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MITRAL
REGURGITATION
Present by
Dionisius Giri S
(C111 09 309)
Supervisor :
PATIENT IDENTITY
Name
: Mrs. DS
Age
: 25 years old
Gender
: Female
MR
: 646185
Day of Admission : January 11th
2014
HISTORY TAKING
Chief Complaint : Shortness of breath
History of illness:
Suffered since 1years ago and got worsen 5
days before admitted to the hospital. It was
experienced while doing minimal activity
walking to the bathroom and relieved with
resting. Sometimes awaked during at night time
that caused by sudden shortness of breath,
patient sleep with sit potition. Chest pain (+), on
the left chest, since 1 month ago before
History
of DM (-)
History of hypertension (-) since
History of smoking (-)
History of medicine (+) treated in RSWS on
February 2013, with VHD, and got
Spironolakton
Family History
RISK FACTORS
Modified
Non- Modified
Hipertension
Gender : Female
Diabetes
Age
Mellitus
General Status
Vital Sign
Pulse Rate
Respiratory Rate
: 32 tpm
Temperature
: 36.8 0C (axilla)
: 114 bpm
PHYSICAL EXAMINATION
Head and Neck Examinations
Eye
: Conjunctiva anemic (-/-), Sclera icteric
(-/-)
Lip
: Cyanosis (-)
Neck
Chest Examination
Inspection : Symmetric between left and right
chest.
Palpation : No mass, no tenderness.
Percussion : Sonor between left and right
chest, lung-liver border in ICS IV right anterior.
Auscultation: Respiratory sound: Vesicular
Additional sound :Ronchi +/+,Wheezing /-
Inspection
Auscultation
Palpation
Percussion
Inspection
: Heart apex was not visible
Palpation
: Heart apex was not palpable
Percussion
: Right heart border in right
parasternal line,
Left heart border in left
midclavicular line
ICS V.
Auscultation
: Heart Sounds : S I/II regular, murmur
(+)
sistolik grade 3/6 apex
s
Extremitie
Abdomen
Heart
Electrocardiogram (ECG)
14/1/201
4
ECG interpretation
Rhythm: Sinus rhythm
Heart rate : 117 bpm
Regularity : reguler
Axis
: RAD
P wave
: P mitral 0,12 s on II,avL lead
PR interval : 0,20 s
Q pathologies
:QRS complex : duration 0,12 s, configuration RS, QS on I,avL, v2 leads
ST Segment
: 0,08 s isoelectric
T wave
: 0,12 s
Conclution :
Sinus tachycardi rhythm, HR 117 bpm, LAE, RAD
Radiology findings
LABORATORIUM
HEMATOL
RESULT
OGY
6/1/2014
NORMAL
UNIT
VALUE
WBC
7,6
4,00-10,0
(10/UI)
RBC
4,42
4,00-6,00
(106/UI)
HGB
12,4
12,0-16,0
(gr/dL)
HCT
38,0
37,0-48,0
(%)
PLT
237
150-400
(103/uL)
GDS
117
140
Mg/dL
Ureum
81
10-50
Mg/Dl
Creatinin
1,1
<1,3
Mg/dL
Na
138
136-145
mmol/L
SGOT
92
<41
mmol/L
SGPT
55
<38
Mg/dL
PT
11.1
10-14
detik
APTT
28,5
22-30
detik
CK
748
L<190,P<18
u/L
CKMB
24
7
<25
u/L
TROPONIN T
<0,02
<0.05
ECHOCARDIOGRAPHY
INTERPRETATION
Conclusion
sistolic LV function is good, EF 63,33%
(on tachicardi)
Dimensional chambers of heart:
LA,RA,RV dilatation
Decrease RV function
MR severe
TR moderate-severe
PR Trivial
PH moderate-severe (mPAP 59 mmHg)
Working DIAGNOSIS
Severe MITRAL
REGURGITATION
CHF NYHA III
MANAGEMENT
Bed rest
Oxygen 3-4 lpm via nasal canule
Cardiac diet
IVFD NaCl 0.9% 500 cc/24 hr
Dobutamin 5 g/kgBB/jam
Lasix 40 mg/8 jam/ SP if BP 90
Spironolakton 25 mg x 1
Simarc 2 mg 1 x 1
DISCUSSION
MITRAL REGURGITATION
of these
components can cause the valve to leak.
