1

Specific Instructional Objective

At the end of the lesson of respiratory physiology, students would be able to illustrate the normal function of respiratory system, rightly

3 TWO DIFFERENT MEANING OF RESPIRATION

Respiration has two quite different meaning:

1. Utilization of oxygen in the metabolism of organic molecules by cells

2. The exchange of oxygen and carbon dioxide between an organism and the external environment

GENERAL FUNCTION
OF RESPIRATORY SYSTEM
1.
2. 3. 4. 5. 6.

Provide oxygen
Eliminates carbon dioxide Regulates the blood concentration of hydrogen ions (pH) Form speech sounds (phonation) Defends against microbes Influences arterial concentration of chemical messenger by removing some from pulmonary capillary blood and producing and adding others to this blood Traps and dissolves blood clots

7.

THE SUBTOPICS
1. Structure of the Respiratory System

2. The Pulmonary Ventilation

3. Lung Volume and Capacity 4. The O2 CO2 Exchange 5. The Transport of O2 and CO2 6. The Control of Respiration 7. Exercise and The Respiratory System 8. Aging and Respiratory System

STRUCTURE OF RESPIRATORY SYSTEM

7 Structures of The Respiratory System Upper R.S Nose Pharynx Associated structure Lower R.S

Larynx Trachea Bronchus Lungs

Bronchiole

Artery & Vein

Terminal bronchiole Capillary vessel

Respiratory bronchiole
Alveolar duct

Alveolus

CONDUCTING ZONE 1. Trachea 2. Bronchus 3. Bronchiole 4. Terminal bronchiole 4 RESPIRATORY ZONE 5. Respiratory bronchiole 6. Alveolar duct 7. Alveolus 2 3 5 1 7 6

TRANSVERSE SECTION OF AN ALVEOLUS

1. Type II alveolar cell

1 2 6 7 8 9 10 11

2.

Alveolar capillary membrane

3. Type I alveolar cell 4. Alveolar macrophage

3 4 5

5. Red blood cell

TRANSVERSE SECTION OF AN ALVEOLUS

DETAILS OF ALVEOLAR CAPILLARY MEMBRANE

6 7 8 9 10 11

Red blood cell Capillary endothelium Capillary basement membrane Epithelial basement membrane Type I alveolar cell Surfactant layer

Muscular Control of Breathing Inspiration muscles:

Diaphragm External Intercostals Sternocleido-mastodeus Scalenes

Abdominal muscles

Expiration muscles:
Internal Intercostals Abdominal Muscles

Extrinsic elastic recoil Intrinsic elastic recoil

Abdominal muscles

STERNUM AND DIAPHRAGM DURING INSPIRATION AND EXPIRATION

S.E = Sternum during Expiration S.I = Sternum during Inspiration D.E = Diaphragm during Expiration D.I = Diaphragm during Inspiration

REVIEW QUESTION

1. List the function of the respiratory system 2. List the anatomical portion of the respiratory tract from upper to lower 3. List the muscles act during forced inspiration and during forced expiration

PULMONARY VENTILATION

PULMONARY VENTILATION
Or BREATHING
1. Inspiration 2. Expiration 3. Breathing Patterns

4. Alveolar Surface Tension

5. Compliance 6. Airways Resistance 7. Modified Respiratory Movements

Pulmonary Pressure * The movement of air into and out of the lung depends on pressure change (Boyles law)

