Acute Lung Edema - R. Mohammad Budiarto, MD, FIHA PDF

ACUTE LUNG
OEDEMA
M. Budiarto
CARDIOVASCULAR EMERGENCIES COURSE
Bumi Surabaya Hotel, November 7-8th, 2015
INTRODUCTION
Acute Lung edema :
Condition characterized by fluid accumulation in lungs caused by
extravasation of fluid from pulmonary vasculature into the
inerstitium and alveoli of the lungs.
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
CARDIOGENIC PULMONARY
EDEMA
Defined as pulmonary edema due to increased

capillary hydrostatic pressure secondary to
elevated pulmonary venous pressure
McMurray JJ, 2012
CARDIOGENIC LUNG OEDEMA
(18-25 mmHg normal)
Lung Capillary Pressure
CAD
Decreased Oncotic
Plasma Pressure
Myocarditis
Cardiomyopathy
LA pressure > 25 mmHg
LV dysfunction
Negative Pressure of
lung inters al
Lympha c Drainage
HT
CHD
Hydrosta c pressure
Lung Oedema
Oedema Fluid Through

Lung Epitelium
Alveoli drowned by low

protein fluid
PATHOPHYSIOLOGY
Pathophysiologic mechanisms :
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
The progression
Elevated LA pressure distension and opening of
small pulmonary vessels
Blood gas exchange does not deteriorate
Fluid and colloid shift into the lung interstitium
Lymphatic outflow removes the fluid
Filling interstitial space (can contain up to 500mL)
Alveolar flooding
Abnormalities in gas exchange

Vital capacity and respiratory volumes
CARDIOVASCULAR
Severe
hypoxemia EMERGENCIES COURSE
MECHANISM OF CARDIOGENIC PULMONARY EDEMA
Increased Pressure in Pulmonary Vascular Bed
CARDIOVASCULAR
COURSE
Increased Permeability ofEMERGENCIES
Alveolar-Capillary Walls
HOW TO MAKE THE DIAGNOSIS
CLINICAL MANIFESTATION
Breathlessness
develops
suddenly
Anxious
Feeling of drowning
Coughs
Expectorates pink, frothy
liquid
Sitting bolt upright or may

stand
S3 gallop
Raised jugular
venous
pressure
Peripheral edema
History past illness
:
cardiomypathy,
valvuler
heart
disease,
hypertension,
MI,
congenital heart disease
LABORATORIUM STUDIES
Complete blood count
Electrolyte
Blood urea nitrogen (BUN) and
creatinine serum
Blood gas analysis
LABORATORIUM STUDIES
Brain-type natriuretic
peptide (BNP)
High negative predictive value

Cutoff value : 100 pg/mL
BNP value of under 100
pg/mL heart failure is
unlikely
N -terminal pro BNP

(NT-pro BNP)
Well correlated with BNP

levels
NT-proBNP > 450 pg/mL (in

patients <50 years) ~ BNP >
100 pg/mL
The level of BNP increase:

age, renal dysfunction
ELECTROCARDIOGRAPHY
Sign of hypertrophy, enlargement cardiac chronic LV
dysfunction
Sign ischemia or infarction

conduction disturbance tachydysrhytmia or bradysrhytmia
X RAY
ECHOCARDIOGRAPHY
Establish the etiology of pulmonary edema

Evaluate LV systolic and diastolic function,
valvular function, and pericardial disease.
Non-invasive hemodynamic parameters

appropriate therapy
Pulmonary Arterial Catheter

Helps in differentiating CPE from Non Cardiogenic Pulmonary
Edema (NCPE).
A PCWP exceeding 18 mm Hg indicates CPE

