Tujuan dari Respirasi

adalah untuk menyediakan oksigen bagi

seluruh jaringan tubuh dan membuang
karbon dioksida ke atmosfer

Hidung
Udara masuk disaring,
dihangatkan dan
dilembabkan oleh
mukosa respirasi.
Partikel kasar disaring
oleh rambut hidung.
halus: terjerat
dalam lapisan mukus.
Udara masuk faring:
bebas debu, suhu
sebanding suhu tubuh,
kelembaban hampir 100
%

Rongga torax
Paru adalah organ elastis terletak pada rongga
dada/torax.
Paru dilapisi oleh lapisan tipis kontinu yg
mengandung kolagen & jar elastis yg disebut PLEURA
Pleura Parietalis melapisi rongga dada sedang
Pleura viseralis melapisi paru .
Rongga pleura: ruangan yg memisahkan pleura
parietalis & viseralis
Cairan pleura: lapisan tipis antara pleura parietalis dg
viseralis berfungsi memudahkan kedua permukaan
tersebut bergerak selama pernapasan & untuk
mencegah pemisahan torax & paru.
Tekanan rongga pleura < tekanan atmosfer: untuk
mencegah kolaps paru.

Rongga torax

3 faktor yg mempertahankan tekanan

negatif intrapleura normal:
1. Jaringan elastis paru memberikan kekuatan
kontinu yg cenderung menarik paru menjauh dr
rangka torax.
2. Kekuatan osmotik yg terdapat di seluruh
membran pleura.
3. Kekuatan pompa limfatik.

Diafragma: otot berbentuk kubah yg

membentuk dasar rongga torax &
memisahkan rongga tersebut dari rongga
abdomen.

Anatomi Saluran
Pernapasan

Anatomi Saluran
Pernapasan

Alveoli
Terdapat 2 tipe sel alveolar:
Pneumosit tipe I: lap tipis menyebar &
menutupi > 90% daerah permukaan.
Pneumosit tipe II: tanggung jawab pada
sekresi surfaktan.
Alveolus: suatu gelembung gas yang dikelilingi
oleh jaringan kapiler
batas antara cairan &
gas membentuk tegangan muka yang
cenderung mencegah pengembangan saat
inspirasi & cenderung kolaps saat ekspirasi.
Alveolus dilapisi zat lipoprotein (surfaktan)
dapat mengurangi tengangan permukaan &
resistensi saat inspirasi & mencegah kolaps
alveolus (expirasi).

LUNGS 2
Bronchopulmonary segments
Lobules
Alveolar wall cell types
simple squamous epithelial cell
macrophage (dust cell)
septal cell (produces surfactant)

Type II alveolar cell

making surfactant

Type I alveolar
cell
respiratory
membrane

terminal
bronchiol
e
pulmonary
artery
branch
alveolar
sac

surfactan
t

macrophag
e
blood
capillary
endothelial
cell

respirato
ry
bronchiol
e

Alveoli
Pembentukan & pengeluaran surfaktan oleh
pneumosit tipe II disintesis secara cepat dari
asam lemak yang diekstraksi dari darah, dg
kecepatan pergantian yg cepat. Bila aliran
darah ke paru terganggu (emboli) akibatnya
jumlah surfaktan pada daerah tersebut
berkurang.
Produksi surfaktan dirangsang oleh ventilasi
aktif, volume tidal yg memadai, hiperventilasi
periodik (cepat & dalam) yg dicegah oleh
kons O2 yang tinggi (inspirasi).
Pemberian O2 kons tinggi jangka lama (pasien
dg ventilasi mekanik) menurunkan produksi
surfaktan & menyebabkan kolaps alveolar.

Pernafasan terdiri dari 4

proses :
1. Ventilasi : Keluar masuknya udara karena adanya
selisih tekanan yang terdapat antara atmosfer dan
alveolus
2. Distribusi : Pembagian udara ke cabang -cabang
bronkhus
3. Transportasi dan Difusi
- Transport O2 dan CO2 dalam darah dan cairan tubuh ke
dan
dari sel
- Difusi O2 dan CO2 antara darah dan alveoli

Pertukaran gas-gas antara alveoli dan kapiler

dipengaruhi oleh tekanan parsial O2 & CO2 dalam
atmosfer
4. Perfusi : Aliran darah yang membawa O2 ke
jaringan

JENIS RESPIRASI
1. RESPIRASI EXTERNAL
O2 DIBAWA DARI UDARA
LUAR SAMPAI KE
KAPILER
2. RESPIRASI INTERNAL
O2 DARI KAPILER SAMPAI
KE
SEL PADA JARINGAN.

RESPIRASI EXTERNAL

RESPIRASI INTERNAL

INSPIRATION
Active process
Boyles Law
Inspiratory muscles
Phrenic nerves (C3-5)
Thoracic nerves (T1
T11)

Process
thoracic volume
pleural volume
intrapleural pressure
lung volume
intrapulmonic pressure
air flow into the lungs
760 mmHg

760 mmHg

760 mmHg
BEFORE INSPIRATION

FORCED INSPIRATION

758 mmHg
DURING INSPIRATION

EXPIRATION
Passive process at rest
elastic recoil
surface tension
internal
intercostals
(11 pairs)

Process
thoracic volume
pleural volume
intrapleural pressure
lung volume
intrapulmonic pressure
air flow of the lungs

Forced expiration
internal intercostals (11 pairs)
rectus abdominis
abdominal obliques
transversus abdominis

external abdominal
oblique
internal abdominal
oblique
transversus abdominis
rectus abdominis
760 mmHg

762 mmHg

Perubahan diafragma saat

inspirasi & ekspirasi

Otot Pernapasan

COMPLIANCE
Compliance is the ease with which the lungs and
thoracic wall can be expanded during inspiration.
Related to two factors:
elasticity
surface tension

Compliance is decreased with any condition that:

destroys lung tissue (emphysema)
fills lungs with fluid (pneumonia)
produces surfactant deficiency (premature birth, near-drowning)
interferes with lung expansion (pneumothorax)

