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Surgery 4.

3a

Dr. Villanueva
November 10, 2014

ACQUIRED CARDIAC DISEASES


OUTLINE
I.

Cardiac Assessment
a. Cardiac Function Disability
b. Diagnostics and Ancillary Procedures
II. Coronary Artery Disease
a. Coronary Anatomy
b. Coronary Angiography
c. Viability Studies
d. Revascularization
III. Valvular Heart Diseases
a. Mitral Valve Diseases
i. Mitral Stenosis
ii. Mitral Regurgitation/Insufficiency
iii. Mitral Valve Operative Techniques
b. Aortic Valve Diseases
i. Aortic Stenosis
ii. Aortic Regurgitation/Insufficiency
c. Tricuspid Valve Disease
i. Tricuspid Stenosis and Insufficiency
ii. Multivalve Disease
*Most of the things discussed here are from Schwartz and powerpoint

CARDIAC ASSESSMENT
Symptoms
o Chest discomfort, fatigue, edema, dyspnea, palpitations, syncope.

Family history

Past medical history


*Sample Case at the appendix

Personal habits

Functional capacity

Review of systems
Physical examination foundation for evaluation with acquired cardiac
diseases (ACD) requiring surgical intervention.

Appropriate diagnostic studies

CANADIAN CARDIOVASCULAR SOCIETY (CSS) ANGINA CLASSIFICATION


Ordinary physical activity, such as walking or climbing stairs,
Class
DOES NOT CAUSE angina. Angina may occur with strenuous or
I
rapid or prolonged exertion at work or recreation.
There is SLIGHT limitation of ordinary physical activity. Angina
may occur with walking or climbing stairs rapidly, walking
Class uphill, walking or stair climbing after meals or in the cold, in
II
the wind, or under emotional stress, or walking more than two
blocks on the level, or climbing more than one flight of stairs
under normal condition at a normal pace.
There is MARKED limitation of ordinary physical activity.
Class Angina may occur after walking one or more blocks on the
III
level or climbing one flight of stairs under normal conditions at
a normal pace.
Class There is INABILITY to carry on any physical activity without
IV
discomfort. Angina may be present at rest.

Grading system for patients with ischemic heart disease

Mainly referred for surgery of coronary artery disease


Used to incorporate angina symptoms into the functional assessment
for prognostic value.

CARDIAC FUNCTION DISABILITY


NEW YORK HEART ASSOCIATION (NYHA) FUNCTIONAL CLASSIFICATION
Patients with cardiac disease but WITHOUT resulting
Class I
limitation of physical activity. Ordinary physical activity does
not cause undue fatigue, palpitation, dyspnea, or angina pain.
Patients with cardiac disease resulting in SLIGHT limitation of
physical activity. They are comfortable at rest. Ordinary
Class II
physical activity results in fatigue, palpitation, dyspnea, or
angina pain.
Patients with cardiac disease resulting in MARKED limitation of
physical activity. There are comfortable at rest. Less than
Class III
ordinary physical activity causes fatigue, palpitation, dyspnea,
or angina pain.
Patients with cardiac disease resulting in an INABILITY to carry
on any physical activity without discomfort. Symptoms of
Class IV cardiac insufficiency of the angina syndrome may be present
even at rest. If any physical activity is undertaken, discomfort is
increased.

Used to determine the functional capacity of the patient

Used for evaluating patients severity of disability, in comparing


treatment regimens, and in predicting operative risk
The NYHA is the most widely used classification system in categorizing
patients based on their functional status.

DIAGNOSTIC AND ANCILLARY PROCEDURES


ELECTROCARDIOGRAM AND CHEST X-RAY

Figure 1. The PA (left) and Lateral views (right)


ECHOCARDIOGRAPHY (TTE/TEE/DOBUTAMINE STRESS ECHO)
Utilizes reflected sound waves to image the heart.
Evaluate structural diseases of the heart.

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ECG
o Summary of electrical impluses generated by the heart
o Used to check for rhythm disturbances, heart block, ventricular
strain, signs of atrial and ventricular enlargement, and signs of
ischemia
Stress ECG- requires a patient to exercise to a target rate to help
diagnose ischemic pathologies
Chest X-ray
o detect pulmonary pathology, sequelae of heart failure, as well as
hardware from previous procedures (e.g. prosthetic valves)
a) PA view

Cardio-thoracic ratio of >0.5= cardiac enlargement

Lung pathology such as pleural effusion and congestion


b) Lateral view

Substernal fullness = right ventricular enlargement

Retrocardiac fullness= left atrial enlargement

STANDARD TRANSTHORACIC ECHOCARDIOGRAPHY (TTE)


Excellent non-invasive screening test to evaluate cardiac size, wall
motion, and valvular pathology
Used for viewing LV enlargement and thickening, nature of the 4
cardiac valves, any fluid accumulation, ascending aorta and the aortic
root

Page 1 of 15

SURGERY 4.3A
1.

Parasternal Long Axis View

Cuts the areas of the heart longitudinally

TRANSESOPHAGEAL ECHOCARDIOGRAPHY (TEE)


Invasive test used when more precise imaging is required or when the
diagnosis is uncertain after a transthoracic study
Better used for viewing posterior structures of the heart
Probe inserted via the mouth and it goes behind the heart to check the
structures near the esophagus like the left atrium and the mitral valve

3D ECHO
Useful in the evaluation of mitral regurgitation

Figure 2. Parasternal Long Axis View

2.

Parasternal Short Axis View

A series of views from apex to the pulmonary artery may be


obtained by tilting and shifting along the line of the long axis

STRESS ECHO
For patients with signs of ischemia and cardiac dysfunction

RADIONUCLIDE STUDIES (THALLIUM SCAN/PET SCAN)


Thallium Scan
Currently the most widely used myocardial perfusion screening
study to assess myocardial ischemia.
The amount of uptake at both rest and stressed states are
compared to assess ischemia and viability of myocardium
Initial uptake of thallium into myocardial cells is dependent upon
myocardial perfusion while delayed uptake depends on
myocardial viability
PET Scan
o Used to assess myocardial viability in underperfused areas of the
heart
o More sensitive than thallium scan
o Most useful in determining whether patients with CHF might
improve with operative revascularization

MRI
Delineates the transmural extent of MI
Distinguishes bet. reversible and irreversible myocardial ischemic injury
Useful in the assessment of patients with myocardial scarring and
ventricular aneurysms when ventricular remodelling surgery is an
option
Use of gadolinium can enhance scar tissue and are very useful in
viability assessment

Figure 3. Parasternal Short Axis view (top left); Parasternal Short Axis view at
the level of the aortic valve (top right); Parasternal Short Axis view at the
level of the papillary muscles. It is used to check for weakness of the
myocardium, as well as thickening or thinning of the cardiac muscle walls
(bottom)
3.

