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Homeostasis > Respiration > Flashcards

Respiration Flashcards

1
Q

What are the 2 major components of the respiratory system?

A
  1. Lungs: Gas exchange organ designed to maximise the rate if O2 intake.
  2. Cardiovascular system: Transports O2 to all tissues in the body.
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2
Q

What is the structure of the airway?

A

The airway is divided into 24 generations divided into 2 groups:

  1. 0-16 is the conducting zone. No gas exchange occurs here so it is termed the anatomical dead space.
  2. 17-23 is the respiratory zone. Alveoli are located on the branches of airway in these generations and gas exchange occurs.
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3
Q

What are the functions of the conducting zone?

A
  1. Warms and humidifies air before it enters lungs. This prevents excess water/heat loss from the alveoli exchange surface.
  2. Distributes air across the alveoli.
  3. Removes dust and pollutants from the air before it reaches alveoli.
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4
Q

What are the consequences of the very large total cross-sectional surface area in the respiratory zone?

A
  • Substantial decrease in velocity of air.
  • Movement of air becomes dependent on diffusion.
  • Pollutants drop out of the air and are trapped by mucous lining the bronchioles.
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5
Q

How are the lungs adapted to maximise gas exchange?

A
  1. Ventilation ensures that the alveoli are constantly supplied with air saturated in O2. This ensures there is high [C1].
  2. High blood flow (entire CO) in pulmonary circulation ensures that the alveoli are constantly supplied with blood low in O2, minimising [C2].
  3. Large number of alveoli maximises surface area.
  4. Intimate relationship between alveoli and capillaries minimises diffusion distance.
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6
Q

What is the purpose of the respiratory system?

A

Acts as an evolutionary adaptation to the limitations of gas exchange by simple diffusion across the external surface of larger organisms.

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7
Q

What is the purpose of ventilation?

A

To generate pressure gradient between the atmosphere and alveoli required for air flow.

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8
Q

What are the sequence of events during inspiration?

A
  1. Respiratory muscles cause an expansion in the volume of the pleural cavity.
  2. This causes a decrease in intrapleural pressure from -5 cmH2O to -8 cmH2O..
  3. Transpulmonary pressure becomes more +ve, causing the lungs to expand until the elastic properties of the lungs matches new intrapleural pressure.
  4. Expansion of the lungs causes intra-alveolar pressure to fall below atmospheric pressure (-1 cm H2O).
  5. Pressure gradient is generated between the atmosphere and alveoli.
  6. Air flows into the alveoli, from the atmosphere, down the airway.
  7. Air continues to flow into the alveoli until intra-alveolar pressure equilibrates with atmospheric pressure.
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9
Q

Why is such a small pressure gradient needed in order to generate airflow during inspiration?

A

Because the airway offers very little resistance to airflow.

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10
Q

What is the importance of the pleural cavity at end-expiration?

A

At end-expiration, the chest wall has a natural tendency for outwards elastic recoil. Lungs have tendency for inwards elastic recoil. This causes expansion of the pleural cavity, which generates -ve intrapleural pressure that opposes elastic recoil of chest wall and lungs. This keeps lungs expanded.

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11
Q

What is the clinical significance of the pleural cavity?

A

When the pleural cavity becomes punctured, the intrapleural pressure is lost and the lungs deflate. This is called a pneumothorax.

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12
Q

What are the different transmural pressures?

A

Transpulmonary pressure = P(A) - P(pl)
Trans chest wall pressure = P(pl) - P(B)
Trans system pressure = P(A) - P(B)

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13
Q

What is a capacity?

A

A volume which is a function of 2 or more basic volumes.

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14
Q

What is the process of expiration?

A
  1. Inspiratory muscles relax and/or expiratory muscles contract.
  2. Volume of pleural cavity decreases.
  3. Intrapleural pressure becomes less negative.
  4. Intrapleural pressure no longer large enough to oppose the elastic recoil tendencies of the lungs and/or intrapleural pressure becomes positive and forces lungs to shrink.
  5. Lungs decrease in volume.
  6. Intra-alveolar pressure increases above atmospheric pressure.
  7. Pressure gradient set up between alveoli and atmosphere.
  8. Air flows out of alveoli into the atmosphere.
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15
Q

What is STPD?

