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