Apical 4-Chamber View


Useful window for visualizing all four cardiac chambers
simultaneously as well as the tricuspid and mitral valves.

Figure 4. Apical 4-Chamber view


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CARDIAC CATHETERIZATION
Measures intercardiac pressures and cardiac output
Localizes and quantifies intercardiac shunts
Determines internal cardiac anatomy and ventricular wall motion by
cineradiography
Determines coronary anatomy by coronary angiography
o Coronary angiography = primary diagnostic procedure for
determining degree of coronary artery disease
CT CORONARY ANGIOGRAPHY
Less invasive imaging of coronary anatomy
Extremely sensitive in detecting coronary stenosis
CORONARY ARTERY DISEASE (CAD)
Multifactorial disease in which the primary etiology is atherosclerosis.
Risk factors include hyperlipidemia, smoking, diabetes, hypertension,
obesity, sedentary lifestyle, male gender, and elevated levels of Creactive protein, lipoprotein A, and homocysteine.
Most important factor in long term treatment is the modification of
risk factors such as immediate cessation of smoking, control of
hypertension, weight loss, and reduction of serum cholesterol.
Myocardial ischemia from CAD may result in angina pectoris, MI, CHF,
cardiac arrhythmias, and sudden death.
Angina pectoris (periodic substernal chest pain that typically appears
with exertion and may radiate to the left upper extremity) is the most
common manifestation.
Page 2 of 15

SURGERY 4.3A
Myocardial infarction is a serious consequence of CAD occurring when
ischemia results in myocardial necrosis.

Pre-operative evaluation includes complete history and PE, chest X-ray,


ECG, and baseline ECG.
Patients functional status is of importance because quality of life
improvement and symptomatic relief are both goals of therapy.
Cardiac catheterization (coronary angiography) is the GOLD
STANDARD. Shows coronary anatomy and degrees of stenosis are
delineated allowing for planning of surgical revascularization.

CORONARY ANATOMY
HEART
Base lies opposite the middle thoracic vertebra
th
Apex at 5 intercostal space, 10 cm from the midline
Measures 12 cm in length, 8 cm in width, and 6 cm in thickness
Weighs 280 grams

FIgure 5. The coronary artery and its branches.

RIGHT CORONARY ARTERY


Arises from the anterior/right coronary aortic sinus
Runs forward between the pulmonary trunk and right atrium.
Descends in the right coronary sulcus to reach right (acute) cardiac
order and continues posteriorly.
Does not reach crux of heart (junction of interatrial and interventricular
grooves) in 20%, reaches cruz and extends slightly beyond in 60%, and
may reach left heart border in 20%.
BRANCHES:
1. Atrial branches
o Supply
the
anterior
and
the
lateral
surface
of the right atrium
o One branch supplies the posterior surface of both left and
right atria
2. Right anterior ventricular branches
o Usually 2 to 3 branches
3. Right marginal branch
o Considered by some to be the largest anterios right
ventricular artery often reaching the apex
o Size often reciprocal to that of other anterior ventricular
branches
4. Posterior descending (or interventricular) artery
o Supplies both ventricles
o Anastomoses with the anterior interventricular branch of the
left coronary artery
5. Atrioventricular nodal artery
o Arises from the right coronary artery in 80-85% of patients
(right-dominant)
LEFT CORONARY (MAIN) ARTERY
Passes forward between pulmonary trunk and left atrium
Varies from a few mm to a few cm in size
Usually has no branches

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Occasionally gives rise to an atrial branch


Rarely gives rise to sinoatrial artery
Supplies the major part of the heart, including the greater part of the
left atrium, left ventricle and ventricular septum
LEFT CORONARY ARTERIES
Larger than the right coronary artery
Arises from the left posterior (left coronary sinus)
Enters the anterior interventricular groove and divides into anterior
descending and circumflex arteries.
In 30% of cases, there is a 3rd branch called ramus intermedius
LEFT ANTERIOR DESCENDING ARTERY
Runs towards the apex in the anterior interventricular groove
Sometimes embedded in or crossed by bridges of myocardium (5-12%)
Passes around the apex 2/3 of the time, traversing 1/3 to of posterior
interventricular septum to anastomose with the PDA
Anterior ventricular branches
o Diagonal branches
Septal branches
o Anterior septal branches supply ventral 2/3 of interventricular
septum
o Posterior septal branches supply posterior septum a variable
distance from apex
LEFT CIRCUMFLEX ARTERY
Following the atrioventricular groove, it winds around the left margin
of the heart and anastomoses with the right coronary artery
BRANCHES:
1. Left marginal branches
2. Anterior ventricular branches
o Usually 2 to 3
o Course parallel to diagonal artery and replace it when absent
3. Atrial branches
4. Artery to sinus node (35%)
o Passes over and supplies the left atrium
o Encircles the superior vena cava, supplying the SA node and
the right atrium
5. Artery to AV node (20%)
o When left circumflex artery provides posterior interventricular branch
CORONARY ANGIOGRAM

Figure 6. Coronary Angiogram

In this invasive technique, the coronary arteries are approached using


catheters inserted via the femoral artery or the radial artery. The
selective Judkins Left/Right coronary catheters used in this technique
have pre-formed curvatures such that when the catheter is inserted, its
tip will lodge in the ostium of the left/right coronary artery.
In this procedure the coronary arteries are filled up with dye
introduced via the catheters.
Hypodense areas or irregularities seen are those portions in the blood
vessels which some dye or none at all can pass through. Therefore
irregularities signify partial or complete obstruction of the arteries
with calcifications
Page 3 of 15

SURGERY 4.3A

SELECTIVE JL4 CATHETER


Judkins Left coronary catheter (JL4) have special pre-shaped double
curve and end-hole tip
The size of the segment between the primary and secondary curve
determines the size of the catheter (3.5, 4.0, 5.0, 6.0)
The size of JL is selected depending on the length and width of the
ascending aorta (small person needs JL 3.5 while a large person or
dilated asceding aorta needs 5.0 or 6.0)
JL4 fits most patients
Technique for cannulation is simple: catheter tip follows ascending
aorta border and falls into left main coronary ostium (should happen
without an abrupt jump)

o TECAB total endoscopic coronary bypass


PCI (angioplasty) percutaneous coronary intervention
Others
o TMR transmyocardial laser revascularization
o Biomolecular therapy and tissue engineering

Figure 9. Grafts in CABG


Figure 7. JL4 catheter

SELECTIVE JR4 CATHETHER


Is sized by the length of the secondary curve and it comes in 3.5, 4.0
and 5.0
JR is advanced into ascending aorta (usually LAO projection) with the
tip directed caudally
Cannulating right coronary artery:
o Advance into right coronary cusp and rotate 45 to 90 clockwise
while the tip is pulled back -3cm
o JR tip is advanced 2-4 cm above the valve and rotated clockwise
45o to 90o, with tip rotating downward
o JR4 does not use contralateral wall support
o Nylon vs polyurethane catheters feels different

CARDIOPULMONARY BYPASS/HEART-LUNG MACHINE

Figure 10. Heart-lung machine. Diagrammatic llustration of blood


coming from right pumped back to the aorta. After it is
oxygenated will go through roller pump and brought to aorta. In a
heart lung machine, there are lines to drain the blood and a line to
pump the blood back to the patient.

