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Flashcards in Respiratory Deck (16):

What is the alveolar gas equation? How do you calculate the alveolar-arterial gradient? What is the physiological significance of the A-a gradient?

1. Alveolar gas equation is
- Alveolar partial pressure of O2 (PAO2) = Inspired air partial pressure of O2 (PIO2) - [Alveolar partial pressure of CO2 (PACO2)]/Respiratory Quotient (RQ)]

2. A-a gradient is
- PA02 - PaO2
- Alveolar partial pressure of oxygen - arterial partial pressure of oxygen

3. Ventilation/perfusion mismatch
- Ventilation mismatch: Pneumonia, dead space
- Perfusion: PE


Describe the normal relationship between ventilation and perfusion in a normal upright lung. What conditions can increase V/Q mismatch? Which test can be done in clinical practice to demonstrate a V/Q mismatch?

1. V/Q in normal lungs is affected by pulmonary circulation which is dependent on gravity
A. Apex
- Less perfusion, slightly reduced ventilation
- Ventilation > Perfusion
- V/Q ratio is high
B. Middle
- Ventilation = Perfusion
- V/Q ratio is 1
C. Base
- High perfusion
- Slightly high ventilation
- Perfusion > ventilation
- V/Q ratio is low

2. V/Q mismatch
- Low V/Q ratio -> ventilation problem -> Pneumonia, emphysema, pulmonary edema
- High V/Q ratio -> Perfusion problem -> PE

3. V/Q mismatch can be identified by
- Calculating the A-a gradient
- V/Q scan


What happens to the V/Q ratio from the top to bottom of upright lungs? Explain the reasons for the normal A-a gradient?

1. V/Q ratio in normal upright lung
- Ventilation and perfusion increases from apex to base but
- Perfusion increases more than ventilation (Perfusion > Ventilation)
- V/Q ratio decreases from apex to base

2. A-a gradient
- The difference between alveolar oxygen concentration and arterial oxygen concentration
- Normal gradient is 5 - 10 mmHg
- Occurs because although alveolar O2 concentration in the apex is good, the arterial O2 concentration sampled comes from the base of the lungs where alveolar O2 concentration is lower -> Reduced arterial O2 concentration
- Due to non-linear shape of the O2-dissociation curve where addition of shunted blood with lower O2 concentration results in great decrease in arterial O2 concentration


What does Ventilation/Perfusion ratio mean?

- Ratio of ventilation/air flow into the alveolus over perfusion/blood flow into the pulmonary capillaries


What are the causes of hypoxia in a patient breathing room air? What is the effect of ventilation/perfusion inequality on arterial PO2 and PCO2? What is the effect of ventilation/perfusion inequality on gas exchange? What effect does increasing ventilation to the lungs have on arterial PO2 and PCO2?

1. Causes of hypoxia
- Hypoventilation
- Diffusion limitation
- Reduced perfusion
- Ventilation/perfusion mismatch
- Shunting

2. V/Q inequality has greater effect on PO2 than CO2
- Due to non-linear shape of O2 dissociation curve and linear shape of CO2 dissociation curve

3. V/Q inequality causes
- Impaired/reduced uptake and exchange of O2 and elimination of CO2
- Reduced PaO2 -> Perfusion to the lungs are mainly in the bases where PAO2 is lower

4. Increasing ventilation
- Reduces PCO2 more than increasing PO2
- Hypoxia cannot be corrected by increasing ventilation -> Due to non-linear shape of O2 dissociation curve
- Hypercapnia can be corrected by increasing ventilation -> Due to linear shape of CO2 dissociation curve


How is oxygen transported in the blood? Please draw the oxygen dissociation curve. What are the implications of this curved shape? What factors cause shift to L and R?

1. Oxygen transported in blood
- Binding to Hb haem molecule (majority) -> 20.8mg/100mls blood
- Dissolved in blood (small amount) -> concentration dependent on Henry’s Law

2. Oxygen dissociation curve
- 97% sats = 90 pO2
- 60% sats = 30 pO2
- 50% sats = 27 pO2

3. Curved shape of oxygen dissociation curve
- Top/plateau part represents O2 loading into blood -> small drop in alveolar O2 concentration has little impact on O2 loading in blood
- Lower/steep part represents O2 unloading in tissues -> small drop in capillaries O2 concentration unloads large amount of O2 to metabolically active tissues

3. Curve shift to
- R: Reduce pH, increase CO2 + temp + 2,3 DPG
- L: Increase pH, reduce CO2 + temp + 2,3 DPG


Please draw the curve representing O2 concentration vs pO2. How does this change in anaemic and polycythaemic individual? What is the effect of carbon monoxide on haemoglobin oxygen transport capacity?

