Dr.

Kamrans PBL
Significance of Topic Zindagi Dhoan Dhoan
As the Subject lives his/her Life in Smoke.
As the Smoke is of temporary existence, so the subjects life
would get shorted due to Smoking.
Relation of Flu with Emphysema
If the Subject have emphysema or chronic bronchitis, She/he
needs to be extra vigilant in preventing flu. As in emphysema
or chronic bronchitis it's difficult to breathe under normal
circumstances. This serious infection occurs because of the
airway obstruction and inability to cough out infected mucus.
Pack Year
The pack-year is a unit for measuring the amount a person
has smoked over a long period of time. It is calculated by
multiplying the number of packs of cigarettes smoked per day
by the number of years the person has smoked. For example,
1 pack-year is equal to smoking 20 cigarettes (1 pack) per day
for 1 year, or 40 cigarettes per day for half a year, and so on.
One pack-year is the equivalent of 365.24 packs of cigarettes
or 7,305 cigarettes.
For example: a person who has smoked 15 cigarettes a day
for 40 years has a (15/20) x 40 = 30 pack-year smoking
history.

Respiratory Acidosis
Respiratory acidosis, also called respiratory failure or ventilatory
failure, is a condition that occurs when the lungs cant remove

enough of the carbon dioxide (CO2) produced by the body.

Excess CO2 causes the pH of blood and other bodily fluids to
decrease, making them too acidic. This is because the body
must balance the ions that control pH. Respiratory acidosis is
typically caused by an underlying disease or condition.
Normally, the lungs take in oxygen and exhale CO2. Oxygen
passes from the lungs into the blood. CO2 passes from the
blood into the lungs. However, sometimes the lungs cant
remove enough CO2. This may be due to a decrease in
respiratory rate or decrease in air movement due to an
underlying condition such as Emphysema asthma, COPD,
pneumonia, or sleep apnea. This may cause respiratory
acidosis.
How does the renal system or Buffer System compensate for
conditions of respiratory acidosis?

Buffers help resist a decrease in pH, and

the kidneys help compensate for failure of the lungs to
prevent respiratory acidosis by increasing the rate at which they
secrete hydrogen ions into the filtrate and reabsorb bicarbonate
ions.
Blood Gas Measurement
Blood gas is a series of tests used to measure oxygen and
CO2 in the blood. A healthcare provider will take a sample of
blood from your artery. High levels of CO2 can indicate acidosis.
What is a barrel chest?

Some people who have chronic obstructive pulmonary

disease such as emphysema develop a slight barrel
chest in the later stages of the disease. It occurs because the
lungs are chronically overinflated with air, so the rib cage
stays partially expanded all the time.

 Signs of Emphysema
Symptoms of emphysema describe what a person with emphysema
feels. Signs of emphysema are what doctors look for to help
identify emphysema and its severity. Signs of emphysema
include:
Barrel chest: People with emphysema may have a rib cage that's
larger than normal, especially from front to back. This results from the
lung expansion in emphysema.

Clubbing: The tips of the fingers may become rounded, because

of low blood oxygen levels in advanced emphysema.

Pursed-lip breathing: To make breathing easier in severe

emphysema, people may breathe rapidly through pursed lips.

Polycythemia: The body produces an excessive amount of

hemoglobin and red blood cells, thus High PCV; which carry oxygen
in the blood.
Hypoxemia (hypoxia): Low oxygen levels in the blood, detected on
pulse oximetry or arterial blood gas testing.
The inspired air has reduced oxygen content (e.g., at high altitude or
due to other causes).
2) Insufficient gas exchange is caused by alveolar hypoventilation (or
breathing too little) with chest breathing. It can happen, for example,
during sleep or during physical exercise for people with lung diseases.
3) Some parts of the lungs are obstructed, or damaged, or have
insufficient ventilation (e.g., as for emphysema, COPD and other
conditions).
4) Blood shunting causes the arterial and venous blood to mix and
this causes reduced oxygenation of the arterial blood.

Hypercarbia: High levels of carbon dioxide in the blood. This

results from an inability to exhale carbon dioxide properly in
emphysema.

Cyanosis: Blue-tinged lips, from low blood oxygen in severe

emphysema. Ventilation/perfusion mismatch resulting from
progressive airflow limitation and emphysema is the key driver of this
hypoxia, which may be exacerbated by sleep and exercise.

Malnutrition: Muscles slowly waste away in advanced

emphysema.

