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Respiratory Flashcards

1
Q

what is cellular respiration?

A

the cellular reactions and processes that occur in the CAC to convert chemical energy from nutrients into ATP

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2
Q

what are the fuels used for cellular respiration?

A

primarily glucose, other sugars, fats, ketone, proteins

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3
Q

how much CO2 is formed for each molecule of O2 consumed in carbohydrate respiration?

A

1 CO2 molecule

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4
Q

how many CO2 molecules are formed for each molecule of O2 consumed in fat respiration compared to carbohydrate metabolism?

A

more oxygen molecules are consumed than CO2 produces

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5
Q

what is the respiratory quotient?

A

ratio of CO2 output to O2 usage

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6
Q

what is the RQ of carbohydrates?

A

1

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7
Q

what is the RQ of fats?

A

0.7

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8
Q

what is the RQ of protein?

A

0.8

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9
Q

what is the typical RQ assumed in the alveolar gas equation?

A

0.8

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10
Q

how can RQ be used in physiological experiments?

A

to give an insight into substrate use in the body

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11
Q

what are the functions of the respiratory system?

A

gas exchange, acid base balance, phonation, pulmonary defence, metabolism, handling bioactive materials, thermoregulation

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12
Q

how does the respiratory system meet the requirement for high rate of gas exchange?

A

large SA for gas exchange between inspired air and blood in lungs, maintaining pressure gradient by lung ventilation and blood flow past the alveolar exchange surface

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13
Q

how does the respiratory system meet the need to match supply and demand?

A

central and peripheral regulation of breathing, ventilation/perfusion

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14
Q

how does the respiratory system deliver oxygen to respiring cells?

A

transport of gases in the blood

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15
Q

what makes up the upper respiratory tract?

A

nares, nasal passages, pharynx, larynx

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16
Q

what makes up the lower respiratory tract?

A

trachea, bronchi, bronchioles

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17
Q

how do the branches of the respiratory tract receive blood?

A

from bronchial arteries, and pulmonary circulation

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18
Q

what makes up the conducting zone of the respiratory tract?

A

the nares to the terminal bronchioles

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19
Q

what is the conducting zone?

A

the conducting airways that aren’t involved in gas exchange

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20
Q

what are the secondary bronchi?

A

lobar bronchi

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21
Q

what are the tertiary bronchi?

A

segmental bronchi

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22
Q

what are the smallest airways without gas exchanging capability?

A

terminal bronchioles

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23
Q

what resists thoracic pressure changes in the conducting airways?

A

cartilage support in walls

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24
Q

what is the cartilage support in the walls of the upper 4 generations of the conducting airways?

A

C/U shaped hyaline rings

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25
Q

what is the cartilage support in the lobar and segmental bronchi and further branches before bronchioles?

A

cartilaginous plates

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26
Q

how are bronchiolar airways kept open?

A

by elastic connections between the airways and lung parenchyma

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27
Q

what is the vascular system of the conducting zone?

A

bronchial circulation

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28
Q

what is the purpose of the bronchial circulation?

A

to support gas exchange at level of lung tissues making up the conducting zone

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29
Q

what are the conducting airways lined with?

A

pseudostratified columnar ciliated epithelium

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30
Q

what do the conducting airways do?

A

conduct air to depths of the lung, enable phonation, control air flow via bronchoconstriction, warm inspired air and extract heat from expired air as part of thermoregulation, humidify air, filter and clear particles

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31
Q

how do the conducting airways filter and clear particles?

A

hairs in nostril filter large particles from air, in small airways where flow is slow particles settle out. particles cleared by coordinated action of motile cilia beat to propel mucus and entrapped particles on the mucociliary elevator. mucus propelled by ciliary action at up to 20 mm/min towards pharynx to be expelled from body or swallowed

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32
Q

what is the anatomic dead space?

A

the conducting airways- because they have no exchange function

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33
Q

what is the last gas to be breathed in and first to be breathed out?

A

dead space gas

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34
Q

what is alveolar dead space?

A

the volume which reaches the alveoli but doesn’t participate in gas exchange as the alveolus isn’t perfused

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35
Q

what is the physiological dead space?

A

the anatomical and alveolar dead space combined

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36
Q

what is the respiratory zone?

A

airways where gas exchange occurs

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37
Q

what are the respiratory airways?

A

respiratory bronchioles, alveolar ducts, alveoli

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38
Q

why is the pulmonary circulation’s flow very high?

A

receives the entire cardiac output

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39
Q

how quickly can red blood cells pass through pulmonary circulation?

A

less than a second

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40
Q

what makes up the majority of the lung volume?

A

the respiratory zone

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41
Q

what is the volume of the respiratory zone in humans?

A

2.5-3 litres

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42
Q

what is the volume of the conducting zone in humans?

A

150 ml

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43
Q

why is velocity of flow lower in the respiratory airways than the conducting airways?

A

respiratory airways have much greater cross-sectional area due to branching

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44
Q

what is the movement of gas by predominantly in the respiratory zone?

A

diffusion

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45
Q

why is diffusion very rapid in the respiratory zone?

A

distances are very short

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46
Q

what is an advantage of the dramatic reduction in air velocity in the respiratory zone?

A

inhaled dust and pollutant frequently settle out prior to the alveoli

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47
Q

what is the functional gas exchange unit of the lung?

A

alveoli

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48
Q

how many alveoli are there per human lung?

A

300-500 million

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49
Q

what are alveoli connected by?

A

septa

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50
Q

what are alveoli like?

A

polyhedral with cup-like openings which fold along septae when lung is deflated

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51
Q

how close is blood in pulmonary circulation to the air in alveoli

A

within 0.5 micrometers

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52
Q

what is within alveolar walls?

A

a dense network of tiny capillaries forming an almost continuous sheet of blood

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53
Q

what is the size of the SA for gas exchange between alveoli and the blood in humans?

A

75-140 m2

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54
Q

what is the driving force for diffusion of O2 into blood/CO2 into alveoli?

A

pressure gradient across the alveoli/blood interface

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55
Q

what are alveoli lined by?

A

type 1 and type 2 cells

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56
Q

what are type I cells in alveoli?

A

flat, branched, very thin cells with few organelles

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57
Q

what are type II cells in alveoli?

A

cells which secrete surfactant, have a role in immune function and are progenitors that can repopulate alveolar lining after injury

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58
Q

how thick is the alveolar blood gas barrier?

A

0.2-2 micrometers

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59
Q

what are the 3 layers of the alveolar wall?