PULMONARY VOLUMES, CAPACITIES, AND

RATES
maximum
Volumes

tidal volume (500 ml)

anatomical dead space (150 ml)
alveolar ventilation (350 ml)
physiological dead space
inspiratory reserve volume (3000 ml)
expiratory reserve volume (1200 ml)
residual volume (1300 ml)

Capacities
total lung capacity (TV+IRV+ERV+RV)
vital capacity (TV+IRV+ERV) (4700
ml)
inspiratory capacity (TV+IRV)
functional residual capacity (RV+ERV)

Rates

6000 ml

inspiration

5000 ml

IRV
VC

4000 ml

TLC

3000 ml

TV
2000 ml

ERV

1000 ml

maximum
expiration

RV

SPIROGRAM

maximum voluntary ventilation = TV x breaths/minute

alveolar ventilation rate = alveolar ventilation x breaths/minute

Kontrol Pernapasan
Otot pernapasan diatur oleh neuron &
reseptor pada pons & medula
oblongata.
Faktor utama pengaturan pernapasan:
respon dari pusat kemoreseptor dalam
pusat pernapasan terhadap tekanan
persial CO2 dan pH darah arteri

Kontrol Pernapasan
Persarafan parasimpatis/ kolinergik (mll nervus fagus)
menyebabkan kontraksi otot polos bronkus shg
menyebabkan bronkokonstriksi & peningkatan sekresi
kel mukosa & sel goblet.
Rangsangan simpatis ditimbulkan epinefrin mll reseptor
adrenergik-beta2 menyebabkan relaksasi otot polos
bronkus, bronkodilatasi, & berkurangnya sekresi
bronkus.
Sistem saraf nonkolinergik non adrenergik (NANC):
melibatkan berbagai mediator seperti ATP, oksida nitrat,
substance P, dan VIP (vasoactive intestinal peptide)
respon penghambatan, meliputi bronkodilatasi, dan
diduga berfungsi sebagai penyeimbang terhadap fungsi
pemicuan oleh sistem kolinergik.

Kontrol Pernapasan

Signs and Symptoms of

Pulmonary Disease
Dyspnea subjective sensation of
uncomfortable breathing, feeling
short of breath
Ranges from mild discomfort after
exertion to extreme difficulty
breathing at rest.
Usually caused by diffuse and
extensive rather than focal
pulmonary disease.
26

Derajat Dyspnea
Tingkat

Derajat

Kriteria

Normal

Tidak ada kesulitan bernapss kecuali

dengan aktivitas berat.

Ringan

Terdapat kesulitan bernapas, napas

pendek-pendek ketika terburu-buru atau
ketika berjalan menuju puncak landai.

Sedang

Berjalan lebih lambat daripada kebanyakan

orang berusia sama karena sulit bernapas
atau harus berhenti berjalan untuk
bernapas.

Berat

Sangat berat

Berhenti berjalan setelah 90 meter untuk

bernapas atau setelah berjalan beberapa
menit.
Terlalu sulit bernapas bila meninggalkan
rumah atau sulit bernapas ketika memakai
baju atau membuka baju.

Dyspnea cont.
Due to:
Airway obstruction
Greater force needed to provide
adequate ventilation
Wheezing sound due to air being
forced through airways narrowed due
to constriction or fluid accumulation
Decreased compliance of lung tissue

28

Signs of dyspnea:
Flaring nostrils
Use of accessory muscles in
breathing
Retraction (pulling back) of
intercostal spaces

29

BATUK
Batuk merupakan gejala tersering
penyakit pernapasan
Batuk merupakan reflex pertahanan yang
timbul akibat iritasi percabangan
trakeobronkial
Batuk yang berlangsung lebih dari 3
minggu harus diselidiki untuk memastikan
penyebabnya.
Bronkhitis kronik, asma, tubercolosis dan
pneomonia merupakan penyakit yang
secara tipikal memiliki batuk sebagai
gejala yang mencolok

Cough may result from:

Inflammation of lung tissue
Increased secretion in response to
mucosal irritation
Inhalation of irritants
Intrinsic source of mucosal disruption
such as tumor invasion of bronchial wall

Excessive blood hydrostatic pressure

in pulmonary capillaries
Pulmonary edema excess fluid passes
into airways
31

 When cough can raise fluid into

pharynx, the cough is described as a
productive cough, and the fluid is
sputum.
Production of bloody sputum is called
hemoptysis
Usually involves only a small amount
of blood loss
Not threatening, but can indicate a
serious pulmonary disease
Tuberculosis, lung abscess, cancer,
pulmonary infarction.
32

 Cough that does not produce sputum

is called a dry, nonproductive or
hacking cough.
Acute cough is one that resolves in 23 weeks from onset of illness or
treatment of underlying condition.
Us. caused by URT infections, allergic
rhinitis, acute bronchitis, pneumonia,
congestive heart failure, pulmonary
embolus, or aspiration.

33

 A chronic cough is one that persists

for more than 3 weeks.
In nonsmokers, almost always due to
postnasal drainage syndrome,
asthma, or gastroesophageal reflux
disease
In smokers, chronic bronchitis is the
most common cause, although lung
cancer should be considered.

34

SPUTUM
Pembentukan sputum:
Orang dewasa normal
mukus
sekitar 100 ml dalam saluran napas
tiap hari
Mukus diangkut menuju
faring dengan gerakan pembersihan
silia yang melapisi saluran pernapasan
bila mukus berlebihan
proses
pembersihan tidak efektif
mukus tertimbun
membran mukosa
akan terangsang
mukus
dibatukkan keluar sebagai sputum.

