Download 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. 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.
• 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.
COUGH REFLEX:
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, underventilated 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?
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 / 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 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
1L
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.