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).


Bronchopulmonary segments
Lobules
Alveolar wall cell types
LUNGS 2
terminal
bronchiole
respiratory
bronchiole
pulmonary
artery branch
alveolar sac
simple squamous epithelial cell
macrophage (dust cell)
septal cell (produces surfactant)
Type I alveolar cell
Type II alveolar cell
making surfactant
blood capillary
endothelial cell
macrophage
surfactant
respiratory membrane
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 O
2
yang
tinggi (inspirasi).
Pemberian O
2
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 O
2
dan CO
2
dalam darah dan cairan tubuh ke
dan dari sel
- Difusi O
2
dan CO
2
antara darah dan alveoli
Pertukaran gas-gas antara alveoli dan kapiler dipengaruhi
oleh tekanan parsial O
2
& CO
2
dalam atmosfer

4. Perfusi : Aliran darah yang membawa O
2
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
Active process
Boyles Law
INSPIRATION
FORCED INSPIRATION
Inspiratory muscles
Phrenic nerves (C3-5)
Thoracic nerves (T1 T11)
thoracic volume
pleural volume
intrapleural pressure
lung volume
intrapulmonic pressure
air flow into the lungs
760 mmHg
760 mmHg
760 mmHg
758 mmHg
BEFORE INSPIRATION DURING INSPIRATION
Process
Passive process at rest
EXPIRATION
internal intercostals
(11 pairs)
internal intercostals (11 pairs)
rectus abdominis
abdominal obliques
transversus abdominis
Forced expiration
thoracic volume
pleural volume
intrapleural pressure
lung volume
intrapulmonic pressure
air flow of the lungs
Process
external abdominal oblique
internal abdominal oblique
transversus abdominis
rectus abdominis
760 mmHg
762 mmHg
elastic recoil
surface tension
Perubahan diafragma saat inspirasi & ekspirasi
Otot Pernapasan
Compliance is the ease with which the lungs and thoracic wall can
be expanded during inspiration.
COMPLIANCE
elasticity
surface tension
Related to two factors:
destroys lung tissue (emphysema)
fills lungs with fluid (pneumonia)
produces surfactant deficiency (premature birth, near-drowning)
interferes with lung expansion (pneumothorax)
Compliance is decreased with any condition that:
PULMONARY VOLUMES, CAPACITIES, AND RATES
SPIROGRAM
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
maximum voluntary ventilation = TV x breaths/minute
alveolar ventilation rate = alveolar ventilation x breaths/minute
IRV
ERV
TV
RV
maximum
expiration
VC TLC
6000 ml
5000 ml
4000 ml
3000 ml
2000 ml
1000 ml
maximum inspiration
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 CO
2
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-beta
2
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
0 Normal Tidak ada kesulitan bernapss kecuali dengan aktivitas
berat.
1 Ringan Terdapat kesulitan bernapas, napas pendek-pendek
ketika terburu-buru atau ketika berjalan menuju
puncak landai.
2 Sedang Berjalan lebih lambat daripada kebanyakan orang
berusia sama karena sulit bernapas atau harus
berhenti berjalan untuk bernapas.
3 Berat Berhenti berjalan setelah 90 meter untuk bernapas
atau setelah berjalan beberapa menit.
4 Sangat berat 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 2-3 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 (O
2
yang tidak adekuat dalam tingkat jaringan) dan
Hipoksemia (PaO
2
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 PaCO
2
<35
mmhg. Penyebab langsung selalu hiperventilasi alveolar
(eliminasi CO
2
lebih cepat daripada produksinya).
Hiperkapnia / asidosis respiratorius merupakan meningkatnya
PaCO
2
>45 mmhg. Penyebab langsung adalah selalu
hipoventilasi alveolar (kegagalan dalam mengeliminasi CO
2
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..

eosinophils
epithelial cells

neutrophils
Macropha-
ges
T lympho-
cytes

mast cells

Cells
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)
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
Cont
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 non-
allergic 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
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
gambar
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)
V
o
l
u
m
e

(
l
i
t
r
e
s
)

Time (second)
1 2 3 4
Asthma patient
Normal subject
FEV1
FVC
Component
of
Severity
Classification of Asthma Severity (>12 yrs)
Intermittent
Persistent
Mild 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
SABA use <2 d/wk
>2 d/wk
but not daily &
not >1x on any day
Daily
Several times
per day
Interference
with activity
NONE Minor limitation Some limitation
Extremely
limited
Lung function
Normal FEV
1

between
exacerbations
FEV
1
:

>80%
predicted
FEV
1
/FVC:
normal
FEV
1
: >80%
predicted
FEV
1
/FVC: normal
FEV
1
: >60% but
<80% predicted

FEV
1
/FVC:
reduced 5%
FEV
1
:

<60%

FEV
1
/FVC:
reduced 5%

RISK
Exacerbations
requiring
oral steroids
0-1/yr 2/yr
Consider severity and interval since last exacerbation as
they may fluctuate over time in any severity category
Recommended
Treatment Step
Step 1 Step 2 Step 3 Step 4 or 5
& consider short OS burst
I
m
p
a
i
r
m
e
n
t

Leukotriene receptor antagonists Direct antagonist
of mediators responsible for airway inflammation in asthma
Bronchodilators Provide symptomatic relief of
bronchospasm due to acute asthma exacerbation (short-acting
agents) or long-term control of symptoms (long-acting agents)
Drug categories
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).
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
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
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 anti-
inflammatory 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
Recent studies have shown that it can reduce oral prednisone use
while improving asthma control.
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 anti-inflammatory
drugs have failed
leukotriene receptor antagonists,
Specifically, LTD4 receptor antagonist and 5-
lipoxygenase inhibitors can completely block the
acute phase response and block part of the
delayed phase response
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.

The theory of interplay
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.
Neutrophils

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 .



KLINIS

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
Noxious particles
and gases
Lung inflammation
Host factors
COPD pathology
Proteinases Oxidative stress
Anti-proteinases
Anti-oxidants
Repair mechanisms
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.
VENTILATION
WORK OF
BREATHING
NORMAL COPD
SEVERE COPD
MODERATE COPD
The cost of work at a
given ventilation for
normal and COPD
patients (ACSM,
1998)
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 anti-proteinases


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
h dead space
Impaired passive expiration
Impaired gas exchange


Impaired gas exchange
impaired expiration
h CO2
Hypercapnia
Respiratory acidosis

Damaged pulmonary
capillary bed
h pulmonary pressure
h 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."

109
SYMPTOMS
cough
sputum
dyspnea
EXPOSURE TO RISK
FACTORS
tobacco
occupation
indoor/outdoor pollution
SPIROMETRY
Diagnosis of COPD

GAS DARAH ARTERI
LABORATORY TEST
CHEST X-RAY
Spirometry: Normal and COPD
0
5
1
4
2
3
L
i
t
e
r
1
6 5 4
3 2
FVC
FVC
FEV
1
FEV
1
Normal
COPD
3.900
5.200
2.350
4.150 80 %
60 %
Normal
COPD
FVC FEV
1
FVC FEV
1
/
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


Productive cough
bronchitis

Classic sign
emphysema

Late in common with
infection
Dyspnea Late in course Common
Wheezing Intermittent Mild
H/O smoking Common Common
Barrel chest Occasionally classic
Prolonged expiration Always present Always present
Cyanosis Common Uncommon
Chronic hypoventilation Common Late in course
Ploycythemia Common Late in course
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 %
( A X B )
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