X-Ray Findings in Emphysema

Lungs are large and hyper inflated.
Bullae and avascularity in the peripheral third of lung are findings
in emphysema.
Signs of hyperinflation are:
Low set diaphragm
Flat diaphragm best determined by lateral chest
Hyper lucent lung fields
Increased AP diameter
Increased retrosternal air
Vertical heart
We can call it emphysema only when hyperinflation is associated
with blebs and paucity of vascular markings in the outer third of
the film.

Findings of hyperinflation are:

Dark lung fields.
Low set diaphragm in 11th or 12th posterior rib.
Heart is vertical and narrow. This is the result of downward push
of diaphragm by lungs.
Flattened diaphragms in lateral chest.

 Infra cardiac air: Left diaphragm is seen in its entirety.

Retrosternal air is increased.
Increased AP diameter.
Lateral chest is best to evaluate flattening of diaphragm, AP diameter
and retrosternal air.
This lateral chest shows:
Increased AP diameter
Low set flat diaphragms
Hyper lucent lung fields
Increased retrosternal air encroaching on heart density
Multiple blebs: Avascular zones surrounded by thin wall.

MUSCLES OF RESPIRATION

Respiration involves Inspiration and Expiration which are

accompanied by the alternate increase and decrease of the volume of
thoracic cavity.
Inspiration is an active process and is achieved by increase in all
diameters of thoracic cavity. (Thoracic cavity has three diameters
vertical, transverse and anteroposterior.)
The muscles involved in inspiration are:
Diaphragm:
Diaphragm is the primary muscle of inspiration.It increases all
the three diameters of thorax.
When the diaphragm contracts in inspiration, initially the lower
ribs are fixed and the dome of the diaphragm descends, thus
increasing the vertical diameter of thorax.
Intercostal muscles:
With the first ribs fixed by neck muscles (scalene muscles and
sternocleidomastoid
muscle), the intercostals muscles
(especially external intercostal muscles and interchondral part of
internal intercostal muscles of opposite side), elevate the 2nd to
12th ribs and thus act as inspiratory muscles.
If, on the other hand, 12th rib is fixed by quadratus lumborum
and oblique muscles of anterior abdominal wall, the intercostal
muscles (especially internal intercostal) lower the 1st to 11th

ribs, as in expiration. However, quiet expiration is a passive

process achieved by the elastic recoil of the lungs, the relaxation
of intercostal muscles and diaphragm and an increased in tone
of anterior abdominal wall muscles, which forces the relaxing
diaphragm upward.
They are three types: External intercostal muscles, internal
intercostal muscles and innermost intercostal muscles.
How elevation of rib increases the thoracic diameter?
The ribs are attached to vertebra behind. From there, they move
forward and downward and attach to sternum in front. The ribs
are thus directed forward and downward obliquely. So the
elevation of ribs at their sternal ends (primarily 2nd through 6th)
results in forward thrust of sternum, thus increasing the
anteroposterior diameter of thorax (Pump handle movement).
On the other hand, elevation of these obliquely placed ribs also
raises their middle part or lateral most part (is an active process
in the 7th to 10th ribs), thus increasing the transverse diameter
(bucket handle movement).
When patients with respiratory problems struggle to breath, they
use their accessory respiratory muscles to assist the expansion
of thoracic cavities. They lean on a table or put their hands on
the knees to fix their scapulae and clavicles, so these muscles
are able to act on their rib attachments and expand the thorax.
Accessory muscles involved in forced inspiration are
Pectoralis major and minor, Serratus anterior, Scalene group of
muscles and sternocleidomastoid
By elevation of first and second ribs by scalene muscles which is
otherwise fixed in quiet respiration, by elevation of clavicle by
sternocleidomastoid and other muscles also elevate the ribs,
thus help expanding the thoracic cavity and ultimately in
inspiration.
Accessory muscles involved in forced expiration are
Muscles of anterior abdominal wall, quadratus lumborum,
latissimus dorsi and serratus posterior inferior
Flat muscles of anterior abdominal wall compress the lower part
of thorax and increased the intra-abdominal pressure whereas
quadratus lumborum fixes the 12th rib Latissimus dorsi and