Figure 8. JR4 Catheter


Note: Judkins LEFT catheter = LEFT coronary artery
Judkins RIGHT catheter = RIGHT coronary artery
VIABLE STUDIES (discussed above):

Thallium Scan

PET Scan

MRI
REVASCULARIZATION
Prolong life and reduce major cardiovascular events
Improve the quality of life and functional status
o Decrease the possibility of a heart attack in the future
o Symptoms like chest pain will disappear in 80-90% of cases
*Refer to appendix for guidelines for revascularization w/ percutaneous
coronary intervention & coronary artery bypass grafting in patients
w/angina

OPTIONS FOR REVASCULARIZATION


Surgical (CABG)
o Conventional ON-pump coronary artery bypass
o Off-pump coronary artery bypass
o MIDCAB minimally invasive direct coronary artery bypass

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ACCESS: MEDIAN STERNOTOMY


In coronary artery bypass grafting, the entire chest is opened from
suprasternal notch to xiphoid process, then cut by using a sternal saw
to split open the sternum. And then a retractor is placed to separate
the sternum.

MYOCARDIAL PROTECTION (not discussed)

Cardioplegia was developed as a protective solution to induce both cardiac


asystole and protect the myocardium from ischemic injury.
When infused through the coronary circulation, cold high-potassium
cardioplegic solution produces diastolic arrest and slows metabolic activity,
protecting the heart from ischemia.
The arrested heart allows the surgeon to work precisely in the heart in a
motionless, bloodless field.

OPERATIVE TECHNIQUES
Bypass Conduit Selection
o The most important criterion in conduit selection is graft patency.

Internal thoracic artery - conduit with the highest patency


rate which is commonly left attached proximally to the
subclavian artery and anastomosed distally to the target
coronary artery.
o Arterial grafts: internal thoracic a., internal mammary a. radial a.,
R gastroepiploic a., free inferior epigastric a., splenic a.
o Venous grafts: greater saphenous v., lesser saphenous v.
Page 4 of 15

SURGERY 4.3A
o

Indications: chronic angina, unstable angina, post-infarction


angina, asymptomatic patients with atypical symptoms who have
easily provoked ischemia during stress testing
Conventional Coronary Artery Bypass Grafting (CABG)
o Performed with median sternotomy, cardiopulmonary bypass, and
cardioplegia/myocardial protection.
o Proximal anastomoses are then performed directly onto the
ascending aorta or onto pre-existing grafts.
o The left internal thoracic artery to left anterior descending graft is
frequently performed to avoid kinking or disruption of the bypass.
Off-pump Coronary Artery Bypass (OPCAB)
o To avoid the adverse consequences of cardiopulmonary bypass.
o With OPCAB the heart is left beating
o Requires use of myocardial stabilization devices which help
portions of the epicardial surface to remain relatively immobile
while anastomoses are being performed.
o Creative maneuvers have been developed, including repositioning,
opening the right pleural space to allow for cardiac displacement
in exposing various surfaces of the heart.
o Temporary proximal occlusion of the coronary artery being grafted
is necessary to provide a bloodless target.
*On-pump CAB- uses cardiopulmonary bypass

Figure 11. Off-pump Coronary Artery Bypass (OPCAB) (left) Involves


performing coronary bypass surgery on a beating heart, without the use of a
cardiopulmonary bypass. The use stabilization devices (right) allows the
surgeon to make precise anastomoses while the heart remains beating.
Minimally Invasive Direct Coronary Artery Bypass (MIDCAB)
o An extension of the off-pump coronary revascularization
technique.
o Performed using a left anterior mini-thoracotomy through which
mobilization of the left internal thoracic and direct in situ
anastomosis to the left anterior descending artery
o Applicable to single-vessel disease.
Other operative techniques
o Total Endoscopic Coronary Artery Bypass
o Hybrid Coronary Revascularization
o Transmyocardial Laser Revascularization
o Regenerative Medicine and Tissue Engineering
VALVULAR HEART DISEASE

Figure 12. Valves of the heart


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Age-associated and acquired conditions represent the primary causes


of valvular heart disease.
The most common screening method for valvular heart disease is
cardiac auscultation, with murmurs classified based primarily on their
timing in the cardiac cycle, but also on their configuration, location and
radiation, pitch, intensity and duration.
Although auscultation may provide initial evidence of valvular disease,
associated signs and symptoms may help narrow the diagnosis.
Several diagnostic/imaging examinations to evaluate valvular disease
o Electrocardiogram
o PA and L view X-ray
o Transthoracic echocardiography (gold standard)
Regardless of etiology, valvular heart disease can produce a myriad of
hemodynamic drangements.

Valvular heart diseases:


o Mitral stenosis, mitral insufficiency, aortic stenosis, aortic
insufficiency, tricuspid stenosis and insufficiency, multivalve ds.

MITRAL VALVE DISEASES


MITRAL STENOSIS

ETIOLOGY
o Rheumatic Heart Disease/Rheumatic fever (60% of cases of
acquired mitral stenosis)
o Other causes:

Left atrial myxoma

Ball valve thrombus

Mucopolysaccharidosis

Previous chest radiation

Severe annular calcification

CLASSIFICATION
o Normal Mitral Valve Area: 4 -6 cm2(Schwartz 4-5 cm2)
o Mild MS: 1.6 2.5 cm2
Begin experiencing symptoms upon exertion
o Moderate MS: 1 1.5 cm2
Symptoms may begin at rest
2
o Severe MS: <1 cm
Any physical exertion is typically limited
o NOTE:

1 cm2 is the critical point such that less than this, surgery is
already needed in which the patient requires valve repair or
replacement.
When the valve area is reduced to <2.5 cm2, patients may
begin to experience symptoms when the transmitral gradient
is exacerbated by conditions that either increase transmitral
flow or decrease diastolic filling time.
Symptoms may begin to occur at rest with the onset of
moderate stenosis.
Any physical exertion is typically limited by the time the MV
area is <0.8 to 1.0 cm2

Initial Event: fibrous thickening & commissural fusion followed by


fibrosis & shortening of the subvalvular apparatus (chordae tendineae)
and calcification of the valve and subvalvular apparatus
The resulting stenotic MV has a funnel-shaped apparatus/ with a
significantly narrowed orifice obliterated by interchordal and
commissural fusion.

