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Acquired Heart

Disease
Dr. Aulia janer
Supervised by :
Dr. Juli Ismail, Sp.B, Sp.B TKV

Cardiac Assesment
History
Symptoms
:
Chest
discomfort,
fatigue,
edema,
dyspnea,
palpitations, and syncope
paying particular attention
to
onset,
intensity,
radiation, duration, and
exacerbating/alleviating
factors
Beware

diabetics,
females, and the elderly
silent angina

Functional
Disability and
Angina

Physical Examination
General appearance : pale, diaphoretic, and
obviously uncomfortable patient
Vital sign, mental status, skin
Palpation : deviation punctum maximum
Auskultation: murmur, rubs, gallop
Extracardiac manifestations and examination of the
other organ systems should not be neglected

Cardiac Risk Assessment in General


Surgery Patients
Surgical procedures have been categorized based
on cardiovascular risk into low and moderate risk,
and vascular procedures
Considered one or more : unstable coronary
syndrome,
decompensated
heart
failure,
significant arrhythmias, or severe valvular heart
disease intensive evaluation even delayed
If theres no and functional capacity greater than
or equal to 4 metabolic equivalents (or METs),
low risk surgery plan operation

for
further evaluation and risk
management
risk factors are:
history of ischemic heart
disease
history of prior or
compensated heart
failurehistory of
cerebrovascular disease
diabetes mellitus
renal insufficiency

Diagnostic Studies
Electrocardiogram
and Chest X-ray
Echocardiography
Radionuclide Studies
myocardial
perfusion imaging
Magnetic Resonance
Imaging
Cardiac
Catheterization
Cardiac Computed
Tomography

Diagnostic Studies
ECG & Chest xray
Non invasive, simple
useful in detecting old myocardial infarction, dilation or hypertrophy of
cardiac chambers, arrhythmias, and conduction Abnormalities
Xray detect pulmonary pathology, sequelae of heart failure (e.g.,
pulmonary edema, cardiac enlargement, pleural effusions)

Echocardiography

Reflected sound waves to image the heart


primary diagnostic tool used to evaluate structural diseases of the heart
Doppler technology -> flow pattern, velocity measurement
Transthoracic echocardiography (TTE) & transesophageal
echocardiography (TEE)

Radionuclide Studies myocardial perfusion imaging (MPI)

assess myocardial ischemia


Thallium 201 (201Tl), Technetium-99m,
single-photon emission computed tomography (SPECT)
The distribution of radionuclides depend on perfusion
sensitivity and specificity of exercise SPECT are 90% and 70%

Diagnostic Studies
Magnetic Resonance Imaging
global chamber function and valvular pathologies
contrast agents such as gadolinium can enhance scar
tissue and are very useful in viability assessment
Cardiac Catheterization
access to the cardiac chambers and great vessels with a peripherally inserted catheter under
fluoroscopic guidance
the gold standard for the assessment of coronary artery disease
cardiac chamber pressures, valvular abnormalities, wall motion assessment, and coronary artery
anatomy
LH percutaneous access of the femoral, or less commonly, the radial artery
RH Pheripheral vein, Jugular
Opportunity for interventional therapy

Cardiac Computed Tomography


used to assess the coronary vasculature

EXTRACORPOREAL PERFUSION
History
John
Gibbons

cardiopulmonary bypass
(CPB) 1953 repair a
large atrial septal defect
in an 18-year-old female
Bubble oxygenators
Now a day search for
minimal
inflammatory
effect

Technique CPB
The basic CPB circuit consists of the venous cannulae, a
venous reservoir, pump, oxygenator, filter, and the arterial
cannula
Anticoagulation is required during CPB, and 300 to 400
units/kg of heparin CT 450
Distal ascending aorta, femoral artery, axillary artery, or the
distal aortic arch
Arterial cannulation is performed through a purse-string
suture, or through a side graft which is sewn on to the
native artery
Venous cannulation Purse-string sutures right atrium
single cannula or for two separate cannulae extending into
the superior and inferior vena cava, respectively
Alternative : femoral vein and right atrium

Technique CPB
Flow 2,4L/min/m2 Normothermia
with hypothermia, oxygen consumption is reduced by
50% for every 10C drop in temperature, and a flow of
only 1L/min/m2 is required at 18C.
The oxygenator PaO2 150 mmHg and normocarbia
After procedur : rewarm, lung ventilated, heart
defibrillated.
venous return to the CPB machine is gradually
reduced allowing the heart to fill
Inotropic and vasopressor support
The heparin anticoagulation is reversed with
protamine and hemostasis is achieved

