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CARDIOLOGY:
VALVULAR HEART DISEASE I
AORTIC STENOSIS
ETIOLOGY
Occurs in about of patients with chronic valvular heart disease
Approximately 80% are male
Causes:
1. Adults - degenerative calcification of the aortic cusps
Age-related degenerative calcific AS (senile or
sclerocalcific AS) most common cause of AS in
adults in North America & Western Europe
Risk factors same as those for atherosclerosis
30% of persons > 65 y/o with aortic valve sclerosis
2% with frank stenosis
2. At birth - Congenital
Stenosis present at birth become progressively
more fibrotic, calcified and stenotic
Congenital valve deformity normally it is
tricuspid, but in this condition, usually bicuspid,
without serious narrowing of aortic orifice during
childhood, but they are later prone to develop
calcific changes
Most common congenital disease
3. Rheumatic endocarditis of aortic leaflets
Produce commissural fusion, resulting in bicuspid
valve leaflet more susceptible to trauma
lead to fibrosis, calcification and further
narrowing
Almost always associated with involvement of
mitral valve and severe AR
PATHOPHYSIOLOGY
(+) obstruction to LV outflow produce systolic pressure
gradient between the LV and aorta
There is increased afterload. What do you mean
by afterload? Miki?hahaha
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DR.
BARTOLOME
Can you imagine a stenotic valve? A thickened
arortic valve.. can you imagine yung bisagra?
Ayaw bumukas kasi matigas na sya. So even if you
contact, hirap na hirap lumabas kasi yung bisagra
matigas na (yun po yung joint ng door haha)
Yung sinabi na systemic vascular resistance is
another cause of increased afterload. This time it
is the aorta that produce the after load problem.
Peak systolic pressure gradient > 50 mmHg with normal cardiac
2
output or an effective aortic orifice less than 1.0 cm or < 0.6
2 2
cm /m body surface area = severe obstruction to LV outflow
Elevated LV end-diastolic pressure in severe AS signifies LV
dilatation and/or decreased compliance of hypertrophied LV wall
increased myocardial oxygen demand
What would be the problem of the patient with
increased oxygen demand? They could be
complaining of chest pain. And your patient will
end up having Myocardial Ischemia
Cardiac output at rest within normal but fails to rise normally
during exercise
SYMPTOMS
Rarely of clinical importance until valve orifice has narrowed to
2 2
approximately 0.5 cm /m body surface area in adults
th th
Symptoms gradually appear until 6 8 decades
1. Reduced compliance elevated LV diastolic pressure
elevated pulmonary capillary pressure exertional
dyspnea
2. Inc. Myocardial oxygen demand + reduced O2 availability
angina pectoris
3. Vasodilation in exercising muscles & inadequate
vasoconstriction in non-exercising muscles decreased
arterial pressure exertional syncope
Once you have all these three, these are
indications for you to replace your
aortic valve
If you have syncopal attack and angina
pectoris and will not replace the valve,
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CARDIOLOGY:
VALVULAR HEART DISEASE I
within 2-3 years time, 50% of them will
die
On the other hand, if you have the left
sided failure manifestation like the
exertional dyspnea 50% of them will die
within 1 year if you dont change the
valve
It is important to undergo left heart
catheterization to identify the severity
of the aortic stenosis and identify if ever
they have CAD. Class magkaiba pa yung
CAD at yung aorti stenosis. Magkaiba
nnamng gastos yun
CO at rest usually well maintained until late in the course
Marked fatigability
Weakness
Peripheral cyanosis
Other manifestations of low CO
Advanced stages symptoms of LV failure
Orthopnea
Paroxysmal nocturnal dyspnea
Pulmonary edema
Isolated, severe AS
Severe pulmonary HPN leading to RV failure
Systemic venous HPN
Hepatomegaly
AF and TR
AS + MS decreased pressure gradient across the aortic valve
clinical findings produced by AS are masked
Left heart catheterization helpful in defining the relative
importance of each valvular abnormality
PHYSICAL FINDINGS
1. Rhythm generally regular until late in the course
(+) AF suggests associated MV disease
2. Systemic arterial pressure usually within normal limits
In late stages stroke volume decreased dec.
Systolic pressure + narrowing of pulse pressure
Example of narrowing of pulsepressure
110/100 binibigyan kayo ng clue non
actually, mas malaki ang pulpressure
nyo ibigsabhn you heart is still
contracting and there is a large amount
of fluid coming out. Diastolic pressure is
the minimum pressure in your counduit
then on the other hand, your systolic
pressure is the cardiac output plus your
minimum pressure.
3. Peripheral arterial pulse rises slowly to a delayed sustained
peak - pulsus parvus et tardus basta pag aortic class, there
are a lot of peripheral signs
4. Palpable systolic arterial pulse (bisfiriens pulse) excludes
pure or predominant AS; signifies dominant AR
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DR.
BARTOLOME
5. Late stages of AS pulse pressure reduced pulse
amplitude small
6. Bulging, hypertrophied intraventricular septum
diminished distensibility of RV cavity accentuated a wave
in the jugular venous pulse
7. LV impulse active and laterally and inferiorly displaced
(+) LVH PMI is more than 2.5cm
8. Double apical impulse with the patient in the left lateral
recumbent position
9. Systolic thrill at base of heart, in the jugular notch, and
along carotid arteries
You can appreciate thrills on aortic and pulmonic
area and in the carotid
-right sided and left sided failure manifestation
Auscultation
1. Early systolic ejection sound (OS of the aortic valve) in
children and adolescents with congenital non-calcific
valvular AS disappears when valve becomes calcific and
rigid
2. Paradoxic splitting of S2
3. S4 audible at apex reflects presence of LVH and elevated
LV end-diastolic pressure
Eccentric LVH lumalakinat kumapal ang puso
Concentric LVH kumakapal lang
Dilated LV lumaki lang, you see in MI kasi dead
heart muscles na.. di na sya naghyhypertrophy
4. (+) S3 when LV dilates
5. Murmur
Ejection mid-systolic murmur
Commences shortly after the S1
Ends just before aortic valve closure
Low-pitched, rough and rasping in character,
loudest at the base of the heart, most commonly
nd
in 2 right intercostal space
Transmitted upward along the carotid arteries
At least grade III/VI with severe obstruction
Best heard on a leaning forward position and you
need to use the bell because it is low pitched
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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

