CONGESTIVE HEART FAILURE (CHF)

NYHA III e.c Coronary Artery

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

By :
Mohamad Nuramin bin
Masrom
C 111 12 817

Patient Identity
Name
Gender
Age

: Mr. E
: Male
: 49 years old

Anamnesis (1)
Chief Complaint

: Shortness of breath
Shortness of breath has been experienced
since 2 months ago and worsen 3 days
before entering RSWS. It was experienced
while doing minimal activity such as
walking to the bathroom and relieved with
resting. There is complain of sudden
shortness of breath during night time that
cause her to be awaken. He also had to use
at least 2 pillows to sleep during night time.

Anamnesis (2)
There is also history of chest pain which has

been experienced since several months ago.

Chest pain was felt like being as punch like
pain spread to the neck until her arms
and last for less than 5 minutes of duration.
Chest pain was also relieved by resting.
There is no complaint of palpitation, fever,
cough, nausea, and vomit.
There is no complaint of urination and
defecation.

Past Medical History

There is history of hypertension since 10

years ago but he doesnt take the drugs

regularly.
History of diabetes mellitus type II.
History of smoking since 20 years ago (1
pack a day average).
There is no history of fever, congenital
heart disease, thyroid disease, and
diabetes mellitus.
There is also no family history with
cardiovascular disease and thyroid disease.

Risk Factors
Cigarette smoking (+)
Alcohol consumption(-)
Hypertension(+)
Diabetes Mellitus(+)
Cardiovascular disease (+)
Thyroid disease (-)
History of cardiovascular disease and

thyroid disease in family (-)

Physical Examination
General Status:
Severe ill
Nutritional Status: Good
Consciousness: Conscious
Vital Signs:
Blood Pressure : 130/90 mmHg
Pulse Rate
: 78 bpm, regular
Respiratory Rate : 26 bpm
Temperature
: 36.5 C

Physical Examination
Head and Neck Examinations:
Eye
Lip

: Conjunctiva anemic (-/-), sclera icteric (-/-)

: cyanosis (-)
Neck : No mass, no tenderness, JVP : R + 3 cmH2O

Chest Examination
Inspection : Symmetric left=right
Palpation : No mass, no tenderness, vocal fremitus

left=right
Percussion: Sonor left = right, lung-liver border in ICS
VI right anterior
Auscultation:
Breath sound
: vesicular
Additional sound : Ronchi : (positive) regio

mediobasal at

left and right lung

Wheezing : negative (-)

Physical Examination
Cardiac Examination
Inspection

: Ictus cordis was not visible

Palpation
: Ictus cordis was not palpable
Percussion
:Right heart border in right
parasternal line, left heart border two
fingers from left midclavicular line ICS
VI.
Auscultation
:
Heart sound

: S I/II regular, no gallop, no additional sound

Physical Examination
Abdominal Examination
Inspection

: flat, following breath movement

Auscultation : Peristaltic sound (+), normal

Palpation

: No mass, no tenderness, no palpable

liver and spleen

Percussion

: Tympani (+), ascites (-)

Extremities Examination
Pretibial edema -/ Dorsum pedis edema -/-

Electrocardiography(ECG)
Interpretation:
Rhythm: sinus
HR/QRS rate:75

x/minutes
Regularity: regular
P wave & PR
interval: 0,08s and
0,2 s
QRS Complex: 2
small
squares(0.08s),
Axis: Normal
ST segment: St
depression on V5
and V6
T wave: Normal

Conclusion of ECG
Sinus rhythm, HR 75 bpm, reguler ,

normoaxis,Myocardia ischemic on lateral

wall (V5and V6), LVH

Chest X-rays
Interpretation :
Suprahilar vascular dilatation at right and
left lung
Cor expand with CTI 0,72 with aorta
dilatation
Sinus diafragma sharp and bones intact
Conclusion :
Cardiomegaly with sign of pulmonary edema
with dilatation and elongation aortae

Echocardiography
Echocradiography (02/10/2016)
Left systolic ventricle function normal, fraction ejection 60%
Heart chamber dimension : In normal state
Left ventricle hypertrophy: Negative (LVMI 175.72,RWT :0.56g/m2)
Miocard movement :global normokinetik
Heart Valve: Mitral : MR Trivial
Aorta ,Trikuspid, Pulmonal : Function and movement good
Conclusion :
Left systolic ventricle function normal, ejeksi fraksi 60%
LV dilation
LVH consentric
Disfungstion diastolic grade II