serratus posterior inferior help in forced expiration by depressing

the ribs.
Oxygen Therapy in COPD
Oxygen is usually prescribed to raise the PaO2 to between 60 and 65
mm Hg or the saturations from 90% to 92%. Higher flow rates usually
do not help, and they can even be dangerous. In most cases, oxygen
(O2) is delivered through a small tube (called a nasal cannula) from an
oxygen tank to the patient's nose. Some patients require extra oxygen
while walking, exercising, or sleeping, and others require it
continuously. Portable oxygen units also are available. It is important
to follow instructions carefully when using supplemental oxygen.
Ideally, the patient should receive enough oxygen to keep the oxygen
level at 65 mm HG, but no less than 60 mm HG, or at an oxygen
saturation level of at least 90%. Additional oxygen flow may be
needed during sleep or exertion (physical activity).
Short-burst oxygen therapy,
Short-burst oxygen therapy (SBOT) is typically given to patients
for the relief of breathlessness not relieved by any other
treatments.
It is used intermittently at home for short periods - for example,
10-20 minutes at a time.

Assess the need for oxygen therapy in people with any of the
following:
Very severe airflow obstruction - forced expiratory volume in one
second (FEV1) less than 30% predicted.
Cyanosis.
Polycythaemia.
Peripheral oedema.
Raised jugular venous pressure.
Oxygen saturation 92% or below when breathing air.

Medications to Treat Emphysema Symptoms

There are a number of different types of medications that can be
used to treat emphysema. Some types are inhaled (e.g., through
an inhaler or a nebulizer), and others are taken orally (e.g., in pill
form).

 Inhalers and nebulizers deliver medication directly into the lungs,

which can result in fewer side effects; however, if these devices
are used incorrectly, the medication may be ineffective. A spacer
device is a tube that can be used with an inhaler to help patients
take the medication correctly.
Bronchodilators (e.g.,
anticholinergics,
beta
agonists,
theophylline) can be used to treat acute exacerbations
(called short-acting medications) or to prevent symptoms from
worsening (called long-acting medications). Antibiotics (e.g.,
penicillin) often are used to treat infections that cause acute
exacerbations and anti-inflammatory drugs (e.g., steroids
[prednisone]) can be used to reduce lung inflammation.
Short-acting bronchodilators include albuterol (Ventolin,
Proventil), pirbuterol (Maxair), terbutaline (Brethine), and
metaproterenol (Alupent). Long-acting medicines include
sustained-release albuterol, salmeterol (Serevent), ipratropium
bromide (Combivent), and theophylline (Bronkodyl, Theolair).
Long-acting medications should not be used to treat acute
symptoms because they take longer to work and symptoms may
continue to worsen in the meantime.
Patients who have familial emphysema (alpha-1 antitrypsin
deficiency emphysema) may be treated with an alpha-1 protease
inhibitor (e.g., Aralast, Prolastin), which usually is administered
intravenously (i.e., through a vein).
Forced vital capacity (FVC)
Forced vital capacity (FVC) is the volume of air that can forcibly be
blown out after full inspiration,measured in liters. FVC is the most
basic maneuver in spirometry tests.
Forced expiratory volume in 1 second (FEV1)
FEV1 is the volume of air that can forcibly be blown out in one
second, after full inspiration.[9] Average values for FEV1 in healthy
people depend mainly on sex and age, according to the diagram at
left. Values of between 80% and 120% of the average value are
considered normal.[10] Predicted normal values for FEV1 depend on
age, sex, height, mass and ethnicity as well as the research study that
they are based on.

 FEV1/FVC ratio (FEV1%)

FEV1/FVC (FEV1%) is the ratio of FEV1 to FVC. In healthy adults this
should be approximately 7085% (declining with age).[11] In
obstructive diseases (asthma, COPD, chronic bronchitis, emphysema)
FEV1 is diminished because of increased airway resistance to
expiratory flow; the FVC may be decreased as well, due to the
premature closure of airway in expiration, just not in the same
proportion as FEV1 (for instance, both FEV1 and FVC are reduced,
but the former is more affected because of the increased airway
resistance). This generates a reduced value (<80%, often ~45%). In
restrictive diseases (such as pulmonary fibrosis) the FEV1 and FVC
are both reduced proportionally and the value may be normal or even
increased as a result of decreased lung compliance.
The severity of the obstructive defect. To do this, look at the FEV1

percent predicted:
I.
II.
III.
IV.