TRANSPULMONARY PRESSURE
ALVEOLI

PALV = 0 mm Hg

Chest Wall

Intrapleural fluid
ELASTIC RECOIL

PALV PIP =
4 mm Hg PALV = ALVEOLAR PRESSURE PIP = INTYRAPLEURAL PRESSURE

PIP = - 4 mmHg

THE PRESSURE CHANGES

SEQUENCE OF EVENTS DURING INSPIRATION

NEURAL IMPULSE DIAPHRAGM AND INSPIRATORY INTERCOSTAL MUSCLE CONTRACT

THORAX EXPANDS

PIP BECOMES MORE SUBATMOSPHERIC

TRANS PULMONARY PRESSURE

LUNGS EXPAND PALV BECOMES SUBATMOSPHERIC

AIR FLOWS INTO ALVEOLI

SEQUENCE OF EVENTS DURING EXPIRATION

DIAPHRAGM AND INSPIRATORY INTERCOSTALS STOP CONTRACTING

CHEST WALL MOVES INWARD

PIP BACK TOWARD PREINSPIRATION VALUE

TRANSPULOMONARY PRESSURE BACK TOWARD PREINSPIRATION VALUE

LUNGS RECOIL TOWARD PREINSPIRATION SIZE

AIR IN ALVEOLI BECOMES COMPRESSED

PALV BECOMES GREATER THAN PATM

AIR FLOWS OUT OF LUNGS

Relationship Between Flow and Pressure

P F R
Flow (F) is proportional to the pressure difference (P) between two points and inversely proportional to the resistance (R)

Patm Palv F R
Air moves into and out of the lungs because the alveolar pressure is made alternately less than and greater than atmospheric pressure

BREATHING PATTERNS

Eupnea
Apnea Dyspnea

= Normal quiet breathing

= A temporary cessation of breathing = A painful or labored breathing + tachypnea

Costal breathing = Shallow (chest) breathing Diaphragmatic breathing = Deep (abdominal) breathing

COMPLIANCE The expansibility of the thorax, and thus the lungs. Expressed as the volume increase of the lungs for each unit increase in intra-alveolar pressure (cm3/mm Hg) The greater the increase in volume for a given increase in pressure, the greater the compliance. The Compliance decrease in: Scar lung Pulmonary edema Surfactant deficiency Muscle paralysis , emphysema

V L CL ( Palv Patm )
The greater the increase in volume for a given increase in pressure, the greater the compliance.

Determinants of Lung Compliance The elasticity of connective tissues less elasticity of the lung tissue decrease the compliance Surface tension the higher the surface tension the larger the energy requirement to expand the lung

ALVEOLAR SURFACE TENSION Alveolar fluid surrounds air in alveoli exerts tension (surface tension) Lowered by Surfactant Great surface tension tend to collapse the lung

Some important facts about pulmonary surfactant: 1. Pulmonary surfactant is a phospholipid bound to a protein 2. It is secreted by type II alveolar cells 3. It decreases surface tension of the water layer at the alveolar surface, which increases lung compliance makes the lungs to expand easily 4. Its concentration decreases when breaths are small and constant

AIRWAY RESISTANCE

Patm Palv F R
Factors determine airways resistance: Directly proportional to the magnitude of the frictional interaction between the flowing gas molecules the viscosity of the air which much less than that of blood Directly proportional to the length of the airways Inversely proportional to the fourth power of the airway radius (r4)

Major Factors Influencing the Airway resistance

Physical factors
Airways are held open by transpulmonary pressure and by lateral traction open wider during inspiration and may collapse during forced expiration Airways may partially or totally occluded by mucous accumulation Neuroendocrine agents Prasympathetic nerves (neurotransmitter = acetylcholine) constrict Circulating epinephrine dilates (action is on beta adrenergic) Noncholinergic, nonadrenergic nerves dilate (neurotransmitter = vasoactive intestinal peptide) Paracrine agents

Histamine constricts
Several eicosanoids, notably the leukotrienes, constrict Several eicosanoids dilate

MODIFIED RESPIRATORY MOVEMENT

Coughing: along drown and deep inspiration following by a complete closure
of the rima glottis, which results in a strong expiration that suddenly pushes the rima glottis open and sends a blast of air through the upper respiratory passage. Stimulus for this reflex act may be a foreign body lodged in the larynx, trachea, or epiglotiis

Sneezing: Spasmodic contraction of muscles of expiration that forcefully expels

air through the nose and mouth. Stimulus may be an irritation of the nasal mucosa.