Monitor hemodynamic condition
DIFFERENT 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
INITIAL MANAGEMENT
Airway, breathing and circulation
Oxygen should be administered to all patients to keep oxygen
saturation > 90 %
Method oxygen delivery include : face mask, non invasive

pressure support ventilation (CPAP and BiPAP and mechanical
ventilation.
Oxygen
SaO2
Early
State
BGA
PO2 , PCO2
Hypercapnea (-)
O2 mask
PO2
Yes
(Non Invasif Ventilator)
Late State
PO2 , PCO2
Hypercapnea (+)
O2 Invasif
(mechanical
ventilator)
continue
PO2 > 60
NIV
No
PO2 > 60
Yes
continue
No
PEEP
(5-20 cmH2O)
OXYGEN
Oxygen mask
Oxygen flow 100 %, monitor with oxcimetry
(oxygen saturation)
If still hypoxia; NPPV (Noninvasive Pressure Positive
Ventilation) , intubation
MEDICAL MANAGEMENT
Reduction of
pulmonary
venous
return
(preload)
Main
Goal
Inotropic
support (in
some cases)
Reduction of
systemic
vascular
resistance
(afterload)
Management of ALO
(focus on Cardiogenic Lung oedema)

Many drug are now used in the hospital treatment of acute lung
oedema. These include :
Oxygen
Nitrat
Opiate
Furosemide
ACEi
Inotropic
ARB
CPAP
IABP
Furosemide
Nitrat
Loop Diuretic
CLO
Adrenergik , Aldosteron , RAS
Severe
Vasoconstriction
Nitrat
(vasodilator)
Preload
With caution :
TDS <110 mmHg
Syldenafil Avoid
!!
MS & AS
HCM & Obstructive
Cardiomyopathy
Lung Congestif
Good Response on HT, Coronary ischemic, MR
Block NaCl reabsorption
35-45
minutes
Natriuresis
Diuresis
Add Thiazid
Diuresis
In Patients already taking diuretic, 2.5 times

existing oral dose recommended.
Irrational to use loop diuretic
in vasoconstriction and renal blood ow &
hypotension blood flow optimization
(vasodilator & inotropic)
NITRAT
Nitroprusside sodium
Vasodilatation & increased inotrophic activity
Dose : 10-15 mcg/min IV, titration until efective dose 30-50
mcg/min ( TDS 90 mmHg)
K/I : hypersensitive, subaortic stenosis, atrophy optic, AF or

flutter
Vasodilators ( Nitroglycerin )
Preload reduction
Vasodilation effect lowers preload reduce
pulmonary congestion
Should be avoided : Systolic blood pressure <110
mmHg
DIURETIC
Intra venous loop diuretic (Furosemide)
Doses: 10-20 mg IV (Ps CHF never use diuretic
40-80 mg IV (Ps had been use diuretic)
80-120 mg IV (Ps no respon in first give)
Interaction
concentration
: Metformin decreased diuretic in blood
K/I : hypersensitive, coma hepaticum, anuria, severe

electrolyte depletion
Diuretics
Loop diuretics : Furosemide
Affect the ascending loop of Henle
Diminished renal perfusion
Delay the onset of effects of loop diuretics
Long-term use electrolyte disturbances,
hypotension and worsening renal function
Opiate
ACEi
Morphine
1.
Anxiety, stress
A erload
2.
Preload
1.
Central Sedation
O2 demand
2.
Venodilator
Preload
CO
Prefer on
Ischemic
Myocardium
Intuba on rate
SaO2
CO
&
SV
Renal
Perfussion
Contraindication :
SBP <80 mmHg
Creatinine > 3
Diuresis +
K>5
ACE inhibitor (ACEi)

Hemodynamic effects of ACEI :
Reduce afterload, improving stroke volume and
cardiac output, and slightly reduce preload
improve renal perfusion diuresis
Caution in patients with :

Hypotension (systolic <80 mmHg)
Increased serum creatinine (> 3 mg / dl)
Bilateral renal artery stenosis
Increased blood potassium levels (> 5 mEq / L)
Angiotensin II receptor blockers (ARBs)

