
reduced pulmonary compliance
Thrombi and Emboli
Thrombi formation if left atria, particularly in the enlarged
atrial appendages
Embolization
more common in
1. patients with AF
2. elderly patients
3. patients with reduced cardiac output
May be the presenting complaint in other-wise
asymptomatic patients with mild MS
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DR.
BARTOLOME
this is what im saying earlier, ptx are prone to
develop thrombus and emboli specially in ptx
with atrial fibrillation and low cardiac output.
naimagine nyo yun? Thrombus on you LA will be
dislodged to LV then to the aorta then to
different parts of the body.
if it goes to the brain stroke
if it goes to the eyesblindness
if it goes to the heartMI
PHYSICAL FINDINGS
Inspection and Palpation
1. Malar flush with pinched and blue fascies
2. Jugular venous pulse with prominent a waves due to
vigorous right atrial systole
3. Systemic arterial pressure usually normal or slightly low
4. (+) RV tap along left sternal border signifies enlarged RV
5. (+) diastolic thrill at cardiac apex with patient in recumbent
position
Typical physical signs of mitral stenosis
Irregular pulse of atrial fibrillation
Rise in jugular venous pressure (with coexistent tricuspid
regurgitation)
Parasternal heave with right ventricular hypertrophy
Loud first heart sound
Tapping apex beat (manifestation of a loud first heart sound)
Opening snap, which disappears as the leaflets become rigid
Classic late diastolic murmur with presystolic accentuation (the longer
the murmur, the more severe the lesion)
Auscultation
sa PE, saan mo ilalagay at diaphragm para maapreciate
mo ang Diastolic murmurs (MS)? Sa apical or mitral area
associated with loud s1
-if with PHPN loud S2 specially P2
-place diaphragm on apical area to appreciate
diastolic rumbling murmur
-suration of murmur correlates severity
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CARDIOLOGY:
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o -ibig sabhin if you have HOLOSYSTOLIC
murmur- that is a very significant mitral
stenosis
Other associated murmurs:
- Functional tricuspid regurgitation
o Due to dilatation of the RV and the
tricuspid valve ring
o Thus inadequate tooot
coacrtation yata please check
1:17:55---
o Thus you will have systolic murmur
of the left lower parasternal border
- Left and Right sided murmurs
o Right sided tricuspid and
pulmonic
o Left sided mitral and aortic
o (+) caravallos sign
- Pulmonic regurgitation
o Due to PA HPN. You have dialted
pulmonary valve ring and thus you
end up having inadequate coartation
of the pulmonic valve
o Usually present in ptx with severe
pulmonary HPN
1. Accentuated, slightly delayed and snapping S1
2. Closely split or fixed S2 with accentuated P2
3. Pulmonary systolic ejection click in patients with severe
pulmonary hypertension
4. Opening snap of MV most audible in expiration at or just
medial to cardiac apex
Time interval between A2 and OS varies with
severity of MS
5. Opening snap of MV most audible in expiration at or just
medial to cardiac apex
Time interval between A2 and OS varies with
severity of MS
6. Low-pitched, rumbling, diastolic murmur heard best at apex
with patient in lateral recumbent position
Accentuated by mild exercise carried out just
before auscultation
Duration of murmur correlates with the severity
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BARTOLOME
Associated Lesions
1. Pansystolic murmur along left sternal border
If with severe pulmonary hypertension
Produced by functional TR
Accentuated by inspiration and diminishes during
forced expiration - Caravallos sign
2. High-pitched, diastolic, decrescendo blowing murmur along
