Respiratory 2 Flashcards
Gas diffusion between air and blood
(REFER TO LECTURE IMAGES)
Left images
- 159 mmHg - partial pressure of oxygen in atmosphere
- 100 mmHg - partial pressure of oxygen in alveolar gas
- Positive difference - Diffusion of oxygen into the blood from lungs increased oxygen in blood
Right image
- More carbon dioxide in alveolar gas than in air
- Negative difference - Diffusion of carbon dioxide into the lungs from the blood will increase carbon dioxide in lungs
Lower image
- The sheet are represents the alveoli and the capillaries
- The movement of gases is determined by the area and thickness of the sheet (alveolar capillary interface)
- Vgas - the larger the difference in partial pressure increases the flow of gas
Ventilation and Perfusion
- Normal
- Stop blood flow
- Stop Ventilation
Ventilation: Process of bringing air into and out of the lungs
Perfusion: Blood flow through the pulmonary arteries, pulmonary capillaries & pulmonary veins
Normal
- Ventilation & perfusion
Stop Blood Flow
- Ventilation & no perfusion
- Diffusion of gas from lungs to the blood will decrease
Stop Ventilation
- Perfusion & no ventilation
- Diffusion of gas from the lungs to the blood will eventually slow down and then stop
- Once the oxygen partial pressure in the lungs becomes 40mmHg oxygen will no longer diffuse into the blood because the partial pressure of oxygen in the lungs and blood will be equal
Ventilation and perfusion increase during exercise
- CO
- Alveolar ventilation
- Alveolar PO2
- Cardiac output increases progressively as you work harder during graded exercise and will eventually plateau
- Alveolar ventilation increases in a straight line to a point by which it then increases disproportionally relative to the change in intensity
- Alveolar PO2 increases as a result of exercise
PO2, O2 solubility and haemoglobin
- resting value of oxygen consumption
- Pgas = Total Pressure (mmHg) × Fgas
- PO2 = Total Pressure (mmHg) × FO2
- PO2 of dry air at sea level = 760 mmHg × 0.21 = 159 mmHg
- Resting value of oxygen consumption: 200-400 ml’s per minute
- Plasma can hold some oxygen but not as much as haemoglobin. We need haemoglobin to survive
O2 binding, exercise & altitude
- O2 dissociation curve for Hb. (binging affinity gets stronger the more oxygen it holds. It hold onto the four oxygens very strongly)
- Most of the total O2 content is bound to Hb compared with that dissolved in plasma.
- Anchor points: arterial (100 mmHg); mixed venous (40 mmHg).
- Rightward shift of curve during exercise… less oxygen in the blood - something has weakened the affinity of haemoglobin to bind to oxygen
- ..due to increases in T, [H+ ], PCO2 and 2-3DPG.
- This shift is favourable for unloading of O2 in muscle, but increases the difficulty of O2 binding in the lungs.
- Effect of going to Mt Everest (8848 m, Bar. Pressure = 253 mmHg)?
Oxygenating blood during exercise
- demand
When the demand for oxygen increases, we have the capacity to utilise more oxygen, deliver more oxygen or at a higher rate and transfer at the lungs at a higher rate
1. Pulmonary O2 exchange
2. Circulatory O2 Delivery
3. Cellular O2 utilisation
Pulmonary gas exchange, CaO2 and O2 uptake
- Transit time
Transit time for oxygen exchange during rest is 0.25second, however, during exercise blood flow is much faster so the oxygen exchange may be reduced
Oxygen cascade effectiveness of pulmonary gas exchange
- partial pressures of alveolar PO2 and arterial PO2
- Rest & exercise
HINT: Under normal exercise conditions….
- Under normal exercise conditions (“Exercise”), alveolar PO2 and arterial PO2 are very similar and the arterial PO2 and CaO2 are high.
- Thus, the lung is generally considered not to limit O2 delivery and O2 uptake.
- But…pulmonary gas exchange can become impaired and this is reflected in an increase in the difference between alveolar and arterial PO2 linked to a reduction in the O2 saturation of arterial blood (%SaO2 , next slide) and fall in CaO2
Rest: partial pressure of oxygen decreases as it travels around the body (air -> airway -> alveoli -> systemic arterial -> tissue -> systemic/venous). Cells <1% O2
Exercise: Higher PO2 in airway & alveoli. In blood, less PO2. In tissues, less PO2. Cells «_space;(much less) 1% O2
Arterial hypoxaemia in athletes
- Data taken from two studies.
- Minimal O2 desaturation (normoxaemia) in six male untrained or ‘less-trained’ subjects (UT) under normoxia (FIO2 = 0.21) – continuous line.
- Large O2 desaturation (hypoxaemia) in seven male endurance-trained subjects (ET) under normoxia – dotted line.
- Hyperoxia (FIO2 = 0.26) has no effect on %SaO2 in UT; but it reduces the hypoxaemia in ET (dashed line).
- Maximum O2 uptake is not affected by hyperoxia in UT (57 ml/kg/min);
- But it is increased from 70 to 75 ml/kg/min in ET.
- Arterial hypoxaemia is due to either diffusion limitation (short pulmonary transit time), inadequate ventilation relative to very high CO2 production and/or the extent of mismatching between the ventilation and perfusion of alveoli (“VAQ inequality”).
The paradoxical effect of training on pulmonary gas exchange
- Focus on “maximal exercise” (i.e. at VO2 max)
- In nonathletes (“N.A.”), alveolar PO2 can be increased during exercise; but this has little affect on arterial PO2 .
- In elite athletes (“ATH”) the response of alveolar PO2 is highly variable; but often arterial PO2 is lower than observed in nonathletes.
- Thus, the effectiveness of pulmonary gas exchange can be reduced by training – the paradox.
Automatic (chemical) control of breathing
Breathing is controlled by looking at the O2, CO2 and H+ content of the arterial blood
The controller
- Brainstem
- Pons & Medulla
Effectors
- Phrenic nerves & Diaphragm
- Cervical origin near Medulla
- Accessory muscles
Sensors
- Central chemoreceptors located on ventrolateral surface of medulla (CSA)
- Sensitive to CO2 (and H+ ), not O2 .
- Peripheral chemoreceptors located in aortic arch and carotid sinus.
- Sensitive to CO2 (H+ ), O2 and K+ .
At rest breathing is much more sensitive to changes in CO2 than oxygen
Basic rhythm of breathing at rest
- The central controller generates the basic inspiratory rhythm at rest – another example of a central pattern generator.
- PreBotzinger complex (found in “VRG”) is the key cluster of neurons controlling the rhythm.
- This rhythm is influenced by neural input from the central chemosensors (see “RTN”) which is linked to the sensing of CO2 levels.
- CO2 is the major stimulus for breathing at rest (see next slide).
- CO2 sensing needed to continually tune the basic rhythm.
- Central apnea syndrome is caused by impaired neuronal function in RTN and severely reduced CO2 sensitivity of RTN.
