ACUTE HEART FAILURE

(GAGAL JANTUNG AKUT)

Dr AFDHALUN HAKIM,SPJP,FIHA,FASCC
RS Otorita Batam/BP Batam
 Acute Heart Failure(AHF)
Definition : Rapid onset symptoms and signs secondary
to abnormal cardiac function
May present with several clinical condition:
Acute Decompensated Heart Failure (de novo/acute on
chronic CHF)
Hypertensive AHF
Pulmonary Edema
Cardiogenenic Shock
High Output Failure
Right Heart Failure
 Acute Heart Failure
Heart Failure is a clinical syndrome in which patients have the following features

Symptom typical of heart failure

(breathlessness at rest or on exercise, fatigue, tiredness, ankle swelling)

AND
Signs typical of heart Failure
(tachycardia, tachypnoea, pulmonary rales, pleural effusion, raised jugular venous
pressure, peripheral edema, hepatomegali)

AND
Objective evidence of sructural or functional abnormality of the
heart at rest
(cardiomegaly, third heart sound, cardiac murmurs, abnormality on the
echocardiogram, raised natriuretic peptie concentration
 Clinical presentation of
Acute Heart Failure
1. Acutely
decompensated
Chronic HF
2. Hypertensive AHF
3. Acute Pulmonary
Edema
4. Cardiogenic Shock
5. ACS & Heart Failure
6. Isolated right heart
failure
 Acute Pulmonary Edema
Definisi
Pathophysiology
Mechanism Cardiogenic PE
Signs and Symptoms
Diagnosis and DD
Management
Prognosis
 Acute Pulmonary Edema
Terminology

Cardiogenic Pulmonary Edema

Acute Heart Failure
Decompensated Heart failure
 Acute Pulmonary Edema

Definition :
Pulmonary edema is a condition in wich
fluid accumulates in the
lungs(extavasation of fluid from the
pulmonary vasculature into the intertitium
and alveoli of the lung) ,
usually because the heart’s left ventricle
does not pump adequately
Phatophysiolgy ALE
 Acute Pulmonary Edema
4Major Pathophysiology Mechanism:

• Increased capillary hydrostatic pressure

• Increased capillary permeability
• Decreased plasma oncotic pressure
• Lymphatic Obstruction
 Acute Pulmonary Edema
Classified :
Cardiogenic (Acute Myocardial
Infarct,Crysis Hypertension,Mitral
Stenosis,Aortic Stenosis,Chronic
Heart failure)

Noncardiogenic(ARDS,CRF,Pneumo
nia,Bad Burn,Drug Intoxication)
 Acute Cardiogenic
Pulmonary Edema

• ACPE is caused by elevated pulmonary

capillary hydrostatic pressure leading fluid
into the pulmonary intersitium and alveoli
Mechanism ALE
 Mechanism of cardiogenic pulmonary
Edema

Q=K (P cap - P is)- λ (π cap- π is)

Q= Net fluid filtration

K= Constant called the filtration coefficient
P cap = Capillary hysdrostatic pressure
P is =Hydrostatic pressure in the interstitial fluid
λ coefficient (effectiveness of the capillary wall in prefiltration
π cap=colloid osmotic pressure of plasma
π is = colloid osmotic pressure in the interstitila fluid
Mechanism of cardiogenic pulmonary
Edema
Straling Law
Q=K (P cap - P is)- λ (π cap- π is)

P cap
P is

π is
π cap
Mechanism of cardiogenic pulmonary
Edema
Straling Law
Q=K (P cap - P is)- λ (π cap- π is)

Alveoli
Lymp
π is
π is
Vascular Intertitial space
P cap P is
π cap
Alveoli
 Mechanism of cardiogenic pulmonary
Edema
Dalam keadaan normal:

Tekanan Hydrostatic (P)~ 10 mmHg

Tekanan Onkotic (π ) ~ 25 mmHg
Tekanan Hydros Intertitial ~ -2 to -4 mmHg
Tekanan Onkotic Intertitial ~ 19-25 mmHg
Kemampuan Kel Lymphe mengangkut 20
cc/jam (pada keadaan chronic >200ml/h)
 Mechanism of cardiogenic pulmonary
Edema
Edema paru terjadi bila:

1. Meningkatnya secara berlebihan tekanan

hidrostatic yg melebihi tekanan onkotic (acute
left heart failure, wedge pressure >18 mmHg)
2. Menurunnya tekanan onkotic plasma
(meningkatnya permeabilitas kapiler,rendahnya
albumin atau dilusi plasma oleh cairan
kristaloid)
 Mechanism of cardiogenic pulmonary
Edema
Edema paru terjadi bila:

3. Rusaknya permebalitias membrane alevolar-

capilar,shgg permeabilitas kapiler meningkat
(ARDS,overdosis opiat,toxin)
4. Disfungsi atau sufisiensi lympatic,sehingga
menyebabkan gangguan pengangkutan cairan
ektravascular
 Killip Classification
(ACS STEMI + KOMPLIKASI)
• Stage I : No Heart Failure
• Stage II : Heart Failure (Diagnostic criteria
include rales,S3 gallop and Pulmonary Venous
Hypertension,rales in the lower half of the lung
fields
• Stage III : Severe Hear Failure. Frank
Pulmonary Edema (reles throughout in the lung
fileds
• Stage IV : Cardiogenic Shock
Signs And Symptoms
 Signs and Symptoms
• Rapid development of extreme breathlesstness
• Anxious,coughs &expectorates pink,frothy sputum
• Feel as if drowning
• Increased respiration rate and diaphoresis
• Allae nasi are dilated,retraction intercostal and
supraclaivucular
• Respiration is typically :noisy and patient grab sides of
the bed
• Sweating,skin cold,and cyanotic
 Physical Examination

• Takipnoe and Takikardia • Hypertension cause

• Sitting Hyperadrenergic state,
Upright,demonstrate air may be hypotension
hunger and may become cause LV dysfunction or
agitated shock
• Central Cyanosis • Rales all of the lungs
• Anxious and diaphoretic • S3 Gallops and JVP
• Skin pallor and mottling elevated may be murmur
(+)
• Changes mental status
 Precipitating Factors :

• Noncompliance with • Fluid/Volume

dietary overload (CRF)
• Noncompliance • Alcohol Abuse
medication • Drug Abuse
• Anemia • Phaeochromocytoma
• Sepsis • Myocardial Toxins
Thyrotoxicosis
Differentiation of Cardiogenic from Non
Cardiogenic Pulmonary Edema
• Cardiac • Non Cardiac
History
• Acute Cardiac Event • Underlying Disease

Clinical Examination
• Low flow (cool periphery)
• S3Gallop,Cardiomegali
• JVP elevated
• Crackles wet
• High Flow (warm
periphery)
• Bounding pulses,No
Gallop,JVP normal
• Crackles dry
Differentiation of Cardiogenic from Non
Cardiogenic Pulmonary Edema
Cardiac • Non Cardiac
Laboratory Test
• ECG :ischemia/infarct • ECG :usualy normal
• CXR: perihilar distribution • CXR : peripheral distribution
• Cardiac enzym increase • Cardiac enzym normal
• PCWP >18 mmHg • PCWP<18 mmHg
 Supportive Examination
• Laboratories Study:
- CBC (anemia)
- Electrolytes (hypo kalemia/magnesemia)
- BUN and creatinin
- BGA (Blood Gas Analysis)

• Chest X-Ray : Cardiomegaly,Bilateral Infiltrates (Butterfly

pattern),Kerley B Lines

• ECG: LAE,LVH, ST depresi/elevasi (ACS),arrhytmias

 Supportive Examination
• Echocardiography : Mitral/Aortic
Stenosis,Atrial Tumor,CAD,Pericardial
Effusi(tamponade),LV Fungsi (EF)

