SISTEM RESPIRASI

dr. Dono Indarto, M.Biotech.St.,

PhD, AIFM

Silverthorn D 2009, Human Physiology, an Integrated

Approach, 4th edn, Pearson Benjamin Cummings, San
Francisco.
Homeostasis = maintenance of a stable internal environment
Pathology = changes in structure
Pathophysiology = changes in body function
To understand pathophysiology, we need to understand
homeostasis and the integration of structure and function

Sistem tubuh
manusia

Sistem tubuh
manusia (cont)

Objectives
Anatomi thoraks
Mekanisme respirasi
Hukum-hukum gas
Sistem buffer respirasi

Fungsi sistem respirasi

Ventilasi: udara masuk dan keluar dalam

paru
Pertukaran gas: memasukkan O2 and
melepaskan CO2 dalam darah.
Regulasi keseimbangan asam basa
Melembabkan udara
Berbicara dan penciuman
Pengaturan suhu and keseimbangan
cairan

Pertukaran gas
dengan lingkungan
(external
respiration)

Pertukaran gas
dalam sel (internal

Mekanisme ventilasi
A. Kontraksi diafragma
(60-75% volume)

B. Kontraksi muskuli
dinding dada (25-40%
volume)

Kontraksi muskuli respirasi menyebabkan

perbedaan tekanan antara rongga dada dan
lingkungan (hukum gas Boyle)

Inspirasi (diaphragm
contracts
thoracic volume increases
thoracic pressure
decreases
air flows in)

Ekspirasi (diaphragm
relaxes
thoracic volume
decreases
thoracic pressure
increases

Siklus respirasi
1. Inspirasi (A2)
2. Aliran udara ke dalam alveolus (A3 dan C2)
3. Ekspirasi (A4)
4. Aliran udara keluar alveolus (A5 dan C3)

Tipe ventilasi

Normal
Kontraksi muskuli selama inspirasi
(diafragma dan atau rongga dada)
Ekspirasi pasif (elastic rebound of lung
tissue and muscles)
Hiperventilasi
Inspirasi dan ekspirasi aktif
Kontraksi muskuli tambahan
Kontraksi muskuli dinding abdomen

Ventilasi efektif
Airway resistance:

Lung compliance :
Compliance =
expandability
(capacity to stretch
1. Connective
tissue
2. Lung surfactant
3. Mobility of
thoracic
cage

Hukum gas
Poiseuille
R = x (L x )/r4
R = airway
resistance
= viskositas udara
(humidity and
altitude)
L = panjang
r = diameter

Lung surfactant

1.
2.
3.
4.

Sel-sel alveolar tipe II

Fosfolipid dan protein
Menurunkan tegangan permukaan di dalam alveoli
Menyeimbangkan tekanan parsial alveoli dengan diameter alveoli
yang berbeda (Hukum gas LaPlace)

Diameter organ-organ pada jalan

nafas

 rigid structures with smallest total crosssectional

Approx 90% of airway resistance is
area
normally atributed to trachea and

supported by cartilage and bone so

bronchus
diameters dont
generally change and resistance to airflow
remains
constant
mucus accumulation can significantly
resistance

Bronchioles dont normally

contribute significantly to total
resistance area is about
airway
Total cross-sectional
2000x>trachea
Bronchoconstriction (decreased
diametre) can create
a large increase in airway resistance
Bronchiolar diametre controlled
minute to minute by
local factors (paracrine agents)
CO2 in expired air (bronchodilation)
Histamine from mast cells
(bronchoconstriction)
Parasympathetic neurons mediate
bronchoconstriction
via muscarinic receptors (protective
reflex)
Bronchiolar smooth muscle contains
2 adrenergic
receptors that relax muscle when
stimulated by
adrenaline resulting in
bronchodilation
No significant sympathetic

Not all air we breathe reaches the alveoli as fresh air due to;
anatomical dead space