ACEi intolerance
ACEI and ARBs Preventing remodeling, reduce
arrhythmias
The Valsartan Heart Failure (Val-HeFT) and
Candesartan in Heart Failure: Assessment in
Reduction of Mortality and Morbidity (CHARM)
ARBs lowers the incidence of atrial fibrillation (AF)
ANALGESIC
Morphine IV
Anxiolytic
Venodilatation decreased preload
Artery dilatation decreased systemic vascular resistance &
increased CO
Dose: 2-5 mg IV, every 10-15 minute ( if RR <20 orTDS <100

mmHg )
K/I: hypersensitive, hypotension, respiratory depression,

nausea, emesis, constipation, urine retension, compromised
airway with uncertain rapid airway control
Opiates
Reduce the anxiety associated with dyspnea

Venodilators reduce preload
Reduce sympathetic drive
Depress respiratory drive
Increasing the need for invasive ventilation
ACE INHIBITOR
Decreased vascular sistemic resistance, ????????
Menurunkan tahanan sistemik vaskuler, memperbaiki tekanan
pasak paru, isi sekuncup, curah jantung dan memperbaiki mitral
regurgitasi, tanpa mempengaruhi denyut jantung maupun MAP
Captopril 25-50mg, bila tidak hipotensi
Enalapril 10-20mg
Efek perbaikan dispnea dalam 6-12 menit
INOTROPES
When :
Reduction in preload and afterload still has not improved

Impaired systolic function
Perfusion disturbances and/or congestion
Used only in heart failure patients with low cardiac index and
stroke volume
Inotropic
SBP 70-100 mmHg
Dobutamine
Dopamine
2-20 g/kg/mnt IV
CO , SVR
Shock ( - )
0.5-2 g/kg/mnt IV
CO
5-10g/kg/mnt IV
CO , SVR
>10g/kg/mnt IV
SVR
SBP 70-100 mmHg

Shock ( + )
SBP <70 mmHg
Norepinephrine
0.5-30 g/mnt IV
CO /,SVR
Shock ( + )
INOTROPIC
Dopamin, dobutamin, milrinone
Hypotension with CHF : dopamin & dobutamin
Milrinone: inhibits fosfodiesterase cAMP & change in
calsium transport heart contractility & vascular tonus
(vasodilatation)
INOTROPIC : DOPAMIN
Adrenergic and dopaminergic receptor stimulation
Hemodynamic effect dose dependent
Dose: 5 mcg/kg/min IV, titration
Interacts : phenytoin, & adrenergic blockers, general
anesthesia, MAO inhibitor
prolonged dopamin effect
(anti depressant) &
K/I: hypersensitive, pheochromocytoma, VF

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
Ultrafiltration should be considered in acute heart failure with volume overload who
do not respond to high doses of diuretics or in patients with impaired renal function
Intra-Aortic Balloon Pumping ( 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
Ventilatory Support
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
INOTROPIC : DOBUTAMIN
Vasodilatation & inotropic
Dose: 2.5 mcg/kg/min IV
Interacts: adrenergic blockers antagonism to
dobutamin effect
K/I: hipersensitifity, idiopathic subaortic stenosis, AF or

flutter
Dopamine
Cardiogenic shock
Low dose
dopaminergic
receptors
increasing diuresis
Moderate dose
-receptors
Cardiac
contractility and
Heart rate
High dose
-receptors
Vasoconstriction
(increased afterload),
Blood pressure
Dobutamine
Hypotension due to
decreased
contractility
Positive chronotropic
& inotropic
Moderate or severe
hypotension
should be avoided
Norepine
phrine
-receptors
vasoconstriction
Use in severe
hypotension
Combination with
dobutamine
improve
hemodynamic
Phosphodiesterase inhibitors ( milrinone )

Increase the level of intracellular cyclic adenosine
monophosphate (cAMP)
Positive inotropic effect on the myocardium
Peripheral vasodilation (decreased afterload)
Reduction in pulmonary vascular resistance
(decreased preload)
Improvements in stroke volume, cardiac output,