left sternal border
Graham Steell murmur of PR
Due to dilatation of PV ring
Occurs in patients with mitral valve disease and
severe pulmonary hypertension
LABORATORY EXAMINATION
EKG
1. MS and sinus rhythm
P wave suggestive of left atrial enlargement
2. If with severe pulmonary hypertension, TS and right atrial
enlargement
Tall and peaked P wave in lead II and upright in
lead V1
QRS complex normal
Severe pulmonary hypertension (+) right axis
deviation and RV hypertrophy
Echocardiogram
Most sensitive and specific non-invasive method for
diagnosing MS
Transthoracic 2-D color flow Doppler imaging and Doppler
ultrasound
1. Estimate transvalvular gradient and mitral orifice
size
2. Presence and severity of accompanying MR
3. Extent of restriction of valve leaflets
4. Anatomic suitability for balloon mitral valvotomy
Also provides:
1. Assessment of the size of the cardiac chambers
2. Estimation of LV function
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CARDIOLOGY:
VALVULAR HEART DISEASE I
3. Estimation of PAP
4. Indication of the presence and severity of
associated valvular lesions
Mitral stenosis demonstrated by (a) echocardiography (showing
thickened leaflets that no longer open), (b) electrocardiography
pressure tracing in the left atrium versus left ventricle demonstrating
the gradient between the two cavities (and therefore mitral stenosis),
and (c) chest x-ray.
Roentgenogram
Earliest changes:
1. Straightening of left border of cardiac silhouette
2. Prominence of main pulmonary arteries
3. Dilatation of the upper lobe pulmonary veins
4. Backward displacement of esophagus by an
enlarged LA
Kerley B lines
1. Fine, dense, opaque, horizontal lines most
prominent in lower and midlung fields
2. Due to distention of interlobular septa and
lymphatics with edema when resting LA pressure
> 20 mmHg
Radiograph of the heart: The abnormalities characteristic of mitral
stenosis are more expressed in this case. The heart is enlarged, the
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BARTOLOME
dilatation of the left ventricle (arrow) is associated with the dilatation
of the right ventricle.
Cardiac Catheterization
Useful when there is discrepancy between clinical and
echocardiographic findings
Helpful in assessing associated lesions such as AS and AR
Usually advisable preoperatively to detect patients with
critical coronary obstruction that should be bypassed at the
time of operation
DIFFERENTIAL DIAGNOSIS
Mitral Regurgitation
Diastolic murmur begins slightly later than in patients with
MS
With clear-cut evidence of LV enlargement
(+) apical grade III/VI pansystolic + S3
Aortic Regurgitation
Apical mid-diastolic murmur (Austin Flint murmur)
Atrial Septal Defect
Also with RV enlargement and accentuation of pulmonary
vascularity
Widely split S2 of ASD may be mistaken for mitral OS
(-) LA enlargement and Kerley B lines + fixed splitting of S2
Left Atrial Myxoma
May obstruct LA opening (+) dyspnea, diastolic murmur,
& hemodynamic changes similar to MS
With features suggestive of a systemic disease
Auscultatory findings change markedly with body position
Mitral Regurgitation systolic murmur
Aortic Regurgitation kahit saang auscultatory
area pwede mo sya madinig.
-mitral sounds radiates to the
axilla where as the aortic sounds does
not.
aortic sounds radiates to the carotid
Atrial septal Defect alos with heart
enlargement and accentuation of pulmonary
vascularity.
-associated with fixed splitting of 2nd
heart sound
-no dilatation of LA
LA myxoma tumor within the LA cavity
-it produces obstruction, because it
blocks the mitral orifice
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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

