Respiratory Physiology- II

1. RESPIRATORY PHYSIOLOGY - II
DR. ADNAN MUSTAFA (SENIOR CONSULTANT)
DR. SUMAYYA ABOOBACKER (PGY-1 RESIDENT)
Anesthesiology Department

2. Topics reviewed in the previous session
• Functional Respiratory Anatomy
• Mechanism of Breathing
• Lung Mechanics and Volumes
• Work of Breathing

3. Topics in today’s session
• Compliance & Flow Volume Loops
• Ventilation Perfusion Relationship
• Transport of 𝑶 𝟐 and 𝑪𝑶 𝟐 in Blood
• Regulation of Respiration

4. COMPLIANCE & FLOW VOLUME LOOPS

5. Compliance
• A useful measure of elastic recoil of lung/chest wall or both.
• It is defined as a change in volume divided by the change in pressure.
• Δ𝑉/Δ𝑃

6. Pressure-Volume Curve

7. Flow-Volume Loop

8. Flow-Volume Loop Variants

9. VENTILATION AND PERFUSION

10. Ventilation Distribution
• Ventilation distribution within the lung depends on the compliance of alveoli and the relative
distending pressure.
• Theoretically, the pressure within all the alveoli in the lung is constant, but the pressure outside the
alveoli is heterogenous throughout the lung, resulting in different- sized alveoli.
• Ventilation distribution is also affected by anatomy and flow rates.
• Central regions of the lung are preferentially ventilated, but as flow rates are increased, this
ventilatory difference is minimized.
• Simply stated, during spontaneous ventilation, more gas is distributed to gravity- dependent areas.

12. PERFUSION DISTRIBUTION

13. Pulmonary circulation
• The pulmonary circulation is the portion of the circulatory system which carries deoxygenated blood
away from the right ventricle of the heart, to the lungs, and returns oxygenated blood to the left
atrium and ventricle of the heart. The term pulmonary circulation is readily paired and contrasted
with the systemic circulation. The vessels of the pulmonary circulation are the pulmonary arteries
and the pulmonary veins.
• A separate system known as the bronchial circulation supplies oxygenated blood to the tissue of the
larger airways of the lung.

15. VENTILATION AND PERFUSION RELATIONSHIP

17. The V/Q ratio is the balance between the ventilation (bringing oxygen in to /removing 𝐂𝐎 𝟐 from the
alveoli) and the perfusion (removing 𝐎 𝟐 from the alveoli and adding 𝐂𝐎 𝟐). The V/Q ratio is important
because the ratio between the ventilation and the perfusion is one of the major factors affecting the
alveolar (and therefore arterial) levels of oxygen and carbon dioxide.
Variable Normal Value
PAO2 ~ 100 mm Hg
PACO2 40 mm Hg
PaO2 95 - 100 mm Hg
PaCO2 40 mm Hg

18. • Decrease the V/Q ratio : A decrease in the V/Q ratio is produced by either decreasing ventilation or
increasing blood flow (without altering the other variable). These will both have the same effect - the
alveolar (and therefore arterial) levels of oxygen will decrease and the 𝐂𝐎 𝟐 will increase.
• When you consider a decrease in the V/Q ratio, all you need to remember is:
• Ventilation is not keeping pace with perfusion.
• The alveolar oxygen levels will decrease, which will lead to a decrease in arterial oxygen levels
(Pa𝐎 𝟐)
• The alveolar 𝐂𝐎 𝟐 levels will increase (we're not getting rid of it as fast), also leading to an
increase in arterial 𝐂𝐎 𝟐 .
• To increase the ventilation-perfusion ratio.
• Increase in the V/Q ratio means that ventilation is in excess of the metabolic needs being met by
perfusion, so we blow off 𝐂𝐎 𝟐 (lower PA𝐂𝐎 𝟐 ) and increase our P𝐀𝐎 𝟐 (and Pa𝐎 𝟐).

19. Changing the V/Q Ratio Physiologically
• In the case of standing up, more blood goes to the base of the lung, while relatively less air gets
there. That means we see a LOW V/Q ratio and LOW P𝐀𝐎 𝟐 and Pa𝐎 𝟐. (along with high PA𝐂𝐎 𝟐).
• At the apex of the lung, we get relatively less blood (gravity pulls it down, not up) and relatively high
ventilation, so we have a high V/Q ratio. It leads to an increase in alveolar and arterial oxygen levels
while decreasing the carbon dioxide.