PCWP (preload), and peripheral vascular
resistance (afterload)
increased incidence of arrhythmias
Calcium sensitizers ( Levosimendan )

Inotropic, metabolic, and vasodilatory effects
Binding to troponin C
Not increase myocardial oxygen demand
Not a proarrhythmogenic agent
Effective and safe alternative to dobutamine
PROGNOSIS
Acute lung oedema is a life threatening condition and need
management immediately.
Hospital mortality of ALO are 15-20% mortality of ALO was

reported are 15-20% and it depends on severity when it comes
to ED/ first medical contact.
Infark myocard acute and hypotension will increase mortality
CASE (1)
A man 42 years old, chest pain, dyspnea (+), rales (+),wheezing(-),
BP 70/50, CRT >2 s, SaO2 89%. CKMB 200, Troponin 5, ECG
Sinus rhythm 130x, AMI Inferior-RV-Post. Onset chest pain 4h.
What should we do ?
O2 SaO2 >94%, double IV line, Catheter urine

NE 0.5-30 g/mnt IV, SaO2 >94% anxious
Morphine
TDS 100 Furosemide

PCI
CASE (2)
A man 55 years old, dyspnea (+), rales (+),wheezing(+), BP

190/120, CRT <2, SaO2 90 %, CKMB normal, Troponin normal.
Sinus rhythm 129x/m, OMI anterior. What should we do ?
O2 SaO2 >94%, double IV line, Catheter urine

Furosemide
Nitrate 1 mg/h IV, SaO2 >94% anxious Morphine
Observation Dyspnea (+), rales (),wheezing(-), BP 80/60,
CRT <2, SaO2 94 %. What should we do ?
Dobutamine 2-20 g/kg/mnt IV
CONCLUSION
Acute lung oedema is a severe respiratory distress, tachypnea, orthopnea and
rales on all lung fields 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.
Acute lung oedema requiring individual therapy appropriate clinical presentation.

Quick and precise handling will offer a better prognosis for acute pulmonary
edema patient.
Clinical signs: Shock, hypoperfusion,

Congestive heart failure, acute pulmonary edema
Most likely problem ?
Acute pulmonary edema
Volume problem
Pump problem
Rate problem
Bradicardia
See algorithm
1st Acute pulmonary edema
Furosemide iv 0.5 1.0 mg/kg
Morphine iv 2 4 mg
Nitroglycerin SL
Oxygen/intubation as needed
Administer :
Fluids
Blood transfusions
Cause-specific interventions
Consider vasopressors
Blood
Pressure ?
Tachycardia
See algorithm
Systolic BP
BP defines 2nd
Line of action
(see below)
Systolic BP
< 70 mmHg
Signs/symptoms
of shock
Norepinephrine iv
0.5 30 mcg/min
Systolic BP
70 to 100 mmHg
Signs/symptoms
of shock
Dopamine iv
5 15 mcg/kg/min
Systolic BP
70 to 100 mmHg
No sign/symptoms
of shock
Dobutamine iv
2 20 mcg/kg/min
2nd - Acute pulmonary edema

Nitroglycerin / nitroprusside if BP > 100mmHg
Dopamine if BP 70 100 mmHg, signs/symptoms of shock
Dobutamine if BP > 100 mmHg, no signs/symptoms of shock
Further diagnostic / therapeutic consideration
Pulmonary artery catheter
Intra-aortic balloon pump
Angiography for AMI / ischemia
Additional diagnostic studies
Systolic BP
> 100 mmHg
Nitroglycerin iv
10 20 mcg/min
Consider
Nitroprusside iv
0.1-5 mcg/kg/min
Hemodynamic subsets in acute heart failure

Mor:10.1%
Mor:2.2%
high blood pressure
Normal
Normal
2.2
Mor:22.4%
2.0
1.5
1.0
Pulmonary
edema
normal blood pressure
Hypovolaemic
shock
Cardiogenic
shock
0.5
Mor:55.5%
reduced blood pressure
0
5
10
15
18
20 25
30
35
40
Pulmonary Wedge Pressure