Sighing: A long drown and deep inspiration immediately followed by a shorter

but forceful expiration

MODIFIED RESPIRATORY MOVEMENT, continue

Yawning: A deep inspiration through the widely opened mouth producing an

exaggerated depression of the mandible. It may be stimulated by drowsiness, fatigue, or someone elses yawning, but precise cause is unknown

Sobbing: A series of convulsive inspiration followed by a single prolong

expiration. The rima glottidis closes earlier than normal after each inspiration so only a little air enters the lungs with each inspiration

Crying: An inspiration followed by many short convulsive expirations, during

which the rima glottidis remains open and the vocal folds vibrate; accompanied by characteristic facial expressions and tears

MODIFIED RESPIRATORY MOVEMENT, continue Laughing:

The same basic movement as crying, but the rhythm of the movements and the facial expression usually differ from those of crying. Laughing and crying are sometimes indistinguishable closure of the rima glottidis to produce a sharp inspiratory sound. Stimulus is usually irritation of the sensory nerve endings of gastrointestinal tract

Hiccuping: Spasmodic contraction of the diaphragm followed by a spasmodic

Valsalva maneuver: Forced expiration against a closed rima glottidis during

periods of straining

LUNG VOLUME AND CAPACITY

LUNG VOLUME AND CAPACITIES

6000 ml

5000 ml

4000 ml

3000 ml

2000 ml

1000 ml

LUNG VOLUMES

LUNG CAPACITIES

SPIROGRAM

LUNG VOLUMES

SPIROMETER (RESPIROMETER):
The apparatus that commonly used for measuring the volume of air exchange and the rate of ventilation during breathing.

SPIROGRAM:
The recording picture of breathing

TIDAL VOLUME (VT): The volume of air that moves into and out the airways with each inspiration and expiration during normal quiet breathing (approximately 500 ml) Varies from one person to another and in the same person at different times 70% (350 ml) actually reaches the respiratory zone and participate in respiration

30% (150 ml) remain in conducting zone, known as Anatomic Dead Space (VD)

MINUTE VOLUME of RESPIRATION (MVR) or

MINUTE VENTILATION :
The total volume air taken in during 1 minute Calculated by multiplying the tidal volume by the normal breathing rate per minute An average 500 ml x 12 = 6000 ml/min Not all MVR can be used in gas exchange, some remains in the anatomic dead space

MINUTE VENTILATION (The total ventilation per minute = tidal volume x respiratory rate)

(ANATOMIC) DEAD SPACE [The air that never reach alveoli but is merely moved in and out the airways (conducting zone)]

ALVEOLAR VENTILATION [The volume of fresh air entering alveoli per minute = (tidal volume dead space) x respiratory rate)]

EFFECT OF ANATOMIC DEAD SPACE ON ALVEOLAR VENTILATION Expired air Inspired air Oxygen rich Carbon dioxide rich

Tidal Volume 500 ml

Carbon dioxide rich Anatomic dead space = 150 ml

Oxygen rich Anatomic dead space = 150 ml

Gaseous exchange

End of Expiration

Inspiration

End of Inspiration

INSPIRATORY RESERVE VOLUME: The volume that can be inspired over and above the resting tidal volume approximately 3100 ml

EXPIRATORY RESERVE VOLUME:

The additional volume that can be exhaled over and above the resting tidal volume approximately 1500 ml

FORCED EXPIRATORY VOLUME IN 1 SECOND (FEV1):

The volume of air that can be expelled from the lungs in 1 second with maximal effort following a maximal inhalation Asthma and emphysema can greatly reduce FEV1

FUNCTIONAL RESIDUAL VOLUME:

The volume at the end of an unforced expiration

approximately 2400 ml

RESIDUAL VOLUME:
The volume of air that cannot be measured by spirometry and cannot be expelled even though by forced expiration approximately 1200 ml

MINIMAL VOLUME:
The remaining air volume in the alveoli after opening the thoracic cavity that allows the intrapleural pressure to equal the atmospheric pressure Minimal volume provide a medical and legal tool for determining wither a baby was born dead or died after birth Can be demonstrated by placing a peace of lung in water and watching it float stillborn baby will not float

