1.

Embryological development of the lung and the diaphragm

Origin:
a. Endoderm - tubular ventral growth from foregut pharynx.
b. Mesoderm - mesenchyme of lung buds.
c. Intraembryonic coelom - pleural cavities elongated spaces connecting
pericardial and peritoneal spaces.

Human Lung Stages

Stage Human Features
lung buds originate as an outgrowth from the ventral wall of the foregut
Embryonic week 4 to 5
where lobar division occurs
week 5 to conducting epithelial tubes surrounded by thick mesenchyme are
Pseudoglandular
17 formed, extensive airway branching
bronchioles are produced, increasing number of capillaries in close
week 16 to
Canalicular contact with cuboidal epithelium and the beginning of alveolar
25
epithelium development
week 24 to
Saccular alveolar ducts and air sacs are developed
40
late fetal to secondary septation occurs, marked increase of the number and size
Alveolar
8 years of capillaries and alveoli
 Diaphragm
The diaphragm is formed form a number of composite parts in the embryo. The most
important is the septum transversum. The septum transversum is a thick mass of cranial
mesenchyme that gives rise to parts of the thoracic diaphragm and the anterior mesentery of
the foregut in the adult. After its descent, discussed below, the septum transversum merges
with mesoderm surrounding the oesophagus, the growing pleura and peritoneum
(pleuroperitoneal folds) and the growing muscles of the abdominal wall

2. The structure anatomy of the lung, the pleura, the relational between chest wall, the thorax
and the mediastinum, lungs and their lobes, the vascular system of the thorax, the vagus and
the phrenic nerves, structure of diaphragm, lymphatic system of the lung.
 Border: base diaphragm
Medial heart
Anterior costae
Posterior vertebrae
Right lung 3 lobes, (urutan di hilum dari atas bronchus, artery, vein)
Left lung 2 lobes (karena butuh space utk jantung); (urutan di hilum dari atas
artery, bronchus, vein)
Pleura
o Parietal associated with the wall of pleural cavity
o Visceral adheres and cover to the lung
o Pleural cavity: between parietal and visceral pleural that containing a
monolayer fluid
Structure in the hilum
o Superior: pulmo artery
o Inferior: pulmo veins
o Posterior: main bronchus
o Bronchial vessels, nerves and lymphatics
Vascularization
o artery
Right and left pulmonary artery from pulmo trunk, carry
deoxygenated blood
Bronchial as terbs utk pulmonary tissue
o Vein
Pulmonary vein superior and inferior, carry oxygenated blood to the
left atrium
Bronchial veins drain into azygos or hemiazygos
Lymphatic system
o Drain into tracheobronchial nodes extend to hilum, root, post mediastinum
Innervation
o Spinal nerve T1-T11 costal pleura
o Lower intercostal nerves peripheral diaphragmatic pleura
o Phrenic nerves central diaphragmatic pleura, mediastinal pleura
o Parasympathetic vagus nerve
o Sympathetic splanchnic nerve (anterior and posterior plexus)
3. Pressure differeces in the chest wall, diaphragm, pleura, and airways
Intra-alveolar pressure during inspiration & expiration

As the external intercostals & diaphragm contract, the

lungs expand. The expansion of the lungs causes the
pressure in the lungs (and alveoli) to become slightly
negative relative to atmospheric pressure. As a result, air
moves from an area of higher pressure (the air) to an area
of lower pressure (our lungs & alveoli). During expiration,
the respiration muscles relax & lung volume descreases.
This causes pressure in the lungs (and alveoli) to become
slight positive relative to atmospheric pressure. As a result,
air leaves the lungs

What is Partial Pressure?:

it's the individual pressure exerted independently by

a particular gas within a mixture of gasses. The air we breath is a mixture of
gasses: primarily nitrogen, oxygen, & carbon dioxide. So, the air you blow into
a balloon creates pressure that causes the balloon to expand (& this pressure is
generated as all the molecules of nitrogen, oxygen, & carbon dioxide move
about & collide with the walls of the balloon). However, the total pressure
generated by the air is due in part to nitrogen, in part to oxygen, & in part to
carbon dioxide. That part of the total pressure generated by oxygen is the
'partial pressure' of oxygen, while that generated by carbon dioxide is the
'partial pressure' of carbon dioxide. A gas's partial pressure, therefore, is a
measure of how much of that gas is present (e.g., in the blood or alveoli).

the partial pressure exerted by each gas in a mixture equals the total pressure
times the fractional composition of the gas in the mixture. So, given that total
atmospheric pressure (at sea level) is about 760 mm Hg and, further, that air is
about 21% oxygen, then the partial pressure of oxygen in the air is 0.21 times
760 mm Hg or 160 mm Hg.
Partial Pressures of O2 and CO2in the body (normal, resting conditions): (check
this animation by McGraw-Hill)

