Dr.

Fachrul Jamal, SpAn KIC

SMF ANESTESIOLOGI & ICU
FK-UNSYIAH/BPK RSUZA
BANDA ACEH
 Respiratory System
Functions:
• Remove CO2 & replace O2 needed for

metabolism

• Maintain acid - base balance (pH)

• Maintain body H2O & heat balance

• Production of speech

• Facilitate the sense of smell

SISTIM RESPIRASI
SSPusat (medula)
SSPerifer (n.frenikus)
Otot-otot pernafasan
Dinding dada
Paru
Jalan nafas atas
Cabang-cabang bronkus
Alveolus
Pembuluh darah paru
 Control of Ventilation
• Achieved by a complex network of
chemoreceptors that send message to the
brain, which in turn activates the muscles of
breathing via the phrenic nerve
– **central chemoreceptors in medulla
oblongata & brain stem which are sensitive
to rising H+ concentration in the CSF (CO2
levels provide a stimulus to breathe)
– Peripheral chemoreceptors in the
carotid bodies and aortic bodies which
are sensitive to O2 levels (hypoxia
provides a stimulus to breath)

– especially prominent in those with

chronic CO2 retention, for example,
those with COPD (over time medulla
no longer responds, depend on
HYPOXIC DRIVE )
 Ventilation

The respiratory center

and
Central receptors

Peripheral receptors
Sistim respirasi
 The respiratory tract

The upper airway

Alveolus
The lower airways
 Respiratory Tract

• Upper airway • Lower airway

– nose – trachea
– sinuses (windpipe)
– pharynx – bronchial tree
– larynx – gas-exchanging
lung units (e.g.,
alveolar ducts,
alveolar sacs, &
alveoli)
The upper airway
The lower airways
Larynx

Trachea
Respiration

O2

CO2
Mechanisms of Ventilation:
1. Inspiration
Active process
- diaphragm contracts and lowers
- external intercostals contract, elevating the ribs

Result
-  diameter and longitudinal dimensions of the thorax,
decreasing the intrapulmonic pressure
(now atmospheric pressure > intrapulmonicpressure)
air flows in from the atmosphere until pressures are =
Mechanisms of Ventilation:
2. Expiration
Passive process

- diaphragm relaxes

- this relaxation, along with lung elasticity (a property

of healthy lungs), increases the intrapulmonic
pressure and forces air out of the lungs (now
intrapulmonic pressure > atmospheric pressure)

- becomes an active process with disease & exercise

External intercostal muscles
The mechanics of breathing

Diaphragm
Diaphragm

Inspiration Expiration
 Spontaneous breathing
Pressure
kPa

Intrapulmonary pressure

-1 Intrapleural pressure

Time
Insp. Exp. Insp. Exp. s
Pressure
Controlled ventilation
kPa

+1
Intrapulmonary pressure

Intrapleural pressure
-1

Time
Insp. Exp. Insp. Exp. s
 Pressure
Spontaneous breathing
kPa
Intrapulmonary pressure

0
Intrapleural pressure

s
-1
Time
Insp. Exp. Insp. Exp.

Pressure

kPa Controlled ventilation

+1
Intrapulmonary pressure
0
s
Intrapleural pressure
-1 Time

Insp. Exp. Insp. Exp.

 Static lung volumes
Volume

IRV IC VC TLC
5

VT
3

ERV
2

FRC
1 RV

Time
0 s
 3 Processes:
1. Ventilation - movement of air in & out --
depends on system of open (clear)
airways & movement of respiratory
muscles, primarily the diaphragm which
is innervated by the phrenic nerve.

2. Diffusion - exchange & transport gases

(need perfusion/pulmonary circulation)

3. Perfusion
 PROSES PERNAFASAN
Gabungan mekanisme yang berperan
dalam suplai oksigen keseluruh sel
dan eliminasi karbon dioksida

KOMPONEN YANG BERPERAN

1. Ventilasi
2. Difusi
3. Perfusi
 Ventilasi Semenit ( VE )
= Volume Tidal x Frekwensi

= 500 ml x 12 = 6 L/mnt

Ventilasi Alveolar ( VA )
= VE - Vent. Ruang Mati ( VD )

= 6 L/mnt - 1,8 L/mnt = 4,2 L/mnt

Kapasitas Residu Fungsional = Vol. udara dalam

paru pada akhir ekspirasi ,
• sekitar 3300 ml, pada laki-laki
• sekitar 2300 ml, pada wanita
 VENTILASI
Jumlah udara/gas yang mengadakan
pertukaran dalam alveoli setiap menit

