C A S E P R E S E N TAT I O N

Chf nyha iII ec.

MITRAL
REGURGITATION

Present by
FARINA DWINANDA F
(C111 09 887)
Supervisor :

dr.Khalid Saleh, Sp.PD-KKV,FINASIM

Department of Cardiology and Vascular Medicine

Medical Faculty of Hasanuddin University
Makassar 2014

PATIENT IDENTITY

Name
: TN.M
Age
: 50 years old
Gender
: male
MR
: 669126
Day of Admission : 25 Juni 2014

HISTORY TAKING
Chief Complaint : Shortness of breath
It was felt since 2 month ago and got worsen 3 days before
admitted to the hospital. It was experienced while doing physical
activity. There is no complaint while doing the same activity. Since 2
days ago, patients do nothing but still feel the SOB during rest.
Patient can not sleep since the Sob getting worse with lying flat.
Sometimes awaked during at night time that caused by sudden
shortness of breath. History of chest pain (-). Cough(-), Wheezing (-)
Fever (-), history of fever 1 day before admitted to the hospital.
Nausea (-), Vomite (-), palpitation (-), Cold sweats (-). Oedema
extremities (+) in pretibial. Defecation and urination: Normal.

Past Medical
History
HistoryFamily
of DM
(-)
History
History of
hypertension (+)
History of smoking
(+)

Family
History
History of
cardiovascular
disease in family
(-)

RISK FACTORS

Modified

Non- Modified

Hypertension

Gender : Male

Smoking

Age 50 years old

General Status
* Moderate illness/ Well nourished/ Conscious
* Nutritional Status: Normal
* Weight : 60 kg
* Height :165 cm
: 22,0 kg/m2
* BMI

Vital Sign

* Blood Pressure
:
* Pulse Rate
* Respiratory Rate
* Temperature

: 160/100 mmHg
76 bpm
: 28 bpm
: 36.5 0C (axilla)

PHYSICAL EXAMINATION
Head and Neck Examinations
Eye
: Conjunctiva anemic (-/-), Sclera icteric
(-/-)
Lip
: Cyanosis (-)
Neck

: JVP R+3 cmHO potition 30

Chest Examination
Inspection : Symmetric between left and right
chest.
Palpation : No mass, no tenderness.
Percussion : Sonor between left and right
chest,
Auscultation: Respiratory sound: Vesicular
Additional sound : Ronchi +/+
(mediobasal) ,Wheezing -/-

 Inspection
Palpation
Percussion

Heart

: Heart apex was not visible

: Heart apex was not palpable
: Right heart border in ICS II right
parasternal. Left heart border in ICS 7
midclavicular.
Auscultation
: Heart Sounds : S I/II regular, murmur
(+)
sistolik at apex

Inspection
Auscultation
Palpation

Abdomen

Percussion

: Flat, follows breathing movement

: Peristaltic sound (+), normal
: No mass, no tenderness, liver and
spleen unpalpable
: Tympani (+)

Pretibial edema +/+

Dorsal pedis edema +/+

Extremities

Electrocardiogram (ECG)

ECG interpretation
Rhythm: Sinus rhythm
Heart rate : 70 bpm
Regularity : reguler
Axis
: Right Axis Deviation
P wave
: 0,08 s
PR interval : 0,16 s
QRS complex : duration 0,12 s, configuration QS in II,III, aVF

ST Segment
: 0,08 s
T wave
: 0,12 s
Conclution :
Sinus rhythm, HR70 bpm, RAD, LVH , configuration QS in
II,III,aVF

Radiology findings

THORAX FOTO
INTERPRETATION
Cardiomegaly with lung
oedeme
Bilateral efusion pleura

LABORATORIUM
HEMATOL

RESULT

OGY

NORMAL

UNIT

VALUE

WBC

13,9

4,00-10,0

(10/UI)

RBC

5,46 3

4,00-6,00

(106/UI)

HGB

18,5

12,0-16,0

(gr/dL)

