Cardiology Department

Medical Faculty
Hasanuddin University

Case Report
Oktober 2015

Acute Decompensated Heart

Failure

JAKA HERBIYANTO
C 111 11 299
Supervisor:
dr. Akhtar Fajar M, SpJP.FIHA

Patient Identity

Name
: Mr.Z
Age
: 76 y.o
Gender
: Male
Address
: Makassar
Marital Status
: Married

History Taking
Shortness to breath

Chief complaint :

Experienced since 3 days before admission. Its appear

continously especially at rest or during lying down
position. Dyspneu is not influence by weather and patient
felt more compertable sleeping with 3 pillows. Sometimes
patient awoken at night because of dyspneu.
Intermitten chest pain (+)
Cough (-)
Cold sweat (+)

History Taking

Fever (-), history of fever (-), nausea(-), vomit(-)

Micturition and defecation is normal.
Asthma (-), family history with asthma (-)
Family history with CVD (unknown)
Cigarette smoking (+)
Alcoholism (-)

Previous history

History of hypertension (+): not controlled

History of Cardiovascular disease (+) at 6 years ago.
History of treatment: Simarc 1x20mg and Furosemide 1x
40mg
Hystory of rheumatic fever (unknown)

Physical Examination
General state:
Moderate Illness/ Well nourished/Conscious
Body Weight: 54 kg
Body Height : 168 cm
Body Mass Index : 22,2 kg/m2

Vital state
Blood Pressure : 100/70 mmHg
Heart Rate : 88 x/mnt
Respiratory Rate : 26 x/mnt
Body Temperature : 36,6 C

Physical Examination
Head : Normochepalic
Eye : Anemis (-), Icteric (-)
Pupil : Equal, round, diameter 2,5 mm,
reactive to light
Nares : Appearent is normal
Lip : No cyanosis
Neck : JVP +4 CM H2O, no
lymphadenopathy, no thyroid
enlargement

Physical Examination
Chest Examination
Inspection : Symmetry left=right
Palpation : Mass (-), tenderness (-),
Percussion : Sonor left=right; lung-liver
border in ICS VI anterior
Auscultation: Breath sound;vesicular
Additional sound:
ronchi +/+ (basal)
wheezing -/-

Physical Examination
Cardiac Examination
Inspection : Apex was visible
Palpation : Apex was palpable
Percussion : Right heart border in right
parasternal line,
left heart border in axilla anterior sisnitra
Auscultation: Heart sound: SI/II regular,
Additional sound: murmur (+)
systolic3/6 apex ICS V sinistra and ICS III
parasternal Dextra

Physical Examination
Abdominal Examination
Inspection : Convex, following breath
movement
Auscultation : Peristaltic sound (+), normal
Palpation : Mass (-), tenderness (-), no
palpable
liver and spleen
Percussion : Timpani (+), Ascites (-)

Extremities examination
Pretibial edema -/Dorsum pedis edema -/-

ELECTROCARDIOGRAP
HY (ECG)
Result:

Sinus
Rhythm,
HR
100x/minutes
Normoaxis
LAD

CHEST X-RAY
Result:
Cardiomegaly associated
Atherosclerosis aortae with
Early sign of lungs congestion.

ECHOCARDIOGRA
M
Result:

Dysfunction of systolic and

diastolic of LV and RV.
Ejection Fraction 15,86%
Dilatation at whole chambers.
Akynetic anterior, others
segment Hypokinetic
AS severe
MR severe
TR moderate
PH moderate

