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BIOETHICS

MEDICINE 23

P.08 VALVULAR HEART DISEASES C. CXR – HEART BORDERS


Dr. Olarte | August 27, 2019

OUTLINE
I. Review
II. Mitral Stenosis
III. Mitral Regurgitation
IV. Mitral Valve Prolapse
V. Aortic Stenosis
VI. Aortic Regurgitation
VII. Tricuspid Regurgitation
VIII. Pulmonic Valve Stenosis
IX. Addendum

I. REVIEW
A. HEART CIRCULATION • Left Heart border: Aortic knob, Main Pulmonary Artery,
Left Ventricle
• Right Heart border: Superior Vena cava, Right Atrium,
Inferior Vena Cava

D. 2-D ECHO OF THE HEART

• SVC and IVC – RA – tricuspid valve – RV – Pulmonic valve -


Pulmonary artery – Lungs – Pulmonary vein – LA – mitral
valve – LV – aortic valve – aorta.

B. ECG

E. 4 CHAMBER VIEW IN THE 2D ECHO

• Check for the rhythm and rate then check for abnormalities
in the QRS complex.
• To know if the rhythm is sinus rhythm, look at the P wave,
followed by the QRS complexes
• Check for the regularity of the QRS
• Also check for the rate = 1500/ Number of small squares

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F. AREAS OF AUSCULTATION • Other less common etiologies of obstruction to left


ventricular inflow include congenital mitral valve stenosis,
cor triatriatum, mitral annular calcification with extension
onto the leaflets
• In other patients with rheumatic heart disease, lesser
degrees of MS may accompany mitral regurgitation (MR) and
aortic valve disease

B. CRITERIA
• Normal Mitral Valve Area (MVA) : 4-6cm2
• Mitral Stenosis: <2.0cm2
• Severe: <1.0 cm2 (<1.5 cm2)

C. HEMODYNAMIC HALLMARK
• Hallmark: Elevated Left Atrioventricular pressure
gradient (obstruction of the flow of blood increasing the
• Aortic valve: 2nd ICS R parasternal border pressure in LA higher than LV)
• Pulmonic valve : 2nd ICS L parasternal o When the orifice area is reduced to <~2 cm2, blood can
• Tricuspid valve : 4th ICS L parasternal flow from the LA to the left ventricle (LV) only if
• Mitral valve : 5th ICS L midclavicular line propelled by an abnormally elevated left atrioventricular
pressure gradient, the hemodynamic hallmark of MS.
II. MITRAL STENOSIS • Difference in pressure: pressure gradient
• Stenosis – narrowing of the valves
• In rheumatic MS, chronic inflammation leads to diffuse D. PATHOPHYSIOLOGY
thickening of the valve leaflets with formation of fibrous
tissue often with calcific deposits.
• The mitral commissures fuse, the chordae tendineae fuse
and shorten, the valvular cusps become rigid, and the
pathologic process eventually leads to narrowing at the apex
of the funnel-shaped (“fish-mouth”) valve.
• Calcification of the stenotic mitral valve immobilizes the
leaflets and narrows the orifice further.
• Thrombus formation and arterial embolization may arise
from the calcific valve itself, but in patients with atrial
fibrillation (AF), thrombi arise more frequently from the
dilated left atrium (LA), particularly from within the LA
appendage.

• Decreased Mitral Valve Area ® Increasing the Left Atrial


Pressure
o If you have an obstruction in the Mitral Valve, the Left
Atrium has to pump stronger to force the blood.
A. ETIOLOGES • There will be Left Atrial enlargement, as a compensation to
• Leading cause: Rheumatic Fever decrease the Left Atrial Pressure.
• Congenital • If there is enlargement, the muscle arrangement is deranged
o E.g. Cor triatriatum – The atria is divided by the thin thus giving rise to Atrial Fibrillation and Left Atrial clot.
membrane that results to 3 atrial chambers • Increase in Left Atrial Pressure will be transmitted to the
• Degenerative: Calcification (usually elderly) Pulmonary Venous System.
• Connective tissue diseases: SLE and RA o This now causes Pulmonary Congestion.
• Myxoma o Primary manifestation is dyspnea/exertional
• Infective Endocarditis with large vegetations dyspnea/edema.