20. Changing the V/Q Ratio Pathologically
• Increasing the V/Q ratio to infinity. Pulmonary embolism
• This blood will be very well oxygenated (lots of ventilation, little perfusion) and have a very low
𝐂𝐎 𝟐.
• Not much blood gets through to these alveoli, so the volume of blood in this condition is very
low. However, 5 liters of blood is still coming to the lungs every minute - the blood that can't get
to the area of lung affected by the embolism gets shunted to other parts of the lung (leading to
a low V/Q ratio in those parts of the lung).
• We wasted energy by bringing ventilation to this area - in fact, this is alveolar dead space.

21. Changing the V/Q Ratio Pathologically
• Decreasing the V/Q ratio to zero:
• In this case, we wasted cardiac effort to send the blood to the lungs even though nothing
happened to it as far as oxygen and carbon dioxide go. We call this a physiological shunt -
although the blood travelled to the lungs, it didn't get any oxygen.
• In contrast, an anatomical shunt occurs when the blood physically doesn't enter the lungs (e.g. a
right-to-left shunt - the blood jumps straight from the right ventricle to the left ventricle without
going to the lungs). The end result is- some of the arterial blood has very low oxygen and high
𝐂𝐎 𝟐.

22. Shunt Equation

24. • Steps taken by the body to normalize the V/Q ratio:
• Hypoxic vasoconstriction: In cases where the V/Q ratio is low (lots of blood or too little
ventilation), hypoxic vasoconstriction can occur and cause the blood coming into the area to be
directed to other parts of the lung. Decreasing the perfusion of the hypoxic region will raise the
V/Q ratio and bring the arterial blood gases closer to what we expect.
• Bronchoconstriction: In cases of high V/Q ratio, the bronchi will constrict slightly to increase the
resistance and decrease the amount of ventilation coming into an area that is not well perfused
(although it won't shut it down entirely). This limits the amount of alveolar dead space that
occurs and minimizes the 'wasted' work that occurs with alveolar dead space.

25. A-a gradient
• P𝐀𝐎 𝟐 – Pa𝐎 𝟐
• A normal A–a gradient for a young adult non-smoker breathing air, is between 5–10 mm Hg.
• It gives an idea about the cause of hypoxemia.
• However, the A–a gradient increases with age.

26. Alveolar Gas Equation
• It is used to estimate alveolar partial pressure of oxygen or alveolar oxygen tension

27. Oxygen Cascade
• It It is the process of diminishing or declining O2 tension from :
Atmospheric Air
Alveoli
Arterial Blood Tissue
Capillaries
Mitochondria

29. TRANSPORT OF 𝐎 𝟐 AND 𝐂𝐎 𝟐 IN BLOOD

30. Some Basics.
• The body uses approximately 250 mL O2/min at rest.
• O2 consumption = VA x (Fi – FE)
= 5000 x (0.21 – 0.16)
= 250 mL/min
• 21 % O2 present in air which corresponds to approximately 21 kPa (atmospheric pressure is 101.3 kPa).

31. 𝐎 𝟐 and 𝐂𝐎 𝟐 Transport in Lungs
• 2 modes: Convection and Diffusion
• The pulmonary diffusion capacity/ability of 𝐂𝐎 𝟐 to pass between the alveoli to blood is 20 times more
than Oxygen which allows it to diffuse across the alveolar membrane with greater efficiency.
• Diffusion allows for 𝐎 𝟐 and 𝐂𝐎 𝟐 to be exchanged at the alveoli-pulmonary capillary interface along a
concentration gradient.

32. 𝐎 𝟐Transport in Blood
• 𝐎 𝟐 is carried in blood in 2 forms:
1. Dissolved in plasma (2%)
2. Reversibly bound to Haemoglobin (98 %)
• The Hb molecule consists of four intertwined subunits, each of which consists of a:
• Polypeptide globin chain (alpha or beta)
• Haem group (porphyrin ring containing a Fe2+ ion)
• 𝐎 𝟐 binds reversibly to the Fe2+ ion in the haem group, each Hb molecule holding up to four 𝐎 𝟐
(one to each Fe2+)

33. Oxygen Haemoglobin Saturation Curve
• The pattern of the binding produces the characteristic S shape of the curve relating P𝐎 𝟐 to Hb-𝐎 𝟐 saturation.

