Dr. Fachrul Jamal, SpAn KICSMF ANESTESIOLOGI & ICU

FK-UNSYIAH/BPK RSUZABANDA ACEH

Respiratory SystemFunctions:

• 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 RESPIRASISISTIM RESPIRASI SSPusat (medula)

SSPerifer (n.frenikus) Otot-otot pernafasan

Dinding dada Paru

Jalan nafas atas Cabang-cabang bronkus

Alveolus Pembuluh darah paru

Control of VentilationControl 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 centerandCentral receptors

Peripheral receptors

Sistim respirasi

The respiratory tractThe respiratory tract

The upper airway

The lower airways Alveolus

Respiratory Tract

• Upper airway– nose– sinuses– pharynx– larynx

• Lower airway– trachea

(windpipe)– bronchial tree– gas-exchanging

lung units (e.g., alveolar ducts, alveolar sacs, & alveoli)

The upper airwayThe upper airway

The lower airwaysThe lower airways

Larynx

Trachea

O2

CO2

Respiration

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

The mechanics of breathing

Inspiration

Ext

erna

l int

erco

stal

mus

cles

Expiration

DiaphragmDiaphragm

kPaPressure

Spontaneous breathing

Time

0

-1

Intrapulmonary pressure

Intrapleural pressure

Insp. Exp. Insp. Exp. s

Controlled ventilation

Time

kPa

0

-1

Intrapulmonary pressure

Intrapleural pressure

Insp. Exp. Insp. Exp.

Pressure

s

+1

Spontaneous breathing

Time

kPa

0

-1

Intrapulmonary pressure

Intrapleural pressure

Insp. Exp. Insp. Exp.

Pressure

s

Controlled ventilation

Time

kPa

0

-1

Intrapulmonary pressure

Intrapleural pressure

Insp. Exp. Insp. Exp.

Pressure

s

+1

Static lung volumes

Time0

Volume

s

1

2

3

4

5

6

IRV IC VC TLC

ERV

FRCRV

VT

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 PERNAFASANGabungan mekanisme yang berperan dalam suplai oksigen keseluruh sel dan eliminasi karbon dioksida

KOMPONEN YANG BERPERAN

1.1. VentilasiVentilasi2.2. DifusiDifusi3.3. PerfusiPerfusi

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

VENTILASIJumlah 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

Volume Paru : otot pernafasan penyakit paru space occupying lesion tekanan intra abdominal nyeri, obat

Posisi Tubuh :• tegak• terlentang• miring

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 Pleural Thabesian CHD (Congenital Heart Disease) Tumor Paru Arteriovenous Anastomosis

Atelectasis Pneumothorax Hematothorax Pleural effusion Pulmonary edema Pneumonia 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

VentilationPhysiologicaldead space

Anatomicaldead space

Alveolar 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 ventilation impaired ventilation is compensated for by a reduction in blood flow to the poorly ventilated alveolus, resulting in better oxygenation of the arterial blood.

Impaired perfusionNormal ventilation of poorly perfused alveoli results in a large dead space.

Optimum gas exchange Optimum gas exchange requires: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 mismatchesV/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 GASDETEKSI 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

• 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

Penyebab lain

P (A-a) O2 gradient

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

PAO2 = PO2 alveolar

FiO2 = Oxygen FractionPB = 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

HYPOXEMIA

DiffusionDiffusion• 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 DiffusionFactors 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

Artery

Tissue capillary

Alveolus

Cell

Summary of gas exchange and gas transport

Pulmonary capillary

Vein

Tissue capillary

Alveolus

Cell

ALVEOLUSALVEOLUS

KAPILER PARUKAPILER PARU

UDARA BEBAS:UDARA BEBAS:PiOPiO22 : 21% x 760 = 160 mmHg : 21% x 760 = 160 mmHg

PiCOPiCO22 : 0.04 % x 760 = 0.3 mmHg : 0.04 % x 760 = 0.3 mmHg

PiNPiN22 : 78.6 % x 760 = 597mmHg : 78.6 % x 760 = 597mmHg

PiHPiH22O : 0.46 % x 760 = 3.5 mmHgO : 0.46 % x 760 = 3.5 mmHg NN22 HH22OO

OO22

PAOPAO22::104 mmHg104 mmHg

COCO22

PACOPACO22::40 mmHg40 mmHg

OO22

PvOPvO22: : 40 40 mmHg mmHg

OO22

PcO2: 100 PcO2: 100 mmHgmmHg

COCO22

PcCOPcCO22: 45 : 45 mmHgmmHg

COCO22

PcCOPcCO22: 40 : 40 mmHgmmHg

PROSES DIFUSIPROSES DIFUSIPANPAN22::573 mmHg573 mmHg

PAHPAH22O:O:47 mmHg47 mmHg

PAOPAO22 PcO PcO22

PaOPaO22

PulmonaryPulmonary ArteryArtery

PulmonaryPulmonary VeinVein

Oxygenation

Ventilation

The respiratory centerandCentral receptors

Peripheral receptors

VentilationThe normal regulation of breathing

The bloodReceptors Signal to the respiratory center Muscular activity

PaCO2

Central Low pH Hyperventilation

Peripheral High pH Hypoventilation

The regulation of breathing in a patient withChronic lung disease

The blood Receptors

Signal to the respiratory center Muscular activity

PaCO2

Low PaO2 Hyperventilation

Peripheral

High PaO2 Hypoventilation

The normal regulation of breathing

The blood

Receptors Signal to the respiratory center Muscular activity

PaCO2

Central Low pH Hyperventilation

Peripheral High pH Hypoventilation

The regulation of breathing in a patient withChronic lung disease

The bloodReceptors

Signal to the respiratory center Muscular activity

PaCO2

Low PaO2 Hyperventilation

Peripheral

High PaO2 Hypoventilation

TRAUMA NARKOTIKA DEPRESSANT / ANESTHETIC INFEKSI , PERDARAHAN

GUILLAIN BARRE POLIOMYELITIS , POLINEUROSIS MYASTHENIA GRAVIS

TETANUS RELAXANT / CURARE

OTAK

SYARAF

OTOT

ALVEOLI RONGGA THORAX

FRACTURE COSTAE PNEUMOTHORAX HEMATOTHORAX

EDEMA PARU ATELEKTASIS

GANGGUAN SISTEM PERNAFASAN & PENYEBAB

JALAN NAFAS

• ASTHMABRONCHIALE