LABORATORY EXAM

ECG
1. Left ventricular hypertrophy key finding
2. Advanced cases
ST-segment depression and T-wave inversion (LV
strain) in leads I and aVL and in left precordial leads
When will you say that it is LV? Pag matanda more that
35.. pag bata morethan 40. (height sae cg yata tong
tinutukoy no doc)

Two-dimensional ECHOCARDIOGRAPHY
Eccentric aortic valve cusps characteristic of
congenital bicuspid valves
Can identify cardio megaly. Ang ganda no? kasi ang
goldstandard autopsy haha
Doppler echocardiography
Estimate transaortic valvular gradient
LV dilatation and reduced systolic shortening reflect
impairment of LV function
Chest x-ray: May show a dilated aorta. Calcification of the aortic valve
may be seen. In late disease, pulmonary oedema ("fluid on the lung")
may be seen.
Catheterization and coronary arteriography
Indications:
1. Patients with clinical signs of AS and symptoms of
myocardial ischemia coronary artery disease
suspected
2. Patients with multivalvular disease
3. Young, asymptomatic patients with non-calcific
congenital AS to define the severity of obstruction to
LV outflow
4. Patients in whom it is suspected that the obstruction
to LV outflow may not be at the aortic valve but rather
in the sub- or supravalvular regions

Thickened and stenosed aortic valve seen in parasternal long axis

view on echocardiography. Both the mitral and aortic valves are in
near closed position. IVS: interventricular septum; Ao V: aortic valve;
LV: left ventricle; MV: mitral valve; LA: left atrium.