CLINICAL MANIFESTATIONS
o First clinical signs of MS and are associated with pulmonary
venous congestion

Exertional dyspnea

Decreased exercise capacity

Orthopnea

Paroxysmal Nocturnal Dyspnea (PND)


o Hemoptysis and pulmonary edema may develop as the venous
hypertension worsens
Page 5 of 15

SURGERY 4.3A
o

Advanced MS can cause pulmonary arterial hypertension and


subsequent right heart failure, manifested as:

Jugular Venous Distention (JVD)

Hepatomegaly

Ascites

Ankle edema
o Auscultatory triad: best heard at the apex

opening snap 2o to immobility of chordate

apical crescendo diastolic rumble due to rapid entry of blood


into left ventricle
st

increased 1 heart sound due to rapid closing of MV


o Atrial fibrillation

May develop as left atrial pathology worsens, causing atrial


stasis and subsequent thromboembolism. [4]
DIAGNOSTICS
o Electrocardiogram (ECG) atrial fibrillation, left atrial enlargement
(P mitrale large P wave), right axis deviation
o Chest X-ray

double density sign behind the right atrial shadow (Left


Atrial Enlargement on PA view)
The overall heart size may be normal but the
enlargement of the left atrium and the pulmonary
artery may obliterate the normal concavity between the
aorta and the left ventricle, thus, producing a straight
left border of the heart.

Calcification

Pulmonary congestion

Basal interstitial edema with engorgement of lymphatics


(Kerley B lines)
o 2D Echocardiogram
TEE- diagnostic tool of choice

Left atrium enlargement

Elevated mitral valve gradient (pressure gradient being


produced when the left atrium pushes blood into the orifice)
2

Significantly reduced mitral valve area (<1 cm )


TREATMENT
o Valvuloplasty
o Commissurotomy
o Percutaneous Balloon Mitral Valvuloplasty
o Valve replacement

MOBILITY

Highly
mobile
valve
with
leaflet tips only
restricted

Leaflets mid &


base
portions
with
normal
mobility

Valve continues
to move forward
in
diastole,
mainly from the
base

No or minimal
forward
movement
of
leaflets
in
diastole

LEAFLET
THICKENING
Leaflets near
normal
in
thickness (45mm)
Mid leaflets
normal,
marked
thickening of
margins
(58mm)
Thickening
extended
through entire
leaflet
(58mm)

Marked
thickening of
all
leaflets
tissue (>8mm)

SUBVALVAR
THICKENING
Minimal
thickening just
below the mitral
leaflets
Thickening
of
chordal
structures
extending up to
1/3 of chordal
length

CALCIFICATION
A single area of
increased echo
brightness
Scattered areas
of
brightness
confined
to
leaflet margins

Thickening
extended to the
D/3
of
the
chords

Brightness
extended
into
the mid portion
of the leaflets

Extensive
thickening
&
shortening of all
chordal
structures
extending down
to
papillary
muscles

Extensive
brightness
throughout
much of leaflet
tissue

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MITRAL REGURGITATION/INSUFFICIENCY
ETIOLOGY:
o Myxomatous degeneration
o Rheumatic Fever
o Ischemic heart disease
o Infective Endocarditis
o Congenital abnormalities
o Dilated Cardiomyopathy
o Others: Trauma, collagen vascular diseases, previous chest
radiation, hypereosinophilic syndrome, carcinoid disease and
exposure to certain drugs.
CARPENTIER FUNCTIONAL CLASSIFICATION:
Focuses on the functional anatomic and physiologic characteristics
of the MV pathology, and proposes three basic types of diseased
valves based on the motion of the free edge of the leaflet relative
to the plane of the mitral annulus.
Table 2. Carpentier Functional Classification
Annular dilatation or leaflet perforation with normal
Type I
leaflet motion
Leaflet prolapsed or ruptured chordae tendinae with
Type II
increased leaflet motion, typically occurring in patients
with degenerative disease
Restricted leaflet motion with leaflets not reaching the
Type III
proper plane of closure during systole; occurs in (a)
rheumatic patients and (b) chronic ischemic insufficiency

Table 1. Wilkins Score (MV Morphology)


GRADE

Total score can range from 4 to 16


Treatment based on total score:
o 8 and below PBMV or repair
o 8 and above replace mitral valve
Score of 8 = more favorable candidate for balloon valvuloplasty

PATHOPHYSIOLOGY:
Basic pathophysiologic abnormality: retrograde flow of the
portion of the LV stroke volume into the left atrium during systole
due to an incompetent MV or dilated MV annulus.
Acute severe MR can result from ruptured chordae tendineae,
papillary muscle, or infective endocarditis, and causes a sudden
volume overload on both the left atrium and ventricle.
Chronic MR has indolent course, with increasing volume overload
of the left atrium and ventricle as the effective valve orifice size
becomes larger.

As the left atrium becomes more dilated, the development of


AF becomes more likely, disrupting atrioventricular synchrony
and predisposing to thrombus formation

Chronic volume overload may lead to LV contractile


dysfunction

The changes herald LV decompensation and heart failure, and


indicate significant injury to the ventricular myocardium.
CLINICAL MANIFESTATIONS:
o Exertional dyspnea
o Decreased exercise capacity
o Orthopnea
o CHF
o Apical holosystolic murmur with radiation to axilla
In cases of acute severe MR, patients are often very symptomatic
and present with pulmonary congestion and reduced forward
stroke volume.
In cases of chronic MR, patients may remain asymptomatic for
long periods of time due to the compensatory mechanisms of the
remodeled LV. However, once the LV begins to fail, patients
become increasingly symptomatic.
Page 6 of 15

SURGERY 4.3A

In general, the direction of the mitral valve regurgitant jet is opposite


the leaflet involved.
DIAGNOSTIC:
o 2D Echocardiogram (TTE/TEE)

Left atrium 5 6 cm --> AF

Propensity for atrial fibrillation is greatly increased when the


left atrial size is >4.5 5.0 cm
Coronary angiography must be performed preoperatively in
hemodynamically stable patient rhythm status and the degree of
pulmonary congenstion.
In chronic MR, ECG and chest X-ray are performed to assess
FUNCTIONAL MITRAL REGURGITATION
o Mitral regurgitation secondary to ventricular dysfunction with
structurally normal valve leaflets and subvalvar apparatus.
o Underlying pathology: LV dyssynchrony , annular dilatation, LV
distortion
o Classification:

Ischemic Functional MR (IMR)