A

surfactant, type 1 cells, capillary endothelium

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60
Q

what is the bronchial circulation system?

A

a high pressure, low flow system fed by bronchial arteries delivering oxygenated blood to the conducting airways and supporting structures of the lungs

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61
Q

what % of the left CO does bronchial circulation receive?

A

less than 2%

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62
Q

where does the majority of the bronchial circulation drain into?

A

pulmonary circulation

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63
Q

what does blood draining from the bronchial circulation into the pulmonary circulation cause?

A

small drop in pO2 between blood leaving alveoli fully oxygenated and blood entering left side of heart after mixing with deoxygenated blood from bronchial circulation

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64
Q

what does the pulmonary artery do?

A

receives blood from RV and its arterial branches, carries blood to the alveolar capillaries for gas exchange

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65
Q

what do the pulmonary veins do?

A

return the blood to the left atrium to be pumped by the left ventricle through the systemic circulation

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66
Q

what sort of system is the pulmonary circulation (pressure and flow)?

A

low pressure, high flow

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67
Q

what is the primary function of the capillary bed that places blood in intimate contact with alveoli?

A

facilitates rapid gas diffusion

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68
Q

what are the secondary functions of the capillary bed that places blood in intimate contact with alveoli?

A

blood reservoir, filters blood of emboli, metabolises vasoactive hormones

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69
Q

how does the capillary bed supplying blood close to alveoli act as a blood reservoir?

A

40% of its weight is blood, contains 10% of blood volume in humans- approximately equal to stroke volume of right heart under normal conditions

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70
Q

how does the capillary bed supplying blood close to alveoli filter blood of emboli?

A

emboli (such as blood clots, fat globules, air) are trapped in small pulmonary arterioles and capillaries. pulmonary endothelial cells release fibrinolytic agents to dissolve clots, absorb air emboli

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71
Q

what can emboli cause in the lungs?

A

large emboli can block blood flow to significant areas of lung, many small emboli can significantly compromise lung function, infectious emboli can set up pulmonary abscesses

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72
Q

how does the capillary bed supplying blood close to alveoli metabolise vasoactive hormones?

A

angiotensin I is converted to angiotensin II by angiotensin converting enzyme located on cell surface of the pulmonary endothelial cells- 80% converted during single pass through the pulmonary vasculature. noradrenaline, bradykinin, serotonin, prostaglandin E1, E2 and F2alpha all inactivated. adrenaline, histamine and vasopressin unaffected by passage through pulmonary circulation

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73
Q

where do lymph vessels in the supportive structures of the lung mainly drain into?

A

right thoracic lymph duct

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74
Q

what is the difference between driving pressure and mean capillary pressure in the pulmonary circulation vs systemic circulation?

A

much lower in pulmonary circulation

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75
Q

what is the difference in the resistance to flow in the pulmonary circulation vs the systemic circulation?

A

pulmonary is lower

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76
Q

what is the difference in the compliance of the pulmonary and systemic blood vessels and why?

A

pulmonary vessels much more compliant largely due to less muscle in their walls

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77
Q

what is the response to hypoxia in pulmonary vessels?

A

vasoconstriction

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78
Q

what is the response to hypoxia in systemic vessels?

A

vasodilation

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79
Q

what is the approx. pressure gradient for the entire CO being driven through the lungs vs through systemic circulation?

A

10mmHg vs 85-90mmHg

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80
Q

why is the resistance of the pulmonary circulation lower than the systemic vascular resistance?

A

enormous number of pulmonary vessels to accommodate the flow (dense capillary bed), vessels easily, passively dilated (highly compliant), when CO increases pressure doesn’t increases much as vessels dilate reducing resistance, capillaries that were collapsed are recruited to increase blood flow capacity

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81
Q

what 2 local mechanisms are responsible for reducing vascular resistance when CO increases?

A

capillary recruitment and capillary distension

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82
Q

what influences the extra-alveolar vessels?

A

intra-pleural pressure changes during the breathing cycle

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83
Q

why is alveolar vessel diameter not influenced by intrapleural pressures?

A

the tissue network surrounding the vessels buffers them from the intrapleural influences

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84
Q

what is the likely way alveolar hypoxia leads to vasoconstriction in the pulmonary circulation?

A

probably increases local sensitivity to circulating vasoconstrictive substances/decreases local release of a vasodilator

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85
Q

what is the pulmonary response to regional hypoxia?

A

a localised, regional vasoconstriction which diverts blood away from the affected region with little effect on pulmonary arterial pressure

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86
Q

what is the pulmonary response to general hypoxia?

A

general vasoconstriction which increases pulmonary vascular resistance, increased pulmonary arterial pressure

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87
Q

what can the vasoconstriction caused by general hypoxia lead to?

A

places extra work on right side of heart, can cause right sided heart failure. pressure backing up can cause resistance to venous return and disrupt Starlings forces causing peripheral oedema

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88
Q

what is the mean pulmonary arterial pressure at the top of the lung compared to the middle and base?

A

top is 11mHg less than middle, base is about 11mmHg greater than middle

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89
Q

why are blood flow and pressures within alveolar capillaries higher at the base than the top of the lung?

A

hydrostatic pressure gradient affected by gravity

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90
Q

what provides the driving force to push blood through the blood capillaries as they flow past alveoli?

A

the difference between pulmonary arterial and venous pressure

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91
Q

what does low hydrostatic pressure lead to in the lungs?

A

compressive force from alveoli (PA) may be greater than pressure in alveolar capillary, reduces blood flow to regions of low hydrostatic pressure (top of lung in standing biped)

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92
Q

what are the 3 zones the lungs can be divided into with 3 distinct interactions between alveolar pressure, pulmonary arterial pressure and pulmonary venous pressure?

A

zone 1= upper zone; zone 2= middle zone; zone 3= lower zone

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93
Q

what is the relationship between alveolar pressure, pulmonary arterial pressure and pulmonary venous pressure in zone 1?

A

alveolar pressure is greater than arterial pressure so pulmonary capillaries are collapsed and there is no flow

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94
Q

what is the relationship between alveolar pressure, pulmonary arterial pressure and pulmonary venous pressure in zone 2?

A

arterial pressure is greater than alveolar pressure due to additional hydrostatic influence closer to level of heart. alveolar pressure greater than venous pressure so blood flow determined by difference between arterial and alveolar pressure

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95
Q

what is the relationship between alveolar, pulmonary arterial and pulmonary venous pressure in zone 3?