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o The elevated pulmonary venous and pulmonary arterial


(PA) wedge pressures reduce pulmonary compliance,
contributing to exertional dyspnea.
• Pulmonary congestion now leads to increased peripheral
vascular resistance and pulmonary hypertension.
o Leading to RV pressure overload and exhaustion -> RV
dilates
o There is decreased cardiac output thus manifests as
dyspnea and decreased functional capacity.

E. SIGNS AND SYMPTOMS


• Symptoms usually occur about 2 decades after initial attack
of rheumatic carditis
o Usually it is asymptomatic
o Usually, patient can tolerate MS for a very long time –
most of them are in their 20’s, 30’s, usually they had MS
when they are children
o Repeated episodes of RHD or carditis
o Cause: DENTAL INFECTION
• Presence of Dyspnea and cough
• During the progression of lesion, it manifests as: • “Graham Steel Murmur”
1. Easy fatigability o Murmur of PR (pulmonic regurgitation)
2. Orthopnea o High pitched, diastolic decrescendo blowing murmur
3. Paroxysmal nocturnal dyspnea produced by dilation of pulmonic valve heard best at
4. Hemoptysis – due to rupture of pulmonary-bronchial the base along the left parasternal border this is due to
venous connection due to pulmonary venous the dilatation of the pulmonary valve ring seen in
hypertension severe mitral stenosis as well as severe pulmonary
5. Right sided Heart Failure hypertension
6. Atrial Fibrillation
7. Stroke due to thrombus formation G. ECG
• Recurrent pulmonary emboli, sometimes with infarction, are
an important cause of morbidity and mortality late in the
course if MS.
• Severe MS: malar flush with pinched and blue facies.

F. MURMUR
• Classic MS murmur: Low pitched, rumbling diastolic
murmur heard best at the apex
o Left lateral decubitus position
• Rumbling - Opening snap following the sound of AV opening
o Caused by the thickened valves
• Functional TR that increases in intensity during inspiration
and diminishes during expiration (Carvallo’s sign)
o Used to distinguish it from Mitral Regurgitation
• Caused by the thickened valves
• In patients with calcified valves, it is difficult to hear the
opening snap
• Pre-systolic accentuation just before S1
• The opening snap of the mitral valve is most readily audible
in expiration at, or just medial to, the cardiac apex.
• Mitral Stenosis: enlargement of LA
• The OS is followed by a low-pitched, rumbling, diastolic
• P-Mitrale (leads with most prominent P waves)
murmur, heard best at the apex with the patient in the left
o “M” Pattern: Widened P wave that is usually “M”
lateral recumbent position, it is accentuated by mild exercise
shaped that suggests LA enlargement
carried out just before auscultation
• If with severe pulmonary hypertension, there is
• Duration of this murmur correlates with the severity of
concomitant Right Axis Deviation and RV hypertrophy
stenosis in patients with preserved CO.
• In MS and sinus rhythm, the P wave usually suggests LA
enlargement

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H. CXR • For mild and in favourable valve: Percutaneous Mitral


Balloon Commissurotomy
o We have to do periodic monitoring on these patients
• For Severe: Mitral Valve Replacement
• Heart Rate Control
o Slow down heart rate to give more time for filling.
§ Beta blocker (if patient is in Atrial Fibrillation)
§ Digoxin
§ Diuretics (for congestion)
§ Anti-coagulation
o Since there is an obstruction, increase the flow of blood
from the LA to the LV by slowing down the HR to
increase the amount of time for LV filling
• Penicillin prophylaxis of group A β-hemolytic streptococcal
infections for secondary prevention of rheumatic fever is
important for at-risk patients with rheumatic MS.
• Blue arrow: Straightening and elevation of the left main • In symptomatic patients, some improvement usually occurs
bronchus with restriction of sodium intake and small doses of oral
• Red arrow: Left atrial appendage enlargement diuretics.
• Black arrow: “Double-bubble” sign due to atrial • NOTE: See Addendum for Treatment (This was
enlargement mentioned by Dr. Olarte)
• Dilatation of the Pulmonary Veins
• The earliest changes are straightening of the upper left Mitral Valvotomy
border of the cardiac silhouette, prominence of the main • PTMC – Percutaneous Transverse Mitral Commissurotomy
PAs, dilation of the upper lobe pulmonary veins, and o We use femoral vein put in the balloon - make a
posterior displacement of the esophagus by an enlarged LA. puncture in the inter-atrial septum – insert to the mitral
valves – dilate – break causes valve enlargement.
I. 2-D ECHO • Unless there is a contraindication, mitral valvotomy is
indicated in symptomatic (New York Heart Association
[NYHA] Functional Class II–IV) patients with isolated severe
MS, whose effective orifice (valve area) is < ~1 cm2/m2
body surface area, or <1.5 cm2 in normal-sized adults.
• In addition, the subvalvular structures should not be
significantly scarred or thickened, and there should be no LA
thrombus.