SPUTUM
Sputum yang berwarna kekuning-kuningan
menunjukkan infeksi.
Sputum yang berwarna hijau merupakan
petunjuk penimbunan nanah timbul karena
adanya verdoperoksidase yang dihasilkan
oleh polimorfonuklear (PMN).
Sputum yang berwarna merah muda dan
berbusa merupakan tanda edema paru
akut.
Sputum yang berlendir lekat dan warna
abu-abu atau putih merupakan tanda
bronkhitis kronik. Sedangkan sputum yang
berbau busuk merupakan tanda abses
paru atau bronkiektasis.

Cyanosis
When blood contains a large amount of
unoxygenated hemoglobin, it has a dark
red-blue color which gives skin a
characteristic bluish appearance.
Most cases arise as a result of peripheral
vasoconstriction result is reduced blood
flow, which allows hemoglobin to give up
more of its oxygen to tissues- peripheral
cyanosis.
Best seen in nail beds
Due to cold environment, anxiety, etc.
37

 Central cyanosis can be due to :

Abnormalities of the respiratory
membrane
Mismatch between air flow and blood flow
Expressed as a ratio of change in
ventilation (V) to perfusion (Q) : V/Q ratio
Pulmonary thromboembolus - reduced
blood flow
Airway obstruction reduced ventilation

In persons with dark skin can be

seen in the whites of the eyes and
mucous membranes.
38

Jari Tabuh
Jari tabuh adalah perubahan
bentuk normal falang distal dan
kuku tangan dan kaki serta
ditandai dengan
1.Kehilangan sudut kuku yang
normalnya 160 derajat.
2.Rasa halus berongga pada dasar
kuku.
3.Ujung jari menjadi besar.
jari tabuh berhubungan dengan
peyakit paru (TB, abses paru, atau
kanker paru). Penyakit
kardiovaskuler (tetralogi fallot atau
endokarditis infektif) atau penyakit
hati kronik

Next

2. Hipoksia (O2 yang tidak adekuat dalam tingkat

jaringan) dan Hipoksemia (PaO2 dibawah normal normal
80-100 mmhg).
Tanda dan gejala hipoksemia dan hipoksia tidak
spesifik dan mencakup takipnea, dispnea, sakit kepala,
pikiran yang bingung, takikardi, dan sianosis.
3. Hipokapnia dan hiperkapnia
Hipokapnia didefinisikan sebagai menurunnya PaCO2
<35 mmhg. Penyebab langsung selalu hiperventilasi
alveolar (eliminasi CO2 lebih cepat daripada
produksinya).
Hiperkapnia / asidosis respiratorius merupakan
meningkatnya PaCO2 >45 mmhg. Penyebab langsung
adalah selalu hipoventilasi alveolar (kegagalan dalam
mengeliminasi CO2 secepat produksinya).

Pain
Originates in pleurae, airways or chest
wall
Inflammation of the parietal pleura
causes sharp or stabbing pain when
pleura stretches during inspiration
Usually localized to an area of the chest wall,
where a pleural friction rub can be heard
Laughing or coughing makes pain worse
Common with pulmonary infarction due to
embolism
41

 Inflammation of trachea or bronchi

produce a central chest pain that is
pronounced after coughing
Must be differentiated from cardiac pain

High blood pressure in the pulmonary

circulation can cause pain during
exercise that often mistaken for
cardiac pain (angina pectoris)

42

Respiratory Disorders
Respiratory disorder can be classified into different
group
Respiratory tract infection
Common cold,Influenza,Pneumonias,T.B
Disorder of lung inflation
Pleural pain and pleural effusion
Obstructive air way disorders
Bronchial asthma, COPD, Emphysema, Bronchitis
Pulmonary vascular disorder
Lung cancer

INFLUENZA
Penyakit yang disebabkan oleh virus influenza.
Gejala yang ditimbulkan antara lain pilek,
hidung tersumbat, bersin- bersin, dan
tenggorokan terasa gatal. Perlu diketahui
virus ini
selalu hanya bisa menembus saluran
pernafasan atas saja , sehingga bisa
disimpulkan
saluran respirasi yang lebih dalam sangat
resisten immun terhadap virus ini.

Asthma
is a chronic inflammatory
disorder of the airways in
which many cells and
cellular elements play a
role
In susceptible individuals,
this inflammation causes
recurrent episodes of
wheezing, breathlessness,
chest tightness and
coughing, particularly at
night or in the early
morning..

mast cells

eosinophils

-T lympho
cytes

Cells
epithelial cells -Macropha
ges
neutrophils

Causes and Triggers

oAllergies such as to pollens, mold spores, pet
dander, and dust mites
oInfections (colds, viruses, flu, sinus infection)
oExercise
oAspirin or nonsteroidal anti-inflammatory drug
(NSAID) hypersensitivity, sulfite sensitivity
oUse of beta-adrenergic receptor blockers (including
ophthalmic preparations)

Cont

oIrritants such as strong odors from perfumes or

cleaning solutions, air pollution, and tobacco smoke
oWeather (changes in temperature and/or humidity, cold
air)
oStrong emotions such as anxiety, laughter, crying, and
stress
oIndustrial triggers (wood, grain dust, cotton dust,
isocyanate containing paints, aluminum, hair spray,
penicillins)
oBeta blockers even in form of eye drops

oGastroesophageal reflux disease

oChronic sinusitis or rhinitis
oOSA (obstructive sleep apnoe)
oObesity
oAlergy bronchopulmonary
aspergilosis

COMORBID CONDITION

ASMA
Asma

ekstrinsik (alergik)
(alergen, spt: debu,blu halus,

serbuk)

intrinsik (idiopatik)
(fak nonspesifik spt flu, latihan fisik,
emosi dapat

memicu serangan asma

campuran
(Komponen asma
instrinsik+Ekstrinsik)

Two main pathophysiologic types of

asthma
Extrinsic asthma; common in children,
associated with a genetic predisposition
and is precipitated by a known
allergens. It is related to the formation
of antibody IgE in the body

