Case presentation

CHF NYHA II-III e.c. CAD

BY
INDAH NURMAWATI
C 111 03 134

PATIENT IDENTITY
Name
: Mr. A
Medical Record : 375155
Age
: 54 years old
Address : Bau-bau

HISTORY TAKING

Chief complaint : Shortness of breath

History taking :
- Patient felt shortness of breath since two weeks
ago before admitance. Dyspnea exacerbated by
activity and not by weather change.
change History of
shortness of breath since four years ago,
uncontinuously. He slept with use one pillow. Patient
often wake up in the night because dyspnea.
-Sometimes theres chest pain when dyspnea. Chest
pain was felt in the left chest, not penetrate to back
and pain could be localized.

HISTORY TAKING
-

Swelling in the both of leg since two weeks

ago.
There was no fever, headache.
Theres no cough, nausea and vomit. He
usually felt pain at the upper stomach.
History of increasing micturation in the night
since two years ago, more often thirsty and
hungry.
Urinate and defecate was normal.

PAST MEDICAL HISTORY

The

patient have gone to the doctor with

the same complaint on 2005 and have
had therapy but not regularly.
The patient denied have hypertension,
diabetes mellitus.

RISK FACTOR
He

have smoked since he was young,

1/2 pack/day.
He was not alcoholic.
Man 54 years old

PHYSICAL EXAMINATION

Vital Sign :

Blood pressure
: 130/90 mmHg
Pulse
: 84 x/min
Inspiratory rate
: 28 x/min
Body temperature : 36,5oC

Eyes : there was no anemis, no cyanosis, no icterus

Neck : JVP R+1 cmH20

Inspection
: Symetric
Palpation
: no mass, no tenderness
Percussion
: Sonor
Auscultation : Breath Sound : vesikular
Additional sound :Ronchi +/+ basal, Wheezing -/-

Head Examination :

Thoracal Examination :

PHYSICAL EXAMINATION
Heart

Examination :
Inspection : ictus cordis was no visible
Palpation : ictus cordis was no palpable
Percussion : widening of heart size
Auscultation
: regular of I/II Heart Sound, no murmur

Stomach

Examination :

Inspection : normal
Palpation : no mass, tenderness on regioepigastrium
Percussion : tympani, mild acites (+)
Auscultation : peristaltic sound (+), normal

Extremity

: there was oedema pretibial and dorsum pedis

ADDITIONAL EXAMINATION
Complete blood
WBC
HGB
RBC
PLT
HCT
Blood electrolyte
Sodium
Potassium
Chloride
Heart enzim
CK
CKMB
Troponin-T

: 9,3 x 10 /mm
: 12 g/dl
: 4,44 x 106 /mm3
: 206 x 103 /mm3
: 38,4 %
3

: 125 mmol/l
: 2,7 mmol/l
: 93 mmol/l
: 59
: 33 U/l
: < 0,1 ng/ml

Blood chemistry
Random blood sugar
: 242 mg/dl
Fasting blood sugar : 131 mg/dl
SGOT
: 89 u/l
SGPT
: 1,7 u/l
Cholesterol total
: 201 mg/dl
Cholesterol HDL
: 10 mg/dl
Cholesterol LDL
: 71 mg/dl
Triglyseride
: 203 mg/dl
Protein total : 6,5
Albumin : 2,5
Globulin : 2,8
Ureum
: 34
Creatinin : 0,6
Uric acid : 8.0

ECG :

-Sinus rhytme
-Lateral wall ischemia
-LAD

ADDITIONAL EXAMINATION

Chest x-ray :
Cardiomegaly with
sign of pulmonal
edema

ADDITIONAL EXAMINATION

Echocardiography :
- CHF
-CAD
- PH

SUGGESTION ADDITIONAL
EXAMINATION
Coronary

angiography

DIAGNOSIS
CHF NYHA III-IV e.c CAD
DM type 2

MANAGEMENT

Oxygen : 3-4 L/m

IVFD NaCl 0,9 %
Loop diuretics : Furosemide 2 amp/12 hours/IV
to reduce preload
Aspilets 80 mg 0-1-0
to prevent aggregate platelet
Plavix 75 mg 0-1-0
to prevent production of tromboxane A2, so
platelet not aggregate
ACEI : Captopril 12,5 mg 2x1
arteridilator and venodilator, to reduce afterload
K+ sparing diuretics : Spironolaktone 25 mg 1-0-0
spesifics antagonist of aldosterone

MANAGEMENT...

Nitrat : Farsorbid 10 mg 3x1

Venodilator : to reduce filling pressure
Simvastatin 10 mg 0-0-1
Actrapid 6-6-6

DISCUSSION

CORONARY ARTERY DISEASE

Coronary

artery disease (CAD) occurs

when the arteries that supply blood to
the heart muscle (the coronary arteries)
become hardened and narrowed.The
arteries harden and narrow due to
buildup of a material called plaque (plak)
on their inner walls. The build up of
plaque is known as atherosclerosis

Pathogenesis:
Myocardial O2 supply
Narrow vessel because
flaque
Forming of trombus because
trombosite agregation
Spasme coronaria artery
Myocardial O2 requirements
Activity increase

RISK FACTORS

Risk Factors That Cannot Be Modified:

Age. As you get older, your risk for CAD increases.

Men, risk increases after age 45.
Women, risk increases after age 55.
Family history of early heart disease.
Heart disease diagnosed before age 55 in father or
brother.
Heart disease diagnosed before age 65 in mother or
sister.

RISK FACTORS
Risk

Factors That Can Be Modified:

High blood cholesterol
High blood pressure
Cigarette smoking
Diabetes
Overweight or obesity
Lack of physical activity

 CLINIC

SYNDROM OF CAD :
Angina Pectoris
Infark Miokard

Non-Q wave
Q wave

CONGESTIVE HEART FAILURE

(CHF)
Congestive

heart failure (CHF) is an

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

 When

cardiac output became

inadequate to full fill the requirement of
metabolism, heart would make
mechanism of compensation. But when
the mechanism have been use
maximally and cardiac output still
inadequate, then symptoms of heart
failure would be arise.

NYHA Classification of Heart

Failure
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.

The Framingham criteria for CHF

CHF considered present if two major or one major plus two minor criteria
are fulfilled

Major Criteria

Paroxysmal nocturnal dyspnoea

Neck vein distension
Rales
Radiographic cardiomegaly
Acute pulmonary oedema
S3 gallop
Hepatojugular reflux
Circulation time > 25 seconds
Weight loss 4.5 kg in 5 days in response to treatment of CHF
Pulm.oedema, visc. congestion or cardiomegaly at autopsy

The Framingham criteria for CHF

Minor criteria

Bilateral ankle oedema

Nocturnal cough
Dyspnoea on exertion
Hepatomegaly
Pleural effusion
Heart rate 120 bpm

Manifestations of LHF
Forward effects

Brain
restlessness,
anxiety, generalized
fatigue.
Kidney
low urine output with
subsequent fluid
retention, high
afterload due to RAA
cascade activation,
kidney failure.

Backward effects

Dyspneu
cough

Manifestations of RHF
Forward effects

Peripheral tissue hypoxia

Due to low cardiac output
caused by failure to deliver
enough blood to left atrium

Backward effects

Peripheral subcutaneous tissue

Liver
Portal system
Spleen

TREATMENTS

MANAGING PRELOAD

MANAGING CONTRACTILITY

MANAGING AFTERLOAD

NEUROHORMONAL
MODULATION