1. O2 concentration vs pO2 curve
- Anaemia drops effective Hb percentage/oxygen transport capacity
- Polycythaemic increases effective Hb percentage/oxygen transport capacity

2. Carbon monoxide has 240 x more affinity for Hb than O2
- Significant drop in Hb oxygen transport capacity
- Shifts oxygen dissociation curve to the L, interfering with O2 unloading to tissues


In an alveolus, what affects oxygenation? Describe the oxygen uptake along a pulmonary capillary. How does hypoxia affect oxygenation?

1. Oxygenation affected by
- Ventilation
- Perfusion
- Diffusion across membrane
- Alveolar-pulmonary capillary O2 pressure gradient

2. Oxygen uptake along pulmonary capillary dependent on
- Alveolar-capillary O2 pressure gradient
- Surface area available
- Thickness of membrane/blood gas barrier ~ 0.3microns
- RBC transit time ~0.75s
- Under normal circumstances, O2 uptake is perfusion-limited with alveolar-end capillary O2 pressure gradient being minimal

3. Hypoxia causes
- Decrease in O2 diffusion
- Decrease in alveolar-capillary O2 pressure gradient


How is CO2 transported in the blood? What is the role of RBC in CO2 transport?

1. CO2 transported in
- Bicarbonate buffering system (90%)
- Carbamino compounds (5-10%)
- Diffusion/dissolved in blood (5-10%)

2. RBC in CO2 transport
- Carbonic anhydrase -> Increases the speed of CO2 conversion to carbonic acid
- Haldane effect -> Deoxygenated Hb binds proton and CO2 more readily
- Buffering system -> Proton acceptor -> Binding H+
- Forms carbamino compounds -> Binding CO2 to its amino group
- Chloride shift -> HCO3+ easily diffuses out of cell but cell membrane relatively impermeable to cation (H+) -> Cl- is uptake into cell to maintain plasma ionic neutrality


How is bicarbonate formed in the blood? What is the chloride shift? What is the Haldane effect?

1. In the blood
- RBC has carbonic anhydrase which converts CO2 + H20 H2CO3 H+ + HCO3-

2. Chloride shift is the exchange of HCO3 for Cl- ions to maintain ionic neutrality
- HCO3- readily diffuses out of cell membrane
- Cell membrane is relatively impermeable to cations (H+)
- RBC uptakes Cl- ions in exchange for HCO3- out of cell to maintain ionic neutrality

3. Haldane effect states that deoxygenated Hb has higher affinity for H+ and CO2 than oxygenated Hb
- In tissues, CO2 readily binds to amino group of Hb -> Forms carbamino compounds
- In lungs with presence of O2, CO2 readily dissociates from Hb to be expired from lungs


Draw a diagram that demonstrates the components of total lung volume. What are the typical volumes? Which of these volumes can be measured in the ED?

1. Lung volumes and typical volumes
- TV = 400 - 500mls
- VC = 4.5 - 5L
- TLC = 7L
- Inspiratory reserve volume (IRV)
- Expiratory reserve volume (ERV)
- Residual volume (RV)

2. Volumes measurable in ED
- Spirometry: FEV1, FVC
- Ventilator: TV


Please describe the components of total lung capacity. Name a method to measure each of these. How does physiological dead space differ from anatomical dead space?

1. Total lung capacity consists of
- Tidal volume: Amount of air moved in and out during normal respiration (500mls)
- Vital capacity: Amount of air exhaled after maximum inspiration (4.5 - 5L)
- Residual volume: Amount of air left in the lungs after maximum expiration
- Functional residual volume: Amount of air left in the lungs after normal expiration

2. Measurement of lung volumes
- Spirometry: TV, VC
- Helium dilution: TLC, FRC, RV

3. Dead space
- Anatomical dead space is volume of air in conducting zones of lungs up to division 16 (150mls) -> Does not participate in gas exchange, has ventilation but no perfusion
- Physiological dead space is volume of air in area of lung which does not eliminate CO2 -> Has ventilation but no perfusion


What is anatomical dead space? How does it differ from physiological dead space? How are these different dead spaces measured? What is dead space? What will lead to increased physiological dead space?

