Pulmonary Physiology

Question 1

How does arterial blood differ from venous blood with respect to PO2 and PCO2?

Answer 1

Arterial blood has a higher PO2 and lower PCO2 when compared to venous blood
PO2 arterial = 100, PO2 venous = 40
PCO2 arterial = 40, PCO2 venous = 46

Question 2

Explain gas exchange in the lungs.

Answer 2

Fick’s Law: calculates net diffusion and takes into account the following variables
V = net diffusion
A = area of the diffusing membrane
D = diffusing constant (unique to each gas)
ΔP = concentration difference of the diffusion gas across the membrane
T = thickness of the membrane

Vgas = (A/T) x D x (P1-P2)

Question 3

What characterizes the effects of COPD, particularly emphysema?

Answer 3

COPD: FEV1, FVC, FEV1/FVC all go down. FRC goes up.
FEV1: Forced expiratory volume, max vol of air forcibly exhaled.
FVC: forced vital capacity: Volume of air forcibly exhaled after a maximum inhalation.
FRC: functional residual capacity: Volume of air remaining in lungs at end of normal breath.

Decreases the ability to expel air by blocked airways, increased mucus, inflammation, or increased compliance
Increased airway resistance
Emphysema specifically increases compliance, but makes it more difficult to expel air
Lungs lose natural elasticity due to the destruction of alveoli, thereby also losing gas diffusing surface area

Question 4

Why is mucociliary transport a non-respiratory function of the lung?

Answer 4

Type of pulmonary defence mechanism. Large stuff gets caught in nasal passageway. Mouthbreathing bypasses this. In alveoli, substances can get all the way down there. There are alveolar macrophages that engulf particles. Cannot digest fine rubber particles.

Cilia moves dust towards throat, not towards alveoli. Smokers lose cilia activity. Mucus contains gel layer and sol layer. Dust particles get trapped in this mucous.

Question 5

What is meant by V-Q mismatch and how is it expressed in terms of alveolar and arterial PO2?

Answer 5

A mismatch in alveolar PO2 and arterial PO2 - they should theoretically be the same after perfect diffusion, but this isn’t the case.
This occurs because circulatory shunts bypass gas exchange regions between alveoli and pulmonary blood capillaries (including bronchial circulation in the normal lung).
For example, if PAO2 = 100, then after the shunted blood is mixed in, PaO2 = 97, which is less than the PAO2.

Difference of 5-15 mm Hg is considered normal

Alveolar gas equation: PAO2 = PIO2 - (PACO2 / R)
If PaO2 = 50 and PCO2 = 60, R is .8, what is patient’s arterial PO2 diff?
150 - 60/0.8 = 74. PAO2 - PaO2 = 74 - 50 = 24.

Question 6

How is the breathing cycle regulated?

Central / Peripheral receptors
Medulla, pons, cortex
Glomus cells

Answer 6

• Central controller (pons, medulla and brainstem) output to effector muscles for breathing chemoreceptors send input signals to central controller
• Firing pattern of neurons in the brainstem central controller controls inspiratory and expiratory activity
• Medulla: CPG (central pattern generator located near NTS) – made of:
  DRG (dorsal respiratory group: processes sensory input from peripheral chemoreceptors and lung receptors – inspiratory
  o VRG (ventral respiratory group) – motor function – inspiratory and expiratory
• Pons: basic rhythm of breathing is fine-tuned by apneustic and pneumotoxic centers (these centers are still unknown, we just know that they regulate breathing. Thats it) in the pons
• Cortex: voluntary control over breathing
• Sensory components of breathing:
  o Central (medullary) chemoreceptors – sensitive to pH of CSF – linked to PCO2 through BBB
  o Peripheral chemoreceptors – carotid/aortic bodies sensitive to reduced arterial oxygen
  Glomus cells in carotid bodies depolarize in response to hypoxemia
  In response to low oxygen, glomus cells in peripheral chemoreceptors release acetylcholine and ATP to affect CNS.
  Hypercapnia results in depolarization of glomus cell which is necessary to control breathing

when arterial PO2 falls below 80 mm Hg, or hypercapnia or increased H+ levels, oxygen sensitive potassium channels in GLOMUS CELLS close, causing depolarization and opening of Ca 2+ channels, releasing ATP and ACh. Also occurs with hypercapnia and increased H+.

Central control: central chemoreceptors sensitive to CO2 and H+. BBB permeable to CO2 but not H and HCO3. BBB is selectively permeable to oxygen and co2.

Question 7

Why is hemoglobin important to adequate oxygenation of the body?

Answer 7

binding of one O2 to one Fe2+ heme subunit go into a relaxed state, affinity of other heme subunits for O2 increases

decrease temp, PCO2, 2,3-DPG, or increase in pH(decrease of H+) = increase affinity of oxygen to hemoglobin (left shift).

Right = increase in all (H+ co2 temp dpg)

Carbon monoxide increases affinity of Hb for bound O2. 50% binding of CO to Hb.