LUNG CAPACITIES
INSPIRATORY CAPACITY:
The total inspiratory ability of the lungs, is the sum of tidal volume plus inspiratory reserve volume (3600 ml)

FUNCTIONAL RESIDUAL CAPACITY:

The sum of residual volume plus expiratory reserve volume (2400 ml)

VITAL CAPACITY:
The maximal volume of air that a person can expire after a maximal inspiration that is the sum of expiratory reserve plus tidal plus inspiratory reserve volume (4800 ml)

TOTAL LUNG CAPACITY:

The all volume of air in the lungs (approximately 6000 ml)

PROBLEM
There are three subject that have exactly the same minute volume (6000 ml). Subject A breathes rapidly and shallowly (40 times/min), B normally (12 times/min), and C slowly and deeply (6 times/min). What will be occur?

ANSWER
____________________________________________________________________________ Subject Tidal volume x Frequency, = ml/breath breathe/min Minute ventilation ml/min Anatomic dead space ml/min Alveolar ventilation ml/min

------------------------------------------------------------------------------------------------------------------

A
B C

150
500 1000

40
12 6

6000
6000 6000

150 x 40 = 6000
150 x 12 = 1800 150 x 6 = 900

0
4200 5100

____________________________________________________________________________

Increased depth of breathing is far more effective in elevating alveolar ventilation than is an equivalent increase in breathing rate

ALVEOLAR DEAD SPACE [A quiet small volume (in normal person) of fresh inspired air that is not used for gas exchange with the blood even though it reaches the alveoli, for various reason, have little or no blood supply]

PHYSIOLOGIC DEAD SPACE (The sum of anatomic and alveolar dead space)

THOUGHT QUESTIONS ( homework ) At the end of a normal expiration, a persons FRC (Functional Residual Capacity) is 2 L, his alveolar pressure is 0 mmHg, and his intrapleural pressure is 4 mmHg. He then inhales 800 ml, and at the end of inspiration the alveolar pressure is 0 mmHg and the intrapleural pressure is 8 mmHg. Calculate this persons lung compliance

GASEOUS EXCHANGE

O2 CO2 EXCHANGE
Changes In Partial Pressure During External and Internal Respiration

(Dalton & Henrys laws)

RESPIRATORY QUOTIENT (RQ) The ratio CO2 produced/O2 consumed = approximately 0.8 ( 8 molecules CO2 are produced for every 10 molecules O2 consumed)

TRANSPORT OF OXYGEN AND CARBON DIOXIDE

OXYGEN CONTENT OF SYSTEMIC ARTERIAL BLOOD AT SEA LEVEL

1 L arterial blood contain

3 ml 197 ml O2 physically dissolved (1.5%) O2 bound to Hemoglobin (98.5%)

Total

200 ml

O2

Cardiac output = 5 L/min O2 carried to tissue/min = 5L/min x 200 ml O2/L = 1000 ml O2/min

HEMOGLOBIN AND OXYGEN PARTIAL PRESSURE

O2 Hb dissociation curve at normal body temperature

As pO2 increase, more O2 combines with hemoglobin

HEMOGLOBIN AND OTHER FACTORS

The effect pH on affinity of hemoglobin for oxygen

As pH decrease , the affinity of hemoglobin for O2 is less, so less O2 combines with hemoglobin and more is available to tissue

