respiratory distress syndrome (RDS)

respiratory distress syndrome (RDS)• During intrauterine life surfactant formation begins at 30th 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. Coughing2. Sneezing3. Hiccup4. 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

• 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,

ByDr. 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?

O2 consumption in moderate & severe exercise:

• In healthy athlete alveolar vent. is directly proportional to oxygen metabolism.

• The arterial PO2, PCO2 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 PO2, PCO2 & H+ is minimum to stimulate respiration in exercise because there is increased ventilation so PO2 & PCO2 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 30-40 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 / min2) 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 1.5-2 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 PCO2

• There is initial decrease in arterial PCO2 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 PCO2 remain normal (40 mm Hg) at rest & during heavy exercise.

• If PCO2 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 PCO2

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.