Pure Functional MR (FMR)


o Treatment:

Repair complete semi-rigid or rigid ring

Replacement

+ CABG
LESIONS IN THE MITRAL VALVE

COMMISSUROTOMY
o Open mitral commissurotomy permits direct and careful
examination of mitral valve and chordate tendinae, removal of
atrial thrombus, division of fused commissures and leaflets,
mobilized scarred chordate tendinae, debride calcifications,
correct pre-existent mitral regurgitation.
PERCUTANEOUS BALLOON MITRAL VALVULOPLASTY (PBMV)
o The balloon is introduced via the femoral vein and then inserted
across the mitral valve, breaking the mitral valve leaflets.
o Not a very accurate procedure; can only increase the mitral valve
orifice
o Done in patients who are not good candidates for surgical
procedures (can serve as a bridge to the definitive surgery)
o May be done for uncomplicated mitral stenosis.
o Increases the mitral valve area to approximately 2 cm2 to
significantly cause decline in the left atrial pressure and
transvalvular gradient.
MITRAL VALVE REPAIR
On opening the atrium, the endocardium is examined for a jet
lesion, a roughened area caused by a regurgitant jet striking the
wall.
o Anterior Leaflet Procedures
The anterior leaflet may be repaired via chordal shortening,
chordal transposition, artificial chordal replacement, and
triangular resection of the anterior leaflet.

Figure 14. Anterior leaflet procedure


o
Figure 13. Parts of the Mitral Valve
PART
Leaflets
Chords
Papillary Muscle
Annulus

Posterior Leaflet Procedures


Triangular resection of the posterior leaflet. Excision of the
diseased leaflet tissue extends down towards but generally
not to the mitral annulus.

LESION
Fused, thickened, calcified, redundant
Elongated, shortened, ruptured,
Fused
Dilated, calcified

MITRAL VALVE OPERATIVE TECHNIQUES


Performed in an arrested heart with median sternotomy/minimally
invasive incisions (mini-thoracotomy or partial sternotomy) and the
assistance of cardiopulmonary bypass
MV is commonly exposed through a left atrial incision placed posterior
and parallel to the intra-atrial groove, or through a right atriotomy with
transseptal incision.

Indications for surgery:


o Development of pulmonary hypertension
o Mitral valve area is <1 cm2
o Embolic events

Indications for valvuloplasty


o Mitral stenosis with pliable leaflets
o
No valvular calcifications
o No deformation of chordate tendinae

Contraindication for valvuloplasty


o Presence of moderate mitral regurgitation
o Thickened and calcified mitral valve leaflets
o Scarring and calcification of subvalvular apparatus
Group 14 | QUIJANO, QUIMBO, QUITOY, RAMIREZ

Figure 15. Posterior leaflet procedure


Annuloplasty
Annular dilation is generally corrected using a MV
annuloplasty device, such as a ring or partial band, and is
known to improve the durability of MV repair.
Remodel the annulus, restrict annular dilation while
maintaining the physiologic sphincter motion of the annulus,
and support of physiologic motion.

Figure 16. Annuloplasty


Page 7 of 15

SURGERY 4.3A

Edge-to-edge Repair

Also called double-orifice repair for MR

Involves taking the free edge of the anterior leaflet to the


opposing free edge of the posterior leaflet giving the valve
[4]
a double-orifice bow tie configuration.

Used for anterior leaflet pathology, ischemic insufficiency,


endocarditis, and dilated cardiomyopathy

Late result not well established


o Robotic MV Surgery

Da Vinci Robot

Good results but a disappointingly high early valve repair


failure rate
o Newer techniques:

Pericardial patch augmentation

Tricuspid autographs
o Advantages over MV Replacement:
Preservation of the patients native valve & subvalvular
apparatus

Better (lower) operative mortality


Better postoperative function and survival

Better functional outcomes

Better long-term survival (Degenerative)

Avoidance of complications related to lifelong anticoagulation


or systemic thromboembolism
Lower prosthetic valve failure after surgery
MITRAL VALVE REPLACEMENT
o watch out for the left circumflex artery
o Indication: dense calcification of leaflets or subvalvular apparatus
or with significant mitral regurgitation
o To preserve left ventricular function, the chordate and posterior
leaflet of native valve must be preserved.
o Procedure:
1. Expose the valve, make an incision in the anterior mitral leaflet
at approximately the 12 oclock position, and excise leaflet
tissue as needed.
2. The papillary muscles are reattached to the annulus and, if
possible, the posterior leaflet along with its associated
subvalvular structures are preserved.
3. The annulus is subsequently sized, and an appropriate mitral
prosthesis is implanted using pledgeted horizontal mattress
sutures.
4. The annular sutures may be placed from the atrial to the
ventricular side, seating the valve intra-annularly, or from the
ventricular to the atrial side, seating the valve in a supraannular position.
5. When placing the mattress sutures, care must be taken to stay
within the annular tissue may cause injury to circumflex
coronary artery posterolaterally, the atrioventricular node
anteromedially, or the aortic valve anterolaterally.
6. Sutures are subsequently placed through the sewing ring, and
the valve prosthesis is lowered onto the annulus, where it is
secured.
Factors associated with increased operative risk for MV
replacement include:

Age

Left ventricular function

Emergent procedure status

NYHA functional status

Previous cardiac surgery

Associated coronary artery disease

Concomitant disease in another valve

Group 14 | QUIJANO, QUIMBO, QUITOY, RAMIREZ

NOTE: in the management of mitral stenosis, try the less invasive


procedures first such as PBMV before you move on to the more
invasive procedures.

SURGICAL OPTIONS FOR VALVE REPLACEMENT


Valve repair is increasingly indicated, especially in aortic, mitral or
tricuspid insufficiency, valve replacement may be necessary in certain
patient populations.
Valve replacement can be accomplished with either mechanical or
biological prostheses.
Choice of valve depends many patient-specific factors including age,
health status, desire for future pregnancy, indication or
contraindications to anticoagulation therapy.
Mechanical valves
o Highly durable
o Ex. Ball-in-cage valve, Tilting disk
(monoleaflet/bileaflet)
o Require
permanent
anticoagulation therapy (lifelong)
and careful monitoring of the
International Normalized Ratio
reduces the risk of thromboembolic events and hemorrhagic
complications
o High risk of valve thrombosis and thromboembolic sequelae
o Not advisable to young women who is planning to have future
pregnancies due to use of anticoagulant.
o Patient with indications for systemic anticoagulation may benefit
from mechanical valves.
o For patients with renal failure, on hemodialysis, or with
hypercalcemia.
o Preferred in patients with expected long life spans who are
candidates for anticoagulation therapy and patients in AF
Tissue Valves
o One implanted from another
species, such as porcine xenograft,
bovine, or equine pericardium
o Stented valves are the most
commonly implanted and the most
popular valve in the U.S> is stented
bovine pericardial valve.