1. Anatomical dead space
- Volume of air in conducting zones of lungs up to division 16
- Does not participate in gas exchange
- Has ventilation but no perfusion
- Estimate volume 150mls

2. Physiological dead space
- Volume of air in areas of lungs which does not eliminate CO2
- Has ventilation but not perfusion
- Almost the same as anatomical dead space in healthy individuals
- Marked increase in physiological dead space in individuals with lung diseases

3. Measurements of
- Anatomical dead space: Fowler’s method
- Physiological dead: Bohr’s method

4. Dead space is volume of air in the lungs that does not participate in gas exchange

5. Lung diseases increases physiological dead space
- V/Q mismatch -> Non-perfused but ventilated alveoli -> PE


What is pulmonary compliance? What factors increase or decrease compliance? What are the physiological effects of surfactant? What physiologic factors affect lung compliance? How is lung compliance affected in emphysema? How does compliance vary throughout the upright lung? What are factors affecting compliance. Can you draw the pressure-volume curve of a normal lung.

1. Pulmonary compliance is change of lung volume per unit pressure
- Compliance = V/P
- Measure of distensibility

2. Factors increasing or decreasing compliance
- Increase: Age, emphysema
- Decrease: Acute pulmonary edema, pulmonary HTN, pulmonary fibrosis

3. Effects of surfactant
- Reduces alveolar tension
- Increases compliance
- Reduces WOB
- Increases alveoli stability
- Keeps alveoli dry

4. Physiologic factors affecting compliance
- Age
- Volume of lung
- Phase of respiration
- Surfactant

5. Lung compliance in emphysema
- Increased compliance in emphysema
- Due to loss of lung elasticity
- Easier to inflate but hard to deflate lung

6. In the upright lung, compliance is
- Higher in the base
- Lower in the apex

7. Factors affecting compliance
- Elastic recoil of lungs
- Tension in alveoli -> Surfactant
- Age
- Disease -> COPD, APO, fibrosis

8. Pressure volume curve
- Demonstrate hysteresis of lungs
- Lung volumes are higher in deflation than inflation at any given pressure
- Stiffer at higher volumes


What parts of the brain control respiration? How are chemoreceptors involved in control of ventilation? What other sensors are involved in control of ventilation? How does hypoventilation affect respiration?

1. Brain control of respiration
- Automatic control: Medulla
- Voluntary control: Cerebral cortex
- Pons is the pneumotactic centre modifying medulla activity

2. Chemoreceptors in control of ventilation
- Central chemoreceptors
+ Located in medulla
+ Responds to changes in concentration of H+ -> changes due to CSF pH in response to CO2 concentration -> Increase ventilation in hypercarbia
- Peripheral chemoreceptors
+ Located in sinus bodies and aortic arch
+ Responds to changes in O2 concentration -> Increase ventilation in hypoxia
+ Also responds to changes in pH
+ Minor response to changes in CO2
+ Feedback to medullary respiratory control centre

3. Other sensors in control of ventilation
- Pulmonary stretch receptors -> In lungs, muscles, intercostal -> Vagal afferents
- Irritant receptors -> Upper airway
- Baroreceptors -> Reflex hypoventilation
- Proprioception -> Muscle spindles of intercostal, diaphragm

4. Hypoventilation causes increase CO2
- CO2 readily diffuses across BBB
- Causes high H+ ion concentration and reduce pH of CSF
- Sensed by central chemoreceptors -> Triggers increase in ventilation to expel CO2 -> Reduces H+ and increases pH


What are the initial physiological responses at high altitude? What are the longer term physiological effects of altitude exposure? Describe the symptoms of acute mountain sickness.

1. Initial physiological response to high altitude
- Hypoxia -> Sensed by peripheral chemoreceptors
- Triggers hyperventilation -> Expel more CO2
- Causes respiratory alkalosis -> Inhibits hyperventilation
- Alkalosis sensed by kidneys and increase HCO3 excretion + Brain CSF shifts more HCO3 -> Correct pH to normal
- Normal pH then allows for increase in ventilation again
- Moderate altitude cause increase 2,3 DPG -> Shifts O2 dissociation curve to R
- Higher altitude cause further hyperventilation and decrease in CO2 -> Increase pH -> Shifts O2 dissociation curve to L
- Alveolar hypoxia also causes pulmonary vasoconstriction to reduce shunting -> May get pulmonary HTN

2. Long term physiological effects of altitude
- Polycythaemia due to increased erythropoietin
- Increase O2-carrying capacity of Hb
- Increase blood viscosity
- Pulmonary HTN resulting in RVH
- Increase peripheral capillaries

3. Symptoms of acute altitude sickness
- Dizziness
- Headache
- Fatigue
- Nausea
- Acute pulmonary edema