Respiratory physiology

1. Respiratory physiology
Maqbool Qadir MD

2. Respiratory Physiology

3.  The Lung is for gas exchange
 It allows O2 to move from air into the blood, & CO2
to move out.
 O2 & CO2 move b/w air & blood by simple diffusion,
i.e, from an area of high to low partial pressure.
 Partial pressure= Conc x total pressure
 PO2 at sea level= 21/100 x 760= 159mmHg
 PO2 of inspired dry air =21/100 x 713(760-47)=149 mmHg

4. Respiratory physiology
 Fick’s law of diffusion: amount of gas that
moves across a sheet of tissue is proportional to
the area of the sheet but inversely proportional
to its thickness
 In adults there are 300 million alveoli , each 1/3
mm in diameter. total surface area is approx 85
square meters.
 In newborn at birth have only 150 million
alveoli, with a surface area of 3-5 square meter.

5. Airway
 From trachea to alveolar sac there are 27 generations.
 1-20, trachea-terminal bronchioles, conducting
airways with no gas exchange
Anatomic dead space= 150 ml in adults.*
 21-27 , respiratory bronchioles Alveolar sac,
respiratory zone or acinus ( vol in adults is 2.5- 3 Liters)
 Alveoli could first be counted & measured at 29 wks.
 Lung vol increase by 4 fold b/w 29 wk & term and
further doubled in 4 months after birth.
* ET tubes further increase the dead space

6. Airway development

7. Respiratory physiology

8. Ventilation
how gas gets to the alveoli
 The total vol of gas moving in & out of the
lungs with each breath is Tidal vol ( TV)
 Alveolar vol = TV – dead space vol
 Minute ventilation= amount of air leaving the
lungs in one min= TV x RR= 210 ml/kg/min in
adults ( in NB ~360 ml/kg/min )
 Alveolar ventilation= (TV-DSvol) x RR= 140
ml/kg/min ( 240 ml in NB)

9. Respiratory physiology
Lung volumes

10. Alveolar ventilation
 Intermittent
 During expiration, O2( alveoliblood), CO2 ( bloodalveoli)
 Arterial blood O2 & CO2 are in equilibrium with alveolar gas
 Tissue O2 consumption & CO2 production are continuous
 FRC provides a buffer ( 30 ml/kg body wt)
 During expiration, it continues to provide O2 to capillary blood
& act as a sump for CO2, hence arterial gas tension remains
relatively constant over the respiratory cycle.

11. Alveolar ventilation
 If alveolar ventilation is greater than O2
consumption & Co2 production----
Hyperventilation
 Reverse is hypoventilation---↓O2, ↑Co2
 Measurement of arterial CO2 tension
( PaCO2) can be used to estimate changes in
alveolar ventilation
 PAO2=FiO2 ( BMP- PH2O)- PaCO2/R

12. Alveolar ventilation
Ventilation PaCO2 R FiO2 BMP PAO2
Normal 40 0.8 0.21 760 100
Hypoventil
ation
80 0.8 0.21 760 50
Hyperventila
tion
20 0.8 0.21 760 125
Hypoventilat
ion + FiO2
↑
80 0.8 0.4 760 185

13. Diffusion
How gas gets across the blood –gas barrier
 Fick’s law= rate of transfer of a gas thru a sheet
of tissue is proportional to the tissue area &
differences in gas partial pressures b/w the two
sides, and inversely proportional to the tissue
thickness.
 CO2 diffuses 20 times more rapidly than O2

14. Diffussion

15. Blood Flow & Mtb
How the blood vessels remove gas from the lungs & alter some
compounds
 1 gm of Hgb carry 1.34 ml O2
 The binding of O2 to Hgb is usually expressed
as a % sat
 The % sat is a non-linear function of PaO2( oxy
Hgb dissociation curve)
 Begin to shift to Rt by 1 month
 By 4-6 months it is similar to adults

16. Oxy-Hgb dissociation curve

17. Oxy-Hgb dissociation curve
-Shift to left
 Alkalosis
 ↓ Temp
 ↓ 2-3 DPG conc
 ↑ fetal Hgb
Shift to Rt 
 Acidosis
 ↑Temp
 ↑ 2-3 DPG conc
 ↑ adult Hgb

