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

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 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 mucus retention

• Inhibition of alveolar macrophages Less control of infection

• Infection+ Inflammation Of bronchioles

Chronic obstruction of airways

•Obstruction of airways Difficult expiration

Entrapment of air in alveoli and overstretching

50-80 % of alveolar wall destruction

Lung infection

Physiological abnormalities of emphysema1. Increased air way resistance leads to

increased work of breathing2. Loss of alveolar walls leads to decreased

diffusing capacity3. Hypoxia, hypercapnia death4. Right heart failure.5. Abnormal ventilation perfusion ratio in same

lungPhysiological 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 Bradykinin

EosinophilicChemotactic factor

Slow reacting substance of Anaphylaxis(mixture of leucotrienes)

Edema+mucus

Smooth muscle spasm

(Pollen ,he is sensitive which is inhaled.)

On mast cells

Increased airway resistance

In expiration due to external pressure

• Clinical resultsMaximum expiration rate

Expiration volume

Dyspnea/air hunger

Acute asthmatic attack

Functional residual capacity

Residual volume

Difficulty in expiring

Permanent enlargement of chest over years

Barrel chest

AtelectasisCauses:1) airway obstruction with mucus

and solid object2) Lack of surfactant in fluids

lining the alveoliEffects: 3) Lung collapse lead to

compression of veins 4) increase blood flow resistance 5) 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 toPathology: 1) Macrophage invasion2) 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 cavities6) Late stages= increase fibrous

tissue and decrease function of lung tissue.

Physiologic abnormalities of tuberculosis:1. Increase work of breathing by respiratory

membrane2. Decrease respiratory membrane surface area 3. Increase thickness of respiratory membrane 4. Decrease vital capacity5. Decrease breathing capacity6. Decrease pulmonary diffusion capacity7. 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