Adverse Effects
Derangements in hemostasis Anticoagulation prior to
the commencement of CPB is required
Generation of thrombin plays a major role in both thrombotic and
bleeding phenomena during CPB
heparin induced thrombocytopenia and thrombosis (HITT)

systemic inflammatory response


response of the humoral and cellular immune systems

End-organ dysfunction, etiology CPB surrogates for


regional perfusion and cannot detect end-organ
hypoperfusion directly
Activated cells and circulating cytotoxic products of the immune
response microvascular injury

Myocardial Protection
Pharmacologic agents cardioplegic cardioplegia consists
of potassium-rich solutions that can be mixed with
autologous blood and are delivered into the coronary
circulation
Antegrade cardioplegia is delivered into the root of a crossclamped aorta or directly into the individual coronary ostial
via specialized catheters.
Retrograde cardioplegia catheter is a balloon-cuffed catheter
that is placed through the right atrium into the coronary
sinus and is used to perfuse the coronary circulation in the
opposite direction through the venous circulation
Most surgeons in the United States favor cold blood
potassium cardioplegia

CORONARY ARTERY DISEASE (CAD)


Etiology and Pathogenesis
Atherosclerotic stenoses are the primary
mechanism of coronary artery disease (CAD)
The pathophysiologic process is initiated with
vascular endothelial injury and is potentiated
by inflammatory mechanisms, circulating
lipids, toxins, and other vasoactive agents in
the blood.
Macrophages and platelets are attracted to
this area of endothelial dysfunction inciting a
local inflammatory response

Risk Factors and Prevention


The major risk factors of atherosclerosis include:
age, cigarette smoking, hypertension,
dyslipidemias, sedentary lifestyles, obesity, and
diabetes

Clinical Manifestations
Spectrum of presentations:
angina pectoris pain or discomfort substernal radiate to
left upper extremity, left neck, or epigastrium
myocardial infarction
ischemic heart failure
Arrhythmias
sudden death

CORONARY ARTERY BYPASS


GRAFTING
The indications, categorized by presentation and
angiographic disease burden as well as by
treatment intention (survival improvement and
symptom relief), are summarized later

Intervention vs.
Coronary Artery Bypass
Grafting
The New York State Study (2005) CABG
was associated with higher adjusted rates of longterm survival than PCI
Stent or Surgery Trial (2008) The median
follow-up was extended to 6-years, and a survival
advantage persisted in the CABG group over the
PCI group
(ASCERT Study, 2012) PCI. There was no
difference in adjusted mortality at 1 year, but
there was a significantly lower mortality with
CABG than PCI at 4 years

Operative Techniques
Bypass Conduit Selection
Conventional Coronary Artery Bypass
Grafting
Off-pump Coronary Artery Bypass
Total Endoscopic Coronary Artery Bypass
Hybrid Coronary Revascularization
Transmyocardial Laser Revascularization

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
Another heart sounds, EKG may important
The gold standard for the evaluation of valvular
heart disease is transthoracic echocardiography
(TTE)

Surgical Options
valve replacement can be accomplished with
either mechanical or biological prostheses
Current options for mechanical valve replacement
include tilting disc valves and bileaflet valve

Mechanical vs biological ?

MITRAL VALVE DISEASE


Mitral Stenosis

60% of patients with pure MS presenting


with a positive clinical history of rheumatic
heart disease
The damage caused by endocardial
inflammation and fibrosis is progressive,
causing commissural fusion, subvalvular
shortening of the chordae tendineae, and
calcification of the valve and subvalvular
apparatus

MS

When the valve area is reduced to <2.5 cm2


symptoms

Clinical manifestation
The first clinical signs of MS are those associated
with pulmonary venous congestion, namely
exertional dyspnea, decreased exercise capacity,
orthopnea, and paroxysmal nocturnaldyspnea
Hemoptysis,
jugular
venous
distention,
hepatomegaly, ascites, and lower extremity
edema

Diagnostic Studies
The diagnostic tool of choice is TTE
EKG, chest x-ray should perform

treatment
balloon valvuloplasty,
surgical commissurotomy or repair,
MV replacement may be indicated for the
treatment of MS

Mitral Regurgitation
Etiology :
myxomatous degenerative disease of the MV 2,4 %
rheumatic heart disease, infective endocarditis, ischemic
heart disease, and dilated cardiomyopathy

Pathology
Type I annular dilatation or leaflet perforation
Type II mitral valve prolapse
Type III restricted leaflet motion

