Académique Documents
Professionnel Documents
Culture Documents
Penyakit Saluran Pernafasan Atas
Penyakit Saluran Pernafasan Atas
Penyakit Saluran Pernafasan Atas
Why do we care?
If you understand the basic functions of the
pulmonary system, you’ll be able to:
– relate pathology to function (and assessment)
– identify the basics of unknown pulmonary
diseases
– make logical treatment plans for patients, even
when you don’t have a complete ability to
diagnose their problem
So, here we go!
FAAL PARU
• FAAL RESPIRASI
• FAAL PERTAHANAN
ORGAN PARU
• FAAL ORGAN SEKRESI
FAAL PARU RESPIRASI
Ventilasi
FAAL PERFUSI
Perfusi
FAAL PARU RESPIRASI
FAAL VENTILASI:
PERTUKARAN UDARA
PERNAPASAN ( INSPIRASI DAN Ventilasi
EKSPIRASI )
Otot Bantu
Pernapasan
Tugas Otot
Pernapasan
Ventilasi
Pertahanan
Phonasi
Valsalva
manuver
KONTRIBUSI
DIAPHRAGMA
DALAM
PERNAPASAN
60% VOLUME
ALUN PERNAPASAN
70%-80% VOLUME
KAPASITAS VITAL
BRONCHUS
dan
PERCABANGANNYA
( MANUSIA )
TRACHEA
s/d
BRONCHIOLI
TERMINALIS
IRISAN PARU
(alveoli & saluran napas dilihat
dari dalam )
– Ventilation
– Diffusion
– Perfusion
Ventilation
Definition : movement of
air from the external
environment to the alveoli
Components:
– Brain
– Innervation
– Chest wall
– Upper airways
– Lower airways
The Brain’s Role in Ventilation
Ventilation is primarily
controlled by the pH
of the cerebrospinal
fluid
The brainstem
actually floats in CSF
So, the brainstem
plays a primary role in
initiating ventilation
Message is Transmitted
Two groups of nerves
connect the brainstem
to the muscles of
respiration:
– Phrenic nerve to
diaphragm (C4-C6)
– Thoracic spinal nerves
to intercostal muscles
(T1-T12)
Chest Wall
Chest wall creates
negative
intrathoracic
pressure
– diaphragm (80%)
– increased thoracic
diameter
Air enters airways to
fill the newly created
space
Inspiration
Increased
intrathoracic space
Negative pressure
Bronchioles dilate
Air enters
airways/alveoli
(unless a hole is
present in the chest
wall)
Expiration
Diaphragm &
intercostals relax
Thoracic space gets
smaller
Increased
intrathoracic pressure
Air passively exits via
airways
What Happens to the Airways?
• Smooth-muscle Inspiration
lined airways
(bronchioles)
naturally change
diameter with
inspiration and
expiration
Expiration
• (This will be
important when we
discuss obstructive
lung disease)
TV
PEMERIKSAAN VOLUME
RESIDUAL
( HUKUM GAS BOYLE-GAY LUSAC )
P1.V1 = P2.V2
T1 T2 ,oleh karena
T1 = T2, maka : P1.V1 = P2.V2
V2 = P2 . V1
P1
V1 = Volume Spirometer
V2 = FRC + Volume Spirometer
FRC = V1 ( P1 – P2 )
P1
P1 dan P2 dapat diganti dengan kadar
Gas He pada awal dan akhir
pemeriksaan
RV = FRC - ERV
PEMERIKSAAN VOLUME
RESIDUAL
BODYPLETHYSMOGRAPH
( BODY-BOX )
HUKUM BOYLE
PV = ( P + ∆ P ) X ( V+ ∆V )
Oleh karena Body Box
Volume Tetap, maka :
V = ( P+∆P) X ∆V/∆P
FRC = PBAR X (∆Pb/Pm)
GANGGUAN FAAL PARU RESPIRASI
GANGGUAN DIFUSI
OKSIGEN & KARBONDIOKSIDA SULIT MASUK / KELUAR
PEMBULUH DARAH KAPILER PARU
GANGGUAN PERFUSI
OKSIGEN DAN KARBONDIOKSIDA TERGANGGU
PEREDARANNYA DIJARINGAN TUBUH OLEH KARENA
GANGGUAN SIRKULASI ( GANGGUAN KARDIOVASKULER )
GANGGUAN VENTILASI
OBSTRUKSI RESTRIKSI
VEP1
asma bronkial KV
bronkitis kronis KMP
emphysema
pH
PaO2
PaCO2
½(PEFS+PEFP )
apabila > 15%
hiper-reaktifitas bronchus
SPIROGRAM FAAL PARU
VC 3890 4490 87 %
FVC 3670 4440 83 %
FEV1 3300 3720 89 %
FEV1/ 89.9 83.7 107
FVC
MBC 122.1 163.4 75 %
PF 555 520 107
VENTILASI NORMAL
NORMAL
FFIXED
I EXTRATHORACIC
XOBSTRUCTION
E
D
E
X
T
R
Asthma A
T
H
COPD O
VARIABLE
EXTRATHORACIC
OBSTRUCTION
RESTRICTIVE
INTRATHORACIC
INTRATHORACICI LARGE
LARGE
AIRWAY
AIRWAY OBSTRUCTION
OBSTRUCTION
BRONCHIAL ASTHMA
INTERPRETASI FAAL
RESPIRASI PARU VENTILASI
1. GANGGUAN OBSTRUKSI
2. GANGGUAN RESTRIKSI
3. GANGGUAN CAMPURAN
CATATAN.