Forrester et al: Am J Cardiol 1977; 39:137
Summary
Common cause of acute heart failure, life-threatening and require
immediate action
Defined as pulmonary edema due to increased capillary hydrostatic

pressure secondary to pulmonary venous pressure
High mortality rate

Acute myocardial infarction, hypotension and a history of frequent
acute attacks increase the risk of mortality
BNP and echocardiography Important diagnostic tools

Therapeutic goal :
Improve the patient's symptoms
Improves fluid status
Identification of causalCARDIOVASCULAR
factors
EMERGENCIES COURSE
Cardiogenic LO
The pathogenesis of hydrostatic that accompanies
various disorders of the left side of the heart (coronary
artery disease, myocardiomyopathies, aortic or mitral
valve abnormalities).
Fluid extravasation attributable to an increased

hydrostatic or reduced oncotic pressure gradient across
the intake alveolo-capillary barrier.
Furthermore, capacity of the lymphatic system to

remove fluid from the interstitial space and to drain into
the systemic veins is dependent on systemic venous
pressure and the intergrity of the lymphatics.
Cardiogenic pulmonary oedema

Occurs when cardiac output drops despite an increased
systemic resistance, so that blood returning to the left
atrium exceeds that leaving the left ventricle (LV)
As a result, pulmonary venous pressure increases,

causing the capillary hydrostatic pressure in the lung to
exceed the oncotic pressure of the blood, leading to a
net filtration of protein poor fluid out of the capillaries
LV BACKWARD EFFECTS
Pengosongan ventrikel kiri
Peningkatan volume & tekanan end-diastolic ventrikel kiri
Peningkatan volume (tekanan ) pada atrium kiri
Peningkatan volume pada vena pulmonalis
LV BACKWARD EFFECTS lanjutan
Peningkatan volume pulmonary capillary

bed = peningkatan tekanan hidrostatik
Transudasi cairan dari kapiler ke alveoli
Pengisian cepat rongga alveolar
Edema Paru
NON CARDIOGENIC LUNG OEDEMA
Extravasation
SEPSIS
(Rich Protein Fluid)
Infection
Trauma
Coagulation
impaired
Lung Endotel
permeability
Fill Interstitial Space

& Alveolar
Alveoli drowned by
Rich protein fluid
etc
Lung Oedema
Algorithm for the Clinical Differentation between Cardiogenic and

Noncardiogenic
HOW TO MAKE DIAGNOSIS
Clinical
Features
Clinical features of
left heart failure
Reflect evidence of
hypoxia and
increased
sympathetic tone
History
to determine the
exact cause
Laboratory
Studies
Complete blood
count
Electrolyte
Blood urea nitrogen
(BUN) and creatinine
Blood gas analysis
Electrocardi
ography
LA enlargement and
LV hypertrophy
Chronic LV
dysfunction
Tachydysrhythmia or
bradydysrhythmia or
acute myocardial
ischemia or
infarction
Brain-type
natriuretic peptide
(BNP)
High negative predictive

value
Cutoff value : 100 pg/mL
BNP value of under 100
pg/mL heart failure is
unlikely
The level of BNP increase:
age, renal dysfunction
N -terminal pro BNP

(NT-pro BNP)
Well correlated with BNP

levels
NT-proBNP > 450 pg/mL
(in patients <50 years) ~
BNP > 100 pg/mL
EDEMA PARU AKUT
NON KARDIAK
KARDIAK
Penyebab :
Tanda-tanda :
Tensi/shock
Freq. nafas
Sesak
Sianosis
Ronchi
Hipoksia
Sputum berdarah
TINDAKAN I
-O2 bila perlu intubasi