Roentgenogram
LVH without dilatation produce some rounding of
the cardiac apex
Critical AS associated with post-stenotic dilatation of
AVA, aortic valve area; BP, blood pressure; CABG, coronary artery
ascending aorta
bypass graft surgery; echo, echocardiography; LV, left ventricle;
Aortic calcification apparent on fluoroscopic
Vmax, maximal velocity across aortic valve by Doppler
examination
echocardiography. (From Bonow et al. Modified from CM Otto: J Am
Coll Cardiol 47:2141, 2006.)

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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

TREATMENT a. Cystic medial necrosis of ascending aorta

b. Idiopathic dilatation of the aorta in severe HPN
Medical c. Osteogenesis imperfecta
1. Avoidance of strenuous physical activities in patients with d. Severe hypertension
2 2
severe AS (< 0.5 cm /m ) e. Syphilis
2. Sodium restriction f. Rheumatoid ankylosing spondylitis
3. If with CHF diuretics and digitalis glycosides
4. Nitroglycerin for angina pectoris
5. HMG CoA reductase inhibitors (statins) for slower
progression of leaflet calcification and aortic valve area
reduction hindi ko sinabing standard therapy to, but
probably for patients who are not seeing surgery in the
future, you may want to give this, because thin CAN delay
the problem
6. Digitalis if there is weak contraction of the heart

Surgical: Aortic Valve Replacement (AVR)

Indications:
2
1. Patients with severe AS valve area < 1.0 cm or
2 2
0.6 cm /m body surface area who are
symptomatic
2. Patients who exhibit LV dysfunction
3. Patients with an expanding post-stenotic aortic
root, even if asymptomatic
AORTIC REGURGITATION
Diastolic murmur
Causes:
1. Primary valve disease destruction of the valve, thus
inadequate coarctation or there is an opening within the
AV. Any inflammation of the AV can produce the problem
Males pure or predominant valvular AR
Females primary valvular AR with associated MV
disease
a. 2/3 of patients rheumatic in origin
thickening, deformity and shortening of individual
aortic valve cusps prevent proper opening
during systole and proper closing during diastole
b. Congenital membranous subaortic stenosis thick
aortic valve leaflets valves susceptible to
endocarditis
c. Rheumatoid spondylitis
d. Congenital bicuspid aortic valves
e. Infective endocarditis PATHOPHYSIOLOGY
Can develop on a valve previously affected
by rheumatic disease Increased total stroke volume ejected by LV
f. Traumatic rupture of aortic valve uncommon Entire LV stroke volume ejected into the aorta
cause increased LV end-diastolic volume (increased
preload) major hemodynamic compensation
2. Primary Aortic Root Disease for AR
Aortic root disease without primary involvement of During diastole, there is a regurgitant blood
valve leaflets volume coming from the aorta going to the
Dilatation of aortic annulus may occur secondarily ventricle. You must remember that it is during
and intensify the regurgitation diastole you have left verticular filling. So ang
Patients with marfans syndrome