A 
Temperature = 273 K
Pressure = 1 atm = 760 mmHg
Humidity = 0
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16
Q

Why is lack of humidity important for perfect gas calculations?

A

Water is not a perfect gas in the normal physiological range as n (no. moles) changes with temperature.

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17
Q

What happens to air as it enters the lungs?

A
  1. Air is saturated with water.

2. O2 diffuses from alveolar air to blood while CO2 diffuses from blood to air.

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18
Q

What are the normal values for inspiratory PO2 and PCO2?

A

PIO2 ≃ 149 mmHg (BTPS)

PICO2 = 0.28 mmHg (BTPS) ≈ 0 mmHg

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19
Q

What are the normal values of expiratory PO2 and PCO2?

A

PAO2 ≃ 100 mmHg (BTPS)

PACO2 ≃ 40 mmHg (BTPS)

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20
Q

What are the different types of dead spaces?

A
  • Anatomical dead space = Conducting zone
  • Alveolar dead space = Wasted air in alveoli with no/reduced blood supply
  • Physiological dead space = Anatomical dead space + Alveolar dead space
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21
Q

What is the alveolar ventilation rate (V(A))?

A

Volume of fresh air entering the alveoli per unit time that actually take part in gas exchange.

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22
Q

How can V(A) be changed?

A
  • Increasing breathing frequency (given tidal volume > dead space volume)
  • Increase tidal volume
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23
Q

According to the alveolar ventilation equation, how can PACO2 be controlled?

A
  • By controlling V(A).
  • PACO2 is inversely proportional to V(A).
  • Increasing V(A) decreases PACO2 and vice versa.
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24
Q

What is the significance of PAO2 and PACO2?

A

PAO2 and PACO2 are equal to PaO2 and PaCO2 as they reach equilibrium in the lungs.

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25
Q

According to the alveolar gas equation, how can PAO2 be controlled?

A
  • By controlling PACO2.
  • Increasing PACO2 decreases PAO2 and vice versa.
  • This relationship is purely consequential, not causative.
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26
Q

What are the key features of the static lung compliance graph?

A
  1. Compliance of the lungs is sigmoidal.

2. There is hysteresis depending on inflation/deflation.

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27
Q

What is the shape of the lung compliance curve?

A
  1. Initial stiff phase because alveoli are collapsed.
  2. Middle phase is most compliant (linear relationship).
  3. As the alveoli reach limit of elasticity, they become less compliant and stiff again.
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28
Q

What is the specific compliance of mammalian lungs?

A

0.08/mmHg

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29
Q

What are the factors affecting lung compliance?

A
  1. Lung volume
  2. Elastic properties of lungs
  3. Size of lungs
  4. Surface tension in alveoli
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30
Q

What represents work done in inspiration for a lung?

A

Area between its compliance curve and the y-axis.

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31
Q

What clinical conditions cause increased lung compliance?

A
  • Silicosis

- Fibrosis

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32
Q

What clinical conditions cause decreased lung compliance?

A

Emphysema

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33
Q

What is the functional residual capacity in terms of elastic properties of lungs and chest wall?

A

FRC is the point where the transmural pressure needed to oppose inward elastic tendencies of the lungs is equal to that needed to oppose outwards elastic tendencies of the chest wall.

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34
Q

What factors affect compliance of chest wall?

A
  1. Rigidity/shape of chest wall
  2. Diaphragm
  3. Abdominal contents
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35
Q

What are the 2 factors contributing towards lung compliance?

A
  1. Elastic tissue in lungs

2. Surface tension in alveoli

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36
Q

What are the contributions of surfactant to the properties of the lungs?

A
  1. 2/3-3/4 total lung compliance.

2. Hysteresis of lungs.

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37
Q

What are the roles of surfactants?

A
  1. Reduces surface tension and increases compliance of lungs.
  2. Allows alveoli of different sizes to co-exist.
  3. Keeps alveoli dry.
  4. Immunity.
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38
Q

What is the main surfactant in alveoli?

A

Dipalmitoyl phosphotidylcholine

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39
Q

How does surfactant increase compliance of lungs?