LABORATORY TEST
Complete Blood Count
Test

Result

WBC
RBC
HGB
HCT
PLT

11,6 x 103/ ul
4,2 x 106 / ul
13,2 g/dL
45,5 %
225 x 103 / ul

Electrolyte
Test

Result

Na
K
Cl

189
5,0
114

LABORATORY TEST
Blood Chemistry
Test
GDS

Result
110

Ureum

113

Creatinine

2,56

GOT

219

GPT

56

Test
CK

Result
140

CK-MB

16,6

Troponin

0,51

Cardiac
Enzyme

DIAGNOSIS
Acute Decompensated Heart Failure
AS severe
MR severe

THERAPY

O2 4 lpm via nasal canule

IVFD NaCl 0,9% 500 cc/24jam
Aspilet 80mg/24jam/oral
Clopidogrel 75mg/24jam/oral
Furosemide 40 mg/12jam/iv
ISDN 5mg/ SL

DISCUSSION

Definition
An imbalance in pump function in which
the heart fails to maintain the circulation
of blood adequately or cardiac output
decreases and is unable to meet the
metabolic demands of the body.
Acute heart failure is defined as the rapid
development or change of symptoms and
signs of heart failure that requires urgent
medical attention and usually
hospitalization

Compensatory Mechanisms in HF
1. Frank-Starling Law
2. Neurohormonal system

Sympathetic nervous system

Renin-angiotensin system

3. Ventricular hypertrophy

Increased HR and cardiac contractility

Cardiac dilatation (The Frank-Starling
mechanism)
Myocardial hypertrophy

B-Type natriuretic peptide (BNP)

1. Serum BNP<100
Normal atau gagal jantung terkompensasi dengan baik
2. Serum BNP 100-200
Gagal jantung terkompensasi dengan baik
Normal (usia lanjut)
Cor pulmonal
Hipertensi, dysfungsi sistolik
Penyakit jantung iskemik
3. Serum BNP 200-400
Gagal jajntung terkompensasi dengan ringan sedang
Gagal jantung kronik terkompensasi
4. Serum BNP > 400
Gagal jantung kongesti yang berat (hipovolemi)

Goal terapi ADHF

Stabilize the patient
Reverse acute hemodyna abnormalities

cardiac output

vascular resistance

ventricular filling pressure

Rapidly reverse dyspnea and / or
hypoxemia caused by pulmonary
congestion.
Decrease disease progression and improve
survival.

YA

TIDAK

Profil A

Profil B

warm and dry

warm and Wet

TIDA

Profil L

Profil C

Cold and Dry

Cold and Wet

YA

Perfution
: Cold and Warm
Sign of congesti ve : Wet and Dry

Assessment & Treatment Algorithm for ADHF

DRY WARM
PROFILE

WET WARM
PROFILE

WET-COLD
PROFILE

DRY-COLD
PROFILE

Initial
Management

Initial
Management

Initial Management

Initial
Management

Continue oral
heart failure
medications.

IV loop diuretic

IV nesiritide or IV
vasodilator if high
SVR

Search for other

causes of
symptoms incl
PE, ACS,
depression,
anemia,
hypothyroidism

IV nesiritide or
IV Vasodilator

IV loop diuretic

Oxygen if
indicated

Inotropes or pressor
if low SVR

Admit : telemetry
of observation
unit

Admit :ICU

Oxygen if indicated

Continue RHC
Inotropes and / or
pressor
Consider
decrease of beta
blocker dose
Admit :ICU or
telemetry unit

Optimize oral medications and

discharge
Fonarow et al. Clin Cardiol 2004 ; 27 (suppl V)

THANK YOU

AORTIC STENOSIS
Aortic stenosis is caused by
narrowing of the orifice of the aortic
valve and leads to obstruction of left
ventricular outflow.

Cause of Aortic Stenosis

A. Rheumatic Aortic Stenosis
Usually mild to moderate stenosis
May progress to severe aortic stensos (accelerated valve
aging)
Often combined with aortic regurgitation
Thickened leaflets/focal calcification
Often multivalvular disease
B. Congenital Abnormalities of the Aortic Valve
Unicuspid, bicuspid, quadricuspid
Syndromes (e.g. Downs, Heydes)
May be associated with genetic syndromes (such as Downs,
Heydes)
Shaper et al (1982); Staper et al (1985)

CLINICAL MANIFESTATION