Mitral Valve Replacement


• Necessary in patients with MS and significant associated MR,
those in whom the valve has been severely distorted by
previous transcatheter or operative manipulation, or those in
whom the surgeon does not find it possible to improve valve
function significantly with valvotomy.
• Prosthetic Valves
• Mechanical Prosthetic valves
o Metallic
o From pigs or buffalo

• Classic finding – Doming motion of mitral valves

J. TREATMENT

MILD MODERATE SEVERE


Mean < 5 mmHg 6 – 10 mmHg >10 mm Hg
Pressure
Decrease
Pressure < 139 ms 140–219 ms ≥220 ms
Half-time
Valve Area 1.6 – 2.0 1.5–1.0 cm2 <1.0 cm2
cm2

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WILKINS’ Echo Score A. ETIOLOGIES


• Developed to help guide decision-making.
• The score accounts for the degree of leaflet thickening, ACUTE CHRONIC CHRONIC
calcification, and mobility, and for the extent of subvalvular (PRIMARY)1 (SECONDARY)2
thickening • Usually due to • Myxomatous • Ischemic
• 8 and below - candidate for Valvotomy Infective (MVP, Barlow’s, Cardiomyopat
• > 8 - candidate for valve replacement Endocarditis forme fruste) hy
• Scoring is influenced by the degree of calcification • Papillary • Rheumatic Fever • Dilated
o If hard – valve replacement muscle/chordae • Infective Cardiomyopat
o If soft – valvotomy tendinae rupture Endocarditis hy
(in post- MI: (healed) • Hypertrophic
STEMI) • Mitral annular cardiomyopat
• Blunt Trauma calcification hy with
• Chordal • Congenital (cleft, systolic
rupture/leaflet AV canal) anterior
flail (MVP,IE) • Radiation motion
• Chronic AF
with LA
enlargement
and annular
dilation
1
Chronic Primary – affecting leaflets, chordae tendinae which are
primarily responsible for abnormal valve function
2
Chronic Secondary – leaflets, chordae are “innocent bystanders,
usually normal but the regurgitation is caused by LV remodeling
with annular enlargement, papillary muscle displacement, leaflet
tethering, or their combination
• Mitral annular calcification may include elements of both
III. MITRAL REGURGITATION primary and secondary MR as the disease process may
encroach on the leaflets, impair the normal sphinteric
function of the annulus, or both

B. PATHOPHYSIOLOGY

• Blood goes back to LA during systole


• Blood from LV goes back to LA - regurgitant

• LVEDP – Left Ventricular End diastolic pressure


• LAP – Left Atrial Pressures

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• You can’t distinguish the S1, generally absent and soft, it is


buried to the holocystolic murmur
• It is usually holosystolic, it is decrescendo and ceases in mid-
to-late systole in patients with acute severe MR.
• The systolic murmur of chronic MR not due to MVP is
intensified by isometric exercise (handgrip) but is reduced
during the strain phase of the Valsalva maneuver because of
the associated decrease in LV preload.

E. ECG
• During the contraction of LA, instead of the blood passing
through the aortic valve, some of the blood goes back, plus
the volume coming from the pulmonary circulation, there is
general increase in volume in the LA ® ↑ LVEDP and ↑
LAP
• There’s compensatory mechanism of the LA and LV to
accommodate volume overload which helps relieve
pulmonary congestion ® LV hypertrophy
• Because of the increase in volume that goes back to the LV
and also the LA, it now causes the enlargement of these
chambers
• As the size increases, in time, there will be coaptation of the
Mitral Valve leaflets

C. SIGNS AND SYMPTOMS


• Chronic Mild to moderate MR: May be asymptomatic • There is LA enlargement and LVH (dilatation and thickening
• Chronic severe MR: Symptomatic of the LV) with strain pattern.
o Easy fatigability o There is T wave inversion in the lateral leads and one in
o Orthopnea aVL.
o Exertional dyspnea • Chronic severe MR is frequently associated with AF
• Palpitations are common and may signify onset of AF
• Systolic thrill at the apex F. CXR
• Displaced apex beat
o Due to dilatation of the LV
• Presence of S3
o Poorly functioning LV
• Acute severe MR
o LV is stiff
o Arterial pressure may be reduced.
o (+) S4
o Symptom of CHF is more prominent because the
LV can’t accommodate the increased volume.
o Manifestation is more severe than chronic MR.
• Rupture of chordae tendinae can result in “acute-on-chronic
MR” in patients with myxomatous degeneration of the
valves.

