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OVERVIEW

ARDS
( study guide & practice question )

AHMAD MUSYAFIQ
Ahmad Musyafiq
Institusi :
 RSD KRMT Wongsonegoro Semarang
Pendidikan :
 S1 Keperawatan Karya Husada Semarang
Riwayat pekerjaan :
 Ruang ICU mulai 2003 - sekarang
Organisasi :
 HIPERCCI Jateng
Pelatihan :
 Pelatihan ICU 2006, 2019
 Pelatihan Ventilator 2006
 Pelatihan TPPK 2017
 Pelatihan TOT Kritis 2021
TUJUAN PEMBELAJARAN
• Menjelaskan pathofisiologi ARDS
• Menjelaskan
• Menjelaskan
ARDS (Acute Respiratory Distres Syndrome )
 Asbaugh, Bigelow, & Petty tahun 1967
Adalah sindrom akut respirasi pada pasien dewasa ditandai
oedem paru kardiogenik yang manifestasi hipoxemia karena
sunting dari kanan ke kiri melalui alveoli yang kolaps/diisi air
 The Berlin Definition tahun 2011
Adalah perdangan paru akibat injury yang bersifat difuse &
akut menyebabkan peningkatan permiabilitas pembuluh dara
sehingga meningkatkan lung weight berisi air & hilangnya tissue
dimana oksigen tidak bisa masuk
STAGE of ARDS
 ARDS is multisystem syndrome – not a “ disease “
 Three district stages (or phase) of the syndrome
including :
1. Exudative stage ( 1 – 7 days )
2. Proliferative (or fibroproliferative stage)
( 8 – 21 days )
3. Fibrotic stage
History of diagnosis ARDS
 The first definition of ARDS dates to Asbaugh (1967) :
dari 12 pasien dengan hipoxemia refrakter, bebrapa
responsif terhadap PEEP, dimana ada peradangan
yang meluas, edema & kerusakan membran hyalin

 Over the next 25 years several diferent definitions were


proposed with varying diagnostic criteria
In 1994 broad consensus was achieved with publication of
the American – European Consensus Conference (AECC)
History of diagnosis ARDS

AECC – American – European Consensus Conference 1994


A New Definition
History of diagnosis ARDS

AECC – American – European Consensus Conference 1994


Timing
Variable
that were include Hypoxemia

in the definition
since were Origin of edema

feasible Radiology abnormal

Additional physiological derangement


Common Risk Factors for ARDS

Direct Indirect
1. Non-pulmonary sepsis
1. Pneumonia
2. Major trauma
2. Aspiration of gastric contents 3. Multiple tranfusions
4. Severe burns
3. Inhalation injury
5. Pancreatitis
4. Pulmonary contusion 6. Non cardiogenic shock
7. Drug overdose
5. Near drowning
8. Fluid overload
MANAJEMEN VENTILATOR PADA ARDS
The History of High Tidal Volume in Ventilator Manajemen


In the early 1970s, shortly after ARDS was first describde, Hening Pontopidan a major force in

mechanical ventilation in the 1970s,ponted out that if small tida volume were used in patients with

ARDS, they experienced discomfort and therefore it was better to use tidal volume if 10 mL/kg to 15

mL/kg

Pontopiddan stated that thousand of patirnts were ventilated in this way and that the only major

consequence was hypocapnea, which could easly be treated by adding CO2 to the inspired gas

mixture
Macroscopic aspect of rat lungs after mechanical ventilation at 45 cmH2O peak airway
pressure. Left : normal lung ; middle : after 5 min of high airway pressure mechanical
ventilation. Note the vocal zones of atelektasis ; right : after 20 min the lung were
markedly enlarged and congestive;edema fluid fills the tracheal cannule.
Gross Pathologic Appearance of Rat Lungs Exposed to Various
Inflation Pressure and PEEP
Ventilator – Induced Multiple Organ Failure

Shear – stress injury in ARDS by mechanical ventilation may

induce not only lung injury, but also the production of pro

inflamatory mediators and cellular injury ( biotrauma ).

Biotrauma may lead to the development of multipleorgan failure


TERIMA
KASIH
ARDS ( Acute Respiratory Distres
Syndrome )

Your text here


Gross Pathologic Appearance of Rat Lungs Exposed to Various
Inflation Pressure and PEEP
Ventilator – Induced Multiple Organ Failure

Shear – stress injury in ARDS by mechanical ventilation may

induce not only lung injury, but also the production of pro

inflamatory mediators and cellular injury ( biotrauma ).