Jangan melihat angka, periksa juga :
bentuk spirogram
TABEL KWALITAS & KWANTITAS FAAL PARU
FEV1 < 80 %
RASIO FEV1 / FVC < 80 %
KELAINAN RESTRIKTIF
VC KECIL
RASIO FEV1 / FVC > 80 %
BISA LEBIH BESAR 100 %
KMP ( MBC )
MINIMAL HARGANYA
40 X FEV1
APABILA LEBIH KECIL,
KELEMAHAN
OTOT2 PERNAPASAN
GANGGUAN RESTRIKSI
GANGGUAN RESTRIKSI
schwarte
VAP
efusi pleura
KV
pnemothorax
KMP
tumor rongga
dada
kelemahan
otot-otot
pH atau
PaO2 Phonogram normal
PaCO2 atau
Phonogram abnormal
MESOTHELIOMA
INSPIRASI
EKSPIRASI
GANGGUAN RESTRIKSI
MEMBRAN ALVEOLO-KAPILER
DARAH
TEKANAN GAS
PERFUSI
Diffusion
– Definition of diffusion:
movement of gases between
the alveoli and the pulmonary
capillary bed
– Components:
Alveolus
Basement membrane
(interstitial space)
Capillary wall
Diffusion?
The passive Before diffusion
exchange of gases
along a concentration O2
gradient (high to low) CO2 CO2
O2
Exchange continues
until the
concentrations are
equal After diffusion
O2
O2
CO2
CO2
Basement Membrane
Includes the walls of
the alveolus and
capillary
Most importantly,
includes the interstitial
space between the
walls of the capillary
and alveoli
Drainage via lymphatics
Capillary Wall
If capillary wall is
thickened, diffusion
will be impaired
If capillary wall is
damaged, diffusion
will be impaired
What can go Wrong?
Diffusion may be impaired by the following
disorders :
Alveolar damage
Widened basement membrane
Thickened capillary wall
Why Do We Care?
Understanding these three functions of the
pulmonary system will allow you to:
– Categorize the problem (based on PMH or
chief complaints)
– Perform an intelligent assessment:
Ventilation: look, listen, feel; breath sounds
Perfusion: blood pressure, pulse, evaluation of
blood volume
Diffusion: breath sounds, pulse oximeter
PROSES DIFUSI GAS
1. melalui membran avk dan
plasma
2. masuk dalam eritrosit
Vg= A / T . D ( P1 – P2 )
Vg = volume gas
A = luas permukaan
membran
T = tebal membran
D = kapasitas difusi gas
P1 – P2 = perbedaan tekanan
gas dlm alveoli dan darah
HUKUM P2
FICKS
A V gas = A / T ( P1 – P2 )
P1 T DL = A / T. D
Vgas = DL ( P1 – P2 )
Vg = A / T . D ( P1 – P2 )
dapat pula ditulis sebagai berikut:
Vg = DL ( P1 – P2 )
GANGGUAN SIRKULASI
Simbol
Simbolphonogram
spirogram normal
Simbol
Simbolphonogram
spirogram abnormal
abnormal
SEMBAB PARU
a
a
PENUMPUKAN CAIRAN PADA
DAERAH SENTRAL PARU
PERSELUBUNGAN HILER
GAMBARAN SAYAP
KELELAWAR
b
PENUMPUKAN CAIRAN
MERATA MELUAS TERUTAMA
DAERAH BASAL
b OEDEMA ALVEOLER
GAGAL NAPAS
VENTILASI DIFUSI
GAGAL NAPAS
Blood
flow
5.08
Powdered Dye V
Concentration
V/Q
Water
Q
STIRRER 5.09
O2=150 mmHg
CO2=0
B A C
O2=40 O2=100 O2=150
CO2=45 O2=40 CO2=40 CO2=0
CO2=45
0 NORMAL
DECREASING INCREASING
VA/Q VA/Q
5.10
50
PO2 mmHg
v
0 A
I
0 50 100 150
PO2 mmHg
5.11
MEKANIKA BERNAPAS
( mechanic of breathing )
Otot
Pernapasan
Utama
Otot Bantu
Pernapasan
Tugas Otot
Pernapasan
Ventilasi
Phonasi
KONTRIBUSI
DIAPHRAGMA
DALAM
PERNAPASAN
60% VOLUME
ALUN PERNAPASAN
70%-80% VOLUME
KAPASITAS VITAL
Diaphragm
7.01
Intercostal
Muscles
external
Spine internal
RIBS
Head
Tubercle
Axis of Rotation
7.02
INSP.
EXP.
Abdominal
Muscles
Active
Passive
7.03
Intercostal
Muscles
external
Spine internal
RIBS Head
Tubercle
Axis Of Rotation
7.04
TENAGA PADA SAAT
BERNAPAS BIASA
A. ISTIRAHAT
B. SAAT INSPIRASI
C. SAAT EKSPIRASI
A
C
normal fibrosis paru emphysema
Beberapa kurva simpul-kepatuhan
Ny. Anisa (35 th)
Cl = 0,187 l/cm H2O
Sensor
Efektor
Pusat Kendali Pernapasan
KEMORESEPTOR
Sensoris
KEMORESEPTOR
Efektor BARORESEPTOR
OTOT PERNAPASAN
Control of Ventilation
Chemical Mechanical
Primary: pH of CSF, Stretch receptors in
directly related to the the lung itself
arterial level of CO2 (Herring-Breur
(PaCO2).
receptors) prevent the
Secondary:dissolved lung from over-
oxygen in arterial
bloodstream (PaO2). expanding
This is the hypoxic
drive
Kontrol pernapasan secara kimia
Central Peripheral
chemoreceptors Chemoreceptorts
Pa O2
Pa CO2
pH
H+
Pa CO2