A

arterial and venous pressures greater than alveolar, flow determined by the usual arterial-venous pressure difference

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96
Q

which zone conditions don’t exist in normal healthy individuals?

A

zone 1

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97
Q

when can zone 1 conditions exist?

A

if pulmonary arterial pressure falls, as in severe haemorrhage, or if alveolar pressure is increased, as in forced ventilation

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98
Q

why are alveoli in the base of the lungs usually better ventilated than at the top?

A

gravity related vertical gradient of pleural pressure creates different transpulmonary pressure during normal ventilation; bases have more room to expand than apices; compliance differences between lung regions; pattern of breathing can influence regional distribution of ventilation; regional lung pathology and body position

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99
Q

when is the ventilation/perfusion (V/Q) ratio at 1?

A

at approximately the level of the 3rd rib

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100
Q

when is the ventilation/perfusion (V/Q) ratio >1?

A

higher up in thorax. indicates presence of well-ventilated alveoli with poor blood flow so gas exchange can’t occur- dead space

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101
Q

when is the ventilation/perfusion (V/Q) ratio <1?

A

lower down in thorax, suggests good blood flow but insufficient ventilation (due to alveolar collapse in base of lung, airway obstruction or gas exchange impairment)

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102
Q

what does a V/Q of 0 indicate?

A

complete ‘shunt’ of blood past gas exchange surface

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103
Q

what is venous admixture?

A

blood that hasn’t participated in gas exchange being added to the pulmonary venous (oxygenated) circulation

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104
Q

what is a normal % of venous admixture from bronchial circulation?

A

20%

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105
Q

why do airflow and blood flow both increase down the lung?

A

ventilation and perfusion are gravity dependent

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106
Q

why is blood flow proportionately greater at the base and ventilation proportionately greater at the apex?

A

blood flow shows a 5 fold difference from top to bottom, ventilation shows a 2 fold difference

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107
Q

what determines the pulmonary mixed venous gas concentrations?

A

the relative contribution of the CO exposed to different V/Q rations

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108
Q

what region of the lung does TB tend to localise to?

A

apex, since high V/q ration provides favourable high PO2 environment for the Mycobacterium tuberculosis

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109
Q

how is a low V/Q ratio compensated for?

A

increase in overall ventilation, regional vasoconstriction induced by local hypoxia to shunt blood from poorly ventilated alveoli

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110
Q

how is a high V/Q ratio compensated for?

A

local arterial PCO2 will fall resulting in increase in pH which causes localised increases in airway resistance, shifting ventilation to alveoli with normal V/Q ratios

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111
Q

why does pulmonary fluid accumulation in the interstitial space impair gas exchange?

A

increases the diffusion distances

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112
Q

how is the interstitial pressure in the lungs modulated?

A

by the surface tension of the alveoli (tends to expand fluid volume) and the alveolar pressure (tends to compress fluid volume)

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113
Q

how is net fluid exchange across the capillary determined?

A

difference in hydrostatic and colloid pressure across capillary wall

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114
Q

what counters hydrostatic pressure in the pulmonary circulation?

A

the colloid osmotic pressure difference across the capillary wall

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115
Q

why are there higher concentrations of protein in the interstitial fluid in the lung than the interstitial space in the periphery?

A

the pulmonary capillaries are more permeant to proteins than capillaries in the systemic circulation

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116
Q

where is the colloid osmotic pressure greater, the capillary or the interstitial space?

A

in the capillary

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117
Q

what drains the net flow of fluid into the interstitial space?

A

lymph system in terminal bronchiole region

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118
Q

what is the total outward force of fluid from capillaries into the pulmonary interstitium?

A

29mmHg

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119
Q

what 2 factors serve to ensure interstitial fluid doesn’t enter alveoli?

A

interstitial pressure is negative so pulls water away from alveoli, surfactant acts as barrier to fluid entering alveoli

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120
Q

what can lead to filtration of fluid exceeding removal in the pulmonary interstitium?

A

increased pulmonary capillary pressure, increased pulmonary permeability, decreased capillary colloid osmotic pressure, failure of lymphatic drainage

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121
Q

what is the cause of death usually in fresh water drowning?

A

aspiration of fresh water into lungs accompanied by rapid diffusion of pure water across alveolar membrane into pulmonary capillaries driven by high colloid osmotic pressure in capillary

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122
Q

what does the rapid diffusion of pure water into pulmonary capillaries in fresh water drowning lead to?

A

RBC lysis releasing K+, dilution of extracellular Na+, leading to cardiac fibrillation and death

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123
Q

what is the result of aspiration of sea water with osmolarity greater than plasma?

A

net flow of water out of the pulmonary capillaries into the interstitial space and alveoli after overcoming the negative interstitial pressure, death by asphyxiation

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124
Q

what is flow?

A

change in pressure/resistance

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125
Q

what would happen if the lungs weren’t held partially inflated?

A

would collapse and expel all air from them completely

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126
Q

what is the thoracic cage made up of?

A

12 pairs of ribs, a sternum and a set of internal and external intercostal muscles that lie between the ribs

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127
Q

what encases the lungs?

A

thin visceral pleura

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128
Q

what separates the visceral pleura of the lungs and the parietal viscera of the thoracic cage?

A

thin layer of fluid (approx 10µm thick)

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129
Q

what determines volume of the thoracic cavity at rest?

A

inward elastic recoil properties of lungs, outward elastic recoil tendency of chest wall, meaning there is a small but consistent negative pressure set up within pleural space

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130
Q

what is the transpulmonary pressure?

A

the difference between alveolar pressure and pleural pressure, outward force that keeps alveoli open

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131
Q

what happens if the thoracic cavity is punctured?

A

negative pressure within intrapleural space is lost and lungs collapse to very small volume- pneumothorax. chest wall expands to resting state due to its outwardly directed elastic recoil no longer being opposed by inward elastic recoil of lungs

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132
Q

what is Boyle’s Law?

A

P1V1 = P2V2

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133
Q

what happens to the thoracic cage during inspiration?

A

diaphragm contracts and flattens and pushes abdominal contents down increasing the intrathoracic volume and decreasing the intrapleural pressure, external intercostal and anterior internal intercostal skeletal muscles between ribs contract lifting sternum upwards and widening the thorax

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134
Q

what happens when inspiratory muscles contract?

