Tractus

Respiratorius
dr. Zainuri Sabta
Dep. Anatomi FK UII
Right and Left Pleural Cavities
Parietal Pleura
Visceral (Pulmonary) Pleura
Parietal
Costal

Mediastinal

Diaphragmatic

Cupola

Connecting Pleura
Proyeksi external paru
Lungs
Light, soft, spongy
Conical in shape, apex, base, costal surface, medial
surface, hilus. Note various impressions
Right lung
Three lobes; superior, middle and inferior
Oblique and horizontal fissure

Left Lung
Two lobes; superior and inferior also Lingula and Cardiac
notch, horizontal fissure
Struktur yang keluar/masuk
hilus pulmonis:

1. Bronchi
2. a. & v. pulmonalis
3. a. & v. bronchialis
4. Vasa dan nodi lymphatici
5. nervus
 Lungs formed by
progressive branching,
first 16 generations of
airways = conducting
zone, generations 16-23
= gas exchange zone
300 million alveoli (0.3
mm in diameter), total
surface area 85 m2, 0.4
m2 if lung a sphere
Change in intrathoracic
pressure moves air
inspiratory muscles
(diaphragm, external
intercostals, accessory =
SCM, scalene) size
of thorax
intrathoracic pressure
relative to atmospheric
pressure bulk flow
into airways (flow =
pressure gradient /
resistance)
Inervasi diaphargma
 Trachea

Bronchus:
Vascularisasi a. bronchialis cab. Aorta (2 cabang kiri, 1 kanan)
Drainase vena kanan : v .azygos
kiri: v. hemiazygos
(sebagian kecil via v. bronchiales dan v. pulmonale)

Sympathis vasokonstriksi, bronchodilatasi (beta 2 ), supresi sekresi kelenjar (alpha)

Parasympathis vasodilatasi, bronchokonstriksi, peningkatan sekresi kelenjar , sensasi
 Lungs have large surface area & thin membrane for gas
exchange, formed by progressive branching (vascular and air
spaces brought close together), first 16 generations of airways
= conducting zone, generations 16-23 = gas exchange zone
300 million alveoli (0.3 mm in diameter), total surface area 85
m2, 0.4 m2 if lung a sphere
Change in intrathoracic pressure moves air inspiratory
muscles (diaphragm, external intercostals, accessory = SCM,
scalene) size of thorax intrathoracic pressure relative
to atmospheric pressure bulk flow into airways (flow =
pressure gradient / resistance)
 Airways
Trachea, primary bronchi, secondary bronchi, tertiary
bronchi out to 25 generations
All comprised of hyaline cartilage
Trachea
Begins where larynx ends (about C6)
10 cm long, half in neck, half in mediastinum
20 U-Shaped rings of hyaline cartilage keeps lumen intact
but not as brittle as bone
Lined with epithelium and cilia which work to keep foreign
bodies/irritants away from lungs
 Airways
Primary Brochi
One to each lung continuation of trachea
Right bronchus is wider and shorter 2.5 cm as opposed to
5 cm and branches from the trachea at a greater angle
Secondary bronchi one to each lobe, three in right,
two in left
Tertiary one to each bronchopulmonary segment
approximately 10 per lung
All of the above are hyaline cartilage with no ability
to change diameter
 Bronchioles
First level of airway surrounded by smooth
muscle; therefore can change diameter as in
brocho-constriction and broncho-dilation
Terminal
Respiratory
3-8 orders
alveoli
 Innervation
Pleura via intercostal (thoracic) nerves
Tracheobronchial tree
Parasympathetic via CN X efferent function =
broncho-constriction via smooth mm., also to
epithelial cells in trachea; afferent =
responsible for cough reflex
Sympathetic from T1-T5 efferent = brocho-
dilation
 Blood Supply
Lungs do not receive any vascular supply from
the pulmonary vessels (pulmonary aa. Or
veins)
Blood delivered to lung tissue via the
bronchiole arteries
Vessels evolve from aortic arch
Travel along the bronchial tree
Perkembangan paru,
eophagus dan larynx

Paru berkembang dari Laryngotracheal groove, di mana pada cekungan tsb muncul
laryngotracheal diverticulum yang selanjutnya menjadi Lung bud
Bagian endoderma menjadi: bronchioli, pleura viseral, epithel larynx, trachea, glandula
trachea, dan epithel bronchi.
Trachea dan esophagus dipisahkan oleh septum. Bila gagal memisah akan membentuk
fistula.
Kejadian Pulmo
ventilasi
 Ventilasi paru

Lungs settle in pleural

space, more negative
pressure at apices (alveoli
expanded) at FRC vs.
at bases (weight of lung
collapses alveoli); basilar
alveoli undergo greater
volume increase during
inspiration (more
ventilation at base)
More pulmonary blood Pleural Space between parietal / visceral pleura,
flow to base of lung (due potential space under negative pressure (chest wall
to gravity and high expanding out, lungs collapsing in)
pressure of air in apical Pleural space should be fluid free (sum of hydrostatic
alveoli compressing / osmotic pressures favors fluid removal) 5-10
pulmonary vessels) L/day fluxes through pleural space w/o accumulation
normally
 Obstructive lung disease = problem w/ airflow
function of lung asthma, emphysema,chronic
bronchitis, cystic fibrosis
Restrictive lung disease = problem w/ gas exchange
function of lung pulmonary fibrosis,pulmonary
alveolar proteinosis
 Bronchi / bronchioles have minimal effect on airflow
obstruction (but contribution to COPD via enlargement of
bronchial mucus glands, goblet cells, airway smooth muscle
hypertrophy
Respiratory bronchioles major cause of obstruction
macrophage inflammation, mucus plugs, loss of alveolar
attachments (less alveolar septae tugging on airways and
keeping them open distorted / collapsed bronchioles)
 Tractus Respiratorius