80% = minimal obstructive defect

65 - 80% = mild obstructive defect
50 - 65% = moderate obstructive defect
< 50% = severe obstructive defect

Diffusing capacity (DLCO)

This test measures how the lung surface works and how well the
oxygen you breathe in goes through to the blood. It involves breathing
in a specific mixture of gases. The gases used are all found in normal
room air.
They include Methane and Carbon monoxide but in very, very small
concentrations. Although carbon monoxide is a dangerous gas in
large quantities, the amounts used for this test are very small and
used in controlled conditions so you are safe. Carbon monoxide, is
the same size and shape as oxygen and attaches to red blood cells
faster than oxygen. So carbon monoxide can indirectly measuring how
well oxygen goes through the lung surface

Diffusing capacity (or DLCO) is the carbon monoxide uptake from a

single inspiration in a standard time (usually 10 seconds). Since air
consists of very minute or trace of CO, 10 seconds is considered to be
the standard time for inhalation,then rapidly blow it out (exhale). The
exhaled gas is tested to determine how much of the tracer gas was
absorbed during the breath.
The patient breathe in a nonreactive gas, such as carbon monoxide
(CO), which binds to hemoglobin. In order to reach the hemoglogin,
the CO must diffuse across the alveolar-blood barrier. If there is
thickening of the aleovli or interstitium, the diffusion will be impaired,
resulting in a decreased DLCO.

Histopathology
Emphysema
In the emphysemateous lung, air spaces become enlarged due to
increased compliance and destruction of the alveolar walls.
Proteolysis of connective tissue components, including elastic fibers,
within the alveolar walls increases the compliance of the walls.
Neutrophils secrete a variety proteases that digest connective tissue
fibers and their increased numbers and activity in alveoli are thought
to trigger destruction of the alveolar walls.
Emphysema (40X2.0)

Destruction of tissue leaves little surface

capillaries, and large air spaces. Large
vessel at lower right.
,

Normal lung (40X2.0)

Much normal tissue creates large surface

area with many capillaries, many small air
Spaces. Large vessel at extreme left. Large
airway at extreme right.

Emphysema (100X2.0)

Normal lung (100X2.0)

Destruction of tissue leaves little surface Much normal tissue creates large surface
few capillaries, and large air spaces.
area with many capillaries, filled with RBCs.

Pathology
There is gross destruction of the air sacs or the alveoli in emphysema.
There is persistent over-inflation that leads to damage to the elasticity
of the lungs.
The lungs are like a balloon. In emphysema the lungs are overinflated so that they lose their elasticity and elastic recoil. There are
balloon-like bullae or blisters in the lung tissues. Because carbon
dioxide is trapped in the bullae, the body is deprived of fresh air
flowing into the lungs.
The lungs begin to cope with this lack of fresh air by taking deeper
breaths. This further expands the lung tissues and makes it lose its
elasticity. With loss of elasticity more carbon dioxide accumulates in
the lungs leaving less space for fresh air and this leads to shortness of
breath.
With time the muscles and ribs begin to expand to contain the
expanded lungs. The diaphragm that lies beneath the lungs and is
normally dome shaped also flattens and lose their functional capacity.
Causes of emphysema and its relation with pathology
One of the most important causes of emphysema is cigarette
smoking. Other causes include air pollutants, inhalation of chemicals,
fumes, dust etc.
Cigarette smoke changes the structure and function of the lungs by
causing irritation and inflammation of the narrow airways. This leads

release of enzymes in the lungs that destroy lung tissues and an

increased size in the air sacs eventually leading to emphysema. The
destroyed lung tissues form bullae (holes) and lose elasticity.
Alpha-1 antitrypsin deficiency is a rare genetic condition where there
are decreased levels of the protective protein, alpha-1 antitrypsin.
Alpha-1 antitrypsin protects the lungs from the destructive effects of
enzymes. Patients who lack this enzyme thus have lungs that are
damaged by enzymes called elastases at an early age.
Apart from chronic inflammation caused by irritation there is also a
theory of increased oxidative stress that can contribute to increased
destruction and/or impaired lung maintenance and repair in
emphysema.
The major consequence of the oxidative stress is thought to be the
activation of the transcription factor nuclear factor-kB. This in turn
activates proinflammatory cytokine transcription that causes
destruction of the lungs. Cigarette smoking also inhibits histone
deacetylase. This also promotes the release of proinflammatory
cytokines.
A theory goes that there is an imbalance between proteases (protein
break down enzymes) and antiproteases in emphysema. A delicate
balance between protease and antiprotease activity is required for
proper lung maintenance. When this balance changes there is
increased destruction and inappropriate repair of lungs leading to
emphysema.