A

pleural pressure becomes more negative to point where it overcomes elastic recoil of lungs so lung volume also expands. alveolar pressure drops to below atmospheric pressure, produces pressure gradient between upper airway and alveoli, produces airflow into lungs- ends when alveolar pressure = atmospheric pressure

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135
Q

what happens to the thoracic cage during expiration?

A

diaphragm and intercostal muscles relax, allows the elastic components of the lung to recoil reducing thoracic volume (eupnea), active contraction of abdominal muscles and expiratory muscles to actively compress thoracic space if increased ventilation required

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136
Q

what are transmural pressures?

A

differences in pressure recorded across organ and tissue walls

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137
Q

what are the 3 transmural pressures in the mammalian respiratory system?

A

transpulmonary, trans chest wall and trans total system

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138
Q

how does inspired air flow through the conducting zone?

A

bulk flow

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139
Q

how are transmural pressures calculated?

A

the pressure differential of the inside compartment minus the outside compartment

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140
Q

is the transpulmonary pressure always positive or negative in normal breathing?

A

positive

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141
Q

what is the distending pressure?

A

the transpulmonary pressure keeping the lungs inflated

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142
Q

what determines the volume of the thoracic cavity at end expiration under normal conditions?

A

the outward elastic recoil tendency of the chest wall and the inward elastic recoil properties of the lungs

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143
Q

what is a spirometer used for?

A

measuring the volume of air breathed in and out of the lungs

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144
Q

what is bulk flow?

A

movement of a mass of fluids down a pressure gradient- active process reliant on pressure gradient

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145
Q

what is a fluid?

A

substance that has no fixed shape and yields easily to external pressure- a liquid or gas

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146
Q

what is a gas?

A

substance or matter in a state with no fixed shape and no fixed volume

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147
Q

what is the lung volume at any given pressure like in inflation compared to deflation?

A

smaller in inflation than deflation

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148
Q

what is respiratory compliance?

A

the change in lung volume per unit change in transpulmonary pressure gradient

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149
Q

what is static compliance?

A

the change in lung volume per unit change in transpulmonary pressure in the absence of flow

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150
Q

what is static compliance composed of?

A

chest wall compliance, lung tissue compliance

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151
Q

what is chest wall compliance?

A

relates to the tendency of the chest wall to expand and exert a negative pressure at all lung volumes

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152
Q

what is lung tissue compliance made up of?

A

elastic forces of the lung tissue, elastic forces caused by surface tension of the fluid that lines the inside walls of the alveoli and other lung air spaces

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153
Q

how is lung compliance normalised to correct for differences in size?

A

dividing compliance by FRC yielding value called specific compliance

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154
Q

why is there a lower pleural pressure at the apex than the base of the lungs?

A

the ‘downward pull’ of gravity

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155
Q

what does the higher transpulmonary pressure at the apex of the lungs result in?

A

the alveoli being expanded more than alveoli at the base leading to regional difference in compliance of the lung

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156
Q

what does the greater compliance of the base of the lung compared to the apex of the lung lead to?

A

base of lung undergoes a greater increase in volume for a given pressure change relative to the apex

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157
Q

what is the net result of the greater compliance in the base of the lung?

A

greater proportion of the tidal volume goes to the base of the lung so a greater alveolar ventilation occurs at the base

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158
Q

what generates the elastic forces of the lung tissue?

A

the collagen and elastin fibres within the lung parenchyma

159
Q

why does the compliance curve flatten at greatest lung volumes?

A

when collagen and elastin fibres stretched towards their limit they exert a greater resistance to expansion

160
Q

what proportion of the elastic recoil of the lungs are the elastic forces generated by surface tension responsible for?

A

more than 2/3

161
Q

what is the calculation relating pressure and surface tension?

A

pressure= (2xsurface tension)/radius

162
Q

what is surfactant?

A

mixture of phospholipids, proteins and ions produced by type II alveolar epithelial cells in the alveolus and secreted into the water of the alveolus. acts as a detergent

163
Q

what is the principle agent in surfactant?

A

dipalmitoyl phosphatidyl choline (DPCC)

164
Q

why is surfactant turnover high?

A

continual renewal of surfactant of alveolar inner surface brough about by each expansion of the lungs

165
Q

how does DPPC reduce surface tension?

A

molecules hydrophilic at 1 end and hydrophobic at other, when molecules aligned on inner alveoli surface their intermolecular forces oppose the normal attractive forces between surface water molecules

166
Q

why is the reduction in surface tension by surfactant greatest when the film is compressed?

A

molecules of DPPC crowded together so greater repulsion

167
Q

why is there a smaller amount of surfactant per unit area when the alveoli reinflate and lungs expand, meaning less of an ability to reduce surface tension?

A

some surfactant is squeezed out of the surface layer at low lung volumes

168
Q

where is surfactant positioned in the alveoli and what does this mean?

A

positioned at surface of the alveolar lining fluid so displaces water molecules at the air-liquid interface reducing cohesive forces of the fluid lining the airways

169
Q

how does sighing help to maintain compliance?

A

increases release of surfactant and helps disperse it

170
Q

why is the lung functionally immature prior to 85-90% of the gestation period?

A

doesn’t have adequate surfactant production

171
Q

what causes infant respiratory distress syndrome?

A

low surfactant production reducing lung compliance

172
Q

how is infant respiratory distress syndrome treated?

A

antenatal provision of corticosteroids to mother to prime foetus to produce surfactant, artificial surfactant in pre-term neonates, positive end expiratory pressure ventilation to reduce alveolar collapse and fluid accumulation

173
Q

what is hysteresis?

A

differences between pressure-volume relationships of inflation and deflation portions of compliance diagram

174
Q

why is the compliance diagram shaped the way it is?

A

collapsed alveoli require extra mechanical energy to open than well-inflated alveoli; alveolar surface tension is lower in a deflated lung; stress relaxation (loss of energy in lung parenchyma which occurs with stretch); gas absorption during measurement of volumes in live subjects

175
Q

what are the functional consequences of a loss of lung compliance?

A

stiff lung, more work performed to maintain normal alveolar ventilation so energy cost of breathing increased

176
Q

what are the functional consequences of an increase in compliance?

A

individuals can inflate the lung but have great difficulty exhaling due to loss of elastic recoil properties of lung so extra work needed to force air out of lungs

177
Q

what causes the resistance of the respiratory system?

A

inertia of lung/chest wall tissues, inertia of the gas, gas compression, resistance to deformation of the tissues (non-elastic), resistance from air-flow friction

178
Q

what affects airway resistance?