Immunological Mechanisms in
Respiratory Diseases

Patofisiologi Asma

Intrinsic asthma; tend to develop in

adulthood, and symptoms are triggered by nonallergic factors such as;
1.Viral infection, irritants which cause
epithelial damage and mucosal inflammation
2.Emotional upset which mediates excess
parasympathetic input
3.Exercise which causes water ad heat loss
from the airways

Pathophysiology
Release of inflammatory mediator produce
bronchial smooth muscle spasm
Vascular congestion
Increase vascular permeability
Edema formation
Production of thick tenacious mucus
Impair mucociliary function
Thickening of air way wall
Increase response of bronchial smooth
muscle
Damage epithelium produce hyper
responsiveness and obstruction

gambar

Faktor2 yang mengakibatkan obstruksi ekspirasi pada asma

bronkial. A. Potongan melintang dari bronkiolus yang
mengalami oklusi akibat spasme otot, mukosa yang
membengkak, dan mukus dalam lumen, B . Potongan
memanjang dari bronkiolus

The mechanism of inflammation in

asthma can be
Acute; early recruitment of cells to the airways
Subacute; resident and recruited cells are activated to cause
a more persistent pattern of inflammation

Chronic; cells damage is persistent and subject to ongoing repair,

permanent change in the airway may occur with airway remodelling

Gambaran klinik
Batuk yang memburuk pada malam hari
Sesak nafas
Mengi atau Wheezing (a high-pitched
whistling sound that occurs when exhaling)
due to turbulent airflow through a narrowed
airway
nafas pendek tersengal-sengal.
Produksi sputum meningkat, sulit tidur
Hambatan pernafasanan reversibel
Adanya peningkatan gejala pada saat
olahraga, infeksi virus, eksposur terhadap
alergen dan perubahan musim.
Terbangun di malam hari krn gejala seperti
di atas .

Investigations
Pulmonary function testing
(spirometry) Forced expiratory volume
(FEV)
Methacholine or histamine challenge
testing
Exercise testing
Peak expiratory flow rate monitoring

Forced expiratory volume (FEV)

Volume (litres)

Normal subject

Asthma patient
FVC

FEV1

Time (second)

Classification of Asthma Severity (>12 yrs)

Impairment

Component
of
Severity

Persistent
Intermittent

Moderate

Severe

Symptoms

<2 d/wk

>2 d/wk
but not daily

Daily

Throughout the
day

Nighttime
awakening

<2 d/mo

3-4x/mo

>1x/wk but not

nightly

Often 7x/wk

<2 d/wk

>2 d/wk
but not daily &
not >1x on any day

Daily

Several times
per day

NONE

Minor limitation

Some limitation

Extremely
limited

SABA use

Interference
with activity

Normal FEV1

Lung function

RISK

Mild

Exacerbations
requiring oral
steroids

between
exacerbations
FEV1: >80%
predicted
FEV

1/FVC:
normal

0-1/yr

FEV1 : >80%
predicted
FEV1/FVC: normal

FEV1: >60% but

FEV1: <60%

<80% predicted
FEV1/FVC:
FEV1/FVC:

reduced 5%

reduced 5%

2/yr

Consider severity and interval since last exacerbation as

Drug categories
Bronchodilators

Provide symptomatic relief of

bronchospasm due to acute asthma exacerbation (short-acting
agents) or long-term control of symptoms (long-acting agents)

Leukotriene receptor antagonists

Direct antagonist
of mediators responsible for airway inflammation in asthma

Corticosteroids Highly potent agents that are the primary

choice for treatment of chronic asthma and prevention of acute
asthma exacerbations. Numerous inhaled corticosteroids are used for
asthma and include beclomethasone (Beclovent, Vanceril),
budesonide (Pulmicort Turbuhaler), flunisolide (AeroBid),
fluticasone (Flovent), and triamcinolone (Azmacort).

Mast cell stabilizers

Prevent the release of mediators from

mast cells, which results in airway inflammation and bronchospasm.
Indicated for maintenance therapy of mild-to-moderate asthma or
prophylaxis for EIA

5-Lipoxygenase inhibitors

Inhibit the formation of

leukotrienes. Leukotrienes activate receptors that may be
responsible for events leading to the pathophysiology of asthma,
including airway edema, smooth muscle constriction, and altered
cellular activity associated with inflammatory reactions

Three Steps of Asthma Treatment

Step 1 - Control bronchospasm with short- acting b2 agonists or
long-acting salmeterol

Step 2 - Control inflammation with inhaled corticosteroids or

leukotriene antagonist

Step 3 - Control severe exacerbation with oral corticosteroids

Step 1
Is to control bronchospasm with inhaled b2
agonists. Short-acting b2agonists are
appropriate for patients with mild,
intermittent asthma who do not require daily
maintenance therapy.
Inhaled b2 agonists are effective, work
quickly within 2 to 3 minutes and provide
acute relief for up to 4 to 6 hours
Remember that short-acting b2 agonists are
indicated for use as rescue bronchodilators
during acute attacks of bronchospasm.

When daily maintenance therapy is needed for

more persistent symptoms, the long-acting b2
agonist salmeterol is an excellent and effective
choice in treatment
Salmeterol can be taken once or twice a day as an
inhaled bronchodilator
The bronchodilating action of salmeterol is
delayed in onset (20-30 minutes) but frequently
lasts 8 to 12 hours when taken properly.

Step 2
Is to control inflammation when there is evidence
of persistent or frequently recurring symptoms
with inhaled corticosteroids or leukotriene
antagonists, or the non-steroidal antiinflammatory agents cromolyn sodium or
nedocromil sodium
This is maintenance anti-inflammatory therapy
without any direct bronchodilator effect.

