Curriculum Vitae

Intan Komalasari, MD, FIHA

Cardiologist
Date of birth: Jakarta, may, 1981
Education:
1. Medical School, Faculty of Medicine Trisakti University, Jakarta,
Indonesia
2. National Board of Cardiology, Dr. Soetomo Hospital, Faculty of
Medicine Airlangga University, Surabaya, Indonesia
3. Course of Doppler Vascular at National Cardiovascular Center
Harapan Kita, Faculty of Medicine University of Indonesia,
Jakarta, Indonesia
4. Fellow Indonesian Heart Association

Current Position :
5. Lecturer in Faculty Medicine of Hang Tuah university,
Surabaya, Indonesia
6. Cardiologist in Husada Utama Hospital, Surabaya, Indonesia
7. Cardiologist in Islam Hospital, Surabaya, Indonesia
 How To Deal Acute
Pulmonary Oedem ?
Intan komalasari, dr, . Sp.JP - FIHA

FAKULTAS KEDOKTERAN UNIVERSITAS HANG TUAH –

RUMKITAL dr. RAMELAN SURABAYA
 Definition

Defined as pulmonary edema due to increased capillary hydrostatic

pressure secondary to elevated pulmonary venous pressure
McMurray JJ, 2012

ALO is a severe respiratory distress,

tachypnea, orthopnea and rales on
all lung field verified by chest X-ray
and/or with arterial oxygen
saturation <90 % on room air
 Etiology

Pathophysiological mechanism are

traditionally categorized into two primary
cause :
• Cardiogenic pulmonary edema
• Non cardiogenic pulmonary edema
 Pathophysiology

– Imbalance of Starling forces - Ie, increased

pulmonary capillary pressure, decreased plasma
oncotic pressure, increased negative interstitial
pressure
– Damage to the alveolar-capillary barrier
– Lymphatic obstruction
– Idiopathic (unknown) mechanism
Mechanism Of Cardiogenic Pulmonary Oedem
 How To Deal
The Diagnosis??
 Diagnosis

1 History &
Physical
Examination
2 Laboratory
Studies
3 Electrocardio
graphy
ü Clinical features of ü Complete blood ü LA enlargement and
left heart failure count LV hypertrophy 
ü Reflect evidence of ü Electrolyte Chronic LV
hypoxia and ü Blood urea nitrogen dysfunction
increased (BUN) and ü Tachydysrhythmia or
sympathetic tone creatinine bradydysrhythmia or
ü History ü Blood gas analysis acute myocardial
 to determine the ischemia or
exact cause infarction
 Brain-type
4 natriuretic peptide 5 N -terminal pro BNP
(NT-pro BNP)
(BNP)
ü High negative predictive ü Well correlated with BNP
value levels
ü Cutoff value : 100 pg/mL ü NT-proBNP > 450 pg/mL (in
ü BNP value of under 100 patients <50 years) ~ BNP >
pg/mL  heart failure is 100 pg/mL
unlikely
ü The level of BNP increase:
age, renal dysfunction
 ChestX-RAy

• Enlarged heart,
Kerley lines,
basilar edema,
pleural effusion
(particularly
bilateral and
symmetrical
pleural
effusions)
 Pulmonary Arterial Catheter

• Helps in differentiating CPE from Non

Cardiogenic Pulmonary Edema (NCPE).
• A PCWP exceeding 18 mm Hg
indicates CPE
• Monitor hemodynamic condition
 Differential Diagnosis

• Conditions to consider in the differential diagnosis

of CPE include the following :
• Pneumothorax

• Pulmonary embolism
• Respiratory failure

• Acute Respiratory Distress Syndrome

• Asthma
• Chronic Obstructive Pulmonary Disease
 How To Deal
The Management ??
 Oxygen

↓ SaO2 BGA

Early State PO2 ↓, PCO2 ↓ O2 mask PO2 ↑

Hypercapnea (-)
Yes
Yes
NIV PO2 > 60 continue
(Non Invasif Ventilator)
No
No
Yes
Yes
O2 Invasif PO2 > 60 continue
Late State PO2 ↓ ↓, PCO2 ↑
(mechanical
Hypercapnea (+) ventilator) No
No

PEEP
(5-20 cmH2O)
 Furosemid
Nitrat
CLO Loop Diuretic
Adrenergik ↑, Aldosteron ↑, RAS ↑
Block NaCl reabsorption

With caution :
35-45
Severe • TDS <110 mmHg
minutes Natriuresis
• Syldenafil  Avoid !!
Vasoconstriction • MS & AS Diuresis
• HCM & Obstructive
Nitrat Cardiomyopathy
(vasodilator) Add Thiazid Diuresis ↑ ↑
Lung Congestif
Preload ↓ ↓ • In Patients already taking diuretic, 2.5 times
existing oral dose recommended.
• Irrational to use loop diuretic
Good Response on HT, Coronary ischemic, MR in vasoconstriction and renal blood flow ↓ &
hypotension  blood flow optimization
(vasodilator & inotropic)
 ACE-I
OPIATE i

Morphine 1.
↓ ↓ Afterload
Anxiety, stress ↓
2.
↓ Preload

1. O2 demand ↓
Central Sedation
2.
Venodilator
CO ↑
Prefer on Renal
Ischemic &
& Diuresis +
Perfussion ↑
Preload ↓ Myocardium SV ↑

Contraindication :
CO ↑ Intubation rate ↑ ↑
• SBP <80 mmHg •• K
K >> 5
5
SaO2 ↓ ↓ • Creatinine > 3
 Inotropic
SBP 70-100 mmHg

Dobutamine 2-20 μg/kg/mnt IV CO ↑, SVR ↓

Shock ( - )

0.5-2 μg/kg/mnt IV CO
SBP 70-100 mmHg

Dopamine 5-10μg/kg/mnt IV CO ↑, SVR ↑

Shock ( + )
>10μg/kg/mnt IV SVR ↑ ↑

SBP <70 mmHg

Norepinephrine 0.5-30 μg/mnt IV CO ↔/↑,SVR ↑ ↑

Shock ( + )
Ultrafiltration

• Useful in patients with renal

dysfunction and diuretic resistance
 IABP

• Reducing aortic impedance and systolic pressure

• In cardiogenic shock :
• decreases LV filling pressures by 20-25%
• improves cardiac output by 20%

• Provide hemodynamic support in perioperative

and postoperative period in high-risk patients
• severe coronary disease, severe LV dysfunction, or
recent MI
Noninvasive Pressure - Support Ventilation (NPSV)

• Consider in severe CPE

• Two types :
– CPAP and BiPAP

• Improves air exchange

• Increases intrathoracic pressure 
reduction preload & afterload
• Several studies :
– Decreased length of stay in the ICU
– Decreased need for mechanical ventilation
Mechanical Ventilation

• When :
– Remain hypoxic with noninvasive
supplemental oxygenation
– Impending respiratory failure
– Hemodynamically unstable

• Maximizes myocardial oxygen

delivery and ventilation
• Increase alveolar patency
 Conclusion

• ALO is a severe respiratory distress, tachypnea, orthopnea and rales on all lung
field verified by chest X-ray and/or with arterial oxygen saturation <90 % on room
air

• Two most common forms of lung oedema are cardiogenic and non-cardiogenic.
Based on history taking, physical examination and medical tests, a clinician can
distinguish between the two causes of acute lung oedema

• ALO requiring individual therapy appropriate clinical presentation. Quick and

precise handling will offer a better prognosis for acute pulmonary edema patient.