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

Present by
Fitriani Indah AY
(C111 09 292)

Supervisor :
dr. Pendrik Tandean,SpPD-KKV,FINASIM

Department of Cardiology and Vascular Medicine


Medical Faculty of Hasanuddin University
Makassar 2014
PATIENT IDENTITY
• Name : Mrs. SS
• Age : 54 years old
• Gender : Female
• MR : 682706
• Day of Admission :
September 29 2014
HISTORY TAKING
Chief Complaint : Shortness of breath

• It was felt since ± 1 month ago and got worsen 3 days before admitted to the
hospital. It was experienced while doing minimal activity such as 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 position.

• Cough (+) since 6 days ago with sputum of white coloured.

• history of fever 1 day before admitted to the hospital.

• Cold sweats (+)

• Oedema extremities (+)


Past Medical History

* History of DM (+) since 1 year ago with


uncontrolled therapy
* History of hypertension (+) since 1 year ago
with uncontrolled therapy

Family History

History of cardiovascular disease in family (-)


RISK FACTORS

Non- Modified Modified

• Hypertension • Gender : Female


Diabetes Mellitus • Age 54 years old
General Status
* Moderate illness/ Well nourished/ Conscious
* Nutritional Status: Normal
* Weight : 50 kg
* Height : 155 cm
* BMI : 20.8 kg/m2

Vital Sign

* Blood Pressure : 170/90 mmHg


* Pulse Rate : 100 bpm
* Respiratory Rate : 28 bpm
* Temperature : 36.7 0C (axilla)
PHYSICAL EXAMINATION

Head and Neck Examinations


Eye : Conjunctiva anemic (-/-), Sclera icteric (-/-)
Lip : Cyanosis (-)
Neck : JVP R +3 cmH₂O potition 30º

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 : 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 (+)
Heart sistolik grade 2/6 apex

• Inspection : Flat, follows breathing movement


• Auscultation : Peristaltic sound (+), normal
• Palpation : No mass, no tenderness, liver and
spleen unpalpable
• Percussion : Tympani (+)
Abdomen

• Pretibial edema +/+


• Dorsal pedis edema +/+

Extremities
ECG
interpretation
* Rhythm : Sinus rhythm
* Heart rate : 100 bpm
* Regularity : reguler
* Axis : Normoaxis
* P wave : 0,08 s
* PR interval : 0,16 s
* Q pathologies :-
* QRS complex : duration
0,12s, configuration poor R wave
rogression
* ST Segment : 0,08 s
* T wave : 0,12 s
* Conclution :
* Sinus rhythm, HR 83 bpm,
Normoaxis, poor R-wave
progression (V1-V4).
INTERPRETATION
• Cardiomegaly with lung
edema
• Bilateral efusion pleura
• Atherosclerosis aortae
LABORATORIUM 29/9/2014

HEMATOL RESULT NORMAL UNIT

OGY VALUE

WBC 10,34 4,00-10,0 (10³/UI)

RBC 4,283 4,00-6,00 (106/UI)

HGB 10,1 12,0-16,0 (gr/dL)

HCT 30,0 37,0-48,0 (%)

PLT 396 150-400 (103/uL)

GDS 190 140 Mg/dL

Uric acid 5,7 2,4-5,7 Mg/Dl

Creatinin 2,3 <1,3 Mg/dL


Na 137 136-145 mmol/L

SGOT 24 <41 mmol/L

SGPT 23 <38 Mg/dL

PT 11.1 10-14 detik

APTT 31.1 22-30 detik

CK 280 L<190,P<187 u/L

CKMB 49 <25 u/L

TROPONIN T <0.1 <0.05


ECHOCARDIOGRAPHY
Conclusion
* Decrease of systolic LV function, EF 50%
* Dimensional chambers of heart : normal
* Dysfunction sistolic and diastolic
* LVH (+) LV, EF 50%
* Global normokinetic * LVH (+)
* Adequate RV systolic function, TAPSE 1,7cm * MR moderate
* PH moderate-severe
* Heart valves : * PE moderate
- Mitral: MR moderat
- Aorta : AR trivial –mild
- Tricuspid : TR moderate
- Pulmonal : PR mild, PR moderate severe
(PSAP 61 mmHag)