The effect pCO2 on affinity of hemoglobin for oxygen

As pCO2 increase , the affinity of hemoglobin for O2 decreases

The effect body temperature on affinity of hemoglobin for oxygen

As temperature increase , the affinity of hemoglobin for O2 decreases

FETAL HEMOGLOBIN

Oxygen hemoglobin dissociation curve comparing fetal and maternal hemoglobin

Fetal Hb has a higher affinity for O2 than does adult Hb

TRANSPOR OF HYDROGEN IONS BETWEEN TISSUES AND LUNGS

HYPOXIA 1. Hypoxic hypoxia

Low pO2 in arterial blood: high altitude, airways obstruction, fluid in lung

2. Anemic hypoxia
Low Hb: hemorrhage, anemia, CO poisoning

3. Stagnant (ischemic) hypoxia

Low tissue blood flow

4. Histotoxic hypoxia
Tissue unable uses O2 properly

CARBON DIOXIDE TRANSPORT

1. Dissolved CO2: 7% dissolved in plasma 2. Carbaminohemoglobin Hb + CO2 3. Bicarbonate ions HbCO2

CO2 + H2O

H2CO3

H+ + HCO3-

Summary of Gas Exchange and Transport in Lung and Tissue

CONTROL OF RESPIRATION

CONTROL OF RESPIRATION
Respiratory center 1. Medullary Rhythmicity Area

2. Pneumotaxic Area
3. Apneustic Area

REGULATION OF THE RESPIRATORY CENTER

1. Cortical influences
Voluntary, protective

2. Chemical regulation
Central Chemoreceptors: located in Medulla Oblongata Peripheral Chemoreceptors: Aortic & carotid bodies

3. Neural changes due to movement 4. Inflation reflex

Baroreceptors = Stretch receptors

5. Other influences
Blood pressure, Limbic system, Temperature, Pain, Stretching the anal sphincter muscle, Irritation of airways

Proposed role of the medullary rhythmicity area in controlling the basic rhythm of respiration

Stimulus (stress)

Increase arterial blood pCO2

Central & peripheral chemo-receptor Return to homeostasis

Inspiratory area control center (in MO)

Respiratory muscle: hyperventilation

NEGATIVE FEEDBACK

Decrease arterial blood pCO2; increase pO2

Stimulus (stress)

Decrease arterial blood pO2 (severe hypoxia)

Central chemo-receptor suffer hypoxia Positive feedback further lowers pO2 so hypoxia worsens

Inspiratory area suffer hypoxia (in MO)

Respiratory muscle: hypoventilation

POSITIVE FEEDBACK

Decrease arterial blood pO2

VENTILATION RATE AND DEPTH INCREASE WITH:

1. 2. Voluntary 3. 4. 5. 6. 7. 8. Anticipation Decreasein Increase Prolonged Stretching in anal pain arterial sensory body blood of 3 hyperventilation + activity blood impulses pressure temperature sphincter Hvia detected from level stimulation or p by CO2 controlled by system cerebral of the limbic above proprioceptors baroreceptors 40 mm Hg in and cortex decreaseand muscles in arterial joints and increase blood pO in motor 100 to 2 from 50 mm Hg, impulses from detected the by centralcortex motor and peripheral chemoreceptor

1 15 2 14

13

4 5 6 10 8 9

12 7 11

VENTILATION RATE AND DEPTH DECREASE WITH:

12. 9. 10. 11. Decrease Severe Increase pain of in in pharynx blood body causes 13.Irritation 14. 15. Voluntary Decrease in arterial or apnea temperature pressure larynx detected by (sudden touch by or sensory blood hypoventilation H+ impulses level or from p CO2 chemicals cold baroreceptors stimulus) causes causes 3 proprioceptors below controlled 40 mm by cerebral Hg in apnea and followed apnea byarterial coughing muscles decrease cortex (limited and in joints by and +) or sneezing decrease blood buildup pO of in CO motor 50H mm 2 below 2 and impulses Hg, detected from by the central motor and peripheral cortex chereceptors

15
2 14

13

4
5 6 10 8 9

12 7 11

EXERCISE AND RESPIRATORY SYSTEM

EXERCISE AND THE RESPIRATORY SYSTEM

Exercise

Raises pulmonary perfusion

Pulmonary ventilation

Raises the O2 diffusion capacity

a. Decreased p O2, ,due to 3. Motor impulses from b. Increased p CO due to 2 c. 2. Increased Sensory impulses temperature from 1. Anticipation ofcortex the increased O consumption 2 motor the primary increased CO production by 2 in due proprioceptors to liberation of muscles more activity, which stimulates (precentral gyrus) contracting muscle fibers heat and as joints more O utilized 2 the limbic system