Inhaled corticosteroids and oral corticosteroids

are used to control inflammation in asthma
Corticosteroids prevent the migration of inflammatory
cells and increase the responsiveness of airway b2
receptors
Corticosteroids have been shown to reduce acute
bronchial hyperresponsiveness to irritants and may
chronically blunt the early airway response to irritants
with continued use
The new inhaled corticosteroid, fluticasone propionate,
appears to possess a higher potency than other
inhaled corticosteroids.
Like other inhaled corticosteroids, fluticasone is
indicated for the maintenance treatment of asthma as
prophylactic therapy

Inhaled nonsteroidal anti-inflammatory drugs like

cromolyn or nedocromil may reduce symptoms in
patients with mild to moderate asthma
They are frequently prescribed in children and in
adults with allergic asthma
They inhibit the activation of mast cells and
eosinophils, block inhaled neurogenic stimuli, and
may reduce airway temperature changes that can
trigger an asthma attack
Nedocromil may allow the reduction of
corticosteroid use in selected patients

Step 3
Is to control severe exacerbations with systemic
oral corticosteroids, i.e. prednisone 1 mg/kg or 40
to 60 mg daily for 1 to 2 weeks
Many patients are steroid-dependent and
frequently develop cushingnoid features such as
hyperglycemia, fluid retention, weight gain with
moon facies, and easy bruisability

Anticholingeric drugs like ipratropium

may have an adjunctive role in asthma therapy
They block vagal pathways and produce
bronchodilation by decreasing airway vagal tone
They are less potent than b2 agonists and have a
slow onset of action
While they may reduce mucus secretion, there is no
evidence that they modulate the inflammatory
response

Oral theophylline and intravenous

aminophylline were once the mainstay of
asthma treatment, especially nocturnal asthma
Originally thought to act as a
phosphodiesterase inhibitor to increase cAMP,
these methylxanthines are now though to
antagonize adenosine, a mediator of acute
inflammation
Theophyllines reverse bronchospasm, enhance
mucociliary clearance, and increase
diaphragmatic contraction

However, theophylline is probably useful as an

adjunct to b2 agonists and anti-inflammatory drugs
Any benefit may be diminished somewhat by a
narrow therapeutic range (5 to 15 g/ml) which can
lead to serious and toxic consequences, e. g.
seizures, tachyarrhythmias when exceeded
Its use in the emergency treatment of asthma is not
recommended but recent evidence suggest it may
modulate chronic asthma symptoms more effectively
than is generally perceived.

The use of cytotoxic agents, e. g.

methotrexate, cyclosporine can not
be recommended unless standard
therapy with b2 agonists and antiinflammatory drugs have failed

leukotriene receptor antagonists,

pecifically, LTD4 receptor antagonist and 5lipoxygenase inhibitors can completely block the
acute phase response and block part of the
delayed phase response
S

Blocking the generation of leukotrienes or

blocking their actions on cells may be helpful in
control of asthma and treatment of asthma attacks

DEFINISI PPOM/COPD
Penyakit obstruksi saluran nafas
kronis dan progresif yg ditandai
oleh hambatan aliran udara yg
bersifat non reversibel atau
reversibel sebagian bersifat
progresif & berhubungan dg
respons inflamasi abnormal paru
thd partikel atau gas beracun.

Bronkitis kronik& emfisema

Meskipun bronkitis kronik dan emfisema
merupakan 2 proses yg berbeda, tp
penyakit ini sering ditemukan bersama2
pada penderita COPD.
Merupakan penyebab kematian
terbanyak
COPD mnyerang pria 2x lebih banyak
dari wanita karena faktor perokok
Faktor etiologi utama adalah merokok
dan polusi udara

FAKTOR RISIKO

Host:
- Genetik: Defisiensi
alpha 1 anti tripsin
atau antiprotease
(menghambat aksi
dari enzym protease)

- Hipereaktivitas
bronkus

Lingkungan:
Asap rokok (faktor
risiko utama - sigaret)
Partikel debu & bahan
kimia perindustrian
Polusi udara
Indoor air pollution
from heating and
cooking with biomass
in poorly ventilated
dwellings
Infeksi
Status sosial

PATOGENESA
Inflamasi /Keradangan kronis pd sal.
napas, parenkim paru, sistem vaskuler
paru pe makrofag, limfosit T
(CD8+), netrofil release mediator
LB4, IL8, TNF
Imbalance proteinase anti proteinase
Stres oksidatif
Ketiga faktor diatas akan merusak
struktur paru.

is

that this inflammatory process which

includes alveolar macrophages in some way
releases neutrophil chemotactic factors
known as (IL-8 ) causing neutrophils
to
emigrate from the blood space into the
airspace to release elastase .

In

normal circumstances alpha-1-antitrypsin

binds to the elastase and prevents it from
binding to elastin thus destroying the
structure of the lungs.

The theory of interplay

 in

the blood and air space release more active

oxygen species in smokers, than in non smokers,
these together with the 1017 oxidants in inhaled
cigarette smoke inactivate the alpha-1-antitrypsin
at its active site.
This reduces the ability of alpha-1-antitrypsin to
bind to elastase by a factor of approximately 2000
allowing active ealstase to bind to elastin and
cause the enlargement of the airspace that is seen
in emphysema
P-Selectin , L-seletin adhesions
are important for the transport of inflammatory
cells in the systemic circulation .

Neutrophils

Keluhan utama: sesak napas, batuk, dahak

Sesak timbul progresif sp mengganggu aktivitas,
men-dadak memberat bila tjd eksaserbasi
Batuk kronis, memberat pagi hari, dahak mukoid

purulen bila eksaserbasi

Suara mengi (wheezing)
Batuk darah blood-streaked purulen sputum
(eksa-serbasi)
Nyeri dada (pleuritis, pneumotoraks, emboli paru)
Anoreksi & BB menurun progresif jelek

KLINIS

Noxious particles
and gases
Host factors
Anti-oxidants

Lung inflammation

Oxidative stress

Anti-proteinases

Proteinases
Repair mechanisms

COPD pathology

PATOLOGI
Saluran napas besar
Hipertrofi kelenjar & pe jumlah sel Goblet
hipersekresi mukus
Saluran napas kecil
Recycled injury & repair dinding sal. napas
remodeling (pe kolagen & jar. ikat)
penyempitan lumen & obstruksi sal. napas
Parenkim paru
Destruksi parenkim emfisema sentrilobuler
Vaskuler pulmonal, Penebalan dd pembuluh
darah

Pathophysiology
The different pathogenic mechanisms
produce the pathological changes which,
in turn, give rise to the physiological
abnormalities in COPD:
mucous hypersecretion and ciliary
dysfunction,
airflow limitation and hyperinflation,
gas exchange abnormalities,
pulmonary hypertension,
systemic effects.