Alveoli
o PO2 = 100 mm Hg
o PCO2 = 40 mm Hg
Alveolar capillaries
o Entering the alveolar capillaries
PO2 = 40 mm Hg (relatively low because this blood has just
returned from the systemic circulation & has lost much of its
oxygen)
PCO2 = 45 mm Hg (relatively high because the blood returning
from the systemic circulation has picked up carbon dioxide)

While in the alveolar capillaries, the diffusion of gasses occurs: oxygen diffuses from
the alveoli into the blood & carbon dioxide from the blood into the alveoli.

o Leaving the alveolar capillaries

PO2 = 100 mm Hg
PCO2 = 40 mm Hg

Blood leaving the alveolar capillaries returns to the left atrium & is pumped by the left
ventricle into the systemic circulation. This blood travels through arteries & arterioles
and into the systemic, or body, capillaries. As blood travels through arteries &
arterioles, no gas exchange occurs.

o Entering the systemic capillaries

PO2 = 100 mm Hg
PCO2 = 40 mm Hg
o Body cells (resting conditions)
PO2 = 40 mm Hg
PCO2 = 45 mm Hg

Because of the differences in partial pressures of oxygen & carbon dioxide in the
systemic capillaries & the body cells, oxygen diffuses from the blood & into the cells,
while carbon dioxide diffuses from the cells into the blood.

o Leaving the systemic capillaries

PO2 = 40 mm Hg
PCO2 = 45 mm Hg

Blood leaving the systemic capillaries returns to the heart (right atrium) via venules &
veins (and no gas exchange occurs while blood is in venules & veins). This blood is
then pumped to the lungs (and the alveolar capillaries) by the right ventricle.

Two main disorders in the lung

1. Restrictive
People with a restrictive lung disease have a much more difficult time filling their lungs
with air. This is a result of the lungs being restricted from fully expanding. Most of the time,
restrictive lung diseases occur when there is stiffness in the lungs themselves. Sometimes, this
can occur when there is stiffness in the chest wall, weak muscles or damaged nerves that can
restrict the expansion of the lungs. People with a restrictive lung disease have a much more
difficult time filling their lungs with air. This is a result of the lungs being restricted from fully
expanding. Most of the time, restrictive lung diseases occur when there is stiffness in the lungs
themselves. Sometimes, this can occur when there is stiffness in the chest wall, weak muscles
or damaged nerves that can restrict the expansion of the lungs.
Decreased Total Lung Capacity (TLC)
Cause:
 Intrinsic lung diseases or diseases of the lung parenchyma. The diseases cause
inflammation or scarring of the lung tissue (interstitial lung disease) or result in filling
of the air spaces with exudate and debris
Extrinsic disorders or extra-pulmonary diseases. The chest wall, pleura, and respiratory
muscles are the components of the respiratory pump, and they need to function
normally for effective ventilation.
The distensibility of the respiratory system is called compliance, the volume change
produced by a change in the distending pressure. Lung compliance is independent of the thoracic
cage, which is a semirigid container.
Conditions classified as restrictive lung disease:

Interstitial lung disease

Sarcoidosis
Pneumoconiosis

2. Obstructive
Obstructive lung diseases include conditions that make it hard to exhale all the air in the
lungs. The damage to the lungs or the narrowing of the airways inside the lungs, causes air to come
out a lot more slowly than normal. Usually, by the end of every breath, a lot of air remains in the
lungs.

Common conditions related to obstructive lung diseases:

Chronic obstructive pulmonary disease (COPD), which includes emphysema and

chronic bronchitis
Asthma
Bronchiectasis

Obstructive lung disease makes it harder to breathe, especially during increased activity or
exertion. As the rate of breathing increases, there is less time to breathe all the air out before the
next inhalation.

Types and management of pneumothorax

 Types:
Traumatic pneumothorax. This occurs when an injury to the chest (as from a car wreck or
gun or knife wound) causes the lung to collapse.
Tension pneumothorax. This type can be fatal. It occurs when pressure inside the pleural
cavity is greater than the outside atmospheric pressure. It can force the entire lung to
collapse and can push the heart toward the lung, putting pressure on both.
Primary spontaneous pneumothorax. This happens when a small air bubble on the lung
ruptures. These may happen for no obvious reason or while undergoing changes in air
pressure (like when scuba diving or mountain climbing).
Secondary spontaneous pneumothorax. This typically happens to those who already have
lung disease. As the lung is already compromised by disease and may have diminished
capacity, this can be a serious complication.

The range of medical therapeutic options for pneumothorax includes the following:
Watchful waiting, with or without supplemental oxygen
Simple aspiration
Tube drainage, with or without medical pleurodesis
Surgery
If the patient has had repeated episodes of pneumothorax or if the lung remains unexpanded
after 5 days with a chest tube in place, operative therapy such as the following may be necessary:
Thoracoscopy: Video-assisted thoracoscopic surgery (VATS)
Electrocautery: Pleurodesis or sclerotherapy
Laser treatment
Resection of blebs or pleura
Open thoracotomy
Pharmacotherapy
The following medications may be used to aid in the management of patients with
pneumothorax:
Local anesthetics (eg, lidocaine hydrochloride)
Opioid anesthetics (eg, fentanyl citrate, morphine)
Benzodiazepines (eg, midazolam, lorazepam)
Antibiotics (eg, doxycycline, cefazolin)
Function of chest tube
Chest tube helps drain air, blood, or fluid from the pleural space, which is the space
surrounding your lungs.