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CARDIOLOGY:
VALVULAR HEART DISEASE I
daming volume na nangagaling sa ventricle, so it
will make your left ventricle enlarged now.
Dilatation and eccentric hypertrophy of LV allows LV to
eject a normal effective forward stroke volume and a
normal left ventricular EF
As LV function deteriorates end-diastolic volume rises
further & forward stroke volume and EF decline
Deterioration of LV function precedes development of
symptoms
Reverse pressure gradient from aorta to LV falls
progressively during diastole account for the
decrescendo nature of the diastolic murmur
Patients with severe AR effective forward CO usually
normal or only slightly reduced at rest but fails to rise
normally during exertion
Elevated myocardial oxygen requirements due to LV
dilatation and elevated LV systolic tension myocardial
ischemia
HISTORY
Patients with acute, severe AR
Failure of LV to dilate sufficiently to maintain stroke
volume
LV diastolic pressure rises rapidly with associated
increase of LA and PA wedge pressures
Pulmonary edema and/or cardiogenic shock rapidly
develop
SYMPTOMS
Patients with CHRONIC, severe AR
Long latent period asymptomatic for 10-15 years
1. Uncomfortable awareness of heartbeat especially on
lying down early complaint
2. Sinus tachycardia during exertion or with emotion,
or PVCs produce uncomfortable palpitations and
head pounding
3. Diminished cardiac reserve first symptom is
exertional dyspnea followed by orthopnea, PND,
and excessive diaphoresis
4. Anginal chest pain at rest and during exertion
5. Systemic fluid accumulation, including congestive
hepatomegaly and ankle edema
6. Left and right sided manifestations
PHYSICAL FINDINGS
Patients with severe AR
1. Jarring of entire body and bobbing motion of the head
with each systole parang naghehead bang..
2. Abrupt distention and collapse of the larter arteries
easily visible
3. Arterial pulse
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DR.
BARTOLOME
Rapidly rising water-hammer pulse collapses
suddenly as arterial pressure falls rapidly during
late systole and diastole (Corrigans pulse)
Capillary pulsations
Corrigans pulse
Capillary pulsations
Quinckes pulse alternate flushing and paling of
the skin at the root of the nail while pressure is
applied to the tip of the nail
Traubes sign booming pistol-shot sound over
the femoral arteries
Duroziezs sign - to-and-fro murmur audible if the
femoral artery is lightly compressed with a
stethoscope
4. Palpation
Heaving LV impulse that is displaced laterally and
inferiorly
Diastolic thrill palpable along left sternal border
Prominent systolic thrill in the jugular notch and
transmitted upward along the carotid arteries
Due to markedly increased blood flow across
the aortic orifice
With pure AR or with combined AS and AR
carotid arterial pulse is bisfiriens (two systolic
waves separated by a trough)
5. Auscultation
With severe AR aortic valve closure sound (A2)
usually absent
S3 and systolic ejection sound
Murmur
1. high-pitched, blowing, decrescendo diastolic
murmur
rd
Heard best in 3 intercostal space along
left sternal border
2. Mid-systolic ejection murmur heard best at
base of heart & transmitted along the carotid
vessels
3. Austin Flint murmur soft, low-pitched,
rumbling mid-diastolic bruit
If murmur is soft heard best with diaphragm of
stethoscope and with patient sitting up, leaning
forward, and with breath held in forced expiration
If AR due to primary valvular disease diastolic
murmur louder along left rather than right sternal
border suggests that AR caused by aneurysmal
dilatation of aortic root
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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

Eccentric jet of aortic regurgitation cursing along the posterior margin

Severe, ACUTE AR of the left ventricular outflow tract (anterior mitral leaflet).
There is sudden regurgitant blood volume fro the
aorta going to the left ventricle you up have 3. Roentgenogram
sudden elevated end diastolic pressure then LA Apex displaced downward and to the left
HPN thenP venous HPN then P arterial HPN the P Cardiac shadow extends below left diaphragm
edema. LV enlargement in left anterior oblique and lateral
Elevated LV end-diastolic pressure lead to projections LV displaced posteriorly and
early closure of mitral valve (+) mid-diastolic encroaches on spine
sound
Soft or absent S1
Soft, short diastolic murmur of AR
Walang time mag compensate ang puso nyo
Acute pulmonary edema- primary
manifestation
You end up having patient with cardiogenic
shock

LABORATORY EXAM

1. ECG
Severe, chronic AR ECG signs of LVH
ST-segment depression and T-wave inversion in
leads I, aVL, V5 and V6 (LV strain)
Left axis deviation and/or prolonged QRS
denote diffuse myocardial disease poor
prognosis

2. Echocardiogram
Rapid, high-frequency fluttering of anterior mitral
leaflet a characteristic finding
1. Produced by impact of regurgitant jet
Useful in determining cause of AR, by detecting
dilatation of the aortic annulus
Color flow Doppler very sensitive and helpful in
assessing severity

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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