Pathophysiology of COPD

According to GINA
What is the difference between
asthma and COPD (chronic
obstructive lung disease)?
COPD is a collective name for chronic
bronchitis and emphysema, two
diseases that are almost always
caused by smoking. Many of the
symptoms of COPD are similar to
those of asthma (e.g. breathlessness,
wheezing, production of too much
mucus, coughing).

COPD/PPOM

BRONCHITIS
KRONIS atau
COPD type B
Bronkitis kronik adalah
inflamasi kronis saluran
nafas yg ditandai dg udema
dan hiperplasi kelenjar sub
mucosal shg terjadi produksi
mukus berlebihan ke batang
bronchial akibatnya terjadi
peningkatan resistensi sal
pernafasaan
secara kronik atau berulang
dengan disertai batuk, yang
terjadi hampir setiap hari
selama sekurangnya tiga
bulan dalam 1 tahun selama
2 tahun berturut turut. .

Etiologi
Faktor lingkungan :
- Merokok
- Pekerjaan
- Polusi udara
-Infeksi berulang
Faktor host :
- usia
- jenis kelamin
- penyakit paru yang
sudah ada

CHRONIC BRONCHITIS
Chronic bronchitis is defined as "persistent cough
with sputum production for at least 3 months in at
least two consecutive years".
The most important cause of chronic bronchitis is
recurrent irritation of the bronchial mucosa by
inhaled substances, as occurs in cigarette smokers.
The pathological hallmarks of chronic bronchitis are
congestion of the bronchial mucosa and a
prominent increase in the number and size of the
bronchial mucus glands. Copious mucus may be
seen within airway lumens. The terminal airways
are most susceptible to obstruction by mucus.

Pathophysiology of chronic bronchitis

Irritants

Hyperplasia and hypertrophy of

mucous secreting cell

Thick mucous

Air trapping
Sticky coating

Air way obstruction

Impaired ciliary function

Edema
Decrease mucous clearance

Bronchial wall thickness and

Lung defense system compromise
inflammation

Vulnerable for infection

More infection more mucus

CHANGES IN LUNG
VOLUMES

VENTILATION COST
In COPD work of breathing is greater for
any given level of ventilation than normal.

SEVERE COPD

WORK OF
BREATHING

The cost of work at a

MODERATE COPD
given ventilation for
normal and COPD
NORMAL COPD patients (ACSM,
1998)
VENTILATION

 Damage to the epithelium impairs the

mucociliary response that clears
bacteria and mucus. Inflammation and
secretions provide the obstructive
component of chronic bronchitis.

In contrast to emphysema, chronic

bronchitis is associated with a
relatively undamaged pulmonary
capillary bed.

Emphysema
or type A
COPD
Definition
Abnormal permanent
enlargement of air
spaces distal to the
terminal bronchioles,
accompanied by the
destruction of the walls
and without obvious
fibrosis
Emphysema is
characterized by loss of
elasticity of the lung and
abnormal permanent
enlargement of air
spaces with destruction
of the alveolar walls and
capillary beds.

Etiologi
Emphysema

Smoking

the primary risk factor

Long-term smoking is
responsible for 80-90 %
of cases.
Prolonged exposures
to harmful particles
and gases from:

passive smoke,
Industrial smoke,
Chemical gases, vapors,
mists & fumes
Dusts from grains,
minerals & other
materials

Alpha 1-antitrypsin
deficiency
>>emphysema
Genetics
Bronchitis
Asthma

Pathophysiology
Exposure to inhaled noxious particles &
gases
inflammation
imbalance of proteinases and antiproteinases

Dilatation & destruction

mucus secretion+

FIG. 1. Inflammatory mechanisms in COPD. Cigarette smoke (and other

irritants) activate macrophages in the respiratory tract that release
neutrophil chemotactic factors, including IL-8 and LTB4. These cells then
release proteases that break down connective tissue in the lung
parenchyma, resulting in emphysema, and also stimulate mucus
hypersecretion. These enzymes are normally counteracted by protease
inhibitors, including 1-antitrypsin, SLPI, and TIMP. Cytotoxic T cells (CD8)
may also be recruited and may be involved in alveolar wall destruction.
Fibroblasts may be activated by growth
factors releases from macrophages and epithelial cells. CTG, connective
tissue growth factor; COB, chronic obstructive bronchiolitis.

Pathophysiology
Affects alveolar
membrane
Destruction of alveolar
wall
Loss of elastic recoil
Over distended alveoli

Over distended alveoli

Damage to adjacent
pulmonary capillaries
dead space
Impaired passive
expiration

Impaired gas
exchange

Impaired gas exchange

impaired expiration
CO2
Hypercapnia
Respiratory acidosis

Damaged pulmonary
capillary bed
pulmonary pressure
work load for right
ventricle
Right side heart failure
(due to respiratory
pressure)
Cor Pulmonale

Gas Exchange is poor

because
Loss of alveolar structure base thereby
causing decreased gas exchange
surface area
Mechanically, elastance is lost due to
the constant stretching of distal airways
Consequently, these patients are very
compliant, because the natural
tendency for the lung to collapse is
inadvertently lost

 This V/Q mismatch results in relatively

limited blood flow through a fairly well
oxygenated lung with normal blood
gases and pressures in the lung, in
contrast to the situation in blue
bloaters. Because of low cardiac output,
however, the rest of the body suffers
from tissue hypoxia and pulmonary
cachexia. Eventually, these patients
develop muscle wasting and weight loss
and are identified as "pink puffers."

