3. kuliah fisiologi respirasi
DESCRIPTION
fisiologi respirasiTRANSCRIPT
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