A

Surfactant dramatically decreases the surface tension caused by air-water interface in the alveoli, which increases the compliance of the lungs and thus decreases work done in inspiration.

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40
Q

How does surfactant allow alveoli of different sizes to exist?

A
  • Same amount of surfactant produced in small alveoli compared to large (on average).
  • Smaller surface area of means that there are more surfactant molecule per unit area in smaller surfactants.
  • This results in smaller alveoli having lower surface tension and thus producing smaller pressure, preventing their collapse.
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41
Q

How does surfactant keep alveoli dry?

A
  1. Acts as physical barrier to fluid in the interstitium.
  2. Decreases surface tension and tendency for alveoli to collapse. This results in less negative interstitial pressure which prevents excess fluid from leaving the blood to enter interstitium and thus the alveoli.
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42
Q

How does surfactant promote immune function?

A

Other components of surfactant include IgA (antibodies) and apoproteins (SP-A, SP-D), contributing to direct and innate immunity. SP-A and SP-D act as opsonins, coating pathogens to promote phagocytosis.

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43
Q

What causes infant respiratory distress syndrome and what are the symptoms?

A 
Cause: Type II pneumocytes have not matured in premature babies and do not produce surfactant. This results in these babies having an increased alveolar surface tension and decreased lung compliance.
Symptoms:
- Breathing difficulties
- Atelectasis
- Pulmonary oedema
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44
Q

How does surfactant cause hysteresis?

A
  1. As surface area decreases, the ability for surfactants to reduce surface tension increases as the surfactant molecules are more compressed and there are more surfactant molecules per unit area.
  2. When surface area is too low, some surfactant molecules are forced out of the layer of surfactant on surface of water, reducing the number of surfactant molecules per unit area and thus decreasing the ability for surfactant to reduce surface tension.
  3. As the surface area suddenly increases, there is a dramatic increase in surface tension because of this.
  4. As the surfactant molecules become redistributed in the surfactant layer, surface tension reducing ability of surfactant increases and so there is a smaller increase in surface tension as surface area increases.
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45
Q

What types of flow occur in the airways?

A
  1. Laminar: Occurs in small airways (bronchioles) where the flow velocity of the air is low.
  2. Turbulent: Occurs in larger airways (trachea, bronchi) where the flow velocity of air is high.
  3. Transitional: Shows properties of both types of flow above and occurs at the bifurcation of the airways.
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46
Q

What factors influence airway resistance?

A
  1. Lung volume
  2. Dilation/constriction of airway by smooth muscles
  3. Density of air
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47
Q

How does lung volume affect airway resistance?

A

Increasing lung volume decreases resistance. This is because the bronchi and bronchioles are attached to the lung parenchyma. This means that as lung volume increases, the parenchyma pulls the bronchi and bronchioles outwards, increasing their radius and thus decreasing their resistance.

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48
Q

How does dilation/constriction of airways affect airway resistance?

A
  • Constriction of the airways caused by smooth muscle contraction (especially in bronchioles) is caused by parasympathetic stimulation, through the release of ACh. This decreases their radius and thus increases the resistance.
  • Dilation of the airways due to relaxation of smooth muscles is caused by sympathetic stimulation via noradrenaline and β2 adrenoreceptors. This increases the radius and thus decreases the resistance. Drugs like isoproterenol can also be used to induce bronchial dilation (in patients with asthma).
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49
Q

How does air density affect airway resistance?

A

Decreasing the density of air will decrease the effective resistance experienced by it (because it reduces the tendency for it to undergo turbulent/transitional flow). Breathing in low density air (e.g. containing helium) with thus increase flow and decrease work done in respiration.

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50
Q

What is the main determinant of maximum flow rate during expiration?

A

End-inspiratory lung volume

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51
Q

What are the effects if emphysema on the equal pressure point (EPP)?

A

In emphysema, the compliance of the lungs increase, so the elastic recoil potential of the alveoli at a given lung volume decreases, which means the pressure gradient between alveoli and air also decreases, causing EPP reach respiratory bronchioles much more quickly than in normal person. This causes airway collapse and thus great difficulty in expiration.

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52
Q

How do patients with emphysema compensate for their reduced EPP?