Diagnosis of COPD
EXPOSURE TO RISK
FACTORS
tobacco

SYMPTOMS
cough
sputum
dyspnea

occupation
indoor/outdoor pollution

SPIROMETRY

GAS DARAH ARTERI

LABORATORY TEST
CHEST X-RAY
109

Spirometry: Normal and COPD

0

FEV1

Normal
COPD

Liter

FVC

FEV1/ FVC

4.150

5.200

80 %

2.350

3.900

60 %

FEV1

COPD
4

FEV1

Normal

5
1

FVC

FVC
4

6 Seconds

Normally, the left side of the

heart produces a higher level
of blood pressure in order to
pump blood to the body; the
right side pumps blood
through the lungs under
much lower pressure. Any
condition that leads to
prolonged high blood
pressure in the arteries or
veins of the lungs (called
pulmonary hypertension) will
be poorly tolerated by the
right ventricle of the heart.
When this right ventricle fails
or is unable to
properly pump against these
abnormally high pressures,
this is called cor pulmonale.

Prognosis ?
Indikator: umur dan keparahan
Jika ada hipoksia dan cor pulmonale
prognosis jelek
Dyspnea, obstruksi berat saluran
nafas, FEV1 <
0.75 L (20%) angka kematian
meningkat, 50% pasien berisiko
meninggal dalam waktu 5 tahun

Tujuan Terapi
Memperbaiki keadaan obstruksi saluran
nafas
Mencegah dan mengatasi eksaserbasi akut
Menurunkan progresivitas penyakit
Meningkatkan keadaan fisik dan psikis
Menurunkan jumlah hari tidak masuk kerja
Menurunkan lama tinggal di RS
Menurunkan angka kematian

NON FARMAKOLOGI
Menghentikan kebiasaan merokok
Rehabilitasi paru-paru secara
komprehensif dengan OR dan latihan
pernafasan
Perbaikan nutrisi
Tidak ada obat yang dapat menunda
memburuknya fungsi paru jika pasien
tetap merokok

 Kortikosteroid benefit is very limited, laporan

tentang efektivitasnya masih bervariasi, kecuali
jika pasien juga memiliki riwayat asma
Oksigen untuk pasien hipoksemia, cor
pulmonale. Digunakan jika baseline PaO2 turun
sampai < 55 mmHg
Antibiotik digunakan bila ada tanda infeksi,
bukan untuk maintenance therapy
Vaksinasi direkomendasikan untuk high-risk
patients: vaksin pneumococcus (tiap 5-10 th) dan
vaksin influenza (tiap tahun)
1-proteinase inhibitor utk pasien yang
defisiensi 1- antitripsin digunakan per minggu,
masih mahal contoh: Prolastin

Tahap terapi pada PPOK yang

stabil
Tahap 1 : Ipratropium bromida (MDI) atau
nebulizer, 2-6 puff 4 x sehari, tunjukkan cara
penggunaan yang tepat, advis pasien ttg
pentingnya penggunaan teratur dan efek
samping yg mungkin timbul (mulut kering &
rasa pahit), jika hasil trial : perbaikan FEV1 <
20% step 2
Tahap 2 : Tambahkan -agonis MDI atau
nebulizer, tunjukkan cara penggunaan yang
tepat, advis pasien ttg pentingnya penggunaan
teratur dan efek samping yg mungkin timbul
(takikardi, tremor) jika tidak ada
perkembangan: hentikan -agonis, jika ada
perbaikan tapi kecil step 3

 Tahap 3: Tambah teofilin,mulai dari 400 mg/hari

dlm bentuk sustained released, sesuaikan dosis
setiap interval 3 hari untuk menjaga serum
level antara 10-15 g/ml, pantau ESO takikardi,
tremor, nervous, efek GI; jika tidak ada
perbaikan hentikan teofilin dan go to step 4
Tahap 4: Coba dengan kortikosteroid :
prednison 30-40 mg/hari selama 2-4 minggu,
cek dengan spirometer (perbaikan 20%),
titrasi dosis ke dosis efektif terkecil (< 10 g
sehari), pertimbangkan penggunaan
kortikosteroid inhalasi jika pasien tidak
berespon baik kembali ke steroid oral

Terapi antibiotika
Berdasarkan evidence terbaru yang tersedia,
antibiotika harus diberikan pada pasien-pasien
PPOK yang :
Pasien dengan eksaserbasi akut dengan 3 tanda
utama yaitu : increased dyspnea, increased
sputum volume, increased sputum purulence
(Evidence B), atau
Pasien dengan eksaserbasi akut dengan 2 tanda
utama, jika peningkatan purulensi sputum
merupakan salah satunya (Evidence C)
Pasien dengan eksaserbasi parah yang
membutuhkan ventilasi mekanik, baik invasif
maupun non-infvasif (Evidence B)

Key points
PPOK adalah penyakit yang
sebenarnya secara potensial dapat
dicegah stop smoking
Sekali PPOK terjadi penderita akan
memerlukan terapi yang kompleks
yang efikasinya masih diperdebatkan
para ahli
Penyakit ini bersifat progresif dan
ireversibel berbiaya besar baik baik
personal maupun masyarakat

Difference between bronchitis

and emphysema
bronchitis

emphysema

Productive cough

Classic sign

Late in common with

infection

Dyspnea

Late in course

Common

Wheezing

Intermittent

Mild

H/O smoking

Common

Common

Barrel chest

Occasionally

Prolonged expiration

Always present

Always present

Cyanosis

Common

Uncommon

classic

Chronic hypoventilation Common

Late in course

Ploycythemia

Late in course

Common

Bronchitis v. Emphysema
Easy to
decompensate
Usually relatively
easy to treat
Can cause
emphysema
Rarely are these
patients ever
having normal
blood gases

Usually more
difficult to
decompensate
Difficult to treat
Can be caused by
bronchitis
Early, blood gases
are normal