Conducting airways contain

about 150ml of air not
involved in gas exchange

anatomical dead space

- when we breathe in 500ml, the air
that
reaches the alveoli is a mixture of
used or
stale air from the dead space (150ml)
and
fresh air (350ml)
- mixing of inhaled air with the

Volume of alveolar air replaced

by fresh air each breath is about
1/7th of the total alveolar volume

Mengapa tekanan O2 alveolar

100mmHg?
Rate of entry of new O2 (ventilation)
mixing of fresh and stale air
influence of humidification
Rate of absorption of O2 (gas exchange)
Hukum gas Dalton:
Total pressure exerted by a mixture of
gases is the sum of the pressures exerted
by the individual gases

Aplikasi hukum gas Dalton dalam

sistem respirasi

Partial
pressure of
gases
in air

Gas
exchange
+
Perfusion

Struktur alveoli

Membrane
respirasi

Kecepatan difusi gas

Thickness of respiratory membrane - due

to interstitial oedema or fibrosis
Surface area of respiratory membrane due to tissue destruction
Diffusion coefficient of gases O2 and CO2
are lipid soluble so diffusion through the
membrane is equivalent to water (CO2
20x>O2)
Individual gas pressure difference across the
membrane alveolar PP vs capillary blood
PP

O2 supply = O2 demand

Respirasi eksternal:
Adequate alveolar ventilation within a range manageable by
compensatory
mechanismsReflex changes to
respiratory rate/depth
Adequate gas exchange
across the respiratory
membrane
Adequate pulmonary blood
flow - within a range
manageable by local
autoregulatory
mechanisms
Respirasi internal:
Adequate delivery of O2 to
the tissue
Adequate perfusion of
capillary bed
Metabolism within a range
manageable by local
compensatory mechanisms
temp -O2 /Hb dissociation
pH -O2 /Hb dissociation
CO2 -O2 /Hb dissociation
blood flow

Normoksia
Oksigenasi
jaringan

Difusi
95 Capillary
40 - Interstitial
fluid

Pengeluaran karbon dioksida

jaringan

23 - Intracellular
average (range 540)
46
Intracellular
45 - Interstitial
fluid
40 Capillary

Hipoksia
O2 supply < O2
demand in the
tissue

Low O2
supply:

hypoxaemia
low
perfusion

High O2 demand:
increased activity
increased
metabolism

Darah: transport O2 dan CO2 ke dan dari

jaringan
Dissolved gas
O2 1.5%
CO2 7%
Bound to haemoglobin
O2 98.5%
CO2 23%
Bicarbonate (HCO3-)
CO2 70%

Hemoglobin (Hb) peran penting

sebagai pembawa O2

4 Heme per Hb
4 x O2 molecules per Hb
> 1 billion O2 molecules/RBC
> 6 billion ATP molecules generated by
the O2 carried/RBC (ie 6xATP/O2)
maximum 20ml O2 carried/100ml blood
Cardiac output = 5L/min
1L/min O2 carried to tissues

Heme + O2 (HbO2) oxyhaemoglobin

CO2 carried by haemoglobin does not bind to the heme

Fe2+ - binds to amino groups on Hb
carbaminohaemoglobin (CO2 +HbNH2 HbNHCOOH)
CO (carbon monoxide) does bind heme higher affinity
than O2 O2 unable to bind difficult to displace CO
Ability of Hb to bind O2 is determined by its shape
affected by:
Blood PO2
Blood PCO2
Blood pH
Blood temperature
RBC metabolic activity formation of 2,3
bisphosphoglycerate
(BPG)

Transport CO2 dari jaringan ke dalam

darah

Transport CO2 dari jaringan ke dalam

darah
acts as a
buffer
absorbing
H+
generated
by
metabolism
Internal
buffering of
H+ - if
CO2 levels
increase
above
normal
(hypercapnia
) H+
accumulates
in plasma

acidaemia

Refleks pengaturan respirasi via

Khemoreseptor perifer
khemoreseptor
(carotic and aortic
Khemoreseptor
sentral
(medulla oblongata)

bodies)