chf nyha iiii

8/13/2019 Chf Nyha Iiii

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KONSULEN:

Dr. dr. Idar Mappangara, SpPD,

SpJP.FIHA.FINASIM

PRESENTER:

NOR HAZIRAH BINTI OMAR

C 111 09 846


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IDENTITY OF PATIENTName : Mr. R

Age : 64 y.o

Gender : MaleAddress : Daya

MR : 443141

Date of admittance : 9 September 2013


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ANAMNESIS Chief Complaint :Shortness of breath (SOB)

Brief Anamnesis :

The onset of SOB was 1 month before admittingin hospital. It worsens 1 day before admitting inhospital. It worsens during any physical activitiessuch as lifting up things (DOE). He also

experiences SOB whenever he lies down and withmild exertion. Patient complains that he oftenwakes up in the middle of night and gasps for air(PND) and he feels better if use two to threepillows while sleeping (orthopnea). He says that

wheather does not influence SOB.


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ANAMNESIS Patient complaints that his both legs was swollen.

The onset was 1 week before admitting in hospital.

Cough (+), white serous, appears since 1 week ago Chest pain (-), History of chest pain (+), 10 years ago,

doctor advise the patient to do catheterization to putin two stent but the patient refuse to do so.

Fever (-), History of fever (-) Nausea (-), Vomit (-)


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PAST MEDICAL HISTORY History of shortness of breath in June 2013 (+) was

admitted in hospital

Hypertension (-)

Diabetes mellitus (-)

Cigarette smoking (+) 20 years


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Present status:

Moderate illness / Well-nourished / Conscious

Vital signs:

BP : 100/70mmHg

HR : 92bpm

RR : 36x/minT : 36,5C


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Regional status

Head Examination

- Eyes : Anemis (-), Icterus (-)

- Lip : Cyanosis (-)

- Neck : JVP R +2 cmH2O, enlargement of thyroid gland (-)

Chest Examination

- Inspection : Symmetric sinistra et dextra

- Palpation : No mass, no tenderness, VF sinistra = dextra

- Percussion : Sonor sinistra et dextra

Lung-liver border in ICS VI right anterior

- Auscultation : Breath Sound = Bronchovesicular

Additional Sound = Rh , Whz -/-


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Cardiac Examination

Inspection : Ictus cordis not visible.

Palpation : Ictus cordis not palpable

Percussion : Right heart border in right parasternal line,left heart border in left midclavicle line ICS V.

Auscultation : Heart Sounds = S I/II regular , murmur (-)


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Abdominal- Inspection : flat, following breath movement,

ascites (+)

- Auscultation : peristaltic sound (+), normal

- Palpation : liver unpalpablespleen unpalpable

- Percussion : shifting dullness (+)

Extremities

- Oedema pretibial +/+

- Oedema dorsum pedis +/+

- Cyanosis (-), Clubbing finggers (-)


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ELECTROCARDIOGRAPHY


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Intrepetation of ECG :Rhythm : Sinus

Heart rate : 104 bpm

Regularity : Reguler

PR interval : 0,08

P wave : Normal

Axis : RAD (180)

Complex QRS : The height of R wave > S wave at V1

: Pathologic Q wave at V2

V4Duration QRS : 0,08

T wave : inverted at V1V3

Conclusion : Sinus tachicardia, HR 104/mnt, RAD,

RVH, OMI anteroseptal, low voltage


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Types of test Results Normal Value

Routine Blood Test WBC 7,26 x 10^3/uL 4,00-10,00

PLT 121 x 10^3/uL 150-400

RBC 5,2 x 10^6/uL 4,00-6,00

HGB 15,9 13,0-16,0 g/dL

HCT 24,7 37,0-48,0 %

Blood Chemistry GDP 76 110 mg/dl

Ur 52 10-50 mg/dlCr 1,1


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Types of test Results Normal Value

Cardiac Enzyme CK 60


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CHEST-XRAYConclusion:

Cardiomegaly with signs

of pulmonary edema

Dilatation of aortae

Right pleural effusion


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USG Bilateral Pluera Effusion

especially at right

Ascites


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WORKING DIAGNOSIS

1. Congestive Heart Failure NYHA III ec

CAD

2. Hipoalbumin


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MANAGEMENT

Heart Diet

IVFD NaCl 0,9% 10 drips/min O2 24 liter/min

Furosemide 200mg/24h/IV

Aspilet 80mg 1-0-0

Farsorbid 10mg 1-1-1 Captopril 6,25mg 1-1-1

Alprazolam 0,5mg 1-0-0

Simvastatin 20mg 0-0-1

Laxadin Syrup 0-0-2C

Infus albumin 20% 1 bottle/24 hours


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PLANNING

ECG Control

Chest X-Ray

Lab Examination


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Ong, WT; Patacsil, GB. Cardiology Blue Book: 148

Heart no longer able to pump an

adequate supply of blood in

relation to the venous return and inrelation to the metabolic needs of

the body tissues at the particularmoment

HeartFailure

The state in which abnormal

circulatory congestion occurs asthe result of heart failure.