• Cor-Angiogram: Right Heart Cath

(PCWP),Senosis Koroner,Cardiac Index
 Causes
• Acute Coronary • Cardiac Tamponade
Syndrome • Aortic Dissection
(STEMI/NSTEMI)
• Post Partum
• Crisis Hypertension Cardiomyopati
• Valvular Heart • Acute Severe
Disease (MS,AS) Myocarditis
• Arrhythmias
• Chronic CHF
 Diff.Diagonosis (DD)

• ARDS • Cardiogenic Shock

• Asma Bronchial
• Emphysema
• COPD
• Pulmonary Embolism
 Precipitating Factors :

• Noncompliance with • Fluid/Volume

dietary overload (CRF)
• Noncompliance • Alcohol Abuse
medication • Drug Abuse
• Anemia • Phaeochromocytoma
• Sepsis • Myocardial Toxins
Thyrotoxicosis
Management ALE
ALE MANAGEMENT
 Medical Therapy Focus :
2 Main Goals

• Reduction of Pulmonary Wedge

Pressure(Preload Reduction):
reduce amount of fluid in the lungs,improve gas
exchange
• Reduction of Systemic Vascular
Ressisrance (Afterload Reduction):
Improve heart function(cardiac output) and renal
perfusion
 General management
• “Oxygen-IV-Monitor : (O-I-M)
• O2 high flow ( NR bag mask): 6-10 L/m
• Sit Upright with legs dependent
• IV Line (Ringer Lactat/Asering)
• Monitor Patient (ECG monitoring)
• Oxy-Haemoglobin Saturation monitoring
• Intubation if needed
 Indication of Intubation :
• PaO2 cannot be maintained above 60
mmHg,despite 100% Oxygen
• Sign of cerebral hypoxia (lethargy or
confusion)
• PaCo2 increases progressively
• Respiratory Acidosis Develops
 First Line Action:

•MONF
 First Line Action:
• O2 Sungkup (NRM) 10-12 L/min
• Nytroglycerin SL (NTG 0,4 mg,cedocard 5
mg)
• Nitrat IV (ISDN Nitrat) mulai dosis 10
mcg/min
• Furosemide IV (0,5-1 mg/Kg>> Maks 2
mg/KgBB)
• Morphine IV (2-4 mg )

• NTG and MO : CI BP < 90 mmHg

 Second Line Action:
• NTG or Nitroprusside IV : if BP>100
mmHg
• Dopamine if BP 70-100 mmHg signs or
symptoms of shock
• Dobutamine if BP>100 mmHg, No signs or
symptoms of shock
• Furosemide :
has biphasic action
1.Decrease venous tones and an increase
venous capacitance - to Fall LV End Filling
Pressure(Preload)
2.Produces Diuresis (doses 0,5-1 mg/Kg) if no
response in 20 min,repeat with increase dose
2 mg/Kg
Morphin Sulfate
Remain a part of Th/ for ALE
Dilates the capacitance vessels of the
peripheral venous bed.reduces venous
return to central circulation and preload
Reducing afterload by causing mild arterial
vasodilatation
Sedative effect
Nitroglycerin
Potent Vasodilator
Reduces Pulmonary Congestion by dilating
venous vessels-reducing preload
Dilates systemic arteriesdecrease systemic
vascular resistance -decrease afterload and
increase cardiac output
Sublingual/IV ( IV: initiated at 10
mcg/minincrease by 5-10 mcg every 3-5
minute
Nitroglycerin
Avoid NTG :
Use Viagra within the previous 24 hrs
BP <90 mmHg
Bradicardia (HR <50 mmHg)
RV Infarction
 Further Diagnostic and Theraphy