-Nitroglycerin SL
-Furosemide IV 0,5-1 mg/kg
-Morphin IV 2-4 mg titrasi
(kecuali pada non cardiac)
Komplikasi IMA
AF VR cepat
Takiaritmia
Hipertensi
Kx. Katub : MR/MS/AR
Dilated cardiomyopathy
TINDAKAN II
Pada Edema Paru Akut

sebab cardiac
..continue.. COURSE
CARDIOVASCULAR EMERGENCIES
Tindakan II
Pada Edema Paru Akut sebab Kardiak
..lanjutan..
TDS > 100 mmHg
Nitroglycerin 10-20 /mnt IV

Nitropruside 0,1-5 /kg/mnt IV
TDS 70-100 mmHg

Gejala shock
Dobutamin 2-20 /kg/mnt IV
TDS 70-100 mmHg

Gejala shock +
Dopamin 5-15 /kg/mnt IV
Selanjutnya Dx. dan Tx. :

1.
2.
3.
4.
5.
6.
7.
Identifikasi penyebab yang reversible

Kateterisasi A. Pulmonal
IABP
Angiografi & PCI
Surgical interventions
Tambahan pemeriksaan untuk Dx
Tambahan terapi CARDIOVASCULAR EMERGENCIES COURSE
th
Bumi Surabaya Hotel, November 7-8 , 2015
Hemodynamic subsets in acute heart failure

Mor:10.1%
Mor:2.2%
high blood pressure
Normal
Normal
2.2
Mor:22.4%
2.0
1.5
1.0
Pulmonary
edema
normal blood pressure
Hypovolaemic
shock
Cardiogenic
shock
0.5
Mor:55.5%
reduced blood pressure
0
5
10
15
18
20 25
30
35
40
Pulmonary Wedge
Pressure
Surabaya
Hotel,
November 7-8th, 2015
Forrester et al: Am Bumi
J Cardiol
1977;
39:137
MAIN GOALS OF TREATMENT

1.Reducing pulmonary venous return
(pre-load reduction)
2.Reducing systemic vascular resistance
(after-load reduction)
3.Maintaining adequate blood pressure by
inotropic support
4.Preventing and treating respiratory
distress with ventilatory support

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ACUTE LUNG

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Bumi Surabaya Hotel, November 7-8th, 2015

are traditionally categorized into

Cardiogenic pulmonary edema

Bumi Surabaya Hotel, November 7-8th, 2015

Defined as pulmonary edema due to increased

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

CARDIOGENIC LUNG OEDEMA

(18-25 mmHg normal)

Lung Capillary Pressure

LA pressure > 25 mmHg

Oedema Fluid Through

Alveoli drowned by low

Bumi Surabaya Hotel, November 7-8th, 2015

Imbalance of Starling forces - Ie,

Bumi Surabaya Hotel, November 7-8th, 2015

Abnormalities in gas exchange

Bumi Surabaya Hotel, November 7-8th, 2015

MECHANISM OF CARDIOGENIC PULMONARY EDEMA

Increased Pressure in Pulmonary Vascular Bed

Bumi Surabaya Hotel, November 7-8th, 2015

HOW TO MAKE THE DIAGNOSIS

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Sitting bolt upright or may

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Blood gas analysis

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

High negative predictive value

N -terminal pro BNP

Well correlated with BNP

NT-proBNP > 450 pg/mL (in

The level of BNP increase:

Bumi Surabaya Hotel, November 7-8th, 2015

Sign ischemia or infarction

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Establish the etiology of pulmonary edema

Non-invasive hemodynamic parameters

Bumi Surabaya Hotel, November 7-8th, 2015

Pulmonary Arterial Catheter

A PCWP exceeding 18 mm Hg indicates CPE

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

Bumi Surabaya Hotel, November 7-8th, 2015

Method oxygen delivery include : face mask, non invasive

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

(Non Invasif Ventilator)

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015

CARDIOVASCULAR EMERGENCIES COURSE

Bumi Surabaya Hotel, November 7-8th, 2015