Pathophysiology
basic pathophysiologic abnormality of MR is the
retrograde flow of a portion of the LV stroke volume into
the left atrium during systole due to an incompetent MV
or dilated MV annulus

Clinical Manifestations
Exertional dyspnea, decreased exercise capacity,
orthopne
Pulmonary Congestion
cardiogenic shock
systolic murmur of MR may be holosystolic or absent
a third heart sound and/or diastolic flow murmur

Diagnostic Studies
Doppler TTE
EKG and chest X-ray
Coronary angiography should be performed prior to valve
surgery

Mitral Valve Operative


Techniques
Commissurotomy
Mitral Valve Replacement
Mitral Valve Repair
Mitral valve surgery is performed on the arrested
heart with the assistance of cardiopulmonary
bypass
A median sternotomy incision, mini thoracotomy,
and partial stenotomy

Commissurotomy
Mitral commissurotomy is used to repair mitral
stenosis associated with rheumatic disease. The
commissuresopenings between the valve leaflets
are manually separated by the surgeon. Fused
chordae tendineae (cords of connective tissue that
connect the mitral valve to the papillary muscle of
the heart's left ventricle) are separated, along with
papillary muscles. Calcium deposits may be
removed from the valve leaflets. The left atrial
appendage is removed to reduce the risk of future
thromboemboli (blood clot) generation.

Mitral Valve Repair

SURGERY FOR PERICARDIAL DISEASE


Acute Pericarditis
Pericarditis is characterized by infiltration of the
cellular and fibrous pericardium by inflammatory
cells
1% of autopsies and accounts for up to 5% of
presentations of nonischemic chest
Etiology :
Primary
Secondary from systemic illness

Clinical Presentation and


Diagnosis
Diagnosis of acute pericarditis typically requires
the identification of at least two of four cardinal
features
Echocardiography is routinely performed in the
evaluation of acute pericarditis

Treatment
Short course of nonsteroidal anti-inflammatory
agents (NSAIDs)
Steroid
Antibiotics
Surgical exploration and drainge
Pericardiocentesis if occure tamponade

Relapsing Pericarditis
one-third of patients with acute pericarditis will
develop at least one episode of relapse
Recurrence may develop either from the original
etiology or from an autoimmune process that
occurs as a consequence of damage from the
initial episode
Can be treated by NSAID (colchicine) and steroid
for rapid response
Even pericardiectomy if relapse with severe
symptom and no response to medication, also
have recurrence tamponade

Chronic Constrictive
Pericarditis
Can occur after any pericardial disease process,
idiopathic and after cardiac surgery, mediastinal
radiation, and pyogenic infectio. Tuberculosis in
immunocompromise patient
It resulted when chronic pericardial scarring and
fibrosis cause adhesion of the visceral and parietal
layers and resultant obliteration of the pericardial
space
Clinically pericardial contriction limits diastolic
filling of ventricel rise filling pressure mimic
RHF

Clinical and Diagnostic


Findings
Classic physical exam findings :

Jugular venous distention with kussmauls Sign


Cardiac apical impulse
Peripheral edema
Acites
Pulsatil liver
Pericardial knock early diastolic sound that reflects a
sudden impediment to ventricular filling, similar to an S3
but of higher pitch.
Liver dysfunction : jaundice and cachexia

CVP elevated 15-20 mmHg or higher


ECG low voltage QRS
Chest x-ray calcification of the pericardium
CT or MRI (cMRI) increased pericardial thickness
(>4mm) , calcification, deformed ventricular contours
and flattening or leftward shift of the ventricular
septum, even pericardial adhesions may seen
Echocardiography mitral inflow velocity, preserved
or increased mitral annulus, early diastolic filling
velocity, and increased hepatic vein flow
Right heart catheterization increased atrial
pressures, equalization of end-diastolic pressure and
early ventricular diastolic filling

Surgical Treatment
Transient constrictive pericarditis self limiting
only medical therapy
If hemodynamic was stable conservative
managemet for 2-3 months prior to a
pericardiectomy
Surgery approached in patients :
Very advanced end stage constrictive pericarditis
Mixed constrictive restrictive disease

In order to minimize recurrence following


pericardiectomy, complete pericardial resection is
desirable
performed through either a median sternotomy or
left anterolateral thoracotomy while on

Surgical result
following pericardiectomy, symptomatic relief may
take several months
Between 1970 and 1985, the operative mortality
was reported to be 12%
but a lower mortality of approximately 4% to 8%
was noted between 1977 and 2006 at several
experienced centers

THANK YOU

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