-associated with systemic diseases like Sodium restriction and diuretics

Digitalis glycosides slow ventricular rate of patients
fever with AF
-associated with platypnea dyspnea in Beta blockers or nondihydropyridine calcium
upright position antagonists (e.g. Verapamil or diltiazem)
Warfarin
-more symptomatic pag nakatayo At least 1 year if systemic and/or pulmonary
embolization occurred
Permanently in patients with AF

Surgical Mitral Valvotomy

Indicated in
1. symptomatic patients with isolated MS whose
2 2
effective orifice is < 1.0 cm /m body surface area
2
2. normal-sized adults with orifice < 1.7 cm
Ideal patients:
1. With relatively mobile, thin leaflets with no or
little calcium
2. Without extensive subvalvular thickening
3. With no or mild MR
No evidence that the procedure improves the prognosis of
patients with slight or no functional impairment
NOT recommended in asymptomatic patients
In pregnant patients valvotomy carried out if pulmonary
congestion occurs despite intensive medical treatment
Indications:
1. MS with significant associated MR
2. Valves severely distorted by previous trans-
catheter or operative manipulation
3. Those in whom the surgeon does not find it
possible to improve valve function significantly
Overall 10-year survival of surgical survivors = 70%

Mitral balloon Mitral balloon

valvulo-plasty valvuloplasty with
with Inoue Inoue Balloon. Mitral
TREATMENT Balloon by valve area increase
Toray Company. from 0.7cm2 to 2.3
Medical
1. Penicillin prophylaxis of beta-hemolytic Strep infection
cm2
2. Prophylaxis for infective endocarditis
3. If patient symptomatic MITRAL REGURGITATION

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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

ETIOLOGY LV volume increases progressively as severity of

regurgitation increases accompanied by reduced
1. Chronic RHD in 1/3 of cases; males > females forward CO
2. Congenital defect of endocardial cushions Severe MR ejection fraction increases in the presence
3. Frequently secondary to ischemia of normal LV function
Consequence of ventricular remodelling or with v wave in the LA pressure pulse usually prominent
fibrosis of a papillary muscle in patients with healed MI As distended LA empties during early diastole rapid y descent
Acute infarction of base of a papillary muscle In chronic MR increased LV compliance LV volume increase
4. Hypertrophic cardiomyopathy displacement of anterior leaflet with little elevation in LV diastolic pressure
of MV during systole Effective forward CO usually reduced in seriously symptomatic
5. Calcification of mitral annulus most common in elderly women patients
6. Infective endocarditis involving valve leaflets or chordae LV contractility reduced, sometimes irreversibly, with long-
tendinae standing MR
7. Trauma Pressure-volume relationship (compliance) of the LA and
pulmonary venous bed affects the clinical picture
systolic murmur that radiates to the axilla Acute MR:
o normal or reduced LA compliance with little
-heard on the apex enlargement of LA
-ano ang lalaki dito? LAor LV? O both? o Marked elevation of LA pressure, particularly of the
v wave
BOTH pag regurgitant flow before and after the
Pressure-volume relationship (compliance) of the LA and
valve ang affetcted pulmonary venous bed affects the clinical picture
-Most common cause is Mitral valve prolapsed Severe MR:
o Marked increase in LA compliance
followed by MI (it is the mechanical complication o Marked enlargement of LA
of mi) o Normal or only slightly elevated LA and PA pressures
o Low cardiac output severe fatigue and exhaustion
-mycardial hypertrophy can also cause MR
AF almost invariably present
-you have increased volume in both LA and LV
ACUTE VS CHRONIC AMR
-no ventricular compensation di na sya
nagdialte kasi acute nga
-pulmonary edema
-decreased cardiac output
-hypotension
-always remember that LV pressure is higher
than the LA = LA HPN
CMR- pag ngkaron ka ng regurg ng dahan dahan..
mag cocompensate then mag ddilate yung
chambers.. Pathophysiology of mitral regurgitation. In mitral regurgitation (MR),
a portion of the LV output is forced retrograde into the LA, so that
forward cardiac output into the aorta is reduced. In acute MR, the LA
is of normal size and is noncompliant, such that the LA pressure rises
PATHOPHYSIOLOGY
markedly and pulmonary edema may result. In chronic MR, the LA
has enlarged and is more compliant, such that LA pressure is less
Patient with MR reduced resistance to LV emptying LV
elevated and pulmonary congestive symptoms are less common if LV
decompressed into the LA during ejection rapid decline in LV
contractile function is intact. There is LV enlargement and eccentric
tension
hypertrophy due to the chronic increased volume load.
Initial compensation more complete LV emptying

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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

Chronic decompensated stage of mitral

regurgitation (MR).
Acute stage of mitral regurgitation (MR).
SYMPTOMS

Most prominent complaints in chronic, severe MR

1. Fatigue
2. Exertional dyspnea
3. Orthopnea
MR with associated pulmonary vascular disease and marked
pulmonary hypertension:
1. Right-sided heart failure ankle edema, distended neck
veins, ascites
2. Painful hepatic congestion
3. TR
Acute, severe MR LV failure with acute pulmonary edema

PHYSICAL FINDINGS

1. Arterial pressure
Usually normal
If severe MR sharp upstroke
2. Jugular venous pulse
Chronic compensated stage of mitral Abnormally prominent a waves in patients with
sinus rhythm and marked pulmonary HPN
regurgitation (MR). Prominent v waves if with accompanying TR
3. Systolic thrill
Palpable at cardiac apex
4. Hyperdynamic LV with brisk systolic impulse and palpable
rapid-filling wave
5. Laterally displaced apex beat
6. RV tap and the shock of pulmonary valve closure palpable in
patients with marked pulmonary HPN