A
  1. Breathing at higher FRCs to increase the elastic recoil of the lungs and thus move EPP into supported airway, which prevents airway collapse.
  2. Breathing with pursed lips creates backlog of pressure which also keeps the airways expanded.
53
Q

What is Henry’s law?

A

Concentration = Partial pressure x solubility

54
Q

What is the solubility of CO2?

A

0.7 ml/l plasma/mmHg

55
Q

What are the ways by which O2 is transported in the blood?

A
  1. Dissolved (~3%)

2. Bound to haemoglobin (~97%)

56
Q

What is the O2 binding capacity of haemoglobin?

A

1.39 ml/g Hb

57
Q

Why is Hb contained in red blood cells?

A

To prevent excretion by the kidneys.

58
Q

What is the loading plateau of haemoglobin?

A
  • Point beyond which increases in PO2 has little effect on O2 saturation of blood.
  • ~60 mmHg.
59
Q

What are the benefits of having loading plateau?

A
  1. Allows blood O2 content to stay constant despite variations in barometric pressure (and thus atmospheric PO2).
  2. Allows blood O2 content to stay constant despite variations in ventilation rate.
60
Q

Why isn’t all Hb-bound O2 released from Hb?

A

To prevent over-saturation of tissue with O2 and subsequent formation of reactive oxygen species.

61
Q

What factors influence Hb-O2 binding affinity?

A
  1. Temperature: Increasing temperature decreases Hb affinity.
  2. pH: Increasing pH increases Hb affinity.
  3. PCO2: Increasing PCO2 Decreases Hb affinity.
  4. DPG: Increasing level of blood DPG decreases Hb affinity.
62
Q

What does H+ ions bind to on haemoglobin?

A

His residues

63
Q

How does PCO2 affect Hb binding affinity?

A
  1. pH-Bohr effect

2. Co2-Bohr effect

64
Q

What is the physiological function of DPG?

A

Keeps Hb-O2 affinity relatively low in normal state to allow efficient O2 unloading at tissues.

65
Q

What is the clinical function of DPG?

A

DPG levels need to be maintained in blood banks.

66
Q

What are the conditions in tissues that allow for efficient O2 unloading?

A
  1. Low PO2
  2. High temperature
  3. High PCO2
67
Q

Why does foetal haemoglobin have higher O2 affinity than adult haemoglobin?

A

It has γ subunits less sensitive to DPG

68
Q

What are the different types of hypoxia?

A
  1. Hypoxic hypoxia: Inadequate ventilation of the lungs.
  2. Anaemic hypoxia: Reduced O2 carrying of blood.
  3. Circulatory hypoxia: Inadequate perfusion of tissues.
  4. Histotoxic hypoxia: Inability for cells to utilise O2.
69
Q

Why is CO poisoning dangerous?

A
  1. Decreases the O2 carrying capacity of Hb due to binding more tightly to Hb than O2.
  2. Increases Hb affinity for O2 by locking it in high affinity T-state.
  3. No effect on blood PO2 and so prevents detection by body.
  4. Colourless and odourless so presence in inhaled air cannot be detected.
70
Q

What are the ways in which CO2 is transported in the blood?

A
  1. Dissolved - ~5%
  2. Bicarbonates - ~5%
  3. Carbamino compounds - ~90%
71
Q

Why is CO2 transport described as opportunistic compared to O2 transport?

A

Unlike O2 transport, there is no buffering of CO2 transport. Instead, all transport mechanisms rely on natural equilibria determined by the relative concentrations of CO2 in tissue and blood.

72
Q

What are the consequences of CO2 carriage as bicarbonate in the blood?

A

As more CO2 is carried in the blood as bicarbonate, the pH decreases.

73
Q

What is the Haldane effect?

A

CO2 carrying capacity of blood increases as PO2 decreases.

74
Q

What is the mechanism behind the Haldane effect?

A

This is because as PO2 decreases, the amount of O2 saturated Hb molecules also decreases. Since deoxyhaemoglobin is a weaker acid and so are less dissociated (bound to more H+) at physiological pH. This allows it to bind to more H+ ions released by:

  1. Conversion of CO2 to HCO3-.
  2. Binding of CO2 to proteins to form carbamino compounds.
75
Q

What are the physiological importances of the Haldane effect?