D. MURMUR • Displacement of apex toward the lateral and downward


• Systolic murmur at least grade III/VI • Late in the course of the disease, there is enlarged LV and it
usually holosystolic heard at the apex (blowing) forms the right border of the cardiac silhouette
• Most prominent at the apex radiating to the axilla • There is cardiomegaly in this patient.
• LA and LV are the dominant chambers in MR.
• Calcification of the mitral annulus may be visualized,
particularly on the lateral view of the chest

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G. TREATMENT A. MURMUR
• Heart Failure Regimen (treat HF first) • Mid or late (non-ejection) systolic click occurring
o Diuretics 0.14 secs or more after S1
o ACEI/ARBs: dilators - decreases afterload(resistance o Mid-systolic click - Due to sudden tensing of slack,
after LV), SV will move forward and will go back to LA elongated chordae tendinae or by the prolapsing
o Beta blockers: slow down heart rate mitral leaflet on maximum excursion
§ But not as low as in Mitral Stenosis, you don’t • 2nd heart sound is the click followed by the
want a low HR in MR, because there will be more blowing murmur
volume in your LV and that will make the patient o A high pitched late systolic murmur heard best at the
go to CONGESTION. apex (left lateral decubitus position)
• Mitral Valve Replacement

IV. MITRAL VALVE PROLAPSE

• The murmur can be affected by position.


o In a filled up heart the mitral valves gets farther so the
click moves closer to S1 and the S2 or the following
systolic murmur is longer.
o In an empty heart the click is more prominent thus
giving a louder systolic click.
o Radiation of the murmur will depend on the involved
leaflet.
§ Posterior Leaflet Prolapse: radiate to the base of
the heart
• Systolic displacement of the mitral valve leaflets that is 2 mm § Anterior Leaflet Prolapse: radiate to the axilla
to the left atrium. o The click and murmur occur earlier with standing,
• Aka Systolic click murmur syndrome or Barlow’s syndrome, during the strain phase of the Valsalva maneuver, and
floppy valve syndrome or billowing mitral leaflet syndrome with any intervention that decreases LV volume
• Usually attributed to Myxomatous Degeneration, (preload), exaggerating the propensity of mitral leaflet
osteogenesis imperfecta, and Ehlers-Danlos syndrome prolapse.
• o Conversely, squatting and isometric exercises, which
May be associated with certain conditions
increase LV volume, diminish MVP; the click-murmur
o Connective tissue diseases including Marfan’s syndrome
o Rheumatic fever complex is delayed, moves away from S1, and may
even disappear
• Women > Men: 15-30 y/o (most are tall, thin women)
• May be asymptomatic - pt comes with nonspecific
B. PATHOPHYSIOLOGY
symptoms: chest pain, difficulty of breathing, palpitation,
• The valves are prolapsing towards the LA during systole.
easy fatigability)
There will be poor co-optation of mitral valve so that some
• Symptoms are associated with SEVERE Mitral Regurgitation
blood will go back to LA causing Mitral Regurgitation.
o More severe, more symptoms
C. TREATMENT
• Determined by the severity of mitral regurgitation
• Mild to mod MR: Treat medically
• Symptomatic from Severe MR: Valve replacement

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V.AORTIC STENOSIS • In AS, the heart should pump stronger to overcome the
pressure from the stenosis. There is ventricular wall
hypertrophy.

