CH F N YH A IV ec CH D

BY : NADIA TARMIZI
SUPERVISOR :
Prof dr. Peter Kabo PhD,
SpFK,SpJP,FIHA

Patient identity

Name : Mr. S
No.MR
: 380809
Age
: 58 years old
Gender
: Male
Date of admittance :07th June 2009

H istory taking
Chief complaint: Shortness of breath
History taking:
Experienced 5days ago, worsen 2 days
before
admitted
to
hospital.
Precipitated by light exertion & lying
position, not by cold weather.
Frequently waking up in the night
gasping for breath, usually needs two
pillows or more to sleep

Crushing like chest pain (+) ,

intermitten radiates to the left arm.

Cough(+), white sputum ,

fever(-), history of fever(-),
nausea(-), vomiting(-), epigastric
pain(+)
Defecation and urination is
normal

Past Illness H istory

History of heart disease (+).Patient had been admitted

to Wahidin .S. Hospital in 1998 and diagnosed CAD

Family history of heart disease (-)
Diabetes mellitus (+) since 2004 did not control his

medication
Family history of DM (+) his brother.
Hypertension (-)
Gastritis (+)

Risk Factor

Gender : Male
Age : 58 years old
Ex-Smoker until 9 years previously.

Until then had smoked 5-10 cigarrettes

per day for 30 years
Past history of cardiovascular
disease(+)
Diabetes mellitus (+)
Family history of DM (+)

PhysicalExam ination
General Appearance :

Severe-illness/normal weight/conscious

Vital Sign :
Blood Pressure
: 140/100 mmHg
Pulse
: 130 bpm, regular
Respiratory rate : 32 tpm
Body temperature : 37 C (axilla)
Head Examination :
Eyes : anemia(-), icterus(+), cyanosis(-)
Neck : JVP R+2 cmH20
Thoracic Examination :
Inspection
: Symmetric sinistra et dextra
Palpation : No mass, no tenderness
Percussion
: Sonor
Auscultation : Breath Sound was bronchovesicular, rales +/+,

wh -/-

PhysicalExam ination
Cardiac Examination :

Inspection
: Ictus Cordis wasnt visible
Palpation
: Ictus Cordis wasnt palpable
Percussion
: normal heart size
Upper border : ICS II sinistra
Lower border : ICS V sinistra
Right border : right parasternalis line
Left border : left medioclavicular line

Auscultation : Regular of I/II Heart Sound, no

murmur

 Abdominal Examination :
Inspection
Palpation

: Normal
: palpable tender liver 2
cm
b.r.c.m

spleen wasnt palpable

Percussion : Tympani , Ascites (-)
Auscultation: peristaltic sound (+) ,
normal

Extremities :

Oedema pretibial -/-

Laboratory fi
nding
Complete blood count
WBC:10.5 x103/ul
RBC: 4.67x106/ul
HGB:.014.1gr/dl
HCT: 41.5%
PLT: 235x103/l
Electrolyte
Sodium:135 mmol/l
Potassium : 3.7
Chloride: 98 mmol/l

Blood chemistry:
FPG : 335mg/dl
GD2PP : 353 mg/dl
Ureum : 33 mg/dl
Creatinine : 0.7 mg/dl
SGOT/SGPT: 39 / 48 u/dl
Total Prot : 296 mg/dl
HDL: 43 mg/dl
LDL:218 mg/dl
Tg: 181 mg/dl
CK: 113
CK-MB : 24 u/dl

Electrocardiogram

Electrocardiogram
Atrial Fibrilation rapidrespond
Heart rate 120 bpm
Axis : Normoaxis
LVH

Echocardiogram

Echocardiogram
Dilatation of LV
LVH (+)
Global Hypokinetic
EF 30%
Mitral valve: Trivial MR
Aortic valve: Normal
Conclusion:
LV Dilatation
Global hypokinetic
EF 30%

Chest XRay
Cardiom egal
y and sign of
pulm onary
edem a

U ltrasonography

CONGESTIVE
LIVER

W orking D iagnosis
CHF NYHA III ec CAD
DM type II non obess

M anagem ent

Bed rest
Diabetic diet 1700 kkl
Cardiac Diet
O2 3-4 Lpm
IVFD NaCl 0.09% 10 dpm
Lasix 2 amp/12 hours/iv
Lasix 2 amp/
NTG 20 mg/min
Captopril 6.25 mg 1-0-1
Laxadyn syr 3x1 ts

Aspilet 80 mg 0-1-0
Digoxin 0.25mg 1 x 1
Lansoprazole 30 (1-0-0)
Simvastatin 20 (0-0-1)
Homolog 10-10-10
Lantus 0-0-10

DISCUSSION

W H AT IS CH F ?
imbalance in pump function in which the

heart fails to maintain the circulation of

blood adequately.
When CO became inadequate to fulfill the
requirement of metabolism, heart would
make mechanism of compensation.
But when the mechanism have been use
maximally and CO still inadequate, then
symptoms of heart failure would be arise.

 Contractility disturbance (eg.

myocardial infarction; temporary

myocardial ischemia; chronic
volume overload such as mitral &
aortic regurgitation).
Pressure overload (eg. aortic stenosis;
uncontrolled hypertension)
Arrhythmias

NYHA Classification of Heart

Failure
I

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.

Framingham Criteria for Congestive Heart Failure

Major Criteria
paroxysmal nocturnal dyspnea
or orthopnea
neck-vein distension
crackles
cardiomegaly
acute pulmonary edema
S3 gallop murmur
increased venous pressure > 12
mmHg
circulation time > 25 sec
hepatojugular reflex

Minor Criteria
ankle edema
night cough
dyspnea on exertion
hepatomegaly
pleural effusion
vital capacity decreased by
1/3 from maximum
tachycardia (HR > 120 bpm)

2 major or 1 major + 2 minor criteria have to be present concurrently.

* major or minor criteria: weight loss > 4.5 kg in 5 days in response to
treatment

H ow is C H F treated?
Prevention of initial cardiac injury:
Coronary artery disease and hypertension are the two commonest causes of
CHF. Dietary restrictions, exercise, weight reduction in obese individuals,
cessation of smoking, and treatment of risk factors like a high cholesterol
level and diabetes are important cornerstones in the prevention of CAD. Use
of medications to control blood pressure also goes a long way in preventing
CHF. Since heavy use of alcohol can contribute to the development of CHF,
such a tendency needs to be discouraged.
Prevention of further injury: Aggressive early treatment of a heart attack
reduces the amount of damaged muscle and decreases the likelihood and
severity of CHF.
Prevention of post-injury deterioration: Studies have shown that patients who
have suffered considerable muscle damage after a heart attack tend to do
better if they are maintained on a class of drugs known as ACE inhibitors. It
is believed that these medications prevent further deterioration.
General treatment of CHF.

TR EATM EN T

Managing
preload
Managing
contractility
-Cardiac glycosides
- adrenergic
-Phosphodiesterase
inhibitors

-diuretic
-venodilators

Managing
afterload
-Ca2+
channel
blockers
-Anti
adrenergic
-Vasodilators

Neurohormonal
modulation
- blockers
-ACE
inhibitors
-Angiotensin
receptor
blockers

Coronary H eart D isease

Relating to disease processes that

affect the coronary arterial

circulation with consequenses that
affect the coronary arterial
circulation ,the heart and its
function.
This term is generally restricted to
apply only to atherosclerotic
coronary artery disease with the
consequence of ischemic heart

thank you