Biotrauma may lead to the development of multipleorgan failure


Indications for Mechanical Ventilation:
GAGAL NAFAS (Respiratory Failure):

Hypoxemic Failure: Ventilatory Failure:

V/Q Mismatch vs. Shunt vs. Hypoventilation Altered Respiratory Mechanics

PaO2<60mmHg on 100% NRB Acute  pCO2 with Resp. Acidosis

Pneumonia COPD/Asthma
ARDS Acute Intoxication
Congestive Heart Failure Neuromuscular Disease
Pulmonary Embolism Sepsis
Obesity Hypoventilation

T. Sisson
Ventilator – Induced Multiple Organ Failure

Shear – stress injury in ARDS by mechanical ventilation may

induce not only lung injury, but also the production of pro

inflamatory mediators and cellular injury ( biotrauma ).

Biotrauma may lead to the development of multipleorgan failure


LANGKAH-LANGKAH OPERASIONAL

 Menentukan BB ideal
 Menentukan siklus
 Menentukan gangguan
 Menentukan mode
 Menentukan setting
Cara kerja
ventilasi
mekanik
Normal breath
Normal breath inspiration animation, awake

Lung @ FRC= balance


Diaghram contracts
-2cm H20

Chest volume

Pleural pressure

-7cm H20

Alveolar
Air moves down pressure falls
pressure gradient
to fill lungs
Normal breath
Normal breath expiration animation, awake

Diaghram relaxes

Pleural /
Chest volume 

Pleural pressure
rises
Alveolar
pressure rises

Air moves down


pressure gradient
out of lungs
Ventilator breath inspiration animation

Air blown in
0 cm H20

 lung pressure Air moves down


pressure gradient
to fill lungs

+5 to+10 cm H20
 Pleural
pressure
Ventilator breath expiration animation
Similar to spontaneous…ie passive

Ventilator stops
Pressure gradient
blowing air in
Alveolus-trachea

Air moves out


Down gradient  Lung volume
INITIATION / TRIGER
Siklus
Ventilasi
Mekanik
VOLUME
)
Himpunan Perawat Critical Care Indonesia ( HIPERCCI

ADA 4 TIPE /
SIKLUS PRESSURE
POSITIVE
PRESSURE
VENTILATOR:
FLOW

TIME
Siklus pernapasan dengan ventilator
LIMIT PRESSURE
VOLUME

CYCLING
• TIME
TRIGGER • FLOW
• PRESSURE
• MESIN • VOLUME
• PASIEN (FLOW
ATAU PRESSURE
PEEP

TIME INSPIRASI TIME EKSPIRASI


Common Risk Factors for ARDS

Direct Indirect
1. Non-pulmonary sepsis
1. Pneumonia
2. Major trauma
2. Aspiration of gastric contents 3. Multiple tranfusions
4. Severe burns
3. Inhalation injury
5. Pancreatitis
4. Pulmonary contusion 6. Non cardiogenic shock
7. Drug overdose
5. Near drowning
8. Fluid overload
PEMILIHAN SIKLUS MEMPERTIMBANGKAN

1. Apakah pasien tampak nyaman


2. Apakah kebutuhan TV atau MV optimal terpenuhi
3. Apakah dengan mode volume tekanan Ppeak berada dalam batas aman
4. Apakah dengan mode tekanan Tv dan MV berada dalam batas aman
5. Apakah frekuensi nafas pasien berada dalam batas yang diharapkan
6. Apakah saturasi O2 dan nilai nilai AGD menunjukan perbaikan
JENIS MODE DASAR

SECARA UMUM

1. ASSIST MODE

2. SIMV MODE

3. SPONTAN MODE
ASSISTED
MODE 1. Assisted Volume mode

2. Assisted Pressure mode

Himpunan Perawat Critical Care Indonesia ( HIPERCCI )


( ASSIST / CONTROL)
 Semua pernapasan, baik berupa pernapasan volume atau tekanan semuanya diatur.

volume

pressure
TV / Pressure Inspirasi

Time Plateau

RR

setting PEEP

Fi02

Peak flow / Flow max

I:E Ratio

Sensitiviti < 5 cmH20


Synchronized Intermitten Mandatory Ventilation (SIMV)

Mengkombinasikan periode ventilasi assist-control


dengan periode pernapasan spontan pasien
vvvvvvv volume
pressure
Volume
Pressure
TV / Pressure Inspirasi

Pressure Suport

RR

PEEP

setting Fi02

Peak flow / Flow max

Time Inspirasi

Sensitiviti < 5 cmH20


SPONTAN
 Triger, Limit, Cycling
berasal dari pasien
 Proses weaning SBT,
Ekstubasi
Timing
Variable
that were include Hypoxemia

in the definition
since were Origin of edema

feasible
Radiology abnormal

Additional physiological derangement


RR .