C. SIGNS AND SYMPTOMS

Cardinal Ave. time to


Symptoms death if
untreated(yrs)
Dyspnea 2 Results from elevation of
pulmonary capillary
pressure caused by
elevations of LV diastolic
pressures secondary to
impaired relaxation and
• Normal aortic valve area= 2-4 cm2 reduced LV compliance
• Moderate Aortic stenosis = < 1.5 cm2 Angina pectoris 3 Reflects an imbalance
• Severe: <1.0cm2 between augmented
myocardial oxygen
A. ETIOLOGY requirements and
• Congenital (bicuspid and unicuspid): reduced oxygen
o Bicuspid aortic valve - Most common Congenital availability
heart valve defect (this is a board exam question)
• Degenerative/calcific - in elderly
• Rheumatic Fever - almost always associated to mitral valve
involvement (developing countries)
• Radiation Exertional 3 Decline in arterial
Syncope pressure caused by
B. PATHOPHYSIOLOGY vasodilation in the
exercising muscles and
inadequate
vasoconstriction in non-
exercising muscles in the
face of a fixed CO, or
from a sudden fall in CO
produced by arrhythmia
• Sudden cardiac death - occurred in 10-20% of severe AS
o MC cause of death in severe AS
o There could also be hemoptysis as a symptom that is
secondary to rupture of pulmonary bronchial venous
connections due to pulmonary hypertension.
• Late stages
o ↓ systolic pressure
o Narrow pulse pressure due to low systolic pressure
§ Pulsus parvus et tardus - Slow rise of peripheral
arterial pulse with delayed peak; Felt at the pulse
o Thrill or “shrudder” palpable in the carotid arteries
o Thrill or palpable S4 in the base

D. MURMUR
• Usually ejection mid systolic murmur
• Crescendo-decrescendo murmur (diamond shape)
• Intensity may decrease as severity increases
• Loudest at base most commonly at 2nd right ICS RPSB
• Valve obstruction ® ↑ LVEDP ® ↑ muscle bulk of LV ® radiating to the carotids
• Gallavardin effect
subendocardial ischemia ® obstruction ® LV failure ®
o Transmission of murmur towards the apex
increased wall stress ® angina/syncope/dyspnea.
• In patients with severe obstruction and preserved cardiac
o Angina: due to ischemia
output, murmur is at least 2/6 and with the Gallavardin
o Syncope: due to less blood to the brain
Effect radiating to the apex, it should be differentiated from
o Dyspnea: due to increase pressure within LA and LV
mitral murmur.

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o Don’t need to open up the patient


o Using Femoral artery going up in the aorta. They place
a pacemaker to increase HR when they do dilation of
stenotic valve to prevent balloon going in and out of the
valve. And after dilation of the balloon, there is now a
new valve

E. ECG
• SOKOLOW’S Criteria - S wave in V1 + R wave in V5
or V6 is ≥ 35 mm
• Axis: LAD
o Classic signs of Left Ventricular Hypertrophy

VI. AORTIC REGURGITATION

F. CXR
• Apex displaced laterally
• Enlarged ascending part of aorta
• Left Ventricular Hypertrophy
• If hypertrophy is present without dilatation, this produces
the rounding border of the cardiac apex in the frontal
projection

• Backflow of blood to left ventricle during diastole


• Widened pulse pressure
o There is backward flow of blood from the aorta into the
left ventricle during diastole. What happens is, there is
increase left ventricular volume and pressure. So when
left ventricle contracts, there is also increase in the
corresponding stroke volume and systolic pressure. This
will increase your blood pressure. However, there is
also a rapid fall of your aortic pressure during diastole.
o If there is fall in the diastolic pressure, and increase in
your systolic pressure, it will create a characteristic
WIDENED PULSE PRESSURE, a situation where
there is increase in pulse pressure. These patients can
have diastolic pressure. There is widened pulse
G. TREATMENT pressure.
• Avoid heavy physical activity § Example: 170/30, 150/40.
• Medication in the treatment of co morbid conditions § Increased LV volume/pressure – increased
including beta-blockers and ACEI can be continued in pulmonary venous pressure – HF symptoms.
asymptomatic § End result of these valve lesions would be heart
o Vasodilation – Increased pressure in LV. Difference in failure
the pressure between LV and aorta will be now
increased. So be cautious giving ACEI/ARBs
• TAVI (Transcatheter Aortic Valve Implantation)

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A. ETIOLOGY C. SIGNS AND SYMPTOMS