Patofisiologi pneumotoraks
Akibat peningkatan tekanan
Intrabronkial ( batuk/ bersin )

Tekanan diteruskan s/d alveoli

( locus minoris / Bullae - fibrotik pada alveoli )

Alveoli robek sehingga

merobek pleura di sekitarnya

Udara masuk intrapleura

Pneumotoraks

Berdasarkan penyebab
terjadinya
PNEUMOTORAKS ARTIFISIAL
Bedakan Tu-pleura dan Tu-paru ( dx )
Proteksi Radioterapi Ca mamae ( tx )
Haemoptisis Profuse ( tx )
. PNEUMOTORAKS TRAUMATIK
Akibat trauma pada dada
. PNEUMOTORAKS SPONTAN
Iatrogenik causa ??
Penyakit kronis TB, COPD, Asma

Berdasarkan jenis fistel

PNEUMOTORAKS TERBUKA
P. Intrapleura = P. dunia luar ( two way )
Tekanan ekspirasi + 2 = + 2
Tekanan inspirasi 2 = - 2
PNEUMOTORAKS TERTUTUP
P. Intrapleura P. dunia luar (no way )
P awal + resorbsi paru P jadi
paru belum ngembang sempurna.
Tekanan ekspirasi 4 =- 4
Tekanan inspirasi 12 = - 1

BERDASARKAN DERAJAT
KOLAPS
Pneumotoraks Totalis
Pneumotoraks Partialis

% Kolaps = ( A X B ) ( a X b ) X
100 %
(AXB)

Pneumotoraks parsial

Pneumotoraks total

Gejala Klinik
Sesak mendadak & memberat
- Sesak tak di pengaruhi Posisi
- Batuk
- Dada terasa nyeri / kram / kemeng
- Nampak sakit berat, keluar keringat
dingin s/d syok
- Napas tersengal sengal s/d sianosis

Penatalaksanaan
Pneumotoraks
Antibiotika ~~ penyebab
Anti Tuberkulosa ( OAT )
Anti Tusif ( codein )
Bronkhodilator
Pencahar / Laxan
Bed Rest / hindari kegiatan yang akibatkan
peningkatan tekanan intra pleura ( teriak,
bersin
keras, mengejan dan batuk keras )

Komplikasi Pneumotoraks
* Terjadi Infeksi
Efusi Pleura ( Fluidopneumotoraks )
Empyema ( Pyopneumotoraks )
Terjadi Trauma
Hematotoraks
Udara dari cav. Pleura meluas
Pneumomediastium Emfisema Cutis
* Udara menekan ke organ sekitar
Tamponade Jantung
Gagal napas

Efusi Pleura

Efusi Pleura

Adanya Cairan Pleura yang Volume nya

lebih dari Normal ( Vol. normal: 1 20
cc )

Fisiologi cavum Pleura

Fisiologi Efusi Pleura

Volume cairan pleura selalu konstan,
akibat dari:
# P. hidrostatik : 9 mmHg
produksi
oleh pleura parietalis
# P. koloid osmotik : 10 mmHg
absorbsi oleh pleura viseralis

Penyebab akumulasi cairan

Pleura
Tekanan koloid osmotik ( Hypolbuminemia )
Permeabilitas kapiler ( Radang, Neoplasma
)
Tekanan hirostatik ( Gagal jantung )
Tekanan negatip intrapleura ( Atelektasis )

Pemeriksaan Fisik Efisi

Pleura
- Inspeksi
nampak sakit, gerak dada
sisi sakit tertinggal,nampak lebih
cembung
- Palpasi
gerak dada sisi sakit
tertinggal, Fremitus raba sisi sakit turun
- Perkusi
suara ketok sisi sakit redup
pd.bag.bawah garis Ellis Damoiseau
- Auskultasi
suara napas sisi sakit turun
/hilang

Sitologi cairan Pleura

- Lekosit > 25.000 / mm3 Empyema
- Netrophil > Pneumonia, TBC,
Pancreatitis
- Limphosit > TBC, limphoma,
keganasan
- Eosinophil > Emboli , Parasit, Jamur
- Eritrosit 5 10 ribu/mm3 Pneumoni,
Keganasan
- Eritrosit 100 ribu / mm3 Keganasan,
Trauma,
Infark Paru
- Sel ganas ditemukan pada 50 60 %
Keganasan

Gambaran Radiologi Efusi

Pleura
< 300 CC : Secara fisik tak ada perubahan.
Foto PA: sinus masih nampak lancip.
Foto Lat: sinus nampak mulai tumpul
> 500 cc : Gerak dada/ fremitus
suara/fremitus raba menurun,suara ketok
redup
> 1000 cc: dada cembung, egofoni positip
> 2000 cc: mediastinum terdorong

Foto Thorax

Foto Thoraks:
Perselubungan Pada
hemitoraks
Dextra dengan sinus
frenicus costalis kanan
tumpul

Penatalaksanaan Efusi
Pleura
- Evakuasi cairan pleura /
torakosentesis
volume pengambilan maksimal 1000 cc
setiap kali pengambilan
- Pemasangan WSD
# Efusi Pleura massive
# Efusi Pleura haemorhagic
# Hematotoraks, Empyema
# Chylotoraks, Chiliform

FARMAKOLOGI
Antikolinergik inhalasi first line therapy, dosis
harus cukup tinggi : 2 puff 4 6x/day; jika sulit,
gunakan nebulizer 0.5 mg setiap 4-6 jam prn, exp:
ipratropium or oxytropium bromide
Simpatomimetik second line therapy : terbutalin,
salbutamol
Kombinasi antikolinergik dan simpatomimetik
untuk meningkatkan efektifitas
Metil ksantin banyak ADR, dipakai jika yang lain
tidak mempan
Mukolitik membantu pengenceran dahak, namun
tidak
memperbaiki aliran udara masih kontroversi,
apakah bermanfaat secara klinis atau tidak