Oxygen Debt:
Definition:
Extra amount of oxygen, that must be supplied
to body after exercise, in order to restore
metabolic system back to pre-exercise state.
• During exercise  oxygen consumption is
increased by skeletal muscle.
Oxygen is present:
• In combination with Hb
• In myoglobin &
• In dissolved form
Oxygen used in severe exercise:
0.3 L
O2 combined with
Myoglobin
1L
O2 combined with
Hemoglobin
0.5 L
O2 in
alveolar air
0.25 L
O2 in
dissolved form
TOTAL OXYGEN = 2 L (approx.)
This much oxygen must be repaid.
Debts:
• To restore phosphagen & glycogen system: 2 L is
required.
• To restore Aerobic system: 8 L is required.
• So, a total of 10-12 L oxygen is used in exercise & is
paid in 90 min after exercise  respiratory rate
remain increased for 90 min after exercise to repay
oxygen debt = 10-12 L.
Chronic Obstructive Pulmonary Disease (COPD)
• Chronic pulmonary emphysema
– It is one of the obstructive respiratory diseases in
which lung tissue is extensively damaged.
– This literally means that air is trapped in the lungs.
• Chronic bronchitis
– excessive mucus production
• Asthma
– bronchiole constriction
CHRONIC PULMONARY EMPHYSEMA
•Airway obstruction disease
Etiological factor : Long term smoking
Extensive alveolar
destruction
Pathological changes in the lungs:
•Chronic infection due to irritant smoke
•Stimulation of excess mucus
• Inhibition of alveolar macrophages
Less control of infection
•(partial paralysis of the cilia of the respiratory epithelium by the nicotine
mucus retention
effects
• Infection+ Inflammation
Of bronchioles
•Obstruction of airways
Chronic obstruction of airways
Difficult expiration
Entrapment of air in alveoli
and overstretching
Lung infection
50-80 % of alveolar wall
destruction
Physiological abnormalities of emphysema
1. Increased air way resistance leads to increased
work of breathing
2. Loss of alveolar walls leads to decreased
diffusing capacity
3. Hypoxia, hypercapnia
death
4. Right heart failure.
5. Abnormal ventilation perfusion ratio in same
lung
Physiological dead space(
Va/Q)
• Loss of alveolar wall
No. of pulm. capill
Pulm. Vasular
resistance
Pulmonary
hypertension
Right heart failure
ASTHMA
• Severe airway obstruction
due to spastic contraction
of the smooth muscle in the
bronchioles which leads to
the difficulty in breathing.
• Etiology
• hypersensitivity of the
bronchioles in response to
the foreign substances in
air.
• Allergic hypersensitivity
(plant pollens)- YOUNG
• Non –allergic irritants -OLD
• Specific Ag + IgE
On mast cells
(Pollen ,he is
sensitive which is
inhaled.)
Increased airway
resistance
In expiration
due to external
pressure
Allergic reactions
Histamine
Edema+
mucus
Smooth
muscle
spasm
Bradykinin
Eosinophilic
Chemotactic factor
Slow
reacting
substanc
e of
Anaphyl
axis(mixt
ure of
leucotrie
nes)
• Clinical results
Maximum expiration rate
Dyspnea/air hunger
Expiration volume
Acute asthmatic attack
Functional residual capacity
Difficulty in expiring
Residual volume
Barrel chest
Permanent enlargement of chest over
years
Atelectasis
Causes:
1)
airway obstruction with mucus
and solid object
2)
Lack of surfactant in fluids
lining the alveoli
Effects:
1)
Lung collapse lead to
compression of veins
2)
increase blood flow resistance
3)
Additional vasoconstriction
due to hypoxia in collapsed
alveoli
Atelectasis
• Vasoconstriction lead to
decrease blood flow
through Atelectasis lung:
– 1)blood5/6 passes to
aerated lung
– 2)Blood 1/6 passes to
unaerated lung
– V/Q ratio is moderately
compromised
– only mild oxygen
desaturation in aortic
blood despite total loss of
ventilation in an entire
lung
Lack of surfactant as a cause of lung
collapse
• Special alveolar epithelial cells secrete surfactant leads to fluid that coat
inside surface of alveoli lead to 2-10 times decrease surface tension in
alveoli which prevents alveolar collapse
• In case of RDS in newborn premature babies, alveoli lead to decrease
surfactant result in increase surface tension lead to lung collapse patient
may die due to suffocation with Atelectasis.
Tuberclosis
•
A constrictive lung disease
Etiology:
tubercle bacilli lead to tissue
reaction in lungs lead to
Pathology:
1) Macrophage invasion
2) Walling off of lesion by fibrous
tissue leading to tubercle
formation
3) If untreated in 3% walling off
fails
4) Massive destruction of lung
tissue
5) Large abcess cavities
6) Late stages= increase fibrous
tissue and decrease function of
lung tissue.
Physiologic abnormalities of tuberculosis:
1. Increase work of breathing by respiratory
membrane
2. Decrease respiratory membrane surface area
3. Increase thickness of respiratory membrane
4. Decrease vital capacity
5. Decrease breathing capacity
6. Decrease pulmonary diffusion capacity
7. Abnormal ventilation perfusion ratio
pneumonia
• It is an infection of
pulmonary parenchyma.
• It may involve primarily the
interstium or alveoli
• Caused by viruses,fungi,and
parasites.
Pneumonia
• Involvement of entire
lobe is called LOBAR
PNEUMONIA
• Involvement of alveoli
contiguous to bronchi is
called
BRONCHOPNEUMONIA
pneumonia
• Abnormalities of function
(Pathology):
– Consolidation of lung occurs
i.e, alveoli are filled with
blood cells and fluids
– Pulmonary membrane
becomes inflamed and
porous so leaking occurs.
– Decrease total surface area
of respiratory membrane
– Decrease V/Q ratio which
results in hypoxemia and
hypercapnia