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Anatomi dan Fisiologi

The Primary Function of the Lung
The respiratory system exists for exchange of gases between
blood and the environment
Gas exchange between venous blood and inspired air
It is importance to the anesthesiologist since a large number
of anesthetic drugs are given by inhalation
The anesthesiologist is also responsible for adequate
oxygenation of patient during, immediately after operation,
and in ICU.
Airways: Tracheobronchial Tree
Trachea: divides into 23 increasingly smaller
Trachea right & left mainstem bronchus
lobar, segmental, and subsegmental bronchi
bronchioles and terminal bronchioles (the
smallest airways without alveoli)
Conducting zone: airway without alveoli =
anatomic dead space, +/- 150 ml in N adult
Terminale bronchioles
Respiratory bronchioles alveolar duct alveolar sac: 17
alveoli, each +/- 0.3 mm
Approximately 150 million alveoli
Area contain alveoli respiratory zone. +/- 3000 ml
Mucosa changes: ciliated columnar cuboidal flat
alveolar epithelial cells
Upper airway wall to distal : lose support of cartilaginous
Smaller airway: without support, depend on airway pressure
to maintain patency
Gas exchange unit
Close contact with pulmonary capillaries
O2 and CO2 move between air & blood by simple diffusion, by partial
pressure gradients
Ficks law: amount of gas moves across a sheet of tissue is proportional to
area of sheet and inversely proportional to its thickness.
Alveolar-capillary membrane less than 0,4 mm, 50 100 mm2.
Alveolar surface tension is high, promotes alveolar collapse
Surfactant (lipoprotein complexes): type II pneumocytes lower alveoli
surface tension, counter collapse
Chest and Muscle of Respiration
Inspiration is initiated by dome-shaped diaphragm, innervated by phrenic nerve
(C3 C5)
Diaphragm contraction forces abdominal content downward and forward, ribs are
lifted up and put, increasing volume of the chest
Thorax expansion lowers intrapleural pressure, generating a pressure gradient
air move into the lungs.
Normal breath: diaphragm descend +/- 1 cm, at forced inspiration diaphragmatic
excursion can be 10 cm
External intercostal m. also aid in inspiration by pulling the ribs up and out.
Increasing respiratory effort, other accessory muscle are recruited. Scalene m.
elevates 1st two ribs and sternocleidomastoid, platysma, and pectoralis m. raises
sternum. Alae nasi flare the nostril augment inspiration by maintaining upper
airway patency
When diaphragm is paralysed or fatiqued (after prolonged
tachypnea or synchronized intermittent mechanical
ventilation), it may not function properly. diaphragm
cannot mechanically fix the thorax (the generation of negative
intra-thoracic pressure cause cephalad movement of
diaphragm and inward movement of abdomen with
inspiration paradoxical breathing, upper thoracic and neck
accessory muscles are required to expand the chest.
Hyperventilated patients (asthma and COPD): in inspiration:
flat diaphragm pull the chest inward rather than outward
(Hoovers sign)
In the absence of airway obstruction is a passive process. Lung and chest
wall are elastic and return to baseline positions to maintain pressure
Exercise, voluntary hyperventilation, certain disease states, expiration
becomes an active process. Muscle for active process: rectus abdominis,
transverse abdominis, and internal & external oblique muscle. Contraction
of these pulls the sternum down and increases intraabdominal pressure,
forcing diaphragm upward. Internal intercostal muscles also help active
expiration by pulling the ribs down and out.
Pulmonary Circulation
The lungs are supplied by 2 arterial circulation, the pulmonary and
bronchial. Pulmonary circulation receives entire output of mixed venous
blood from right heart via main pulmonary artery. Blood travels through
the alveolar capillary bed to pulmonary veins, to left atrium.
Large cross sectional area of pulmonary arterial circulation results in low
arterial pressures compared to the mean systemic arterial pressure (15
mmHg vs 90 mmHg). a capillary segment is +/- 10 m, just enough for a
red blood cell. Blood in the capillaries usually passes through 2 3 alveoli,
take about second, before it reaches pulmonary circulation
Bronchial circulation
Systemic in nature, arises from left heart.
It supplies metabolic needs of trachobronchial tree to the level of terminal
and respiratory bronchioles. This blood returns to left heart via the
pulmonary system.