1. Identify and treat reversible causes(consider

6 H and 6 Ts)
2. Intra Aortic Baloon Pump (IABP)
3. Angiography / PCI
4. Surgical Intervension
5. Additional drug therapy:
-Amrinone (0,75 mg/Kg)5-15mcg/Kg/min
-Fibrinolytic Th/
-Anti Arrhytmias
Next slide 
 Further inpatient care

• When the patient has been stabilizedCVCU

• Monitoring With patient monitor (arrhytmias)
• Complete Supportive Exam (ECG,Enzyme)
• Vasodialtor Therapy
• Diet
• Counselling and education
 Prognosis

• In General Mortality rate 15-20%

• Acute MI and Severe Heart Failure 30%
mortality in 12 Month
• CPE cause of Acute Myocardial Infarction (Killip
III) mortality rate 80 % if patient also is
Hypotension (Shock cardiogenic)
• 45% of pts hospitalized with Acute Heart Failure
will be re-hospitalized at least once (and 15 % at
least 2x)
 Kasus
• Tn.A/65 th/Lk
• KU : Sesak napas berat,tiba2 ,terbangun
saat tidur subuh,harus duduk dan
bertambah berat
• Riw.HT lama (kontrol tak teratur),perokok

• BB : 60 kg TB : 160 cm
 Kasus
• Pem.Fisik
• CM, TD 220/120 HR 110x/m RR 40x/m
• Sat O2 : 90%
• Cor :S1S2 N,Reguler, M(-), Gallop (+)
• Pulmo : Ronchi seluruh lap paru
• Abd/Ext : N
• D/ : Acute Lung Edema ( ec Hipertensi
Emergensi)
• T/:
• O – I – M (Oksigen,IV line ,Monitor)
• Nitrat (ISDN 5 mg ) SL (ulang sp 3x)
• Nitrat (ISDN) IV mulai 10 mcg/m titrasi s/d
maks 200 mcg/m
• Furosemide 40 mg/kgg, sampai 80 mg
• Morphine IV (2-4 mg ) pelan2
 Acute Pulmonary Edema,Hypotension and Shock Algoritm

Clinical Sign:Shock,Hypoperfusion,
1 CongestiveHeart Failure,APE
Most likely Problem?

2 6 8 14
APE Volume Problem Pump Problem Rate Problem
7
Administer Bradicardia Tachycardia
-Fluids
-Blood Transfusions 9
-Cause specific Intervention
Consider: Vasopressor Blood Pressure
3

First-Line Action
-O2 and Intubation as needed
-NTG SL
-Furosemide IV 0,5-1 mg/Kg
-MO IV 2-4 mg
 First-Line Action
-O2 and Intubation as needed Blood Pressure
-NTG SL
-Furosemide IV 0,5-1 mg/Kg
-MO IV 2-4 mg

Syst BP Syst BP<70 mmHg SBP 70-100 mmHg SBP 70-100 mmHg
BP defines 2nd Signs or Symptoms Signs and Symptoms No Signs or
SBP
Line of action Of shock Of shock Symptoms of shock >100 mmHg

Norepinephrine Dopamine Dobutamine NTG 10-20 mc/min

0,5-30 mcg/min 5-15 mcg/Kg/min 2-20 mcg/Kg/min Consider :
Nitroprusside
0,1-5 mcg/Kg/min

Second-Line Actions-APE
-NTG or Nitroprusside if BP >100 mmHg
-Dopamine if BP 70-100,signs or symptoms .shock
-Dobutamine if BP >100,no signs or symptoms shock
 Second-Line Actions-APE
-NTG or Nitroprusside if BP >100 mmHg
-Dopamine if BP 70-100,signs or symptoms .shock
-Dobutamine if BP >100,no signs or symptoms shock

Further Diagnostic and

Theraupetic Considerations :
-Idnetify and treat reversible causes
-Pulmonary artery catheterization
IABP*
Angiography and PCI
Additional diagnostic studies
Surgical Interventions
Additional drug therapy

AHA ACLS-The Reference Texbook,2003