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ACUTE LUNG

OEDEMA
M. Budiarto

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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

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ETIOLOGY

Pathophysiological mechanism
are traditionally categorized into
two primary cause :
Cardiogenic pulmonary edema
Non cardiogenic pulmonary
edema

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CARDIOGENIC PULMONARY
EDEMA

Defined as pulmonary edema due to increased


capillary hydrostatic pressure secondary to
elevated pulmonary venous pressure
McMurray JJ, 2012

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LA pressure > 25 mmHg
CARDIOGENIC LUNG OEDEMA (18-25 mmHg normal)

Lung Capillary Pressure


CAD
Decreased Oncotic
Myocarditis Plasma Pressure

Negative Pressure of
Cardiomyopathy LV dysfunction lung inters al

Lympha c Drainage
HT

CHD Hydrosta c pressure


Lung Oedema
Oedema Fluid Through
Lung Epitelium
Alveoli drowned by low
protein fluid
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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
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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
Severe hypoxemia EMERGENCIES COURSE
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MECHANISM OF CARDIOGENIC PULMONARY EDEMA

Increased Pressure in Pulmonary Vascular Bed CARDIOVASCULAR


Increased Permeability ofEMERGENCIES COURSE
Alveolar-Capillary Walls
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HOW TO MAKE THE DIAGNOSIS

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CLINICAL MANIFESTATION

Breathlessness develops S3 gallop


suddenly Raised jugular venous
Anxious pressure
Feeling of drowning Peripheral edema
Coughs History past illness :
Expectorates pink, frothy cardiomypathy, valvuler
liquid heart disease,
Sitting bolt upright or may hypertension, MI,
stand congenital heart disease

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LABORATORIUM STUDIES

Complete blood count


Electrolyte
Blood urea nitrogen (BUN) and
creatinine serum
Blood gas analysis

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LABORATORIUM STUDIES

Brain-type natriuretic N -terminal pro BNP


peptide (BNP) (NT-pro BNP)
High negative predictive value Well correlated with BNP
Cutoff value : 100 pg/mL levels

BNP value of under 100 NT-proBNP > 450 pg/mL (in


pg/mL heart failure is patients <50 years) ~ BNP >
unlikely 100 pg/mL

The level of BNP increase:


age, renal dysfunction
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ELECTROCARDIOGRAPHY

Sign of hypertrophy, enlargement cardiac chronic LV


dysfunction

Sign ischemia or infarction


conduction disturbance tachydysrhytmia or bradysrhytmia

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X RAY

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ECHOCARDIOGRAPHY

Establish the etiology of pulmonary edema


Evaluate LV systolic and diastolic function,
valvular function, and pericardial disease.

Non-invasive hemodynamic parameters


appropriate therapy
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Pulmonary Arterial Catheter
Helps in differentiating CPE from Non Cardiogenic Pulmonary
Edema (NCPE).

A PCWP exceeding 18 mm Hg indicates CPE


Monitor hemodynamic condition

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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
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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.

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Oxygen

SaO2 BGA

Early
PO2 , PCO2 O2 mask PO2
State
Hypercapnea (-)
Yes

NIV PO2 > 60 continue


(Non Invasif Ventilator)
No

Yes
O2 Invasif PO2 > 60 continue
Late State PO2 , PCO2 (mechanical
Hypercapnea (+) ventilator) No

PEEP
(5-20 cmH2O)

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OXYGEN
Oxygen mask
Oxygen flow 100 %, monitor with oxcimetry
(oxygen saturation)
If still hypoxia; NPPV (Noninvasive Pressure Positive
Ventilation) , intubation

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MEDICAL MANAGEMENT

Reduction of
pulmonary
venous
return
(preload)

Main
Goal Reduction of
Inotropic systemic
support (in vascular
some cases) resistance
(afterload)

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Management of ALO
(focus on Cardiogenic Lung oedema)
Many drug are now used in the hospital treatment of acute lung
oedema. These include :

Oxygen Furosemide

Nitrat ACEi ARB

Opiate Inotropic CPAP IABP

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Nitrat Furosemide

CLO Loop Diuretic


Adrenergik , Aldosteron , RAS
Block NaCl reabsorption

With caution :
TDS <110 mmHg 35-45
Severe Syldenafil Avoid minutes Natriuresis
Vasoconstriction !!
MS & AS Diuresis
HCM & Obstructive
Nitrat
(vasodilator)
Cardiomyopathy 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 ow &
hypotension blood flow optimization
(vasodilator & inotropic)

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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

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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 : Metformin decreased diuretic in blood
concentration
K/I : hypersensitive, coma hepaticum, anuria, severe
electrolyte depletion
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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.
A erload
Anxiety, stress
2.
Preload

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

Contraindication :
CO Intuba on rate
SBP <80 mmHg K>5
SaO2 Creatinine > 3

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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
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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

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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

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Inotropic

SBP 70-100 mmHg

Dobutamine 2-20 g/kg/mnt IV CO , SVR


Shock ( - )

0.5-2 g/kg/mnt IV CO
SBP 70-100 mmHg

Dopamine 5-10g/kg/mnt IV CO , SVR


Shock ( + )
>10g/kg/mnt IV SVR

SBP <70 mmHg


Norepinephrine 0.5-30 g/mnt IV CO /,SVR
Shock ( + )

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INOTROPIC

Dopamin, dobutamin, milrinone


Hypotension with CHF : dopamin & dobutamin
Milrinone: inhibits fosfodiesterase cAMP & change in
calsium transport heart contractility & vascular tonus
(vasodilatation)