• Valvular • Chronic severe AR
o Congenital (bicuspid) o Jarring of the entire body – if you touch the patient
o Endocarditis he/she will vibrate.
o Rheumatic fever o De-Musset’s Sign
o Myxomatous (prolapse) § Bobbing motion of the head
o Traumatic o Water-hammer pulse/Corrigan’s pulse
o SyphiliS § Rapidly rising pulse that collapse rapidly as arterial
o Ankylosing spondylitis affecting the valve pulse drops during late systole and diastole
• Root disease o Quincke’s pulse
o Aortic dissection § Alternate visible capillary pulsation in the nailbeds
o Cystic Medial degeneration after holding the tip of the nail
§ Marfan’s syndrome o Traube’s sign
§ Bicuspid aortic valve § Booming shot (pistol) sound heard over the
§ Nonsyndromic familial aneurysm femoral arteries.
o Infection: Aortitis o Duroziez’s sign
o Hypertension § To and from murmurs heard in the femoral artery
when it is lightly compressed with a stethoscope
B. PATHOPHYSIOLOGY o Other signs
§ Hill’s sign - popliteal systolic blood pressure
exceeding brachial systolic blood pressure by 60
mmHg or greater
o Widened pulse pressure
o LV heave

D. MURMUR
• High-pitched, blowing, decrescendo diastolic murmur
heard best the 3rd ICS Left parasternal border
• A mid-systolic ejection murmur at the base of the heart in
isolated AR
• To-And-Fro murmur
o Forward flow and the backward flow
respectively.
• Austin-Flint murmur
o Soft/Low pitched rumbling
o Beat to beat diastolic murmur due to the anterior
displacement of the anterior leaflet of the mitral valve
by the aortic regurgitation backflow of blood closing the
mitral valve
o During regurgitation of the aorta, the regurgitated jet
causes the anterior mitral valve leaftlet to not fully open
which causes this murmur

NOTE: Read the pathophysiology, This was discussed by


Dr. Olarte

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E. ECG H. TREATMENT
• Left Ventricular Hypertrophy (V1 and V6) • Also depends on the severity
• Left atrial enlargement • TAVI cannot be done
• Left axis deviation • In Severe cases: Do Aortic Valve Replacement
• There is also widening of the QRS complexes meaning there
is already fibrosis and leads to poor prognosis.

VII. TRICUSPID REGURGITATION


F. CXR
• Displaced apex to the lateral and downwards of the left side

A. ETIOLOGY
• Primary
o Rheumatic
o Endocarditis
G. 2D ECHO o Congenital (Ebstein Anomaly)
• Mosaic color flow across the aortic valve during o Trauma
diastole o Papillary muscle injury
• LV size is increased • Secondary
o RV and tricuspid annular dilatation
o Chronic RV apical pacing: MC due to RV
enlargement due to pulmonary artery hypertension
FUNCTIONAL TR
• Most common is RV enlargement – Mitral stenosis

B. SIGNS AND SYMPTOMS


• Signs of Right sided heart failure
• RV pulsation along the left parasternal border
• Carvallo’s sign:
o Functional Tricuspid Regurgitation that increases to
intensity during inspiration and diminishes during
expiration

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C. MURMUR F. 2-D ECHO


• Blowing systolic murmur along the 4th ICS LPSB
• Pansystolic/ holosystolic but differentiate from MR (look for
the Carvallo’s sign)
• RV pulsation/heave can be heard

D. ECG
• Signs of RAE, RVH
• Right atrial enlargement
o Tall R wave in V1 and V2, persistent S wave in V5 and G. TREATMENT
V6 • Treat primary cause
• P waves has increased amplitude more than 2.5 • Treatment of left sided anomaly
• Right Axis deviation
• No placement of metallic valves, they are prone to
• Look for Right Bundle Branch Block blood clots, because it is a low-flow area
• Severe functional TR
o Valve annuloplasty (purse string or insertion of ring)

VIII. PULMONIC STENOSIS

E. CXR
• Bulging portion is more than half of the space
• Shows RA and RV enlargement

• Fusion of pulmonic valves


• Obstruction of the right ventricular outflow tract due to the
fusion of the pulmonic valves

A. ETIOLOGY
• Congenital: more common cause
• Carcinoid

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B. MURMUR C. TREATMENT
• Increased splitting of S2 • NO REPLACEMENT of pulmonic valve
• Harsh crescendo-decrescendo ejection murmur heard best at • Done using Ballooning (dilating the valve)
the left parasternal 2nd or 4th ICS and when the patient leans o Done percutaneously
forward (Diamond shape)

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IX. ADDENDUM

END

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