Transcript Slide 1

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
terminal
bronchiole
pulmonary
artery branch
simple squamous epithelial cell
macrophage (dust cell)
septal cell (produces surfactant)
Type II alveolar cell
making surfactant
Type I alveolar cell
alveolar sac
surfactant
macrophage
blood capillary
respiratory membrane
endothelial cell
respiratory
bronchiole
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
Boyle’s 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
BEFORE INSPIRATION
FORCED INSPIRATION
760 mmHg
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
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)
maximum inspiration
6000 ml
5000 ml
IRV
VC
TLC
4000 ml
3000 ml
TV
2000 ml
ERV
1000 ml
maximum
expiration
SPIROGRAM
Rates
maximum voluntary ventilation = TV x breaths/minute
alveolar ventilation rate = alveolar ventilation x breaths/minute
RV
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
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 (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 lymphocytes
Cells
epithelial cells
Macrophages
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
1
2
Time (second)
3
4
Impairment
Component
of
Severity
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
<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
Lung function
RISK
Classification of Asthma Severity (>12 yrs)
• Normal FEV1
between
exacerbations
• FEV1: >80%
predicted
• FEV1/FVC:
normal
Exacerbations
requiring
oral steroids
0-1/yr
Recommended
Treatment Step
Step 1
• FEV1 : >80%
predicted
• FEV1/FVC: normal
• FEV1: >60% but
<80% predicted
• FEV1/FVC:
reduced 5%
• FEV1: <60%
• FEV1/FVC:
reduced 5%
≥2/yr
Consider severity and interval since last exacerbation as
they may fluctuate over time in any severity category
Step 2
Step 3
Step 4 or 5
& consider short OS burst
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
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 µg/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,
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 (eksaserbasi)
Nyeri dada (pleuritis, pneumotoraks, emboli paru)
Anoreksi & BB menurun progresif jelek
KLINIS
Noxious particles
and gases
Host factors
Lung inflammation
Anti-oxidants
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 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."
Diagnosis of COPD
EXPOSURE TO RISK
FACTORS
SYMPTOMS
cough
sputum
dyspnea
tobacco
occupation
indoor/outdoor pollution

SPIROMETRY
GAS DARAH ARTERI
LABORATORY TEST
CHEST X-RAY
109
Spirometry: Normal and COPD
0
FEV1
Normal
COPD
1
Liter
2
FVC
FEV1/ FVC
4.150
5.200
80 %
2.350
3.900
60 %
FEV1
3
COPD
4
FVC
FEV1
Normal
5
1
2
3
FVC
4
5
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)
• 􀃆 α1-proteinase inhibitor 􀃆 utk pasien yang defisiensi α1antitripsin 􀃆 digunakan per minggu, masih mahal 􀃆 contoh:
Prolastin
Tahap terapi pada PPOK yang stabil
• Tahap 1 : Ipratropium bromida (MDI) atau nebulizer, 26 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 β-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 β-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
μg/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 μg 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