A

airway diameter (greater resistance in narrower airways) and turbulent or laminar flow (greater with turbulent flow)

179
Q

where does turbulent flow occur in the lungs?

A

in the large airways such as the trachea and large bronchi

180
Q

what causes the sounds which can be heard when breathing deeply/with a stethoscope when breathing normally?

A

turbulent air flow

181
Q

what is laminar flow?

A

streamlined flow of air that runs parallel to the sides of the airways and is silent

182
Q

where does laminar flow occur in the airways?

A

the small airways where flow is very slow

183
Q

what is transitional flow?

A

a mix between laminar and turbulent flow

184
Q

what is most of the air flow in the lower airways of the lung?

A

turbulent flow

185
Q

effect of turbulent flow on resistance to flow?

A

increases it

186
Q

what type of air flow does the flow equation used by physiologists to describe airflow in the lungs define?

A

laminar flow

187
Q

what is the most important factor to resistance?

A

tube diameter- small changes will dramatically change resistance

188
Q

where is the greatest resistance to airflow in the lungs?

A

upper respiratory tract

189
Q

why is the resistance in the bronchioles low despite the small individual diameters?

A

very numerous so only tiny amounts of air must flow through each

190
Q

where does most of the pressure drop in the airways occur before?

A

the 7th generation

191
Q

what can regional bronchiole constriction help to maintain?

A

a normal ventilation:perfusion ratio

192
Q

what causes dilation of the bronchioles?

A

sympathetic stimulation of adrenergic fibres by stimulating beta-adrenergic receptors

193
Q

effect of isoproterenol and epinephrine on bronchioles?

A

cause dilation by stimulating beta2-adrenergic receptors in airways

194
Q

what is the effect of PCO2 on conducting airway dilation/constriction?

A

increased PCO2 can induce dilation, decreased PCO2 induces airway constriction

195
Q

what is the effect of parasympathetic stimulation of the bronchioles by the vagus nerve?

A

stimulates cholinergic fibres causing constriction and stimulation of mucus secretion

196
Q

what stimulates parasympathetic nerves in the lungs?

A

local reflexes, noxious stimuli (gases or infection), CNS

197
Q

what does histamine release by mast cells cause in the bronchioles? what condition is this important in?

A

bronchoconstriction, asthma

198
Q

why are helium-oxygen mixtures frequently used in underwater breathing situations?

A

helium reduces resistance of breathing

199
Q

why does resistance in airways decrease as lungs expand?

A

radius of bronchi and small airways increases

200
Q

what do spirometers measure directly and what value is determined from spirometer data?

A

directly measure lung volumes, lung capacities are calculated theoretical values

201
Q

what are the lung volumes measured with a spirometer?

A

tidal volume, expiratory reserve volume, residual volume

202
Q

what is the tidal volume?

A

volume of gas inhaled or exhaled during the respiratory cycle

203
Q

what is the expiratory reserve volume?

A

volume of gas that can be maximally exhaled from the end-inspiratory level during tidal breathing

204
Q

what is the residual volume?

A

volume of gas remaining in the lung after maximal exhalation

205
Q

what standard capacities can be determined from spirometer data?

A

functional residual capacity, inspiratory capacity, vital capacity, total lung capacity

206
Q

what is the functional residual capacity?

A

the volume of gas present in the lung at end expiration during tidal breathing

207
Q

what is the inspiratory capacity?

A

maximum volume of gas that can be inspired from the FRC

208
Q

what is the vital capacity?

A

volume change at the mouth between the positions of full inspiration and complete expiration

209
Q

what is the total lung capacity?

A

volume of gas in the lungs after maximal inspiration

210
Q

why can’t RV and FRC be measured directly from spirometry?

A

the lungs can’t be completely emptied following forced expiration

211
Q

why does the descending portion of the flow-volume curve always take the same path regardless of force of expiration?

A

compression of the airways by intrathoracic pressure during forced expiration

212
Q

what changes occur during the initiation of forced expiration?

A

pleural pressure rises to above atmospheric, alveolar pressure becomes greater than pleural pressure

213
Q

what causes the added pressure in the alveoli during initiation of forced expiration?

A

elastic recoil of the lung acting in series with the positive intrapleural pressure

214
Q

what is the equal pressure point (EPP)?

A

point during maximal forced expiration where the transairway pressure is 0

215
Q

what are the consequences of the large positive intrathoracic pressures produced in forced expiration?

A

elastic recoil means alveolar pressures become even more positive- alveoli remain open; airway resistance means airway pressure reduces as distance from alveolus increases; trans-airway pressure (airway pressure - pleural pressure) will at some point become 0 (EPP), then negative- collapsing airway,

216
Q

why do emphysema patients breath out through pursed lips?

A

this reduces the slope of the pressure gradient between alveoli and the outside- prevents airway collapse by moving EPP towards the mouth into airways supported by cartilage

217
Q

why can’t peak flow rate be increased by increased expiratory effort?

A

the increased effort increases the intrapleural and alveolar pressure so transairway pressure remains constant

218
Q

what primarily determines maximal flow rates and why does maximal flow rate fall with decreased lung volume?

A

elastic recoil of lung which generates the alveolar pressure, decrease in elastic recoil as lung volume decreases

219
Q

what is forced maximal exhalation?

A

when exhalation performed as forcibly and rapidly as possible

220
Q

what is forced vital capacity?

A

the measure provided by forced maximal exhalation

221
Q

how can FEV be normalised for lung size?

A

by expressing it as a percentage of the FVC- approx. 80% under normal conditions

222
Q

what is STPD?

A

standard temperature and pressure dry

223
Q

what conditions are required for STP?

A

273.15 K, pressure of 105Pa, dryness of gas mixture

224
Q

how many litres will a mole of gas occupy at STPD?

A

22.4

225
Q

Ideal gas law?

A

PV = nRT

226
Q

combined gas law?

A

(P1V1)/T1 = (P2V2)/T2

227
Q

what is BTPS?

A

body temperature and pressure saturated- physiological conditions within the body

228
Q

Dalton’s Law?

A

the total pressure of an ideal gas mixture is the sum of the partial pressures of the gases in the mixture. in a mixture of gases the partial pressure is the pressure a gas would exert if it occupied that volume alone

229
Q

calculation for partial pressure of a gas?

A

the fraction of the mixture occupied by the gas x the total pressure exerted by the mixture

230
Q
A
231
Q

why is there (very small) variation of partial pressure of O2 and CO2 around the mean in the alveoli?