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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 (anti depressant) &
prolonged dopamin effect
K/I: hypersensitive, pheochromocytoma, VF
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ULTRAFILTRATION

Useful in patients with renal dysfunction and diuretic resistance

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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

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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

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Norepine
1 Dopamine 2 Dobutamine 3 phrine
Cardiogenic shock Hypotension due to -receptors
Low dose decreased vasoconstriction
dopaminergic contractility Use in severe
receptors Positive chronotropic hypotension
increasing diuresis & inotropic Combination with
Moderate dose Moderate or severe dobutamine
-receptors hypotension improve
Cardiac should be avoided hemodynamic
contractility and
Heart rate
High dose
-receptors
Vasoconstriction
(increased afterload),
Blood pressure
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
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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

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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
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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

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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.
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Clinical signs: Shock, hypoperfusion,
Congestive heart failure, acute pulmonary edema
Most likely problem ?

Acute pulmonary edema Volume problem Pump problem Rate problem

Bradicardia Tachycardia
See algorithm See algorithm

1st Acute pulmonary edema Administer :


Furosemide iv 0.5 1.0 mg/kg Fluids
Morphine iv 2 4 mg Blood transfusions Blood
Nitroglycerin SL Cause-specific interventions Pressure ?
Oxygen/intubation as needed Consider vasopressors
Systolic BP Systolic BP Systolic BP Systolic BP Systolic BP
BP defines 2nd < 70 mmHg 70 to 100 mmHg 70 to 100 mmHg > 100 mmHg
Line of action Signs/symptoms Signs/symptoms No sign/symptoms
(see below) of shock of shock of shock

Norepinephrine iv Dopamine iv Dobutamine iv Nitroglycerin iv


0.5 30 mcg/min 5 15 mcg/kg/min 2 20 mcg/kg/min 10 20 mcg/min
Consider
Nitroprusside iv
0.1-5 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
Hemodynamic subsets in acute heart failure
Mor:2.2% Mor:10.1%

high blood pressure


Normal
Normal
Pulmonary
2.2 edema
Mor:22.4%
2.0
normal blood pressure
1.5 Hypovolaemic Mor:55.5%
1.0 shock Cardiogenic
shock
0.5
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
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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.

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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

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LV BACKWARD EFFECTS
Pengosongan ventrikel kiri

Peningkatan volume & tekanan end-diastolic ventrikel kiri

Peningkatan volume (tekanan ) pada atrium kiri

Peningkatan volume pada vena pulmonalis

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LV BACKWARD EFFECTS lanjutan

Peningkatan volume pulmonary capillary


bed = peningkatan tekanan hidrostatik

Transudasi cairan dari kapiler ke alveoli

Pengisian cepat rongga alveolar

Edema Paru

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NON CARDIOGENIC LUNG OEDEMA

Extravasation
SEPSIS (Rich Protein Fluid)

Infection

Trauma Fill Interstitial Space


Lung Endotel & Alveolar
Coagulation permeability
impaired
Alveoli drowned by
etc Rich protein fluid
Lung Oedema

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Algorithm for the Clinical Differentation between Cardiogenic and
Noncardiogenic

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HOW TO MAKE DIAGNOSIS

1 Clinical
Features 2 Laboratory
Studies 3 Electrocardi
ography
Clinical features of Complete blood LA enlargement and
left heart failure count LV hypertrophy
Reflect evidence of Electrolyte Chronic LV
hypoxia and Blood urea nitrogen dysfunction
increased (BUN) and creatinine Tachydysrhythmia or
sympathetic tone Blood gas analysis bradydysrhythmia or
History acute myocardial
to determine the ischemia or
exact cause infarction

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Brain-type
4 natriuretic peptide 5 N -terminal pro BNP
(NT-pro BNP)
(BNP)
High negative predictive Well correlated with BNP
value levels
Cutoff value : 100 pg/mL NT-proBNP > 450 pg/mL
BNP value of under 100 (in patients <50 years) ~
pg/mL heart failure is BNP > 100 pg/mL
unlikely
The level of BNP increase:
age, renal dysfunction

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EDEMA PARU AKUT

NON KARDIAK KARDIAK

Penyebab :
Komplikasi IMA
Tanda-tanda :
TINDAKAN I AF VR cepat
Tensi/shock
Takiaritmia
Freq. nafas
Hipertensi
Sesak
Kx. Katub : MR/MS/AR
Sianosis
Dilated cardiomyopathy
Ronchi -O2 bila perlu intubasi
Hipoksia -Nitroglycerin SL
Sputum berdarah -Furosemide IV 0,5-1 mg/kg TINDAKAN II
-Morphin IV 2-4 mg titrasi Pada Edema Paru Akut
(kecuali pada non cardiac) sebab cardiac

..continue.. COURSE
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..lanjutan.. Tindakan II
Pada Edema Paru Akut sebab Kardiak

TDS > 100 mmHg TDS 70-100 mmHg


Nitroglycerin 10-20 /mnt IV Gejala shock
Nitropruside 0,1-5 /kg/mnt IV Dobutamin 2-20 /kg/mnt IV

TDS 70-100 mmHg


Gejala shock +
Dopamin 5-15 /kg/mnt IV

Selanjutnya Dx. dan Tx. :


1. Identifikasi penyebab yang reversible
2. Kateterisasi A. Pulmonal
3. IABP
4. Angiografi & PCI
5. Surgical interventions
6. Tambahan pemeriksaan untuk Dx
7. Tambahan terapi CARDIOVASCULAR EMERGENCIES COURSE
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th
Hemodynamic subsets in acute heart failure
Mor:2.2% Mor:10.1%

high blood pressure


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