The amount of blood in the bronchial circulation is small compared to that
in the pulmonary circulation. Most cases of massive hemoptysis are
secondary to erosion into high-pressure bronchial arteries, not pulmonary
Lung can function normally without bronchial circulation, as after lung
transplantation or after therapeutic arterial embolization for massive
Pulmonary Lymphatic System
When fluid leaves capillary network due to hydrostatic and
oncotic pressure, it passes into interstitium of alveolar wall
and into the perivascular and peribronchial spaces within the
lung. Within these spaces the pulmonary lymphatic vessels
run alongside the airways and eventually lead into hilar lymph
nodes. Lymphatic drainage channels from both lungs
communicate along the trachea in the mediastinal lymph
nodes. Pulmonary lymph flow is normally only a few milliliters
/ hr but can increase in pulmonary edema when there is
engorgement of periveascular and peribronchial intersititial
Tidal volume: amount of gas exhaled during a normal breath. VT x RR =
total ventilation (or minute volume). Adult normal VT 500 mL (5-8 mL/kg),
RR 12 /min MV 6.0 L/min. not all this gas participates in gas exchange;
some remains in conducting zone: anatomic dead space; this volume x
RR = dead space ventilation.
Vol of gas actually reaches alveoli (respiratory zone) and involved in gas
exchange = alveolar gas.
Alveolar gas vol x RR = alveolar ventilation.
Normal adult VT 500 mL, 150 mL dead space (VD), alveolar gas (VA) 350 mL
Total ventilation can be measured by
collecting expired gas in a bag. VA is more
difficult to determine unless dead space
fraction is known, Total vent - VD
VCO2 x %CO2 / 100 VA =
(VCO2 x 100/%CO2
VA = (VCO2 / PCO2) x K
Anatomic dead space
Using Fowlers single-breath nitrogen method. Following a single
inspiration 100% O2, N2 concentration measured during exhalation rises as
dead space gas (which should be 100% O2) is washed out by alveolar gas,
which contains N2 from previous inhalation of air. N2 concentration will
plateau when alveolar gas is exhaled (alveolar plateau). The dead space is
found by plotting N2 concentration against expired volume and drawing a
vertical line such that areas A and B are equal.
Dead space or anatomic dead space is volume of gas expired up to vertical
line, which is the midpoint of transition from dead space to alveolar gas.
Physiologic dead space
Consists of both anatomic dead space and alveolar dead
space (vol of gas that does not eliminate CO2 and is not part of
conducting airway).
Bohr method assumes all expired CO2 comes from alveolar
gas and none from dead space. Assuming that no CO2 is lost,
CO2 present before expiration (concent x vol) C1VA + C2VD is
equal to CO2 after expiration C3VT. Since partial pressure of
gas is proportional to its concentration, we can replace C with
VT = VA + VD and VA = VT - VD
VD / DT = (PACO2 PECO2) / PACO2 (Bohr equation)
Normal spontan breathing: VD/VT 0.33 (0.2-0.4)
physiologic dead space
Mechanic of breathing
In order for active inspiration to occur,
respiratory muscle contract to expand the
lung and generate negative intraalveolar
pressure. The work these muscles must
perform is reflection of the forces they must
overcome to expand the lung and chest wall.
These mechanical forces 2 categories:
elastic properties of lung and chest wall, and
airway resistance
Elastic Properties of the Chest Wall

The lung is an elastic organ that recoils inward, or collapse, when not
The chest wall is also an elastic structure; when unrestrained, it recoils
outward. At the end of a passive exhalation, lung volume is determined by
the balance between the tendency lung to collapse and chest wall to
expand. If air enters the intrapleural space (pneumothorax) and
intrapleural pressure becomes zero, lung collapses inward and chest wall
springs out.
After a full inspiration, the inward force of resp system (lung + chest wall)
exceeds the outward force of lungs, and passive expiration results.
Elastic Properties of the Lung
The Pressure-Volume Curve
If the lungs are slowly inflated and deflated,
the pressure-volume curve during inflation
differs from that obtained during deflation
The lung volume at any given pressure is
larger during deflation than during inflation
Elastic Properties of the Lung
Lung compliance (V / P) can be determined from the slope of a pressure-volume
(PV) curve. Normal breathing occurs on the steepest portion of this curve, where
compliance is the greatest (e.g., small changes in pressure produce large changes
in lung volume). At higher expanding pressure, PV curve is flattened as the elastic
fibres of the lung are stretched, causing lung to stiffen and compliance to fall.
Normal compliance +/- 200 mL/cm water.
Restrictive disease: PV curve shifts to the right and the slope becomes depressed,
reducing lung compliance and FRC. Lower compliance: it takes a much larger
change in pressure to change lung volume. In restrictive (pulm edema or
atelectasis, CPAP, or PEEP, expands collapse alveoli, improving lung compliance and
PV curve move to the right
In restrictive diseases due to loss of alveoli (pulmonary
fibrosis), CPAP worsen compliance due to overdistention of
already open alveoli.
In obstructive disease, PV curve shifts to the left and the slope
increases. Less elastic work is required to inspire, but elastic
recoil is reduced significantly and active expiration may
become necessary.
On a ventilator, compliance can easily be measured by
dividing Vt by the airway pressure. Dynamic compliance refers
to Vt divided by the plateau pressure (minus PEEP)