A

because breathing is intermittent and a small amount of air is taken into the lungs with each breath relative to the volume of gas that isn’t exchanged (tidal volume vs FRC)

232
Q

what partial pressure does saturated water vapour exert at atmospheric pressure?

A

47mmHg

233
Q

what happens to the air inhaled into the lungs (temp, composition, etc)?

A

it is warmed to 37 degrees, volume increases, it is humidified until saturated with water vapour which dilutes the original gases, O2 removed and CO2 added

234
Q

what is the major respiratory adaptation to increased metabolic rate?

A

increased ventilation of the respiratory exchange surface- increases delivery of O2 and removal of CO2

235
Q

what is ventilation rate the product of?

A

tidal volume and respiratory rate

236
Q

what does total lung ventilation refer to?

A

the total rate of air flow in and out of the lung during normal tidal breathing. product of the tidal volume and respiratory rate

237
Q

what is the alveolar ventilation?

A

the ventilatory rate of the gas exchange areas

238
Q

what is a person breathing rapid, shallow breaths doing?

A

moving air in and out of their dead space with no alveolar ventilation

239
Q

why doe alveoli with reduced blood flow have alveolar ventilation in excess of what’s needed?

A

to maintain appropriate gas exchange for the reduced blood flow

240
Q

what is the expired minute volume?

A

the volume of air moved out of the lungs in 1 minute- tidal volume x breathing frequency

241
Q

why doesn’t the minute ventilation represent the amount of O2 reaching the alveoli?

A

anatomic dead space

242
Q

issues with correcting tidal volume by dead space volume to estimate alveolar ventilation?

A

it is difficult to quantify dead space

243
Q

what is the alveolar ventilation equation?

A

volume CO2 expired per unit time/fractional concentration of CO2 in alveolar gas

244
Q

what observation does the alveolar ventilation rate equation take advantage of?

A

all of the CO2 exhaled by the body must come from gas exchange in the alveoli- only place where gas exchange occurs and inspired air contains no CO2

245
Q

how can the volume of CO2 expired per unit time be measured?

A

by collecting expired gas over a defined time period and measuring the CO2 concentration within it

246
Q

how is the fractional concentration of CO2 in alveolar gas measured?

A

by sampling the last portion of the tidal volume during expiration which contains pure alveolar gas

247
Q

what values are needed to calculate alveolar pressure of CO2?

A

alveolar ventilation and volume of expired CO2

248
Q

effect of high alveolar ventilation?

A

higher concentration of oxygen, lower concentration of CO2, in alveoli and arteries

249
Q

effect of doubling alveolar ventilation on PCO2?

A

halves alveolar PCO2

250
Q

what is the main use for the alveolar gas equation?

A

calculating a theoretical alveolar oxygen partial pressure to determine the A-a gradient

251
Q

what is the A-a gradient?

A

theoretical alveolar oxygen - actual arterial oxygen

252
Q

what does the alveolar gas equation assume?

A

healthy lung with no ventilation-perfusion mismatch or diffusion defects

253
Q

what does the alveolar gas equation calculate?

A

what the arterial PO2 would be when arterial PCO2 is known

254
Q

what is the difference in alveolar and arterial PO2 a result of?

A

a mixture of factors including venous admixture and ventilation/perfusion mismatching

255
Q

what pathologies can cause ventilation/perfusion mismatch?

A

shunting of blood bypassing the pulmonary circulation, disrupted ventilation (e.g. an occluded airway), perfusion (e.g. a blood clot in the pulmonary vessels)

256
Q

what is Henry’s Law?

A

concentration of gas in liquid= solubility constant x partial pressure of gas in contact with the liquid

257
Q

what is Henry’s Law used for?

A

determining amount of gas in solution where the air meets the layer of liquid in the alveoli

258
Q

what is the amount of gas in solution determined by when a gas and liquid in contact are allowed to equilibrate?

A

partial pressure of the gas in contact with the solution, chemical properties of the gas and liquid (solubility constant), temperature

259
Q

why is haemoglobin needed?

A

to increase the O2 carrying capacity of the blood as O2 is much less soluble in blood than CO2

260
Q

what is Fick’s law?

A

rate of gas diffusion across permeable membrane= diffusion coefficient x solubility coefficient x SA of membrane x difference in partial pressure of gas across membrane/thickness of membrane

261
Q

what determines rate of diffusion across a permeable membrane?

A

chemical properties of diffusing substance and membrane, thickness of membrane, SA of membrane, partial pressure/concentration gradient of gas across membrane, diffusion coefficient, solubility of molecule

262
Q

in what ways can gas exchange at the alveoli be limited?

A

can be diffusion limited or perfusion limited

263
Q

which is more common, diffusion or perfusion limited gas exchange?

A

diffusion limited

264
Q

what is the oxygen cascade?

A

gradual depletion of PO2 in airways as diluted by humidification, then in blood due to venous admixture and ventilation perfusion mismatch, then as it diffuses into metabolising tissues

265
Q

what 2 means is oxygen transported by?

A

dissolved in blood, mostly bound to haemoglobin

266
Q

what does mammalian type A haemoglobin consist of?

A

4 subunits, each has 1 haem associated with globin protein, each subunit has 2 pairs of polypeptide chains- 2 alpha and 2 beta

267
Q

what does mammalian type F (foetal) haemoglobin consist of?

A

4 subunits, each has 1 haem associated with globin protein, each subunit has 2 pairs of polypeptide chains- 2 alpha and 2 gamma

268
Q

differences in haemoglobin S (sickle cell type)?

A

small amino acid substitution in beta chain reduces oxygen affinity of haemoglobin while altering solubility of deoxy form- results in crystallisation of the haemoglobin and sickle shape and fragility of RBCs

269
Q

what is the structure of haem?

A

protoporphyrin consisting of 4 pyrroles with a ferrous iron (Fe2+) at the centre. each ferrous iron can combine reversibly with a single molecule of O2

270
Q

colour of Hb and HbO2?

A

Hb is blue-ish, HbO2 is bright red

271
Q

why do patients with poor lung function tend to have cyanosis (blue tinge to normally pink tissues)?

A

gas exchange compromised, less oxygenated Hb (which is red), more regular Hb which is blue-ish

272
Q

what gives haemoglobin sigmoidal properties?

A

cooperative binding- as each haemoglobin subunit combines with oxygen it increases the affinity for oxygen of the remaining subunits

273
Q

what is anaemia? what effects does it have?