* E/A >1 (pseudonormal)


Chf nyha iII ec. MODERATE
MITRAL
REGURGITATION+PULMONAL
HIPERTENTION
Diabete mellitus
Hipertention grade ii
 Bed rest
 Diuretic
 Oxygen 3-4 lpm via Furosemid 2 amp/8 hr/iv
nasal canule

 Cardiac diet

 IVFD NaCl 0.9% 500


cc/24 hr

 Vasodilator
Cedocard 1 mg/hr/sp

 ARB
Valsartan 1x80 mg
DISCUSSION
HEART FAILURE
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

The state in which abnormal


circulatory congestion occurs as
the result of heart failure.
Myocard Myocard Mechanical
Disease Dysfunction
Pressure overloaded
CAD (Stenosis Aortae, Hypertension,
Coartatio Aortae)
Volume Overloaded
Cardiomyopathy
(Mitral/Aortae Regurgitation,
Congenital Heart Disease,
Hipertransfusion)
Iatrogenic
Miocard Filling Inhibitating
(Cardiac Tamponade, Pericarditis)
Miocarditis
The Framingham criteria for CHF
CHF considered present if 2 major or 1 major & 2 minor
Major Criteria Minor Criteria
• Paroxysmal Nocturnal • Extremity edema
Dyspnea • Nocturnal cough
• Cardiomegaly • Decreased vital pulmonary
• Gallop S3 capacity (1/3 of maximal)
• Hepatojugular reflux • Hepatomegaly
• Increased of JVP • Pleural effusion
• Rales or ronchi • Tachycardia (≥ 120bpm)
• Acute pulmonary edema • Dyspnea d’effort
• Prolonged circulation time(>
25 sec)
• Weigh loss ≥ 4,5 kg in 5 days
in
response to treatment of
CHF
Blood flow to Ischemia of
heart muscle is heart muscle
Plaque in
reduced. Heart can lead to
coronary artery
muscle lacking myocardial
of oxygen infarction

Pulmonary The heart


Symptomatic
edema muscle cant
Congestive
Abnormal Heart pump
Heart Failure
rhythm adequately
Non-
Farmakologi
Farmakologi
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 ventricle.

An imperfection in any one 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 Functional (regional or
disease) global LV remodelling )

* MR is almost always (90%) Structurally normal leaflets


associated with MS in and chordae tendineae
RHD * Ischemic heart disease
* Degenerative processes (Ischemic MR)
of leaflets and chordal
structures * Idiopathic dilated
cardiomyopathy
* Infective endocarditis
* Mitral annular * Mitral annular dilatation
calcification
Etiology
Pathophysiology of MR
Mitral regurgitation

Systolic (Retrograde) ejection into LA

Acute Chronic

Volume overload in LA & LV ↓ed LV afterload (into LA)

↑ed LA, LV Pressure ↑ed LA/LV size/ compliance

Pulmonary edema ↓ed Cardiac output LA dilatation ↓ed contractility


AF ↓ CO
Pulmonary congestion
Symptoms of MR
• Dyspnea
• Fatigue
• Orthopnea
• Palpitation
• Pulmonary edema (often the initial
manifestation)
Clinical Features
Acute Chronic
* Present with sudden * Usually asymptomatic,
onset of pulmonary if there is present with
edema, hypotensio, low CO symptom
cardiogenic shock * Over time  CHF
* Murmur  early features
systolic, soft inaudible * Increased LA size
* Normal LA size and * Lower CO
compliance
Diagnostic Tests
• CXR: LA and LV enlargement
• 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

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