Stage 1
7 microns
& above

Stage 2
4,7-7 microns

Cairan mukus, cilia, reflex

Stage 3 batuk dan sel darah putih
3,3-4,7 microns
(macrophages) merupakan
protector paru terhadap
Stage 4 pengaruh benda asing dari
2,1-3,3 microns
luar misal: debu, kotoran,
Stage 5 bakteri, asap rokok dll.
1,1-2,1 microns
Stage 6
0,6-1,1 microns
Besar-kecilnya dampak partikel yang masuk paru
bergantung pada sejumlah faktor:
konsentrasi partikel di udara dengan diameter
kurang dari 10 mikron,
frekuensi dan lama pemaparan,
kandungan partikel,
cuaca, dan
kondisi kesehatan seseorang.
EFEK TERHADAP KESEHATAN

Inhalasi debu mineral secara umum disebut

Pneumoconiosis.

Silicosis adalah penyakit paru akibat inhalasi debu

yang mengandung cristal silica (alpha-quartz or silicon
dioxide), atau silica tipe polymorphs (tridymite or
cristobalite), yang secara alami terdapat pada dan
memiliki toksisitas sangat tinggi terhadap paru.
Gejala silikosis umumnya muncul beberapa tahun
setelah terkena paparan. Sebagai contoh pekerja
terpapar silica selama 30 tahun, dimana terjadi
fibrosisasi jaringan paru hebat.
 EFEK TERHADAP KESEHATAN
Mekanisme Kerusakan paru
Partikel < 1 mikron
Permukaan partikel merangsang
terbentuknya radikal bebas
(hydroxyl, hydrogen peroxide, and
other oxygen radicals)
Terjadi kerusakan membran sel epitel
alveoli melalui mekanisme peroksidasi lipid
dan dan inaktivasi protein esensial sel
Macrophag alveoli memakan partikel, teraktivasi
dan merangsang pengeluaran cytokines,
termasuk tumor necrosis factor, interleukin-1,
and leukotriene B-4, dan terjadilah proses
radang (inflamasi) yang menyebabkan
kerusakan sel dan matrik alveoli.
Pada tahap selanjutnya merubah growth factor
alpha induces proliferation of type 2
pneumocytes, and other cytokines (eg, platelet-
derived growth factor, insulin - like growth factor)
dan merangsang sel fibroblas berproliferasi
memproduksi collagen dan akhirnya terjadi
fibrosis paru.
 Emphysema protease imbalance destruction of alveolar
tissue loss of elastic recoil hyperinflation flattening
diaphragm ( effort) dyspnea
Dyspnea inactivity deconditioning dyspnea
inactivity deconditioning disability
Airflow limitation during exercise no ventilatory reserve,
flow only by breathing at higher volumes dynamic
hyperinflation; RR time to exhale hyperinflation
SOB
 Emphysema
Abnormal permanent enlargement of alveolar spaces distal to
terminal bronchiole w/ wall destruction, enlargement of alveoli
(overinflation)
Centrilobular involves respiratory bronchiles, upper lobes more
involved, found inassociation w/ CB and smoking, spherical holes 1-5
mm near center of lobu
Panlobular all portions of lobule affected but usually alveolar ducts,
both upper/lower lobes
involved, usually in middle-aged smokers or young pt. w/ antitrypsin
(cotton candy lung)
 Pleuritis painful inflammation, usually w/ viral infections,
also w/ bacteria, TB, PE, tumors
Pneumothorax can have pleuritic pain as well, but dyspnea
most common hyperresonant lung to percussion + breath
sounds
Examine pleural fluid to determine transudate or exudate
(caused by infection, tumor, PE + infarct, collagen vascular
disease, trauma, esophageal rupture, pancreatitis, abscess,
ascites, asbestos, chylothorax, hypersensitivity)
 Exudate damage to pleura, leakage of plasma (protein, RBC, WBC) into
pleural space, meets following criteria fluid protein / serum protein >
0.5, fluid LDH / serum LDH > 0.6, pleural fluid LDH > 2/3 of plasma (200 IU)
continuum from pure transudate to exudates
Empyema pus in pleural space, lots of PMN, seen w/ pneumonia (esp.
anaerobic), occasionally seen w/ trauma, rarely w/ surgery
Hemothorax blood in pleural space, due to trauma excessive blood loss
hypotension
Chylothorax lymph fluid (milky) in pleural space, due to poor lymphatic
drainage (blockage), can be due to congenital atresia of thoracic duct,
trauma from esophageal surgery, or tumor
Pneumothorax injured chest wall (i.e. penetrating wounds, rib fracture),
also due to insertion of central line, IJV or subclavian catheter, chest
surgery, positive pressure ventilation air leaks in; spontaneous
pneumothorax (primary no predisposition,
Pneumothorax injured chest
wall (i.e. penetrating wounds, rib
fracture), also due to insertion of
central line, IJV or subclavian
catheter, chest surgery, positive
pressure ventilation air leaks in;
spontaneous pneumothorax
(primary no predisposition,