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By : Muhammad Fairuz

Supervisor: dr. Abdul Hakim Alkatiri,SpJP

Name
Age
Gender
Address
RM

: Nn. S
: 21 years
: Female
: Pare-Pare
: 38 63 31

Chief complaint: Shortness of breath


History taking:
Experienced 1 month ago, worsen 1 week before
admitted
Precipitated by exertion & lying position, not by
cold weather
Frequently waking up in the night gasping for
breath, usually needs three pillows to sleep
She has been experienced this shortness of
breath since 10 years ago. Her skin usually turn to
blue when she crying when she was still a child.
Fever (+) started last night. There is history of
fever when she was a child and the fever came
and gone whenever she felt shortness of breath.

Cough(-), nausea(-), vomiting(-), chest pain(-),


heartburn(-), abdominal pain (-)
Previously she was admitted to Hospital in Parepare with shortness of breath and swelling all over
her body over 2 month ago.
Swelling on her started from her abdomen then
spread to her lower limbs and her face.
Defecation and urination is normal

DM (-)
HT (-)
History of Reumatic Heart Disease is
unknown

Present status:
Severe illness/ Under nutrition/Conscious
Vital signs:
BP : 100/70 cmHg
HR : 90 bpm regular
RR : 28 x/minute
T
: 37,8C

Head : Anemia (+) Icterus (-) Cyanosis ( - )


Neck :

No mass, no pain
JVP R+4 cmH2O

Chest :
Inspection
: Asymmetrical, left chest is
convex than the right chest
Palpation
: No mass, no pain
Percussion
: Relative Dullness is heard from
ICS
III and below for both
side of the
chest
Auscultation : Vesicular, Rh +/+ (diffuse)

Heart:

Inspection : Visible apex beat at the 5th ICS anterior


axillaries line
Palpation : Palpable apex beat at the 5th ICS anterior
axillaries line
Percussion : Heart widening 3 cm to the left
Auscultation : S1/S2 regular, pansystolic murmur

Abdominal :

Inspection : Convex, moving with respiration


Palpation : Ascites (+), the liver and spleen is hard to
examine.
Percussion : Tympani
Auscultation : Peristaltic sound (+), normal
Extremities : Edema +/+ pretibial and dorsum pedis

Complete blood
count
WBC: 5.800/l
RBC: 3,69x106/l
HGB: 8,7 gr/dl
HCT: 31,0%
PLT: 307x103/l
Electrolyte
Sodium: 130
Potassium: 3.3
Chloride: 101

Blood chemistry:
GDS : 97 mg/dl
Ureum : 17 mg/dl
Creatinine : 0.6 mg/dl
SGOT/SGPT: 17/8 u/dl
Total Prot : 7.0 mg/dl
Albumin : 3.1 mg/dl
Globulin : 3.9 mg/dl
Ck : 27
Ck-MB : 17 u/dl

Interpretation:
Accelerated Junctional Rhytme
HR 100 bpm
Inferior ischemic myocardium.

Conclusion:
Signs of Pulmonal Oedema DD/
Bronchopneumonia
Bilateral diphragma elevation

Conclusion: - Hepatomegaly with congestive


liver
- Acites

Description:

Dilated LA and RA
Good LV Contractile, EF 85%
Mitral Insufisiensi Severe and vegetation
Tricuspidal Insufisiensi
PH (PAP= 27 mmHg)

Conclusion:

MI Severe with vegetation


TI, PH

CHF NYHA IV ec Mitral


Regugitation

Heart Diet
O2 3 4 liter/minute
Lasix 2 amp/12jam/iv
Lasix 2 amp/12jam/sp
NTG 10 ug/mnt
Farsorbid 10mg
3x1
Aspilet 80mg
1x1
Dorner 2 x 1
Alravolam
1/2- 0 1
Laxadyn syr 3 x 1 c
PRC transfusion 1 unit
PCT
3 x1

Congestive
failure (CHF)

heart
is an

imbalance in pump
function in which the
heart fails to maintain
the circulation of blood
adequately.