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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

Clinical signs of chronic mitral regurgitation

Prominent and sustained apex beat

Systolic thrill at the apex

Left parasternal heave resulting from left atrium expansion,

rather than right ventricular hypertrophy

Soft first heart sound

Pansystolic murmur at the apex that radiates into the axilla
Third heart sound that is high pitched due to high early diastolic
filling velocities
Auscultation
1. S1 generally absent, soft, or buried in the systolic murmur
2. Wide-splitting of S2 in patients with severe MR due to
premature closure of aortic valve
3. (+) OS if associated with MS
4. Low-pitched S3 at completion of rapid-filling phase of LV
due to sudden tensing of papillary muscles, chordae
tendinae and valve leaflets - important auscultatory feature
of severe MR
Initially you have left sided manifestations
Then eventually right sided manifestations
On auscultation, arterial pulse will be normal
With minimal JVP initially ( pag may right sided
manifestation na, meron narin JVP)
LV heave
Lateral Displaced apical beat
Sustained parasternal heave
Soft S1
Associated with s3
5. Presystolic murmur in patients with sinus rhythm and
associated MS
6. Grade III/VI holosystolic murmur, most prominent at apex
and radiating to axilla most characteristic auscultatory
finding in severe MR; intensified by isometric strain and
reduced by Valsalva maneuver
If with ruptured chordae tendinae or primary
involvement of posterior mitral leaflet murmur
transmitted to base of heart; with cooing or
seagull quality
LABORATORY EXAM
Electrocardiogram
1. Patients with sinus rhythm evidence of LA enlargement;
RA enlargement if pulmonary HPN severe
2. Chronic, severe MR generally associated with AF
3. May have signs of LV hypertrophy
Echocardiogram
goldstandard
- You can appreciate regurgitant blood flow
- Mosaic pattern of MR
- Normally red and blue only
- -ayan may green, yellow, orange etc theres
mosaic color pattern
1. Color flow Doppler most accurate non-invasive technique
for detection and estimation of MR
2. Two-dimensional echocardiography useful for assessing
the cause of MR and for estimating LV function from end-
systolic and end-diastolic volumes and EF
LA usually enlarged and/or exhibits increased
pulsation
LV hyperdynamic

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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

TREATMENT

Roentgenogram
1. LA and LV the dominant chambers
LA may be massively enlarged and form the right
border of the cardiac silhouette
Pulmonary venous congestion, interstitial edema,
and Kerley B lines sometimes noted
2. Marked calcification of mitral leaflets common in patients
with long-standing combined MR and MS
Medical
1. Restriction of physical activities that produce dyspnea and
excessive fatigue
2. Sodium restriction + diuretics
3. Vasodilators and digitalis glycosides increase forward
output of failing LV
4. IV nitroprusside or nitroglycerin reduce afterload; useful
in stabilizing patients with acute and/or severe MR
5. ACE inhibitors treatment of chronic MR
6. Endocarditis prophylaxis
7. Anticoagulants and leg binders reduce likelihood of
venous thrombi and pulmonary emboli
Surgical
Indications for surgery: severe MR
1. Progressive LV dysfunction, with LV EF declining below
60%
2. End-systolic cavity dimension on echocardiography
rising above 45 mm
Left-sided heart catheterization and angiocardiography may
be helpful in confirming the presence of severe MR if there
is discrepancy between clinical picture and
echocardiographic findings
So how do you treat MR? you can treat it
mediacally initially
decrease your afterload pressure where your
myocardium will pump on
less afetrload = more cardiac output