Dipengaruhi oleh :
 Patensi jalan nafas
 Posisi tubuh
 Volume paru
 “Dead space”
 “Shunting”
 Patensi Jalan Nafas :
 obstruksi
 Infeksi
 tumor

Posisi Tubuh : Volume Paru :

• tegak  otot pernafasan
• terlentang  penyakit paru
• miring  space occupying lesion
 tekanan intra abdominal
 nyeri, obat
 VENTILATION
 Proses transport gas antara alveolus dan
atsmosfir
 Pertukaran gas ini akan berkurang pada ;
 obstructive
 restrictive
 combined ventilation disorders
 Contoh :
 Laparotomi abdomen atas
 COPD (Chronic Obstructive Pulmonary Disease)
 Status Asthmaticus
 CNS dan obat- obatan : sedation, intoxication
 Neuromuscular : myasthenia gravis,
muscle relaxant
 PERFUSION
 Aliran darah paru yang bertanggung jawab
membawa CO2 ke alveoli dan sebaliknya
membawa O2 dari alveoli ke jantung

 Perfusion disorder :
 Pulmonary embolism
 Sumbatan pada mikrosirkulasi paru
karena agregasi platelet dan granulosit :
• septicemia
• peritonitis
• acute pancreatitis
 Extra pulmonary : reduced CO pada gagal
jantung, atau pada kondisi syok
 SIRKULASI PULMONER
 Sifat :
Tekanan pembuluh darah rendah, MAP 8 - 15
mmHg
 Mudah mengembang (distensible)
 Resistensi rendah

 Dalam keadaan istirahat, perfusi pulmoner

sekitar
= 70 ml x 80 x/mnt = 5,6 L/mnt

 Pintasan Fisiologis = jumlah darah yang melintas

dari kanan ke kiri tanpa mendapat oksigenisasi dan
dekarboksilasi paru (sekitar 5 % curah jantung)
 SHUNTING
(Intrapulmonary Right-to-Left Shunt)

ANATOMICAL FUNCTIONAL
 Bronchial  Atelectasis
 Pleural  Pneumothorax
 Thabesian  Hematothorax
 CHD  Pleural effusion
(Congenital Heart Disease)  Pulmonary edema
 Tumor Paru  Pneumonia
 Arteriovenous Anastomosis  Acute Respiratory
 Failure (ARDS)
 DEAD SPACE

Volume udara yang di hirup dalam

satu kali bernafas yang tidak turut
berdifusi dalam alveolus

FUNCTIONAL DEAD SPACE

ANATOMICAL ALVEOLAR
Physiological
Ventilation
dead space

Alveolar dead space

Anatomical
dead space
 Circulation - perfusion

Normal ventilation – perfusion balance Impaired ventilation impaired ventilation of

an alveolus leads to impaired oxygenation.
Physiological shunt.

Compensatory changes in perfusion for impaired Impaired perfusion

ventilation impaired ventilation is compensated for by a Normal ventilation of poorly perfused alveoli
reduction in blood flow to the poorly ventilated alveolus, results in a large dead space.
resulting in better oxygenation of the arterial blood.
 Optimum gas exchange
requires:
• Ventilation/perfusion match (high V/Q
ratio)
• In healthy lungs this ratio is close to 1:1
• Perfusion greater in dependent areas of
the lung
• Ventilation also greater in dependent
areas of the lung
• Measure adequacy of V/Q match through
ABGs
 V/Q mismatches
• In areas where perfusion > ventilation, a
shunt exists. Blood bypasses the alveoli
without gas exchange occurring (e.g.,
pneumonia, atelectasis, tumor, mucus
plug)

• All cause obstruction in the distal

airways, decreasing ventilation
• In areas where ventilation > perfusion,
dead space results. The alveoli do not
have an adequate blood supply for gas
exchange to occur (e.g., pulmonary emboli,
pulmonary infarct, cardiogenic shock).