18. O2 content of blood
 O2 bound to Hgb + dissolve Hgb
( 1.34 x Hgb x SaO2) + ( 0.003 x PaO2)

19. O2 content

20. O2 content

21. O2 delivery
 Arterial O2 content x cardiac output x 10

22. O2 Consumption
 Cardiac output x ( arterial O2 content- venous O2
content)
 If mixed venous O2 tension falls too low, O2 delivery
to mitochondria ↓, leads to ↓O2 consumption----cell
switches from aerobic to anaerobic Mtb
 Anaerobic Mtb generates 2 mol of ATP/mol glucose (
aerobic 38 mol ATP)
 Anaerobic Mtb also generates 2 mol of lactic acid /mol
of glucose

23. Hypoxia
1. Hypoventilation
2. Diffusion block
3. Ventilation –perfusion mismatch V/Q
4. Rt  left shunts

24. hypoventilation

25. Alveolar ventilation
Ventilation PaCO2 R FiO2 BMP PAO2
Normal 40 0.8 0.21 760 100
Hypoventil
ation
80 0.8 0.21 760 50
Hyperventila
tion
20 0.8 0.21 760 125
Hypoventilat
ion + FiO2
↑
80 0.8 0.4 760 185

26. V/Q mismatch
 V/Q >1: single hyperventilated lung unit,
↓ PCO2, ↑PO2
 V/Q <1: poorly ventilated lung, ↑PCO2, ↓
PO2
 The cause of hypoxemia in infants with V/Q
mismatch is perfusion of poorly ventilated but
open alveoli. The only way to ↑ the arterial PO2
in these infants is to ↑ the alveolar PO2

27. V/Q mismatch
underventilated lungs

28. Hyperoxia test

29. RtLt Shunts
mixing of venous blood with arterial blood
1. Through the lungs, past areas of atelectasis
2. Through persistent fetal circulatory pathways
( PFO, PDA) eg, PPHN
3. Congenital heart dis: TOF, TGA, Pul artery
stenosis etc.
* effects of increasing FiO2 on arterial PO2

30. RL Shunt

31. Rt  Lt Shunts
 In most clinical conditions, hypoxemia is a result
of a combination of V/Q mismatch & RL
shunts, when FiO2 equals 1.00, any contribution
to the venous admixture from open poorly-
ventilated alveoli disappears, and any remaining
hypoxemia must be the result of RL
shunts…..Hyperoxia test

32. RL shunts
 Shunt calc : Qp = Aorta sats – SVC sats
Qs Pul V sats - Pul Art sat
LR RL
< 1.5 = small 0.9-1.0=small
1.5-2.5= mod 0.7-0.9= mod
>2.5= large < 0.7= large

33. Alveolar- arterial gradient
A-a DO2
 Increase in both
1. ↑perfusion of poorly ventilated alveoli
2. ↑ blood flow thru the R->L shunts
* In Pt with a RL shunt, the A-aDO2
increases with increasing FiO2 & as such is a
poor estimate of lung disease severity

34. RL Shunt

35. Surfactant
 Laplace equation: P = 2 x T/R
P= pressure needed to resist collapse
T= surface tension
R= radius of alveolus
* Calculations suggest that if the alveoli were lined only with water, it would take
pressures exceeding 55 CM H2O to inflate the lungs.

37. Surfactant
 Prodused in type II alveolar epithelial cells
 Composed of phospholipids, fats, cholesterol &
protein
 The primary active molecule is saturated
dipalmitoyl phosphatidylcholine (DPPC)
lecithin.
 Lowers surface tension by adsorbing to the
surface & displacing water molecule.

38. Surfactant

39. Surfactant Proteins
SP-A
 Most abundant
 Water soluble
 228 amino acids
 Reacts with SP-B & Ca
to form tubular myelin
 Surfactant recycling
 Role in host defense in
lungs
SP-B
 Chromosome 2
 381 amino acid
 Formation of tubular
myelin
 Surfactant recycling
 Congenital SP-B
deficiency, cause severe
RDS

40. Surfactant Proteins
SP-C
 Chromosome 8
 Enhances the rate of
adsorption & spreading
of the surfactant
 May play a role in
surfactant recycling
SP-D
 Similar to SP-A in
structure
 Host defense mechanism

41. Surfactant Synthesis
 Type II alveolar epithelial cells begin to appear
by 20-24 wks
 Corticosteroids & thyroid hormones ↑ the rate
of synthesis.
 L/S ratio ↑ b/w 24-32 wks to about 1
by 34-35 wks ↑ to 2
 Phosphotidylglycerol (PG) also ↑ dramatically
after 35 wks.

43. Compliance
 Change in vol per change in pressure.
*Pressure vol curves of RDS

44. Compliance

45. Compliance