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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

vasodilator therapy
EF ejection
ACE, ARBS, CA2+ Blocker
fraction
-if patient has fluid overload fluid restriction
ESD end-
and diuretics
systolic
-IV NITROPUSIDE dimension
HT
Preload unloader effect hypertension
Afterload unloader effect
MVR mitral
It reduces the amount of blood going back to the
valve repair
heart
Venodilator- less blood will go back to heart MITRAL VALVE PROLAPSE
Use if patient has CHF or P edema already
Also known as:
1. Systolic click-murmur syndrome
-NITROGLYCERINE
2. Barlows syndrome
3. Floppy-valve syndrome
acts the same way 4. Billowing mitral leaflet syndrome
CORONARY ARTERY VASODILATOR Causes:
1. Excessive or redundant mitral leaflet tissue associated
Increase blood flow to the myocardium thus less with myxomatous degeneration and greatly increased
ischemia concentrations of acid muco-polysaccharide
2. Disorders of connective tissue (e.g. Marfans,
osteogenesis imperfecta, Ehler-Danlos syndrome)
3. Acute rheumatic fever
4. Ischemic heart disease & cardiomyopathies

Posterior leaflet usually more affected than the anterior

Mitral valve annulus usually greatly dilated
Reduction in production of type III collagen has been
incriminated
May be associated with thoracic skeletal deformities similar to
Marfan but not as severe
May lead to excessive stress on papillary muscles dysfunction
and ischemia of papillary muscles and subadjacent myocardium

CLINICAL FEATURES

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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

More common in females, usually 14 30 yrs old 2. Two-dimensional echocardiography

May also be observed in older (>50 yrs) patients, usually
males more severe & requires surgical treatment
Increased familial incidence for some patients autosomal
dominant pattern of inheritance
Most patients asymptomatic and remains so for their entire lives
Now considered as the most common cause of isolated severe
MR requiring surgical treatment in North America
a) Identify the abnormal position and prolapse of
the mitral valve leaflets
b) Echocardiographic definition of MVP: systolic
displacement (in parasternal view) of the MV
leaflets by at least 2 mm into the LA superior to
the plane of the mitral annulus

1. Arrhythmias ventricular premature contractions and

paroxysmal supraventricular tachycardia (+) palpitations,
light-headedness, and syncope
Sudden death a rare complication
2. Chest pain that is difficult to evaluate
Substernal, prolonged, poorly related to exertion,
and rarely resembles angina pectoris
3. Transient cerebral ischemic attacks due to emboli from the
MV due to endothelial disruption
4. Infective endocarditis in patients with associated MR

Auscultation
1. Mid- or late (non-ejection) systolic click occurring 0.14 sec
or more after S1 most important finding
2. Multiple systolic clicks followed by a high-pitched, late
systolic crescendo-decrescendo murmur, which is
occasionally whooping or honking, heard best at apex
Occur earlier with standing, during Valsalva
maneuver, and with any intervention that
decreases LV volume
Delayed with squatting & isometric exercise,
which increase LV volume
This patient had a marked prolapse of the posterior mitral valve
leaflet with severe anterior-directed mitral regurgitation. The left
atrium and left ventricle were mildly dilated but the left ventricular
end-systolic dimension was 3.6 cm only. The left ventricular systolic
function was still preserved with an ejection fraction of 63%.
3. Color imaging and Doppler studies
Helpful in evaluating and revealing accompanying
MR

4. Angiocardiography
Shows prolapse of the posterior and sometimes of
mitral valve leaflets

TREATMENT

Medical
1. Infective endocarditis prophylaxis
2. Beta blockers sometimes relieve chest pain
3. Anti-arrhythmic agents if with significant tachy-
arrhythmia
4. Antiplatelet aggregation agents in patients with transient
ischemic attacks
LABORATORY EXAM
5. Anti-coagulants
1. ECG most commonly normal but may show
Surgical
a) Biphasic or inverted T waves in leads II, III, and
If patient is symptomatic with severe MR
aVF
Mitral valve repair
b) Occasionally supraventricular or ventricular
premature contractions

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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

Most important thing about MVP is.. always remember

this one.. board question na yan.. lagi kong tinatanong
yan.. that is what we call dynamic auscultation of MVP

- When you ask yor ptx tostand up and do the

valsava or any intervention that increases
the LV volume
- -the midsystolic click goes nearer to s1
- On the other hand, when you ask your
patient to squat and do isometric
contractions like hand grip
- -midsystolic click goes nearer to s2

Si jlo daw at si nickiminaj(boomboom hAHA) are not

candidates ng straight back syndrome..di ko alam
bakit..hahaha

Confirmation of MVP via ECHO

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