AGING AND RESPIRATORY SYSTEM

AGING AND THE RESPIRATORY SYSTEM

Aging

The airways and tissue become more rigid

Decreases
1. 2. 3. 4. Vital capacity, as much as 35% Blood level of O2 Alveolar macrophage activity Ciliary action

More susceptible to: pneumonia, bronchitis, emphysema, and other pulmonary disorders

SIRKULASI PARU A. Pulmonalis cabang kiri/kanan

- Diameter arteri/arteriol lebih besar dari arteri yang

sederajat - Sangat tipis, dapat mengembang

- Compliance sistem arteri paru 7 ml/mmHg

- Dapat menampung 2/3 volume sekucup dari ventrikel kanan

PEMBULUH BRONCHIAL
Paru mendapat sirkulasi juga dari pembuluh darah bronchial (Teroxigenasi)

Mensupply jaringan penunjang

SALURAN LIMPHE

Terdapat pada semua jaringan penunjang paru mulai dari

jaringan ikat yang mengelilingi bronchialus terminalis Protein plasma yang keluar dari kafiler paru disebabkan dari jaringan paru Membantu mencegah edema

TEKANAN ARTERI PARU

Tekanan sistolik arteri paru rata-rata 25 mmHg Tekanan diastolik arteri paru rata-rata 15 mmHg

TEKANAN KAPILER PARU Kira-kira 7 mmHg

TEKANAN ATRIUM KIRI dan VENA PARU 2 mmHg (1 5 mmHg) Bisa diukur dengan tekanan kapiler paru (Pulmonary Wedge Pressure)

VOLUME DARAH PARU

- 50 ml (9% dari volume darah total

- Paru sebagai tempat penyimpanan darah - Exprirasi kuat (mis. Meniup terompet) 250 ml darah keluar dari paru - Pendarahan berat dikompesasikan dengan otomatis melalui

pergeseran darah dari paru ke pembuluh darah sistemik

Pengaruh kenaikan curah jantung terhadap sirkulasi paru selama kerja berat : 1. Meningkatkan jumlah kapiler yang terbuka (sp 3 x lipat) 2. Meregangkan semua kapiler dan meningkatkan kecepatan aliran darah di setiap kapiler Hasil ini menurunkan tegangan vascular

Fungsi Sirculasi pada Gagal Jantung Kiri Gagal jantung kiri darah terbendung di atrium kiri tekanan atrium kiri sp 40 50 mmHg terjadi peningkatan tekanan kapiler edema paru

EDEMA PARU

Faktor apapun yang tekanan cairan intestitiel paru pengisian memdadak ruang intestitiel paru dan alveolus

Penyebab : 1. Gagal jantung kiri atau penyakit katup metral tekanan kapiler paru cairan masuk ke intestitiel dan alveoli 2. Karusakan membran kapiler paru akibat infeksi (Pneunomia, terhisap bahan beberapa gas klorin, S02 menyebabkan kebocoran protein plasma dan cairan keluar dari kapiler.

Faktor faktor Pengamanan Edema Paru

1. Tekanan negatif cairan intestitiel paru yang normal

2. Pompa limphatik mengeluarkan cairan dari ruang intestitiel

3. Peningkatan osmosis cairan ke dalam kapiler paru. Akibat penurunan konsentrasi protein ke dalam cairan intestitiel ketika aliran lymphe meningkat

Faktor Pengaman pada Keadaan Chronis > 2 mg paru-paru lebih resistent terhadap edema paru pembuluh lymphe mengembang cukup besar (10 x) edema paru tidak jelas walaupun tekanan kapiler 30 35 mmHg

Edema Paru Acut bila 50 mmHg terjadi kematian dalam 20 30 menit

EFUSI PLEURA Pengumpulan sejumlah cairan bebas dalam ruang pleura disebut juga edema rongga pleura