CongestiveHeart

Failure


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EtiologyIschemic heart disease

Valve disease

Hypertensive heart disease

Cardiomyopathy

Coronary artery disease


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NYHA CLASSIFICATION

Classification Description

NYHA I -No limitation o f physical activity

-No symptoms with ordinary exertion

NYHA II -Slight limitation of physical activity

- Ordinary activity causes symptoms

NYHA III -Marked limitation of physical activity-Less than ordinary activity causes symptoms

-Asymptomatic at rest

NYHA IV -Inability to carry out any physical activity without discomfort-Symptoms at rest

i d


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Signs and Symptoms

Company LogoThe National Heart, Blood, and Lung Institute. cited from http://fromyourdoctor.com/.Last updated June 7,


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Diagnosis

NB : To establish a clinical diagnosis of congestive heart failure by these criteria, at least one major

and two minor criteria are required.


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TREATMENT

Managing

afterload

Managing

preload

Neurohormonal

modulation

Managing

contractility

Inotropic agents :Cardiac glycosidesB- adrenergic Phosphodiesteraseinhibitors

Diureticsvenodilator

Ca2+channelblockers

Antiadrenergic

Vasodilators

blockersACE inhibitorsAngiotensinreceptorblockers


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CORONARY ARTERY DISEASE

DEFINITION

Condition in which plaque builds up insidethe coronary arteries. These arteries supply

oxygen-rich blood to the heart muscle.


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CAUSES

The major underlying cause is atherosclerosis.

It is a slow, progressive disease which begins

in childhood and takes decades to advance.

It occurs when plaque builds up in the arteries.

The buildup of plaque occurs over many years. Over time, plaque hardens and narrows your

coronary arteries. This limits the flow of

oxygen-rich blood to your heart muscle.


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Endothelial Injury

Monocytes becomes macrophages

Activate macrophages release free radicals

Oxidize LDL

Toxic to endothelium causing endothelial loss

Exposure of subendothelial connective tissue to blood components

Platelet adhesion & aggregation fibrin deposition

Platelet release various factor

Smooth muscle migrates into intima & proliferate

Smooth muscle cell, macrophages & matrix accumulate LDL from the plasma

ATHEROMATOUS LESION


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PATHOPHYSIOLOGY


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RISK FACTOR

Modifiable:

- Smoking

- Dyslipidemia (Raised LDL-

C, Low HDL-C, Raised

triglycerides)

- Raised Blood pressure

- Diabetes melitus

- Obesity

Non-Modifiable :

Personal History of CVD

Family History of CVD

Age

Gender


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CLASSIFICATION

STEMI NSTEMISTEMI

Non Q wave MI

NSTEMI

Q wave MIUnstable angina pectoris

Coronary Artery Disease

Acute Coronary SyndromeStable angina pectoris


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Unstable Plaque Occlusive Thrombus

Fixed Coronary Obstruction(Chronic Ischemic Heart Disease)

PATOGENESIS

Si &


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Sign & symptoms

Stable angina

Discomfort in the chest, jaw,shoulder, back or arms,

Typically elicited by exertion oremotional stress and relieved by

rest or nitroglycerin.

Less typically, discomfort mayoccur in the epigastric area.

Unstable anginaAngina at rest (> 20 minutes)New-onset (< 2 months)exertional angina (at least CCSCIII in severity)Recent (< 2 months)

acceleration of angina (increasein severity of at least one CCSCclass to at least CCSC class III)

MI

Prolonged chest pain

Associated symptoms from the

autonomic nervous system (nausea,

vomiting, diaphoresis)


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DIAGNOSIS

Electrocardiogram (ECG)

Echocardiogram

Stress test

Cardiac catheterization or angiogram

Magnetic resonance angiography (MRA)


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TREATMENT GOAL:

Improve prognosis by preventing myocardial infarction and

death

Minimize or abolish symptoms.

NON PHARMACOLOGY:

Lifestyle modification

Quit smoking

Exercise regularly

Lose excess weight

Avoid stress


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Nitrates

Beta blockersCa antagonist

HeparinLMWHWarfarin

AspirinThienopiridinesGPIIb/IIainhibitor

Anti CoagulantAnti Platelet

Anti ThromboticAnti Ischemic

Pharmacological


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THANK YOU

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