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 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.

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 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

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

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)

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 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

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

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

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: 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.

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

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