HCT

54

37,0-48,0

(%)

PLT

237

150-400

(103/uL)

GDS

110

140

Mg/dL

ureum

30

10-50

Mg/Dl

Creatinin

2,3

<1,3

Mg/dL

Na

140

136-145

mmol/L

SGOT

3,6

<41

mmol/L

SGPT

99

<38

Mg/dL

PT

11.9

10-14

detik

APTT

31,6

22-30

detik

CK

97,7

L<190,P<187

u/L

CKMB

25,5

<25

u/L

TROPONIN T

0,26

<0.05

ECHOCARDIOGRAPHY

INTERPRETATION
Conclusion

* Decrease of systolic LV function, EF

*
*
*
*

50%
Dimensional chambers of heart : LA
and LV dilatation
LVH (+)
Global hipokinetic
Insdequate RV systolic function, TAPSE
1,3 cm

* Heart valves :
- Mitral: MR mild
- Aorta : 3 cuspis, calsification (-)
- Tricuspid : TR trivial
- Pulmonal : normal function and
*

movement
E/A >2 (pseudonormal)

* Dysfunction sistolic and diastolic

*
*
*
*

LV,
EF 50%
LVH (+)
Dilation of LA and LV
MR mild

Working
DIAGNOSIS

CHF e.c HHD

HT Grade II
MR Mild

MANAGEMENT
Bed rest

Oxygen 3-4 lpm via

Laxative
Laxadyne syr 0-0-II cth

nasal canule

Cardiac diet
IVFD NaCl 0.9% 500
cc/24 hr

Angiotensin receptor
Blocker
Valsartan 1x80 mg

Diuretic
Lasix 2am/8jam/iv

DISCUSSION
HEART FAILURE

DEFINITION
rt
a
e
H
ure Heart failure is no longer able to
l
i
a
F
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
ve
i
t
s
ge
Con art
He e
ur
F ai l

The state in which

abnormal circulatory
congestion occurs as the
result of heart failure.

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)

The Framingham criteria for CHF

CHF considered present if 2 major or 1 major & 2 minor

Major Criteria

Minor Criteria

Paroxysmal Nocturnal Dyspnea

Extremity edema

Cardiomegaly

Nocturnal cough

Gallop S3

Decreased vital

Hepatojugular reflux

pulmonary capacity

Increased of JVP

(1/3 of maximal)

Rales or ronchi

Hepatomegaly

Acute pulmonary edema

Pleural effusion

Prolonged circulation time(> 25

Tachycardia ( 120bpm)

sec)

Dyspnea deffort

Weigh loss 4,5 kg in 5 days in

response to treatment of CHF

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

Sign & symptomp of chf

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

MITRAL REGURGITATION

Normal mitral valve function

depends on perfect function
of the complex interaction
between the mitral leaflets,
the
subvulvar
apparatus
(chordae
tendinae
and
papillary
muscles),
the
mitral annulus, and the left
An imperfection in any one
ventricle.

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

Functional (regional or
global LV remodelling )
Structurally normal leaflets
and chordae tendineae
* Ischemic heart disease
(Ischemic MR)
* Idiopathic dilated
cardiomyopathy
* Mitral annular dilatation

Etiology

Symptoms of MR

Dyspnea
Fatigue
Orthopnea
Palpitation
Pulmonary edema (often the initial
manifestation)

Physical Exam
Palpation may reveal the following:
* Brisk carotid upstroke and hyperdynamic cardiac
impulse
* Prominent LV filling wave
Auscultation may reveal the following:
* Diminished S1 in acute MR and chronic severe MR with
defective valve leaflets
* Wide splitting of S2 as a result of early closure of the
aortic valve
* S3 as a result of LV dysfunction or increased blood flow
across the MV
* Accentuated P2 if pulmonary hypertension is present

* Characteristic murmur

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

CXR: LA and LV enlargement

Echocardiografi:

ECG: LV hypertrophy,
sometimes AF

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%

Thank You