34. Oxygen Haemoglobin Saturation Curve
• The P50 is the P𝐎 𝟐 at which the Hb-𝐎 𝟐 saturation is 50%, normally around 3.5 kPa. It is a reference point that
describes the position of the curve and changes as the curve moves under different conditions.

35. Factors that Influence Oxygen Binding
1. Temperature
2. pH : A decrease in pH by addition of carbon dioxide or other acids causes a Bohr Shift.nA Bohr shift is
characterized by causing more oxygen to be given up as oxygen pressure increases.
3. 2,3-Diphosphoglycerate (DPG) : It is the main primary organic phosphate. DPG binds to haemoglobin
which rearranges the haemoglobin into the T-state, thus decreasing the affinity of oxygen for
haemoglobin

36. 𝐂𝐎 𝟐 Transport in Blood
• 𝐂𝐎 𝟐 is transported in the blood in 3 different forms :-
• Either dissolved in blood (5 %) or
• transported as bicarbonate (90 %) or
• as a carbo-amino (5%) compound.

38. Haldane Effect
• The Haldane Effect describes the phenomenon by which binding of oxygen to haemoglobin promotes
the release of carbon dioxide. In many ways, the Haldane Effect is the mirror image of the Bohr Effect,
making clear that oxygen and carbon dioxide compete for haemoglobin occupancy.

39. REGULATION OF RESPIRATION

40. Regulation of Respiration
• Respiratory Center
• Chemosensitive Area
• Peripheral Sensors
• Peripheral Chemoreceptors
• Lung Receptors

41. Respiratory Center
• The Respiratory Center is located in the Medulla Oblongata and Pons, in the Brainstem and are
made up of three major respiratory groups of Neurons, two in the Medulla and one in the Pons.
• In the Medulla they are the Dorsal Respiratory Group: active during Inspiration, and the Ventral
Respiratory Group: active during both inspiration and expiration
• In the Pons, the Pontine Respiratory Group includes two areas known as the Pneumotaxic Centre
(Inhibitory) and the Apneustic Centre (Excitatory)

42. Chemosensitive Area
• This area located in the Medulla is highly sensitive to PaCO2 or H+ which in turn excites the
other portions of the Respiratory Center.
• The sensory neurons are specifically excited by H+ ions. However, they do not cross the BBB.
But BBB is permeable to dissolved CO2.
• Increase in PaCO2 à Increase in CSF [H+] à Activates Chemoreceptors à Secondary
Stimulation to Medullary Centers à Increase Alveolar Ventilation à Reduce PaCO2 to
normal.

43. • The relationship between PaCO2 and minute ventilation is nearly linear.
• Very high PaCO2 depress the ventilatory response (CO2 narcosis).
• PaCO2 at which ventilation is zero, is called Apneic Threshold.

44. Peripheral Chemoreceptors
• Located in Carotid bodies and Aortic bodies.
• Carotid bodies (Principal Peripheral Chemoreceptors) à Sensitive to changes in PaO2, PaCO2, pH and
Arterial Perfusion pressure.
• Interact with the Medulla via CN IX à reflex increase in Alveolar ventilation in response to decrease
PaO2 and Arterial perfusion, or elevations of [H+] and PaCO2

45. • Carotid bodies are most sensitive to PaO2
• Activity will not appreciably increase until PaO2 decreases below 50 mmHg.
• Anti-dopaminegic drugs, anaesthetics and bilateral carotid surgery abolish the response to hypoxemia.

46. Respiratory Reflexes
• Hering- Breuer Inflation reflex : Overinflated lungs à stretch receptors + à feedback response à
switches off the inspiratory ramp and stops further inspiration.
• Hering-Breuer Deflation Reflex : Marked lung deflation causes a decrease in Expiration time.
• Pulmonary irritant receptors : Stimulated by some types of irritants that enter the tracheobronchial
tree which causes coughing and sneezing.
• J Receptors : Stimulated especially when the pulmonary capillaries become engorged with blood or
fluids which can in turn lead to dyspnea.

47. THANK YOU!
Questions ?
Anesthesiology Department