Laboratory Finding

omplete Blood Count

Test

Result

Normal value

WBC

13.6/ul

4.0 10.0 x 103

RBC

2.77/l

4.0 6.0 x 106

HGB

7.9 gr/dl

12 16

HCT

36.0%

37 48

PLT

348 000/l

150 400 x 103

Test

Result

Normal value

Na

138 mmol/l

136-145

4.8 mmol/l

3.5-5.1

Cl

100 mmol/l

97-111

Electrolyte

Laboratory Finding

Blood Chemistry
Test

Result

Normal value

GDS

156 mg/dl

<140

Ureum

194 mg/dl

10 50

Creatinine

7.42 mgr/dl

< 1.3

SGOT

17 u/l

<38

SGPT

13 u/l

<41

Total Chol
HDL Chol
LDL Chol

183 mg/dl
45 mg/dl
108 mg/dl

<200
> 55
< 130

TG

75 mg/dl

<200

Test

Result

Normal value

CK

402 U/L

<167

CK-MB

31.6 U/L

<25

Troponin-T

<0.1

Negative

Cardiac Enzymes

Diagnosis
CHF NYHA III e.c CAD
Hypertensive Heart Disease
Diabetis Mellitus type II
Acute Kideney injury dd Acute

on Chronic Kidney Disease

Anemia normositik normokrom

Management
O23-4lpm
IVFD Nacl 0,9% 10 tpm
Furosemid 40mg/12hours/iv
Aspilet 80mg/24hours//oral
Simvastatin 20mg/24hours//oral
Nitrokaf r 2,5mg/12hours//oral
Ramipril 2,5mg/24hours//oral
Amlodipin 10mg/24hours//oral
Alprazolam 0,5mg/24hours//oral
Levemir 0-0-10 IU
Novorapid 8-8-8 IU

Planning
Consultation with Kidney and

Hypertension Division
ECG control
Echocardiography

DISCUSSION
Congestive Heart Failure
(CHF)

Definition
Heart Failure

Congestive
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.

Etiology of
Heart Failure
Main Causes
Ischemic heart disease
(35%-40%)

Cardiomyopathy(dilated)
(30-40%)

Hypertension ( 15-20%)

Other Causes
Arrhythmias
Valvular heart disease
Congenital heart disease
Pericardial disease
Hyperdynamic circulation
Alcohol and
drugs(chemotherapy)

The Framingham criteria for CHF

CHF considered present if 2 major or 1 major & 2 minor

Major Criteria
Paroxysmal Nocturnal
Dyspnea
Cardiomegaly
Gallop S3

Minor Criteria
Extremity edema
Nocturnal cough
Decreased vital
pulmonary

Hepatojugular reflux

capacity (1/3 of maximal)

Increased of JVP

Hepatomegaly

Rales or ronchi

Pleural effusion

Acute pulmonary edema

Tachycardia ( 120bpm)

Prolonged circulation time(> 25

Dyspnea deffort

sec)
Weigh loss 4,5 kg in 5 days in
response to treatment of CHF

Classification of CHF

Pathophysiology of Heart Failure

Pathophysiology of CHF
Plaque in
coronary artery

Blood flow to
heart muscle is
reduced. Heart
muscle lacking
of oxygen

Ischemia of
heart muscle
can lead to
myocardial
infarction

Symptomatic
Congestive
Heart Failure

Pulmonary
edema
Abnormal
Heart rhythm

The heart
muscle cant
pump
adequately

Treatment of CHF

Managing
preload
Managing
contractility

Inotropic agents :
Cardiac glycosides
B- adrenergic
Phosphodiesterase
inhibitors

Diuretics
venodilator

Managing
afterload
Neurohormonal
modulation
ACE inhibitors
Angiotensin
receptor
blocker
blockers
CCB

blockers
ACE inhibitors
Angiotensin
receptor blockers

Pharmacologic Management
ACE Inhibitors
Blocks the conversion of angiotensin I to
angiotensin II; prevents functional deterioration
Recommended for all heart failure patients
Relieves symptoms and improves exercise
tolerance
Reduces risk of death and decreases disease
progression
Benefits may not be apparent for 1-2 months after
initiation

Angiotensin-Converting
Enzyme Inhibitors
Recommended as first-line therapy
Should be uptitrated to the dosages shown to be effective

in the large, controlled trials, and not titrated based on

symptomatic improvement

Moderate renal insufficiency and a relatively low blood pressure

(serum creatinine 250 mol.l-1 and systolic BP 90 mmHg) are

not contraindications

Absolute contraindications : bilateral renal artery stenosis

and angioedema

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560

Diuretics
Essential for symptomatic treatment when fluid

overload is present and manifest.

Always be administered in combination with

ACE inhibitors if possible.