A
  • In tissues where PO2 is low, CO2 can be easily loaded into blood and carried away from tissues producing it.
  • In lungs where PO2 is high, CO2 can be easily unloaded into blood and excreted out of the body.
76
Q

Why is more CO2 carried in red blood cells than in plasma?

A
  1. More CO2 is carried in RBCs as bicarbonate.

2. More CO2 is carried in RBCs as carbamino compounds.

77
Q

Why is more CO2 carried in RBCs as carbamino compounds?

A
  1. Presence of haemoglobin means that there is much greater protein concentration in RBCs compared to plasma.
  2. Buffering capacity of Hb (due to imidazole groups on histadine) allows for more of acidic carbamino compounds to be formed.
  3. Hb forms carbamino compounds much more easily compared to plasma proteins.
78
Q

Why is more CO2 carried in RBCs as bicarbonates?

A
  1. Presence of carbonic anhydrase means that HCO3- forms much faster in RBCs compared to plasma.
  2. Buffering capacity of Hb means that p.o.e. for reaction shifts to the right, in favour of HCO3- formation.
  3. Exchangers in plasma membrane of RBCs transport HCO3- out of the cell in exchange with Cl-, which decreases [HCO3-] in RBCs, shifting p.o.e. to the right, in favour of HCO3- formation. As consequence of this, as [HCO3-] increases, [Cl-] increases. This causes phenomenon called a chloride shift.
79
Q

Why does CO2 loading into blood increase in the tissues?

A
  1. High PCO2

2. Low PO2

80
Q

Why does CO2 unloading from blood increase in the lungs?

A
  1. Low PCO2

2. High PO2

81
Q

What are the factors affecting blood CO2 carrying capacity?

A
  1. PCO2
  2. PO2
  3. RBC [Hb]
  4. Plasma pH
  5. [Plasma protein]
82
Q

What is osmotic the consequence of CO2 carriage in RBCs as bicarbonates?

A

As more CO2 converted to HCO3- (replaced by Cl- in chloride shift), osmolality of RBCs increase, causing water to enter and induce swelling.

83
Q

What type of buffering system is the bicarbonate system described as?

A

Open buffering system.

84
Q

What are the types of blood pH disorders?

A
  1. Respiratory alkalosis: Too high VA decreases PCO2, which increases pH for given [HCO3-]. pH decreased by increased excretion of HCO3-.
  2. Respiratory acidosis: Too low VA increased PCO2, which increases pH for given [HCO3-]. pH increased by decreasing excretion of HCO3- and production of more HCO3-.
  3. Metabolic alkalosis: Increase in blood pH due to metabolism, maintains constant PCO2. pH decreased by increasing PCO2 (hypoventilation).
  4. Metabolic acidosis: Decrease in blood pH due to metabolism, maintains constant PCO2. pH increased by decreasing PCO2 (hyperventilation).
85
Q

What are the 2 circulations associated with the lungs?

A
  1. Bronchial circulation.

2. Pulmonary circulation.

86
Q

What are the functions of the bronchial circulation?

A
  1. Supplies lung tissue with O2 and nutrients.

2. Provides heat and moisture to air passing through the conducting zone.

87
Q

What is the structure of the pulmonary circulation?

A
  • Intimately associated with the respiratory tree.
  • Branches in accordance to the branches of the respiratory tree and ends in the alveoli as a network of capillaries also intimately associated with alveoli, facilitating efficient gas exchange.
  • Unlike systemic capillary beds, pulmonary capillary beds are not parallel. Instead, they form complex network of interconnected vessels.
88
Q

What are the functions of the pulmonary circulation?

A
  1. Oxygenation of blood.
  2. Acts as blood reservoir.
  3. Removes emboli.
  4. Metabolism of vasoactive hormones.
89
Q

What features of the pulmonary circulation make it good at removing emboli?

A
  1. Interconnected capillaries mean that there are lots of redundancies. Blockage of one does not cut off blood supply.
  2. Endothelium releases fibrolytic agents to break down blood clots. They also absorb air bubbles.
90
Q

Why are many important vasoactive agents metabolised in the pulmonary circulation?