Generally rheumatic in origin commonly associated with

some degree of TR; females > males
Does not occur as an isolated lesion usually associated with
MS
(+) diastolic pressure gradient between RA and RV
Mean diastolic pressure gradient of 4 mmHg sufficient to
TREATMENT
elevate mean RA pressure systemic venous congestion
(+) ascites and edema
Medical-prevent regurgitant blood volume-goal
Patients with sinus rhythm RA a wave extremely tall and may
-reduce afterload, thats the time you reduce your systemic
approach the level of the RV systolic pressure
vascular resistance.
CO at rest usually depressed and fails to rise during exercise
1. Digitalis glycosides patients with severe regurgitation
Low CO normal or slightly elevated LA, PA, and RV
and dilated LV without frank LV failure
systolic pressures despite presence of MS
2. Salt restriction
Presence of the TS masks the hemodynamic and
3. Diuretics
clinical features of the MS
4. Vasodilators, especially ACE inhibitors
5. Antiarrhythmics
SYMPTOMS
6. Long-acting nifedipine delay the need for operation
Development of MS precedes that of TS initial symptoms of
Surgical definitive treatment following the 55 rule
pulmonary congestion
Consider two points in deciding on advisability and proper
Characteristically complain of relatively little dyspnea for the
timing of surgical treatment:
degree of hepatomegaly, ascites, and edema
Patients with chronic AR usually do not become
Low CO fatigue
symptomatic until after the development of myocardial
Discomfort due to refractory edema, ascites, and marked
dysfunction
hepatomegaly
When delayed too long, surgical treatment often does
Suspected if symptoms of RV failure persist after an adequate
not restore normal LV function
mitral valvotomy
Operation should be carried out even in asymptomatic
patients with progressive LV dysfunction and a left
ventricular ejection fraction < 55% OR a LV end-systolic PHYSICAL FINDINGS
2
volume > 55 mL/m 55/55 rule
Patients with acute, severe AR require prompt surgical Severe TS
treatment 1. Marked hepatic congestion resulting in cirrhosis, jaundice,
serious malnutrition, anasarca, and ascites
TRICUSPID STENOSIS 2. Congestive hepatosplenomegaly with prominent pre-
systolic pulsations of the enlarged liver
3. Distended jugular veins with giant a waves (in patient with
diastolic mumur
sinus rhythm)
right or left sided murmur?
4. Auscultation
Right sided (pulmonic and tricuspid are right sided
Pulmonic valve closure sound not accentuated
murmurs)
Diastolic murmur with many of the qualities of the
Bakit may tinatawag tayong right sided murmurs?
diastolic murmur of MS
Dun pumapasok yung caravllo sign ninyo. When
Murmur heard best over left lower sternal margin and
you ask the patient to inspire and the murmur
over the xiphoid process most prominent during
and the intensity of the murmur
presystole in patients with sinus rhythm
increases(murmur becomes louder), most
Murmur augmented during expiration and during the
probably that is a right sided murmur
strain of Valsalva maneuver
where will you appreciate the murmur?
Left Lower sternal border
Will there be a right ventricular enlargement in TS? LABORATORY EXAM
Will there be asignificant right sided failure manifestation in TS?
Tandaan nyo, hindi makapass ang blood from RA ECG
to RV. RA enlargement tall, peaked P waves in lead II with
So YES merong right sided failure manifestation. prominent, upright P waves in lead V1
You will have RA HPN and then venous HPN
More common in tropical and subtropical climates

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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

Absence of ECG evidence of RVH in a patient with right- intensified during inspiration
sided heart failure believed to have MS should suggest Reduced during expiration and Valsalva maneuver
associated tricuspid valve disease AF usually present

Chest roentgenogram combined TS and MS LABORATORY EXAM

Prominence of RA and SVC without much enlargement of
the PA ECG
Changes characteristic of MI or severe RVH
Echocardiogram
Thickened tricuspid valve Echocardiography
RV dilatation and prolapsing or flail tricuspid leaflets
TREATMENT Diagnosis made by color flow Doppler echo