Contractility

disturbance

(eg.

myocardial

infarction; temporary myocardial ischemia; chronic


volume

overload

such

as

mitral

&

aortic

regurgitation).

Cardiomyopathy

Pressure overload (eg. aortic stenosis; uncontrolled


hypertension)

Major Criteria

Minor Criteria

Paroxysmal Nocturnal

Extremity edema

Dyspnea

Cough

Dyspnea deffort

Decreased vital

Cardiomegaly
Gallop S3
Increased of JVP

pulmonary
capasity (1/3 of
maximal)

Hepatojugular reflux

Hepatomegaly

Rales or ronchi

Pleural effusion

Acute pulmonary edema

Tachycardia

Prolonged circulation
time
(> 25 sec)

No symptoms and no limitation in ordinary physical activity.

II

Mild symptoms and slight limitation during ordinary activity.


Comfortable at rest.

III

Marked limitation in activity due to symptoms, even during


less-than-ordinary activity. Comfortable only at rest.

IV

Severe limitations. Experiences symptoms even while at rest.

Managing
preload
Managing
contractility

Managing
afterload
Neurohormonal
modulation

Diuretics
Venodilators

Ca2+

channel blockers
Anti adrenergic
Vasodilators

Cardiac

glycosides
adrenergic
Phosphodiesterase inhibitors

blockers
ACE inhibitors
Angiotensin receptor blockers

a condition in
which the mitral
valve does not
seal tightly,
which allows
blood to flow
backward in your
heart

Valvular-leaflets
Myxomatous Disease
Rheumatic
Endocarditis
Congenital-clefts

Annulus
Calcification

Chordae
Fused/inflammatory
Torn/trauma
Degenerative

Papillary Muscles
CAD (Ischemia,
Infarction,Rupture)
Infiltrative disorders

the acute stage, which usually occurs with a spontaneous chordae


tendineae rupture secondary to myocardial infarction, a sudden
volume overload occurs on an unprepared left ventricle and left
atrium.

If the mitral regurgitation develops slowly over months to years or if


the acute phase can be managed with medical therapy, the individual
will enter the chronic compensated phase of the Mitral Regugitation.

An individual may be in the compensated phase of mitral


regurgitation for years, but will eventually develop left ventricular
dysfunction, the hallmark for the chronic decompensated phase of
Mitral Regurgitation

Acute mitral
regurgitation

Electrocardiogram

Normal

Heart size

Normal

Systolic murmur
Apical thrill
Jugular venous
distension

Chronic mitral
regurgitation
P mitrale, atrial
fibrilation, left
ventricular
hypertrophy.
Cardiomegaly, left
atrial enlargement

Heard at the base,


radiates to the neck,
spine, or top of head
May be absent

Heard at the apex,


radiates to the axilla

Present

Absent

Present

The mitral component of the first heart sound is usually


soft and is followed by a pansystolic murmur which is
high pitched and extends, as the name suggests, the
whole of systole. The murmur usually radiates to the
axilla. Patients may also have a third heart sound.
Patients with mitral valve prolapse often have a mid-tolate systolic click and a late systolic murmur.

In acute mitral regurgitation secondary to a


mechanical defect in the heart (ie: rupture of a
papillary muscle or chrordae tendineae), the
treatment of choice is urgent mitral valve
replacement.
If the individual with acute mitral regurgitation is
normotensive, vasodilators may be of use to decrease
the afterload seen by the left ventricle and thereby
decrease the regurgitant fraction.
Individuals with chronic mitral regurgitation can be
treated with vasodilators as well. In the chronic state,
the most commonly used agents are ACE inhibitors
and hydralazine.
There are two surgical options for the treatment of
mitral regurgitation: mitral valve replacement and
mitral valve repair.

Indications for surgery for chronic mitral


regurgitation include signs of left ventricular
dysfunction. These include an ejection
fraction of less than 60 percent and a left
ventricular end systolic dimension (LVESD)
of greater than 45 mm.

Thank You!