A

low concentration of RBCs in circulation. means O2 content will be low as less Hb in blood, causes peripheral vasoconstriction so patients tend to be pale

274
Q

why does the spleen contract during exercise?

A

to increase the RBC fraction of the blood and its Hb concentration to increase its O2 carrying capacity

275
Q

what limits the usefulness of splenic contraction during exercise?

A

increased blood viscosity that affects perfusion of peripheral capillaries and increases cardiac work

276
Q

how does Hb maintain the partial pressure gradient at the alveolus?

A

as O2 diffuses into blood it is bound to Hb so doesn’t exert a partial pressure

277
Q

why can changes in ventilation be used to regulate arterial PCO2 without affecting O2 supply?

A

quantity of O2 in arterial blood remains the same over range of high ventilation rates

278
Q

what does a left shift in the haemoglobin O2 dissociation curve signify?

A

greater O2 affinity- more O2 is bound to Hb at a given PO2

279
Q

why is there a left shift in the oxygen dissociation curve of fetal haemoglobin compared to adult Hb?

A

low PO2 within placental circulation so adult Hb isn’t well saturated, CO binding causes the left shift so less oxygen is offloaded in tissues

280
Q

factors that will shift the O2 dissociation curve to the right?

A

H+, CO2, temperature, BPG

281
Q

why does greater metabolic rate tend to increase unloading of O2 from Hb at the tissue?

A

products of metabolism (heat, CO2, H+ in lactic acid) all shift O2 dissociation curve to right

282
Q

what is the Bohr effect?

A

the effect of CO2 and H+ ions on the affinity of haemoglobin for O2

283
Q

what is 2,3-biphosphoglycerate? how does it interact with Hb?

A

metabolite present in RBCs. binds and stabilises Hb so that there is right shift in O2-Hb dissociation curve

284
Q

how does the body use B/DPG to cause better unloading of O2 in hypoxic tissues?

A

conditions that cause low tissue PO2 (e.g. acclimatisation to altitude) stimulate production of B/DPG

285
Q

difference between right shift caused by DPG and right shift caused by pH, CO2 and temperature?

A

DPG causes permanent right shift that will impair O2 loading at lungs- the others are reversed in the lungs

286
Q

effect of pregnancy on maternal BPG and Hb?

A

BPG increases causing right shift in Hb- since fetal Hb relatively left-shifted oxygen transfers to fetal Hb from maternal ensuring fetal Hb saturation is high enough for transport of O2 to fetal tissues

287
Q

effect of CO on Hb-oxygen relationship?

A

CO has an extremely high affinity for Hb, will displace O2 from Hb forming carboxyhaemoglobin so less O2 will bind to Hb, total O2 content of blood will be dramatically reduced. slso causes left shift in oxygen-Hb dissociation curve so bound O2 can’t be offloaded in tissues

288
Q

complications of CO poisoning diagnosis?

A

normal pulse oximetry readings of saturation, normal pink colouring, blood stays red when CO binds Hb, CO is odourless, colourless and non-irritating

289
Q

how is CO2 transported in the blood?

A

produced in the tissues, diffuses into the capillary blood for transport to the lungs. diffuses out of respiring tissues into blood along concentration gradient.

290
Q

what 3 forms is CO2 transported into the blood via?

A

bicarbonate, dissolved and bound to proteins (particularly Hb)

291
Q

how is the majority of CO2 transported into the blood?

A

as bicarbonate

292
Q

why are chloride levels much higher in RBCs than blood or tissues?

A

in RBCs carbonic anhydrase catalyses conversion of CO2 to bicarbonate, which is exchanged for Cl- ions to maintain electrical neutrality

293
Q

what is the Haldane effect?

A

more CO2 is carried in deoxygenated blood than oxygenated blood as O2 displaces CO2 from Hb and deoxygenated Hb is a weaker acid then oxyhaemoglonin so is a better buffer, so more HCO3 is produced as a means of transporting CO2

294
Q

what is the sequence of events for CO2 movement out of the tissues?

A

dissolved CO2 enters plasma down its concentration gradient. some bound to proteins as carbamino compounds, small amount converted to HCO3-. H+ formed from both reactions buffered by blood buffers. dissolved CO2 enters RBC where small fraction remains dissolved. most CO2 is hydrated forming HCO3- and H+- catalysed by carbonic anhydrase. H+ are buffered by the large number of imidazole groups on the His residues of the alpha and beta polypeptide chains of Hb

295
Q

what is Hamburger’s phenomena/the Cl- shift?

A

most HCO3- leaves the RBC down its concentration gradient in exchange for Cl-

296
Q

effect of extra intracellular HCO3- and Cl-?

A

increase the intracellular osmolarity and osmotic pressure resulting in water influx and cell swelling

297
Q

what maintains the concentration gradient for CO2 diffusion into the RBC?

A

efflux of HCO3-, production of carbamino compounds, H+ buffering by Hb

298
Q

what are the 4 general categories of hypoxia?

A

hypoxic hypoxia, anaemic hypoxia, circulatory hypoxia, histotoxic hypoxia

299
Q

what is hypoxic hypoxia?

A

low arterial blood PO2 accompanied by inadequate Hb saturation

300
Q

what is anaemic hypoxia?

A

reduced O2 carrying capacity of the blood

301
Q

what is circulatory hypoxia?

A

when too little oxygenated blood is delivered to the tissues

302
Q

what is histotoxic hypoxia?

A

normal O2 delivery to tissue but cells unable to use the oxygen available to them (e.g. cyanide poisoning)

303
Q

what is hyperoxia?

A

when an above normal arterial PO2 occurs

304
Q

what is hypercapnia?

A

excess CO2 in arterial blood, caused by hypoventilation

305
Q

what is hypocapnia?

A

below normal arterial pCO2 levels brought about by hyperventilation

306
Q

what can override central pattern generator in breathing?

A

cerebrum

307
Q

what monitor movements of the chest wall?

A

proprioceptive receptors

308
Q

what is ‘system control theory’?

A

when a central controller sends signals to effector units such that a controlled parameter is altered with continuous monitoring by specialised sensors fed back to central controller

309
Q

what are the 3 regions of the medulla oblongata and pons that make up the central pattern generator?

A

medullary centre, apneustic centre, pneumotaxic centre

310
Q

what are the 3 major groups of neurons involved in the central pattern generator?