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560

Beta-Adrenoceptor Antagonists (B-Blocker)

Recommended for the treatment of all pts

with stable, mild, moderate and severe

heart failure on standard treatment, unless
there is a contraindication.
Patients with LV systolic dysfunction, with

or without symptomatic HF, following an

AMI long-term betablockade is
recommended in addition to ACE inhibitor.
Guidelines for the diagnosis and treatment of chronic heart failure
European Heart Journal (2001) 22, 1527-1560

Chronic Heart Failure Choice of

Pharmacological Therapy
LV systolic dysfunction

ACE inhibitor

Diuretic

Beta-blocker

Aldosterone
Antagonist

Asymptomatic LV
dysfunction

Indicated

Not indicated

Post MI

Not indicated

Symptomatic HF
(NYHA II)

Indicated

Indicated if
Fluid retention

Indicated

Not indicated

Worsening HF
(NYHA III-IV)

Indicated

Indicated
comb. diuretic

Indicated

End-stage HF
(NYHA IV)

Indicated

Indicated
comb. diuretic

Indicated

Indicated

Indicated

Guidelines for the diagnosis and treatment of chronic heart failure

European Heart Journal (2001) 22, 1527-1560

Chronic Heart Failure Choice of

Pharmacological Therapy
LV systolic dysfunction

Angiotensin
II receptor
antagonists

Asymptomatic LV
dysfunction

Not indicated

Cardiac glycosides

Vasodilator
(hydralazine/
isosorbide
dinitrate)

Potassium
-sparing diuretic

With AF

Not indicated

Not indicated

(a) when AF
If ACE inhibitors
If ACE inhibitors
(b)
when
improved
are not tolerated
and angiotensin
Symptomatic HF (NYHA II)
from
more
and not on betaII antagonists
severe
HF
in
blockade
are not tolerated
sinus rhythm
If ACE inhibitors
are not tolerated
Worsening HF (NYHA III-IV)
and not on betablockade
End-stage HF (NYHA IV)

If ACE inhibitors
are not tolerated
and not on betablockade

If persisting
hypokalaemia

indicated

If ACE inhibitors
and angiotensin
II antagonists
are not tolerated

If persisting
hypokalaemia

indicated

If ACE inhibitors
and angiotensin
II antagonists
are not tolerated

If persisting
hypokalaemia

Guidelines for the diagnosis and treatment of chronic heart failureEuropean Heart Journal (2001) 22,
1527-1560

Coronary Artery Disease

Coronary Artery
Disease
Coronary artery disease is a narrowing of

the
small blood vessels that supply blood and oxygen
to the heart.
(CAD) occurs when the arteries that supply blood
to the heart muscle (the coronary arteries)
become hardened and narrowed due to buildup of
a material called plaque (plaque) on their inner
walls. This is known as atherosclerosis
Eventually, blood flow to the heart muscle is
reduced, and, because blood carries much-needed
oxygen, the heart muscle is not able to receive
the amount of oxygen it needs.

Causes Coronary Artery

Disease
Coronary artery disease (CAD) is caused by

atherosclerosis (the thickening and hardening

of the inside walls of arteries). Some
hardening of the arteries occurs normally as a
person grows older.
In atherosclerosis, plaque deposits build up in
the arteries. Plaque is made up of fat,
cholesterol, calcium, and other substances
from the blood. Plaque buildup in the arteries
often begins in childhood.

Plaque in the arteries can be:

Hard and stable. Hard plaque causes the
artery walls to thicken and harden. This
condition is associated more with angina
than with a heart attack, but heart attacks
frequently occur with hard plaque.
Soft and unstable. Soft plaque is more likely
to break open or to break off from the artery
walls and cause blood clots. This can lead to
a heart attack.

Risk factors
Risk Factors That Cannot Be Modified:
Age and gender. As get older, risk for
CAD increases.
Men, risk increases after age 45.
Women, risk increases after age 55
(or menopause).
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 That Can Be

Modified:
High blood cholesterol
(hyperlipidemia)
High blood pressure
(hypertension)
Cigarette smoking
Diabetes
Overweight or obesity
Lack of physical activity

INVESTIGATION
Electrocardiogram (ECG)
Treadmill Test
Echocardiography
Coronary Angiography
Multi-Slice Computed Tomography

Scan (MSCT)
Cardiac Magnetic Resonance Imaging
(Cardiac MRI)
Radionuclear Medicine

TREATMENT (1)
Lifestyle Changes
Eat a healthy diet
Quit smoking, if you
smoke
Exercise
Lose weight, if you
are overweight or
obese
Reduce stress

Medicines
Cholesterol-lowering
medicines
Anticoagulants
Aspirin
ACE inhibitors
Beta blockers
Calcium channel
blockers
Nitroglycerin
Long-acting nitrates

TREATMENT (2)
Special Procedures
Angioplasty (PTCA)
Coronary artery bypass surgery
Enhanced External Counterpulsation (EECP)
Cardiac Rehabilitation
Exercise training
Education, counseling, and training

THANK YOU