Penyebab :
1. Penghambatan drainase limphatik dari rongga pleura 2. Gagal jantung tekanan kapiler paru tekanan perifer transudasi cairan 3. Tekanan osmotik koloid plasma transudasi cairan 4. Infeksi / peradangan kapiler pengaliran protein plasma dari cairan ke dalam rongga pleura

TEKANAN PLEURA

Adalah tekanan cairan dalam ruang antara pleura visceralis dan pleura parientalis

Pleura normal pada awal inspirasi 5 cm air

Pleura saat inspirasi 7,5 cm air

TEKANAN ALVEOLUS

Adalah tekanan di bagian dalam alveoli paru. Bila tak ada udara yang mengalir tekanan alveoli = 0 cm air

Pada saat inspirasi normal 1 cm air

Pada saat expirasi normal + 1 cm air (Tekanan ini mendorong 0,5 l udara keluar paru)

TEKANAN TRANSPULMONAR

Perbedaan antara tekanan alveolus dan tekanan pleura merupakan perbedaan antara tekanan alveoli dan tekanan pada permukaan luar paru nilai daya elastis paru tekanan daya lenting paru

Gangguan Fisiologis Pernapasan I.Emfisema Paru Kronik Penyebab :

1.
2.

Infeksi kronik ;Merokok,bahan yg mengiritasi bronchus, bronchiolus.

Infeksi ;mucus dan edema epitel bronchus. Menyebabkan in feksi kronis pd sbgn bsr saluran nafas. Obstruksi saluran napas terutama menyebabkan kesukaran ekspirasi, sehingga udara terperangkap dalam alveoli dan menyebabkan alveoli sangat teregang.

3.

Efek Fisiologis dari Emfisema Kronik :

1. Obstruski bronkiolus yang berat meningkatkan tahanan saluran napas dan mengakibatkan peningkatan kerja pernapasan.

2. Hilangnya sebagian besar dinding alveolus akan sangat menurunkan kapasitas difusi paru
3. Proses obstruksi seringkali jauh lebih buruk pada beberapa bagian paru daripada bagian lainnya. menghasilkan rasio vantilasi-perfusi yang sangat abnormal, dengan VA/Q sangat rendah pada beberapa bagian (pintas fisiologik), mengakibatkan aerasi darah yang buruk, dan VA/Q yang sangat tinggi pada bagian lain (ruang rugi fisiologik), menagkibatkan ventilasi yang percuma, kedua efek ini terjadi pada paru-paru yang sama. 4. Hilangnya sebagian besar dinding alveolus juga mengurangi jumlah kapiler paru yang dapat dilalui darah.

II. Pneumonia Mengakibatkan dua kelainan utama paru :

1. Penurunan luas permukaan total membran pernapasan

2. Menurunnya rasio ventilasi-perfusi

III. Atelektasis Akibat : 1. Sumbatan brunkus kecil oleh mukus 2. Sumbatan brunkus besar oleh gumpalan mukus yang besar atau benda padat seperti kanker.

IV. Asma Ditandai dengan kontraksi spastik dari otot polos bronkiolus, yang menyebabkan kesukaran bernapas.

Efek : 1. Edema lokal pada dinding brukiolus kecil maupun sekresi mukus yang kental ke dalam lumen bronkiolus 2. Spasme otot polos bronkiolus

V. Tuberkulosis Basil Tuberkel Menyebabkan : 1. Daerah yang terinfeksi diserang oleh makrofag 2. Daerah lesi dikelilingi oleh jaringan fibrotik untuk membentuk yang disebut tuberkel Tuberlkulosis menyebabkan : 1. Peningkatan kerja pada bagian otot pernapasan yang berfungsi untuk ventilasi paru dan mengurangi kapasitas vital dann kapasitas pernapasan 2. Mengurangi luas permukaan membran pernapasan total dan meningkatkan ketebalan membran pernapasan 3. Kelainan rasio ventilasi perfusi dalam paru