1. 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.

2. During exercise  oxygen consumption is increased by skeletal muscle.
Oxygen is present:
In combination with Hb
In myoglobin &
In dissolved form

3. Oxygen used in severe exercise:
0.3 L
O2 combined with Myoglobin
1 L
O2 combined with Hemoglobin
0.5 L
O2 in
alveolar air
0.25 L
dissolved form
TOTAL OXYGEN = 2 L (approx.)
TOTAL OXYGEN = 2 L (approx.)
This much oxygen must be repaid.

4. Debts: To restore phosphagen & glycogen system: 2 L is required.
To restore Aerobic system: 8 L is required.
So, a total of 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 = L.

5. 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

6. CHRONIC PULMONARY EMPHYSEMA
Airway obstruction disease
Extensive alveolar destruction
Etiological factor : Long term smoking
Pathological changes in the lungs:
Chronic infection due to irritant smoke
Stimulation of excess mucus
(partial paralysis of the cilia of the respiratory epithelium by the nicotine effects
Inhibition of alveolar macrophages
Less control of infection
mucus retention

7. Infection+ Inflammation Chronic obstruction of airways Of bronchioles
Difficult expiration
Entrapment of air in alveoli and overstretching
Lung infection
50-80 % of alveolar wall destruction

9. Physiological abnormalities of emphysema
Increased air way resistance leads to increased work of breathing
Loss of alveolar walls leads to decreased diffusing capacity
Hypoxia, hypercapnia death
Right heart failure.
Abnormal ventilation perfusion ratio in same lung
Physiological dead space(
Va/Q)

10. Loss of alveolar wall No. of pulm. capill Pulm. Vasular resistance
Pulmonary hypertension
Right heart failure

11. 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

13. Specific Ag + IgE Allergic reactions Histamine
On mast cells
(Pollen ,he is sensitive which is inhaled.)
Histamine
Slow reacting substance of Anaphylaxis(mixture of leucotrienes)
Bradykinin
Eosinophilic
Chemotactic factor
Increased airway resistance
Edema+mucus
Smooth muscle spasm
In expiration due to external pressure

14. Clinical results Expiration volume Dyspnea/air hunger
Maximum expiration rate
Expiration volume
Acute asthmatic attack
Functional residual capacity
Difficulty in expiring
Residual volume
Permanent enlargement of chest over years
Barrel chest

15. Atelectasis Causes: airway obstruction with mucus and solid object
Lack of surfactant in fluids lining the alveoli
Effects:
Lung collapse lead to compression of veins
increase blood flow resistance
Additional vasoconstriction due to hypoxia in collapsed alveoli

16. 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

17. 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.

18. Tuberclosis A constrictive lung disease Etiology:
tubercle bacilli lead to tissue reaction in lungs lead to
Pathology:
Macrophage invasion
Walling off of lesion by fibrous tissue leading to tubercle formation
If untreated in 3% walling off fails
Massive destruction of lung tissue
Large abcess cavities
Late stages= increase fibrous tissue and decrease function of lung tissue.

19. Physiologic abnormalities of tuberculosis:
Increase work of breathing by respiratory membrane
Decrease respiratory membrane surface area
Increase thickness of respiratory membrane
Decrease vital capacity
Decrease breathing capacity
Decrease pulmonary diffusion capacity
Abnormal ventilation perfusion ratio

20. pneumonia It is an infection of pulmonary parenchyma.
It may involve primarily the interstium or alveoli
Caused by viruses,fungi,and parasites.

21. Pneumonia Involvement of entire lobe is called LOBAR PNEUMONIA
Involvement of alveoli contiguous to bronchi is called BRONCHOPNEUMONIA

22. 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