Disadvantage: smaller effective orifice area especially with


small prosthetic valve area
o Stentless minimizes the limitations in flow characteristics seen in
patients with small prosthetic valve.
o Less thrombogenic
o Recommended for patients averse to systemic anticoagulation
therapy and for patients >65 years old
o Recommended for women planning pregnancy
o More prone to degeneration especially in the mitral position.

Increased degeneration in patients in renal failure,


hemodialysis, or with hypercalcemia
o Preferred in patients without other indications for anticoagulation
therapy

>60 years of age for aortic position

>70 years for mitral position


Homografts
o From human cadavers, also known as allografts
o Have been used for aortic valve replacement and pulmonary valve
o Risk of thromboembolic complications with homograft is low
o Systemic anticoagulant is not required
o Have been shown to have some advantages in patients with
endocarditis
o Uncertain long-term durability in the face of tissue degeneration

Page 8 of 15

SURGERY 4.3A
Autograft
o The diseased aortic valve is replaced using the patients native
pulmonary valve graft as an autograft. (Ross Procedure)
o Particularly beneficial in children

AORTIC VALVE DISEASES


AORTIC STENOSIS
Calcific aortic valve disease, also known as senile or degenerative
disease, is an age related disorder characterized by lipid accumulation,
proliferative, and inflammatory changes, oxidative stress, upregulation
of angiotensin enzyme infiltration of macrophages, and T lymphocytes.

ETIOLOGY:
o Acquired/Degenerative Calcific Disease most common, affecting
older patients particularly >70 years old 50%
o Bicuspid Aortic Valve 30%
o Rheumatic Disease common in developing countries 10-15%

CLASSIFICATION OF AORTIC STENOSIS:


o Normal Aortic Valve Area: 2.5 3.5 cm2
2
o Mild AS: >1.5 cm
o Moderate AS: 1 1.5 cm2
o Severe AS: <1.0 cm2, transvalvular pressure gradient >50 mmHg
o Critical AS: <0.5 cm2, transvalvular gradient 100mmHg

PATHOPHYSIOLOGY:

NOTE: stenosis = pressure overload (concentric hypertrophy);


regurgitation/insufficiency = volume overload (eccentric hypertrophy)

CLINICAL MANIFESTATIONS:
o Exertional dyspnea classic symptom including angina and
syncope[4]
o Decreased exercise capacity (NYHA Functional Classification II or
III)
o Heart failure
o Angina
Due to the increased oxygen demand of the hypertrophied
myocardium in the setting of reduced oxygen supply
secondary to coronary compression
o Syncope
Most common during exertion, as systemic vasodilation in
the setting of a fixed cardiac output causes decreased
cerebral perfusion. It may also occur at rest secondary to
paroxysmal atrial fibrillation and subsequent loss of atrial
booster pump function.
o Harsh basal crescendo-decrescendo (diamond-shaped) systolic
nd
murmur at R 2 ICS with radiation to carotid arteries
o Diminished and delayed peripheral pulse (pulsus parvus et tardus)
Narrow and sustained peripheral pulse
o S4 gallop at apex with development of left ventricular
hypertrophy)

Group 14 | QUIJANO, QUIMBO, QUITOY, RAMIREZ

As the disease progresses, aortic valve closure may follow


pulmonic valve closure, causing paradoxical splitting of the
second heart sound
DIAGNOSTICS:
o Chest X-ray Normal or enlarged cardiac shadow due to LVH
Usually demonstrates a normal heart size, with rounding of
the left ventricular border and apex
Cardiac enlargement is a sign of left ventricular failure and
cardiomegaly, and is a late finding
o Electrocardiogram (ECG) Normal, LVH, complete heart block or
various forms and degrees of atrioventricular or intraventricular
block (due to calcific infiltration of the conduction system) and
atrial fibrillation
o 2D Echo
o Provides an accurate estimate of the peak and mean systolic
transvalvular gradients, which allows calculation of the aortic
valve area
TTE is indicated in all patients with systolic murmur graded
>2/6, a single second hear sound, or symptoms characteristic
of AS
o Cardiac Catheterization and Coronary Angiography
Since the symptoms of AS oftentimes mimic those of
ischemic disease, these may be necessary at the initial
evaluation in patients with AS.
o Stress-echocardiography
May be useful in the asymptomatic patient with AS in order
to elicit exercise-induced symptoms, or abnormal BP
responses during exertion.
Also useful in the evaluation of low-gradient AS in patients
with depressed LV function.
Contraindicated in patients with ischemic heart disease.
COMPLICATIONS:
o A-S-C survival in 5-3-2 years (angina, syncope, CHF)
TREATMENT:
o Valve Replacement
Based on the severity of AS and the overall physical condition
of the patient, aortic valve replacement may be
recommended for the treatment of AS.
In patients with severe calcific AS, this is the only effective
treatment.
Indicated for all symptomatic patients experiencing exertional
dyspnea, decreased exercise capacity, heart failure, angina,
and syncope.
o Ross Procedure
Better outcome
Involves replacing the diseased AV with the patients native
pulmonary valve as an autograft, which is in turn replaced
with a homograft in the pulmonic position. The autograft may
be implanted in the aortic position directly with resuspension
of the valve commissures, or in association with a root
replacement, which requires reimplantation of the coronary
ostia.(See Appendix for illustration)
The primary benefit compared to traditional AV surgery is a
low risk of thromboembolism without the need for systemic
anticoagulation.

Page 9 of 15

SURGERY 4.3A

Figure 17. Ross Procedure in Aortic Stenosis

A small aortic root may be a particularly difficult problem when tissue


valves are placed, as the stented tissue valves have relatively poor flow
characteristics in smaller sizes. This can potentially result in patientprosthetic mismatch. So, if the annulus is <19mm, aortic enlargement
is needed using the following techniques:
o Kono Right Ventricular Outflow Incision
o Manouguian Procedure incision through the non-coronary cusp
into the anterior leaflet of the mitral valve
o Root replacement with homograft done when the two previous
preocedures failed
The average rate of progression once (+) for Aortic Stenosis:
o An increase in jet velocity of 0.3 m/sec/yr
o An increase in mean pressure gradient of 7 mmHg/year
o A decrease in valve area of 0.1 cm2/year

Figure 21. Algorithm in the treatment of Severe Aortic Stenosis.