PS
Triger / Sensitivitas
PI
PEEP
FiO2
FLOWMAX / PEAKFLOW .

TV
ETS / ESENS
EARLY DETECTION
Tinspirasi
I : E Ratio
Pramp
RR ( Respiratory
RR ( Respirator
Rate )
 Jumlah respirasi d
 Jumlah respirasi
ventilatordalam
dalam 1

1 menit Dilambangkan f

 Dilambangkan dengan
huruf f
VT (RR ( Respirator
Volume Tidal )
 Jumlah respirasi d
 Besaran volume yang
ventilator dalam 1
Dilambangkan
dihembuskan dalam 1 f
inspirasi
 Dilambangkan dengan
huruf VT
 6 – 8 dikalikan BB ideal
Peakflow
RR ( Respirator/
Flowmax /
 Jumlah respirasi d
ventilator dalam 1
Flowrate
Dilambangkan f

 Kecepatan gas untuk


menghantarkan tidal
volume yang disetting

 Mencari I : E ratio
Sensitivitas
RR ( Respirator /
Triger
 Jumlah respirasi d
ventilator dalam 1
Dilambangkan f
 Menentukan jumlah
upaya nafas pasien untuk
memulai inspirasi pada
ventilator
 Ada 2 : Flow & Pressure
FiO2RR ( Respirator
( Fraktio Oksigen )

 Jumlah respirasi d
 Besaran konsentrasi
ventilator dalam 1
Dilambangkan f
oksigen yang
dihembuskan dalam 1
inspirasi
Berkisar 35 – 100 %
PEEP
RR ( Respirator
 Tekanan diakhir
 Jumlahekspirasi
respirasiyang
d
ventilator
diberikan secara sengajadalam 1
Dilambangkan
 Menyebabkan f
alveoli tetap
terbuka diakhir ekspirasi
 Efek : perbaikan oksigen,
mengurangi resiko
atelektases
 Nilai fisiologis dimulai 5
TPL (RR ( Respirator
Time Plateau )
 Waktu  yang
Jumlah respirasi d
dibutuhkan
ventilator dalam 1
untuk mempertahankan
Dilambangkan f
pengembangan paru saat
inspirasi
 10 % dari time cycle
 Difusi oksigen dari alveoli
ke kapiler
Ps ( Pressure
RR ( Respirator
suport )
 Jumlah respirasi d
 Upaya inspirasi pasien
ventilator dalam 1
Dilambangkanpada
dibantu ventilator f

tingkat tekanan yang


telah ditentukan
 Pasien sudah bernafas
spontan
PI ( Pressure
RR ( Respirator
Inspirasi )
 Jumlah respirasi d
 Mengatur ventilator
/ membatasi
dalam 1

jumlah Dilambangkandari
pressure f

ventilator
 Setting tidak boleh > 35
I : ERRRatio
( Respirator
 Jumlah respirasi
 Perbandingan antarad
ventilator dalam 1
nilai inspirasi dan
Dilambangkan f
ekspirasi
 Normal 1 : 2
 Astma / COPD 1 : 3
 ARDS / severe hypoxia
1 : 1, 2 : 1
EtsRR
/ Esens
( Respirator
( ExpiratoriTriger Sensitivity
Jumlah respirasi d
)
 Pemicu ekspirasi
ventilator dalam 1 /

persentaseDilambangkan f
aliran puncak
dimana siklus ventilator
dari inspirasi ke ekspirasi
RiseRRTime /
( Respirator
Ramp
 Jumlah respirasi d
ventilator dalam 1
 Waktu yang dibutuhkan
Dilambangkan f
untuk mengubah dari
tekanan rendah ke
tekanan tinggi
KOMPLIKASI MECHANICAL VENTILATOR

Alveolar Distention Repeated closing and opening of OXYGEN


VOLUTRAUMA collapsed Alveolar unit TOXITY
“ATELECTRAUMA”
Over Pressure
BAROTRAUMA

Lung Inflamatory
BIOTRAUMA
Ventilator Induced
Lung Injury

Multiple Organ Dysfunction Sindrome


SUMMARY
Ventilator (mechanical ventilation) adalah
alat yang digunakan untuk membantu
pasien yang mengalami gagal napas.
Tiap Parameter klinis pasien yang
menggunakan ventilator harus dikonfirmasi
dengan setting yang diberikan

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