A

Pulmonary circulation is only circulation that receives whole of the cardiac output and so will eventually encounter all hormones in the blood. This allows for quicker and finer control.

91
Q

What are the differences between the pulmonary and systemic circulations?

A
  • The SC has high MAP (~95 mmHg) while the PC has lower MAP in comparison (~15 mmHg).
  • The SC has high peripheral resistance (1.1 PRU) while the PC has low peripheral resistance (0.08 PRU).
  • The SC has low compliance while the PC has high compliance.
  • The capillary beds in the SC are parallel while they are interconnected in PC.
92
Q

Why is it important for vascular resistance to be low in the pulmonary circulation?

A

Flow in PC = Flow in SC, but MAP in PC 1/10 of SC, so resistance also has to be 1/10 in order to achieve this flow.

93
Q

What structural features of the PC ensure low vascular resistance?

A
  1. Arrangement of vessels.

2. Structure of vessels.

94
Q

How does the arrangement of vessels reduce resistance in PC?

A
  1. Large number of interconnected capillaries in capillary bed.
  2. Numerous arterioles connected in parallel also decreases resistance offered by arterioles.
95
Q

How does the structure of vessels reduce resistance in PC?

A
  1. Vessels in PC are shorter and wider than vessels in SC.
  2. Arterioles in PC have thinner muscular walls and are more dilated than SC (due to lack of sympathetic tone).
  3. Vessels in PC have thinner walls and are more compliant than vessels in SC.
96
Q

Why does an increase in CO have little effect on PABP?

A
  1. High capillary compliance.

2. Capillary recruitment.

97
Q

What are the types of blood vessels in the lung?

A
  1. Alveolar

2. Extra-alveolar

98
Q

What is the behaviour of alveolar vessels with lung volume?

A
  1. At low lung volumes, alveoli are at rest, which causes the alveolar vessels to be slack (expanded) and thus have low resistance.
  2. At high lung volumes, alveoli are stretched, which causes the alveolar vessels to be stretched (compressed) and thus have high resistance.
99
Q

What is the behaviour of extra-alveolar vessels with lung volume?

A
  1. At low lung volumes, intrapleural pressure is higher (less –ve), which causes the extra-alveolar vessels to be compressed and thus have high resistance.
  2. At high lung volumes, intrapleural pressure is lower (more –ve) to facilitate the expansion of the lungs, which causes the extra-alveolar vessels to expand and thus have low resistance.
100
Q

What factors prevent movement of fluid into alveoli?

A
  1. High intra-alveolar pressure.

2. Surfactant.

101
Q

What pathologies can cause pulmonary oedema?

A
  1. Increase in pulmonary capillary pressure (left heart failure, general hypoxia)
  2. Increase in capillary permeability (oxidant damage by ROS)
  3. Decrease in capillary colloid osmotic pressure (starvation)
  4. Decrease in interstitial pressure (acute respiratory distress syndrome – ARDS)
  5. Lymphatics blockage
102
Q

What is the relationship between height in lungs and blood pressure?

A

Blood pressure increases near the base of the lungs compared to apex.

103
Q

What is the relationship between height in lungs and V_A/Q ratio?

A

V_A/Q increases towards the apex of the lungs.

104
Q

When V_A/Q is low, what are the responses to increase it?

A
  1. Increased ventilation rate to increase V_A and restore V_A/Q.
  2. Decreased blood flow due to vasoconstriction to decrease Q and thus restore V_A/Q.
105
Q

What is the clinical significance of high V_A/Q at apex?

A

High O2 environment favours growth of Mycobacterium tuberculosis. This is why tuberculosis tends to localise at the apex of the lungs.

106
Q

What are the 2 causes of venous admixtures?

A
  1. Wasted air: Air entering lungs but not being used to oxygenate blood.
  2. Wasted blood: Blood not being oxygenated by lungs before passing into arterial circulation.
107
Q

How does wasted blood occur?

A
  1. Left-to-right shunting:
    - Atrial septal defects
    - Bronchial circulation
  2. Alveolar shunting:
    - Collapsed alveoli
    - Pulmonary oedema
    - Atelectesis
  3. Low V_A/Q ratios at the base of the lungs
108
Q

What were the findings of Lumsden’s brainstem transection experiments?