Figure 18. Konno-Rastan Aortoventriculoplasty


Table 3. Classification of the Severity of Aortic Stenosis in Adults (AHA
Guidelines, 2008)
MILD
MODERATE
SEVERE
Valve Area
2
2
>1.5 cm
1 1.5 cm
<1 cm2
(NV: 2.5 -3.5)
Mean Pressure
<25 mmHg
25 40 mmHg
>40 mmHg
Gradient
Jet Velocity
<3 m/sec
3 -4 m/sec
>4 m/sec

Therapeutic decisions, particularly those related to corrective surgery,


are based largely on the presence or absence of symptoms. Thus, the
absolute valve area (or transvalvular pressure gradient) is not the
primary determinant of the need for aortic valve replacement.

Group 14 | QUIJANO, QUIMBO, QUITOY, RAMIREZ

NOTE: Severe aortic stenosis is not an indication to do the surgical


procedure immediately. The presence of signs and symptoms is the
main determinant. In asymptomatic patients, surgery is recommended
when there are already signs of LV dysfunction that can be determined
using 2D Echo.
AORTIC VALVE REPLACEMENT:
o Results:

Operative Risk: 1 5 %

Perioperative Stroke: 2.8 4.8 %

10-yr Survival: >80% in <65 years old


o Major Operative Risk Factors (STS Database)

Age

Cerebrovascular

Body Surface Area


Accidents

Diabetes Mellitus

Infective Endocarditis

Renal Failure

Prior
cardiac

Hypertension
operation

Chronic Lung Disease

Myocardial Infarction

Peripheral
Vascular
Cardiogenic Shock
Disease

NYHA
Functional
Classification
o NOTE: Check risk factors of the patient, note gradient and PA
lower risk 3% and high risk 7-10%
AORTIC REGURGITATION/INSUFFICIENCY
ETIOLOGY:
o May result from disease of the valve leaflets or of the aortic root
due to:

Degenerative

Congenital Disease

Inflammation

Aortoannular Ectasia

Infectious
disease
Aneurysm of aortic
(Endocarditis, Rheumatic
root
Fever)

Aortic dissection
PATHOPHYSIOLOGY:
Basic pathophysiologic abnormality: retrograde flow of a portion
of the LV stroke volume into the left ventricle during diastole,
producing left ventricular volume overload.

Page 10 of 15

SURGERY 4.3A
Left ventricular
volume
overload/
increased
preload

Increased left
ventricular
strokevolume
during systole

Left ventricular
dilatation

Decreased coronary
perfusion,
increased oxygen
demand

Widened pulse
pressure, low
diastolic pressure

"Afterload mismatch"
and progressive systolic
dysfunction

Blood
regurgitation
into left
ventricle in
diastole

Left ventricular
failure, pulmonary
hypertension

CLINICAL MANIFESTATIONS:
o Asymptomatic
o Dyspnea on exertion
o Decreased exercise capacity
o Palpitations
o Left ventricular heave
o High-pitched decrescendo diastolic blowing murmur 3rd left ICS
sternal border

Diastolic murmur may be short and/or soft because the left


ventricular and aortic pressures often equalize before the end
of diastole.[4]
o Wide pulse pressure

Causes a sensation of pounding in the patients head and


peripherally causes a forceful, bounding and quickly
collapsing pulse (Corrigans or water-hammer pulses)
o S3 gallop heart failure; may be indicative of late disease

Table 4. Common Signs of Aortic Insufficiency


Low-pitched rumbling heart murmur which is best
Austin Flint Murmur heard at the cardiac apex (midsystolic rumble at
the apex that stimulate mitral stenosis)
A pulse characterized by a sharp rise to full
Corrigans Pulse
expansion followed by immediate collapse that is
seen in aortic insufficiency
A pistol shot systolic sound heard over the
Traubes Sign
femoral artery
Rhythmic nodding or bobbing of the head in
De Mussets Sign
synchrony with the beating of the heart
A pulse that is bounding and forceful, rapidly
Watsons Waterincreasing and subsequently collapsing as if it were
hammer Pulse
the hitting of a water hammer that was causing the
pulse
A 20 mmHg difference in popliteal and brachial
Hills Sign
systolic cuff pressures
Consists of an audible diastolic murmur which can
Duroziezs Sign
be hear over the femoral artery when it is
compressed with the bell of a stethoscope
Quinckes Sign
Pulsation of the capillary bed in the nail
Mullers Sign
Pulsation of the uvula

DIAGNOSTICS:
o Chest X-ray cardiomegaly
o Electrocardiogram (ECG) normal, LVH, sinus rhythm, atrial
fibrillation
o 2D Echo primary diagnostic tool to evaluate chamber size, left
ventricular function, degree of insufficiency

Group 14 | QUIJANO, QUIMBO, QUITOY, RAMIREZ

TREATMENT:
o Aortic valve replacement

Performed more commonly


AV repair or replacement may be performed based on the
morphology and severity of valve dysfunction.

Procedure:
Aortotomy is performed, extending medially from
approximately 1 to 2 cm above the right coronary artery
and inferiorly into the noncoronary sinus, and the valve
is completely excised.
The annulus is thoroughly debrided of calcium deposits.
After the calcium has been removed, the ventricle is
copiously irrigated with saline. Annulus is sized and an
appropriate prosthesis is selected.
Pledgeted horizontal mattress sutures are then placed
into the aortic valve annulus and subsequently throught
the sewing ring of the prosthetic valve, taking care to
avoid damage to the coronary ostia, the conduction
system, and the MV apparatus.
o Aortic valve repair
The aneurysmal portion of the aortic root is excised, and the
aortic valve is reimplanted inside a tubular Dacron graft, with
concomitant reimplantation of the coronary arteries.

Alternatively, the aneurysmal tissue and supravalvular tissue


can be excised in their entirety, with subsequent implantation
of the Dacron graft onto the superior aspect of the annulus
and the reimplantation on the coronary arteries.
o Ross Procedure
Poor Long-Term Outcome:
o Ejection Fraction <45%
o Fractional Shortening <25%
2
o End-diastolic Dimension >70 mm (40 mm/m )
2
o End-systolic Dimension >55 mm (30 mm/m )
o Pre-operative end-diastolic/end-systolic volume <2..9
NOTE: If the disease had been caught early such that there is still a
good left ventricular function, the outcome would be better. If the LV
function is already decreased by 45 50%, the prognosis is not that
good anymore.

Figure 22. Algorithm for Chronic Severe Aortic Regurgitation.


Page 11 of 15

SURGERY 4.3A

1.
2.
3.
4.
5.