• In areas where both perfusion and

ventilation are limited or absent, a silent
unit exists (e.g., pneumothorax, severe
ARDS).
DETEKSI GANGGUAN PERTUKARAN GAS

 Partial pulmonary failure

 PaO2, PaCO2  (respiratory alkalosis)

 Global pulmonary failure

 PaO2  , PaCO2  (respiratory acidosis)
 ….Hypercapnia

Penyebab :
 VT or f ( )
 Drug
 Anesthesia
 CNS
 Fatigue
 ….Hypercapnia
Penyebab lain
• Tidak mampu merespon terhadap PaCO2 
– Obat-obatan
– Alkalemia
– COPD
• Tidak mampu bernafas ok
– Spinal cord injury
– Neuromuscular blocker
– Guillain-Barre` Syndrome
– Myasthenia Gravis
• Otot pernafasan yang lemah ok
– Fatique, Malnutrition, Dystrophy
 …..Hypoxemia
P (A-a) O2 gradient

PAO2 = FiO2 ( PB - 47 ) – ( 1.25 PACO2 )

PAO2 = PO2 alveolar

FiO2 = Oxygen Fraction
PB = Barometric Pressure

• P (A-a) O2 Adult : < 10 torr (<1,3 kPa )

• Umumnya : < 20 torr ( < 2,7 kPa )
 HYPOXEMIA
• Penyebab “SHUNT EFFECT” yang lain

• Difusi () melalui alveolocapillary

membrane complex :
– interstitial edema
– inflammation
– fibrosis, etc.

• Alveolar hypoventilation

• High Altitude
 Diffusion
• Transport of gases between the alveoli and
(pulmonary) capillaries and eventually from the
capillaries to the tissues

• diffusion dependent on perfusion and the

partial pressure (pp) exerted by each gas
(each gas in a mixture of gases exerts a partial
pressure, a property determined by the
concentration of the gas)

• gases diffuse from area of  conc. (pp) to 

conc. (pp)
•  concentration   pp of gas 
 diffusion

• CO2 more soluble than O2, therefore it

diffuses faster
Factors Affecting Diffusion
•  surface area in the lung (e.g.,
lobectomy, atelectasis, emphysema)
• thickness of alveolar-capillary membrane
(e.g., edema, pneumonia)
• differences in partial pressure of gases
on either side
• Characteristics of the gas (CO2 diffuses
faster)
Summary of gas exchange and gas transport

Pulmonary capillary
Alveolus

Artery

Cell
Tissue capillary
Summary of gas exchange and gas transport

Cell
Tissue capillary

Vein

Alveolus

Pulmonary capillary
 Oxygenation

UDARA BEBAS:
PiO2 : 21% x 760 = 160 mmHg
PiCO2 : 0.04 % x 760 = 0.3 mmHg
ALVEOLUS
PiN2 : 78.6 % x 760 = 597mmHg
PiH2O : 0.46 % x 760 = 3.5 mmHg
N2 H2O
KAPILER PARU
PAN2: PAH2O:
PROSES DIFUSI 573 mmHg 47 mmHg

PAO2: PACO2: Pulmonary Vein

104 mmHg 40 mmHg PaO2
Pulmonary Artery O2 O2 CO2 O2
PvO2:
40 mmHg CO2 CO2
PcCO2: 45 PcCO2: 40
mmHg PcO2: 100mmHg  PAO2  PcO2
mmHg
 Ventilation

The respiratory center

and
Central receptors

Peripheral receptors
 Ventilation
The normal regulation of breathing

Receptors Signal to the respiratory center Muscular activity

The blood
Central Low pH Hyperventilation
PaCO2
Peripheral High pH Hypoventilation

The regulation of breathing in a patient with

Chronic lung disease
Signal to the respiratory center Muscular activity
The blood Receptors
Low PaO2 Hyperventilation
PaCO2 Peripheral
High PaO2 Hypoventilation
 The normal regulation of breathing

Receptors Signal to the respiratory center Muscular activity

The blood Central Low pH Hyperventilation

PaCO2

Peripheral High pH Hypoventilation

 The regulation of breathing in a patient with
Chronic lung disease
Signal to the respiratory center Muscular activity

Receptors Hyperventilation
The blood Low PaO2

PaCO2 Peripheral

High PaO2 Hypoventilation

GANGGUAN SISTEM PERNAFASAN & PENYEBAB

 TRAUMA
OTAK  NARKOTIKA
 DEPRESSANT / ANESTHETIC
 INFEKSI , PERDARAHAN

 GUILLAIN BARRE
SYARAF  POLIOMYELITIS , POLINEUROSIS
 MYASTHENIA GRAVIS

 TETANUS
OTOT  RELAXANT / CURARE

JALAN NAFAS ALVEOLI RONGGA THORAX

• ASTHMABRONCHIALE  EDEMA PARU  FRACTURE COSTAE

 ATELEKTASIS  PNEUMOTHORAX
 HEMATOTHORAX