Medical
Intensive salt restriction and diuretic therapy required
during preoperative period to improve hepatic function
Surgical
Carried out preferably at time of mitral valvotomy in
patients with moderate or severe TS
Open heart repair OR replacement of TV with a large
bioprosthetic valve
TRICUSPID REGURGITATION
Systolic murmur
+ caravallos sign
Always associated with left sided malfunctions or valvular
problems
Usually functional and secondary to marked dilatation of
the tricuspid annulus
May complicate RV enlargement of any cause
Commonly seen in late stages of heart failure due to
rheumatic (TR with TS) or congenital heart disease with
severe pulmonary HPN
Other causes: ischemic heart disease, cardiomyopathy, cor
pulmonale, infective endocarditis, tricuspid valve prolapse,
trauma, carcinoid heart disease
Reversible if pulmonary HPN is relieved
Roentgenogram
Enlargement of both RA and RV
TREATMENT
No operation needed in the absence of pulmonary HPN
Treatment of underlying cause of heart failure reduce
severity of functional TR
Surgical treatment should be carried out in patients with
severe regurgitation secondary to deformity of the TV due
to rheumatic fever
PULMONIC VALVE DISEASE
Less affected by rheumatic fever
Pulmonic regurgitation most common acquired
abnormality affecting the pulmonic valve
Secondary to dilatation of the PV ring as a
consequence of severe pulmonary HPN
(+) Graham Steell murmur
High-pitched, decrescendo, diastolic blowing murmur
along left sternal border difficult to differentiate from
murmur of AR
Usually of little hemodynamic significance

CLINICAL FEATURES
JONES CRITERIA FOR RHEUMATIC FEVER
Clinical features result primarily from systemic venous
congestion and reduced CO
Major Criteria Minor Criteria
TR in patients with pulmonary HPN symptoms of
pulmonary congestion diminish but clinical manifestations
of right-sided heart failure become intensified
Distended neck veins with prominent v waves Carditis Clinical
Marked hepatomegaly, ascites, pleural effusion, Migratory polyarthritis Fever
edema Sydenhams chorea Arthralgia
Systolic pulsations of liver Subcutaneous nodules Laboratory
(+) hepatojugular reflux Erythema marginatum Elevated acute phase
Prominent RV pulsation along left parasternal region reactants
Blowing holosystolic murmur along lower left sternal Prolonged PR interval
margin

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CARDIOLOGY: DR.
BARTOLOME
VALVULAR HEART DISEASE I

Plus
Supporting evidence of a recent group A streptococcal infection
(e.g. (+) throat culture or rapid antigen detection test; and/or
elevated or increasing streptococcal antibody test)
To fulfil the Jones Criteria, either 2 major criteria or 1 major criterion
and 2 minor criteria PLUS evidence of an antecedent streptococcal
infection are required (p1977-1979) read this topic dw haha
Involvement of heart in rheumatic fever is called
pancarditis. There is involvement of the endo, epi and
myocardium.
They can have
o CHESTPAIN
o MYOCARDIAL DYSFUNCTION
o Either SYSTOLIC OR DIASTOLIC PROBLEMS
o Most of the time its CONTRACTION PROBLEMS-
there is inadequate contraction of the heart, so
the patient will start complaining of heart failure
o VALVULITIS namamaga yung mga valves nyo..
hindi pa naninigas yan initially.
During acute rheumatic fever you do
not develop stenotic valve. It is later
after how many years that you develop
stenosis. 15 to 30 years
MIGRATORY POLYARTHRITIS
-involves the large joint and it is migratory
-asymmetrical usually
DERMATOLIGIC MANIFESTATIONS
-nodules
-erythema marginatum
OTHER MANIFESTATION
Arthralgia and fever
- Magkaiba ang arthralgia at ang arthritis.
- In ARTHRALGIA there is only pain
- In ARTHRITIS there is inflammation
LAB
-CBC increase in WBC
- ESR
-C REACTIVE PROTEIN
-ECG - PROLONGED PR INTERVAl
SUPPORTING EVIDENCES OF GROUP B STEP INFECTION
AGES 15 TO 5 YEARS OLD ARE COMMON

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