A
  1. The medullary centre contained the CPG.
  2. The apneustic centre centre prolongued inspiration.
  3. Pneumotaxic centre inhibits inspiration.
  4. Vagal input involved in termination of inspiration.
109
Q

How does the medullary centre generate breathing pattern?

A
  • The medulla contains groups of cells in the VRG and DRG.
  • These cells have self-excitatory properties that may contribute to the central pattern.
  • They communicate with motor neurone pools that innervate the diaphragm.
110
Q

How does the pneumotaxic centre inhibit inspiration?

A

Groups of neurones in centre called the pontine respiratory group (PRG) send inhibitory signals to the VRG and DRG in the medullary centre.

111
Q

What is the interaction between voluntary and involuntary breathing?

A
  • In the short term, voluntary breathing overrides involuntary breathing to allow for activities such as speaking and coughing.
  • In the long term, involuntary breathing always overrides voluntary breathing (as evident with breath holding).
112
Q

How is ventilation controlled?

A
  • Central chemoreceptors

- Peripheral chemoreceptors

113
Q

What factors are detected by the CCRs?

A

CSF pH, which is directly proportional to PaCO2.

114
Q

What types of cells are found in PCRs?

A

Glomus cells

115
Q

What is the relative importance of carotid body PCRs compared to aortic body PCRs?

A

Carotid body PCRs have dominant effect over aortic body PCRs.

116
Q

What factors are detected by the PCRs?

A
  • PO2
  • PCO2
  • pH
117
Q

What is the importance of PCRs?

A
  • They are the only receptors capable of bringing about response to hypoxia since only they detect PO2.
  • They are the only receptors capable of bringing about compensatory response to metabolic acidosis as only they can detect metabolic acids.
118
Q

How does the glomus cells detect low blood PO2?

A
  1. O2 binding Haem protein decreases opening probability of K+ channels.
  2. Low PO2 causes raised cAMP, which inhibits cAMP-dependent K+ channels.
  3. Low PO2 inhibits NADPH oxidase activity in mitochondria which increases levels of oxidised glutathione and inhibits K+ channels.
  4. Depolarisation causes Ca2+ channels to open and stimulates neurotransmitter release.
119
Q

What coordinates the response to respiratory acidosis?

A

Mainly CCRs (~80%), but PCRs have small contribution.

120
Q

What coordinates the response to metabolic acidosis?

A

Mainly PCRs.

121
Q

What coordinates the response to hypoxia?

A
  • Response to hypoxia at altitude purely mediated by PCRs.

- Response to hypoxia due to inadequate ventilation is mediated by combination of PCRs and CCRs.

122
Q

What is the Hering-Breuer reflex?

A

Inspiration activates pulmonary stretch receptors that inhibit inspiration and promote expiration.

123
Q

What is the deflation reflex?

A

Decrease in lung volume causes inhibition of expiration and promotes inspiration.

124
Q

How is the CCR breaking effect towards altitude hyperventilation countered?

A
  1. HCO3- pumped out of the CSF.

2. PCR output increased in response to prolonged hypoxia.

125
Q

What are the long-term effects of high altitude hypoxia?

A
  1. Polycythemia.
  2. Pulmonary hypertension (due to general vasoconstriction).
  3. Increased 2,3-DPG production.
126
Q

What causes the ‘bends’ during scuba diving?

A
  1. As the divers ascend, the pressure decreases, which decreases the solubility of N2. Excess dissolved N2 in the body leaves solution as gas bubbles in the bloodstream. These act as emboli and can result in blockage of the vessels in the brain/heart.
  2. The air bubbles also block arteries in the joints, causing joint pain and classical symptoms of the ‘bends’.
  3. The air bubbles are capable of causing strokes/heart attacks.
127
Q

What are preventative techniques to the ‘bends’?

A
  • Ascend slowly.

- Use oxygen-helium, which is less soluble and has lower density, so makes inspiration easier.

128
Q

What is believed to mediate the response to exercise?

A
  • Mainly feedforward.

- CCRs and PCRs are mainly there to match ventilation rate exactly with O2 consumption rate.

Homeostasis (15 decks)

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