respiratory distress syndrome (RDS) During intrauterine life surfactant formation begins at 30 th week and it can be detected in amniotic fluid. Pre-mature infants do not produce enough surfactant the pressure of -20 to -30 mm of Hg will be required to keep the lungs expanded Amnicentisis can be performed and in that fluid we can estimate the surfactant concentration. Surfactant secretion is stimulated by: – glucoorticoids, – epinephrine, – thyroxine Deficiency occurs in: – premature babies, – babies of hypothyroid, – diabetic mothers. – Smoking decreases surfactant.

Protective Reflexes: Non respiratory air movement into respiratory tract: 1.Coughing 2.Sneezing 3.Hiccup 4.Yawning

There are nerve endings in the epithelium of airways called irritant receptors. These respond to irritants & they may be mechanical as mucus / foreign particle in airways. It may be chemical,e.g., histamine, bradykinin.

COUGH REFLEX: Stimuli: Light touch, very slight amount of foreign matter, or chemical irritants (sulphur dioxide gas, chlorine gas). Cough receptors: on epiglottis, larynx, trachea, bronchi, tonsils. Afferents: vagus nerve Respiratory centre: Neuronal circuits of medulla Events: inspiration followed by forceful expiration. During coughing posterior nares are closed Purpose: to dislodge the irritants from airways.

Sequence of events in cough reflex: 1)Up to 2.5 liters of air are rapidly inspired. 2) Epiglottis closes. 3) Vocal cords shut tightly to entrap the air within the lungs. 4)Abdominal muscles and internal intercostals contract for forceful expiration. 6) Rise in pressure in the lungs to 100 mm Hg or more. 7) The vocal cords & epiglottis suddenly open widely. 8) Air explodes outward (may be at 75 to 100 miles /hr) under this high pressure in the lungs. 9) Rapidly moving air carries with it any foreign matter present in bronchi or trachea.

SNEEZE reflex

Applies to nasal passages Stimulus: irritation in nasal passages/ upper respiratory tract. Afferents: trigeminal nerve Centre: Medulla posterior nares are open. Uvula depressed, air passes through the nose as COUGH reflex Applies to lower respiratory passages. Stimulus: irritation in lower respiratory passages. Afferents: vagus nerve Centre: Medulla Posterior nares: remain closed.

HICCUP: Definition: Abrupt short inspiration due to brief contraction of diaphragm. Glottis becomes closed. There is characteristic sensation & sound. Stimulus: stimulation of nerve endings in GIT & abdominal cavity.

YAWNING: Definition: Deep inspiration followed by expiration. Mouth remains open during yawning. Mechanism: When alveoli become under-ventilated, pO2 falls  yawning Purpose: – By yawning, under- ventilated alveoli become ventilated & collapse of alveoli is prevented. – Yawning also increases venous return.

Respiratory Changes During Exercise, Oxygen Debt, By Dr. Mudassar Ali Roomi

2 main respiratory changes in exercise: 1) increase in pulmonary ventilation 2) increase in both rate & depth of respiration.

Regulation of Respiration during exercise: What causes intense ventilation during exercise?

O 2 consumption in moderate & severe exercise: In healthy athlete  alveolar vent. is directly proportional to oxygen metabolism. The arterial P O2, P CO2 and pH remain almost normal. Conclusion: Hypoxia, hypercapnia & acidosis have no role in inducing hyperventilation during exercise!!

4 main factors that increase rate of respiration during exercise: 1.Anticipatory increase in rate of ventilation: When a person intends to perform exercise impulses from cerebral cortex  skeletal muscle  to initiate contraction & simultaneously collateral impulses  respiratory centre  increase ventilation.

2. Impulses from proprioceptors: (receptors for position & movement present around joints, in the muscles, tendons and joint ligaments). This is the major stimulus for respiratory centre during exercise.

3. Increase in temperature: During exercise  metabolism increases  body temperature increases  stimulates respiration directly & indirectly.

4. Chemical factors: – Decrease in PO2 – Increase in PCO2 – Increase in H+ conc. The effect of P O2, P CO2 & H + is minimum to stimulate respiration in exercise because there is increased ventilation  so P O2 & P CO2 remain in normal limits.

Metabolic systems during exercise: 3 types: 1)Phosphagen system: consist of ATP & Creatine phosphate in muscle (ATP can maintain muscle contraction for 5-6 sec; energy from creatine phosphate can sustain contraction for another 10 sec)

2) Glycogen-Lactic Acid System: (another sec) Glucose stored as glycogen in the muscle undergoes glycolysis  ATP.

3) Aerobic System: (For long long time) Nutrients, Glucose, Amino Acids Fatty Acids are oxidized. It is the ultimate source of energy.

Changes in Respiration during Exercise: 1) Normal respiratory minute volume (RMV) at rest = 500 x 12 = 6 L / min – in severe exercise: RMV = up to 100 – 110 L / min 2) Maximum Breathing Capacity (MBC): Up to 150 – 170 L / min

3) Oxygen Consumption (O.C): It is the percentage of arterial blood which gives its O2 while passing through the tissues. – 250 ml / min (at rest) – may increase to 4-5 L / min in exercise 4) Utilization Co-efficient (U.C): 25% (at rest) 75 – 85 % in severe exercise

5) Diffusion Capacity for O2: – At rest: 20 – 30 ml / mm Hg / min – in exercise: 65 ml / mm Hg / min 6) Chemical parameters in skeletal muscles: – PO2 decreases, – PCO2, H+, Temp increases  Right hand shift of oxy-Hb dissociation curve  easy dissociation of O2 to supply skeletal muscle.

7) Effect on Respiratory Quotient (RQ): – In moderate exercise: RQ remains about 1. – In severe exercise: May increase up to due to extra CO2 formation – After severe exercise: RQ falls up to 0.5.

Interrelation between chemical & nervous factors in control of respiration during exercise: At the onset of exercise  alveolar vent. increases instantaneously, without an initial increase in arterial P CO2 There is initial decrease in arterial P CO2 due to great increase in alv. Vent. Conclusion: brain  anticipatory stim. of resp. at the onset of exercise.

Neuro-genic drive from respiratory centre during heavy exercise Arterial P CO2 remain normal (40 mm Hg) at rest & during heavy exercise. If P CO2 does change from 40, there is stim. of vent. above 40 & depression of vent. below 40. This shift in exercise is partly a learned response that involves cerebral cortex. Conclusion: Neurogenic factor shifts the curve about 20- fold in upward direction so that vent. Matches the rate of CO2 release keeping normal level of Arterial P CO2

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 O 2 combined with Myoglobin 1 L O 2 combined with Hemoglobin 0.5 L O 2 in alveolar air 0.25 L O 2 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 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.