During chest tube insertion, a hollow plastic tube is inserted between your ribs and into the
pleural space. The tube may be connected to a machine to help with the drainage. It will stay in
place until the fluid, blood, or air is drained from your chest.

Chest tube insertion is typically an emergency procedure. It may also be done after surgery
is performed on your organs, such as your lungs, or tissues in your chest cavity.

Chest tubes are used to treat conditions that cause a lung to collapse. Some of these
conditions are:

Surgery or trauma in the chest

Air leaks from inside the lung into the chest (pneumothorax)
Fluid buildup in the chest (called a pleural effusion) due to bleeding into the chest,
buildup of fatty fluid, abscess or pus buildup in the lung or the chest, or heart failure
A tear in the esophagus (the tube that allows food to go from the mouth to the stomach)

The chest tube usually stays in for a few days. After your doctor is sure that no more fluid or
air needs to be drained, the chest tube will be removed.

Lung oedema

Cardiogenic pulmonary edema (CPE) is defined as pulmonary edema due to increased

capillary hydrostatic pressure secondary to elevated pulmonary venous pressure. CPE reflects the
accumulation of fluid with a low-protein content in the lung interstitium and alveoli as a result of
cardiac dysfunction.

Pulmonary edema can be caused by the following major pathophysiologic mechanisms:

 Imbalance of Starling forces - Ie, increased pulmonary capillary pressure, decreased
plasma oncotic pressure, increased negative interstitial pressure
Damage to the alveolar-capillary barrier
Lymphatic obstruction
Idiopathic (unknown) mechanism
Signs & symptoms:
Dyspnea
Orthopnea (inability to lie down flat due to breathlessness)
Paroxysmal nocturnal dyspnea (episodes of severe sudden breathlessness at night)
Coughing up blood (pink frothy sputum)
Excessive sweating
Anxiety
Pale skin
Peripheral pitting edema (due to left ventricular failure)
Raised JVP
Hepatomegaly
End-respiratory crackles and 3rd heart sound on auscultation

Etiology

CPE is caused by elevated pulmonary capillary hydrostatic pressure leading to transudation of

fluid into the pulmonary interstitium and alveoli. Increased LA pressure increases pulmonary
venous pressure and pressure in the lung microvasculature, resulting in pulmonary edema.

The progression of fluid accumulation in CPE can be identified as 3 distinct physiologic

stages.
Stage 1
In stage 1, elevated LA pressure causes distention and opening of small pulmonary
vessels. At this stage, blood gas exchange does not deteriorate, or it may even be slightly
improved.
Stage 2
 In stage 2, fluid and colloid shift into the lung interstitium from the pulmonary
capillaries, but an initial increase in lymphatic outflow efficiently removes the fluid. The
continuing filtration of liquid and solutes may overpower the drainage capacity of the
lymphatics. In this case, the fluid initially collects in the relatively compliant interstitial
compartment, which is generally the perivascular tissue of the large vessels, especially in
the dependent zones.
The accumulation of liquid in the interstitium may compromise the small airways,
leading to mild hypoxemia. Hypoxemia at this stage is rarely of sufficient magnitude to
stimulate tachypnea. Tachypnea at this stage is mainly the result of the stimulation of
juxtapulmonary capillary (J-type) receptors, which are nonmyelinated nerve endings
located near the alveoli. J-type receptors are involved in reflexes modulating respiration
and heart rates.
Stage 3
In stage 3, as fluid filtration continues to increase and the filling of loose interstitial space
occurs, fluid accumulates in the relatively noncompliant interstitial space. The interstitial
space can contain up to 500mL of fluid. With further accumulations, the fluid crosses the
alveolar epithelium in to the alveoli, leading to alveolar flooding. At this stage,
abnormalities in gas exchange are noticeable, vital capacity and other respiratory volumes
are substantially reduced, and hypoxemia becomes more severe.

The initial management of pulmonary edema, irrespective of the type or cause, is supporting
vital functions. Therefore, if the level of consciousness is decreased it may be required to proceed
to proceed to tracheal intubation and mechanical ventilation to prevent airway compromise.
Hypoxia (low O2 level) may require supplementary O2.

Acute cardiogenic pulmonary edema often responds rapidly to medical treatment. Positioning
upright may relieve symptoms. Loop diuretics such as furosemide or bumetanide are
administered, often together with morphine or diamorphine to reduce respiratory distress. Both
diuretics and morphine may have vasodilator effects, but specific vasodilators may be used
(particularly intravenous glyceryl trinitrate or ISDN) provided the blood pressure is adequate.