TRICUSPID STENOSIS AND INSUFFICIENCY


ETIOLOGY:
o Organic: rheumatic fever, endocarditis, rarely trauma
o Functional: mitral valve disease, pulmonary HTN, right ventricular
failure
o Functional is more common than organic tricuspid insufficiency. It
results from dilatation of tricuspid annulus and right ventricle as a
result of pulmonary hypertension and right ventricular failure.
Cross-sectional area:
o Normal tricuspid valve area: 7-9cm2
o Severe tricuspid stenosis: <2cm2
CLINICAL MANIFESTATIONS:
o Jugular vein distention, hepatomegaly, ascites, leg edema, clotting
abnormalities (result from chronic elevation of right atrial pressure
above the range of 15 to 30 mmHg)
o Tricuspid insufficiency produces a prominent systolic murmur
heard best at the left lower sternal border.
o Tricuspid stenosis produces a murmur best heard as a diastolic
murmur at the lower end of the sternum.
DIAGNOSTICS:
o Echocardiography: confirms the diagnosis and differentiates
stenosis from insufficiency
o Chest x-ray: enlargement of the right atrium and right ventricle.
TREATMENT:
o Valve repair (commissurotomy, annuloplasty)
o Valve replacement (necessary when significant tricuspid stenosis is
present, since the entire valve and subvalvular apparatus are
damaged)
INDICATIONS FOR SURGERY:
o Based primarily on clinical findings, which are correlated with
echocardiographic findings and hemodynamics
o Severe insufficiency is indicated by echocardiography when the
regurgitant jet occupies a large part of the atrium, the effective
regurgitant orifice is greater than 40 mm2, or the width of the
vena contracta (narrowest flow) is greater than 6.5 mm.

What does the fox say?? Woof-woof woof-woof woof-woof


What does the heart say??? Beat-Beat-beat-beat-beat-beat

Image from Google

You are like a dictionary.you add meaning to my life

MULTIVALVE DISEASE (CAN BE STENOTIC, INSUFFICIENT, OR BOTH)


Aortic and Mitral Valve Disease
Mitral and Tricuspid Valve Disease
o Most common: mitral disease with functional tricuspid
insufficiency resulting from chronic pulmonary HPN and right
heart failure
Triple Valve Disease
o Usually is a result of chronic aortic and mitral disease with severe
pulmonary HPN, biventricular failure, and functional tricuspid
insufficiency
REFERENCES
Lecture PPT
Lecture recording
2015B trans
th
Schwartzs Principles of Surgery (10 ed.)
th
Sabiston Textbook of Surgery 19 edition

Edited by: Kyle Ompoc

Group 14 | QUIJANO, QUIMBO, QUITOY, RAMIREZ

Page 12 of 15

Surgery 4.3a

Dr. Villanueva
November 10, 2014

ACQUIRED CARDIAC DISEASES


APPENDIX
SAMPLE CASE
GENERAL INFORMATION

C.B.
56 y/o male
Taxi driver
Imus, Cavite
CC: DYSPNEA

HISTORY OF PRESENT ILLNESS


December 2005
December 2010
(+) Submandibular pain
Chest pain noted on exertion
and numbness 40 minutes
Noted also at rest 2-3 times per
after a heavy meal
day, lasting for 10-15 minutes,
(+) Chest tightness with
usually awakening him from
radiation to the left arm
sleep
Admitted for 2 days
(+) Dyspnea on walking 200 m,
and 2 flights of stairs
Prescribed ASA and ISMN x
1 month
Stopped smoking

September 2011
(-) Chest pain
(+) Dyspnea on less than
ordinary
activities;
orthopnea; PND; bipedal
pitting edema

March 2012
(+) Palpitations and respiratory
distress
Admitted
Given Lanoxin and diuretics
incorporated into his chelation
medications
Decided to seek consult at PHC

REVIEW OF SYSTEMS
General: weight loss, loss of appetite
SHEENT: no rash, no visual dysfunction, no redness, no deafness, no
tinnitus, no discharge, no epistaxis, no postnasal drip, no bleeding
gums, no sores
Respiratory: no cough, no hemoptysis, dyspnea on minimal exertion
Gastrointestinal: no nausea, no vomiting, no abdominal pain, no
diarrhea, no hematemesis, no hematochezia, no melena
Genitourinary: no flank pain, no urinary frequency, no hesitancy, no
dysuria, no hematuria
Endocrine: no polyuria, no polydipsia, no polyphagia
Hematologic: no bleeding episodes
Neurologic: no headache, no seizure, no mental changes
Psychiatric: no anxiety, no depression
PAST MEDICAL HISTORY
(+) HPN
(+) DM (2009)
o Metformin 500 mg/tab BID
(-) Asthma/allergy

Group 14 | QUIJANO, QUIMBO, QUITOY, RAMIREZ

PERSONAL/SOCIAL HISTORY AND ENVIRONMENTAL EXPOSURE


(+) 60 pack years smoker
(+) Occasional alcoholic beverage drinker
No illicit drug use
FAMILY HISTORY
(+) CAD
o Sister died of heart attack (<40 y/o)
o Father died of heart attack (<60 y/o)
(+) DM, maternal side
PHYSICAL EXAMINATION
Supple neck, JVP 8 cmH2O, no bruit, no CLAD
Symmetrical chest expansion, no retractions, normal fremitus, no
rales/wheezes
th
Adynamic precordium, AB 6 LICS anterior axillary line, normal rate,
regular rhythm, no heaves nor thrill, soft S1 at the apex, (+) S3, (-) S4,
(+) 2/6 holocystolic murmur at the apex, (-) carvallos
Flabby abdomen, normoactive bowel sounds, soft, no hepatomegaly,
no bruit
No edema, no hyperpigmentation, no cyanosis, pulses full and equal

SALIENT FEATURES
SUBJECTIVE
OBJECTIVE
56 y/o male
2D echo result of MSWA with
depressed EF of 46%
Chest pain and dyspnea on
minimal exertion
Soft S1 at the apex; (+) S3
Orthopnea and PND
2/6 holosystolic murmur at the
apex
Palpitation
Edema
DM
History of previous ACS (Dec
2005, Dec 2010, Apr 2011,
Jun 2011)
60 pack year smoker
Family history of premature
CAD

CLINICAL IMPRESSION
Cardiac Diagnosis:
o Etiology: HCVD
o Anatomic: CAD
o Physiologic: CSA s/p AMI (Dec 2005, Dec 2010, Apr 2011, Jun
2011); functional mitral regurgitation
o Functional: NYHA Class III, CCS III
Other Diagnosis:
o Type II Diabetes Mellitus, controlled

Page 13 of 15

Surgery 4.3a

ACQUIRED CARDIAC DISEASES

Group 14 | QUIJANO, QUIMBO, QUITOY, RAMIREZ

Dr. Villanueva
November 10, 2014

Page 14 of 15

Surgery 4.3a

ACQUIRED CARDIAC DISEASES

Group 14 | QUIJANO, QUIMBO, QUITOY, RAMIREZ

Dr. Villanueva
November 10, 2014

Page 15 of 15