Mitral regurgitation is
retrograde flow of blood from
LV to LA through incompetent
mitral valve during systolic
phase.
Causes by Primary (intrinsic
valvular disease) and
Functional (regional or global
LV remodelling )
Primary (intrinsic
valvular
disease)
MR is almost always
(90%) associated with
MS in RHD
Degenerative
processes of leaflets
and chordal
structures
Infective endocarditis
Mitral annular
calcification
Structurally normal
leaflets and chordae
tendineae
Ischemic heart disease
(Ischemic MR)
Idiopathic dilated
cardiomyopathy
Mitral annular
dilatation
Etiology
Pathophysiology of MR
Mitral regurgitation
Systolic (Retrograde)
Acute
Volume overload in LA & LV
ed LA, LV Pressure
ejection into LA
Chronic
ed LV afterload (into LA)
ed LA/LV size/ compliance
Pathophysiology
Symptoms of MR
Dyspnea
Fatigue
Orthopnea
Palpitation
Pulmonary edema (often the
initial manifestation)
Physical Exam
Auscultation
Clinical Features
Acute
Present with sudden
onset of pulmonary
edema, hypotensio,
cardiogenic shock
Murmur early
systolic, soft
inaudible
Normal LA size and
compliance
Chronic
Usually
asymptomatic, if
there is present with
low CO symptom
Over time CHF
features
Increased LA size
Lower CO
Diagnostic Tests
ECG: LV hypertrophy,
sometimes AF
Echo:
LAE
LV enlargement
Medical Therapy
ACE-Inhibitor
Diuretic
Nitrat
Digoxin
Antibiotic
Surgical intervention
Symptomatic with severe MR
Asymptomatic with severe MR and
preserved LV function
Asymptomatic with severe MR and
LVESD > 45 mm and EF < 55%
DISCUSSION
HEART FAILURE
DEFINITION
rt
a
e
H
ure
l
i
a
F
Heart is no longer able to pump an
adequate supply of blood in relation
to the venous return and in relation
to the metabolic needs of the body
tissues at the particular moment
iv e
t
s
ge
n
o
rt
C
Hea re
u
Fail
ETIOLOGY OF HEARTFAILURE
Miocard
Disease
CAD
Cardiomyopathy
Iatrogenic
Miocarditis
Miocard Mechanical
Dysfunction
Pressure overloaded
(Stenosis Aortae,
Hypertension, Coartatio
Aortae)
Volume Overloaded
(Mitral/Aortae Regurgitation,
Congenital Heart Disease,
Hipertransfusion)
Miocard Filling Inhibitating
(Cardiac Tamponade,
Pericarditis)
Major Criteria
Minor Criteria
Paroxysmal Nocturnal
Extremity edema
Dyspnea
Nocturnal cough
Cardiomegaly
Decreased vital
Gallop S3
pulmonary capacity
Hepatojugular reflux
(1/3 of maximal)
Increased of JVP
Hepatomegaly
Rales or ronchi
Pleural effusion
Tachycardia (
Prolonged circulation
time(> 25 sec)
120bpm)
Dyspnea deffort
clASSIFICATION OF CHF
PATHOPHYSIOLOGY OF CHF
Plaque in
coronary
artery
Symptomatic
Congestive
Heart Failure
Blood flow to
heart muscle
is reduced.
Heart muscle
lacking of
oxygen
Ischemia of
heart muscle
can lead to
myocardial
infarction
Pulmonary
edema
Abnormal
Heart rhythm
The heart
muscle cant
pump
adequately
CHF MANAGEMENT
Optimalized
Oxigenation
NonFarmakolog
i
Reduce Physical
Activity
Low salt, enough
calories and
proteins detary
CHF MANAGEMENT
Farmakologi
Managing
preload
Managing
afterload
Managing
contractility
Neurohormonal
modulation
Diuretics
Venodilator
Inotropic agents :
Cardiac glycosides
B- adrenergic
ACE
inhibitors
ARB
blockers
CCB
blockers
ACE
inhibitors
ARB
Thank You