A

dorsal respiratory group, ventral respiratory group, pneumotaxic centre

311
Q

location and role of dorsal respiratory group of neurons?

A

dorsal medulla, primarily nucleus of solitary tract. mainly causes inspiration

312
Q

location and role of ventral respiratory group of neurons?

A

ventral medulla, mainly causes expiration

313
Q

location and role of pneumotaxic centre neurons?

A

dorsal pons, mainly controls rate and depth of respiration

314
Q

what does the nucleus of the solitary tract contain?

A

dorsal respiratory group of neurons, termination of vagal and glossopharyngeal nerves

315
Q

what are the 2 groups in the medullary respiratory centre?

A

dorsal and ventral

316
Q

what group in the medullary respiratory centre is most important in normal inspiration?

A

dorsal respiratory group

317
Q

pattern of firing of dorsal respiratory group?

A

rhythmic pattern independent of other inputs, which ramps up over time then abruptly stops for approx. 3 seconds

318
Q

where are APs from the dorsal respiratory group transmitted to? what is their effect?

A

the diaphragm and intercostal muscles, gradually increase their contraction causing steady inspiration followed by rapid relaxation which enables elastic recoil of chest wall and lungs to cause expiration

319
Q

what is responsible for the entirety of exhalation in quiet breathing?

A

passive exhalation

320
Q

when does the ventral respiratory group become active?

A

only when there is greater demand on respiratory system such as in intense exercise

321
Q

what is the effect of the neurons in the ventral respiratory group?

A

some cause inspiration, some cause expiration

322
Q

what do the neurons in the ventral respiratory group appear to be particularly important in?

A

increasing the depth of inspiration and force of exhalation by activating the contraction of abdominal muscles to cause rapid, active exhalation

323
Q

function of the pontine respiratory group of pneumotaxic centre?

A

appears to switch off inspiration thereby regulating tidal volume and breathing frequency

324
Q

what are the neurons in the pneumotaxic centre called?

A

pontine respiratory group

325
Q

effect of a strong or weak pneumotaxic signal?

A

strong can increase respiratory rate to 40 breaths pm, weak may be associated with very slow breathing rate

326
Q

effect of direct electrical stimulation of the pneumotaxic centre?

A

attenuates the inspiratory ramp-may play roles in fine-tuning/controlling period of respiratory rhythm

327
Q

possible role of neurons in the apneustic centre?

A

may be prolonging the ‘inspiratory ramp’ in the medullary inspiratory centre as intact apneustic centre causes regular inspiratory phase of breathing cycle and severed results in irregular breathing cycle

328
Q

why is positioning the central pattern generator in the brain stem ideal?

A

it is under autonomic neural control and requires no consciuous input

329
Q

interaction of voluntary and automatic use of respiratory muscles?

A

can override automatic control of breathing by breath holding but automatic system will eventually override voluntary one

330
Q

evidence that the central pattern generator is located within the medullary centre?

A

transection below the medulla results in complete cessation of breathing, sectioning above pons (with vagus nerve intact) leaves breathing unaffected

331
Q

evidence that vagal afferent input is important in terminating inspiration?

A

if vagus nerve intact sectioning above pons leaves breathing unaffected but vagotomy results in reduction in breathing frequency and increase in tidal colum, if both vagus nerves cut breathing stops at full inspiration or see inspiratory spasms interrupted by intermittent expirations

332
Q

evidence that the pneumotaxic centre inhibits the inspiratory phase?

A

transection at level of upper pons leads to slowing of respiration and increase in tidal volume

333
Q

effect of sectioning above the medulla + then of vagotomy?

A

rhyhmic but irregular breathing, vagotomy slows irregular pattern

334
Q

role of stretch receptors in influencing ventilation?

A

in muscular walls of bronchi and bronchioles. detect overinflation of lungs at high tidal volumes, trigger termination of inspiratory ramp via vagal and dorsal respiratory group

335
Q

roles of irritant receptors and mechanoreceptors in influencing ventilation?

A

detect chemicals or particulates in airways, can trigger sneezing and coughing reflexes aimed at dislodging foreign material from airway

336
Q

role of proprioceptive receptors in influencing ventilation?

A

detect mechanical distortion of the respiratory muscles and their connective tissue components- information integrated to alter strength of contraction of muscles to maintain ventilation

337
Q

effect of anaesthetic drugs on respiration?

A

depress the function respiratory centre, hypoventilation common without mechanical ventilation

338
Q

why do opioids cause respiratory arrest?

A

medulla is rich in opioid receptors

339
Q

why can raised intracranial pressure impair ventilation?

A

caudal position of pons/medulla makes it susceptible to compression by back of skull

340
Q

coupling of respiratory rhythm to movement in galloping horses and dogs?

A

as forequarters lift up the abdominal contents move backwards, diaphragm flattens and lungs expands. when stride completed forequarters are lower, diaphragm moves forward and is more domed, air forced out of lungs

341
Q

what variable is under closest control in the respiratory control system?

A

arterial pCO2

342
Q

relation of breathing to arterial blood PO2, PCO2 and [H+]

A

inversely related to pO2, directly related to PCO2 and [H+]

343
Q

proof that breathing is more related to pCO2 than PO2?

A

if PaCO2 rises without accompanying hypoxia then pulmonary ventilation rises

344
Q

what lies directly below respiratory centre on ventral aspect of medulla?

A

chemosensitive area important in regulation of respiration

345
Q

what is the blood brain barrier?

A

highly selective semipermeable border of endothelial cells that regulates the transfer of solutes and chemicals between the circulatory system and CNS

346
Q

effect of CO2 crossing the blood brain barrier?

A

reacts with water in CSF leads to increased [H+] in CSF, HCO3- moves across BBB and neutralises acidic pH produced so little effect on ventilatory response

347
Q

role of peripheral chemoreceptors?

A

primarily detect changes in O2 in the blood (lesser extent detect changes in CO2 and H+). stimulation results in inhibition of K+ channels, cell depolarisation, Ca2+ entry and neurotransmitter release leading to afferent signaling to medulla + increased ventilation

348
Q

where are peripheral chemoreceptors located?

A

aortic bodies located in aortic arch, carotid bodies located bilaterally in bifurcations of carotid arteries

349
Q

what performs sensing in peripheral chemoreceptors?

A

glomus cells have O2 sensitive potassium channels inactivated when PaO2 decreases causing depolarisation of the glomus cell

350
Q

how much of the ventilatory response to hypercapnia can be attributed to peripheral chemoreceptors?

A

20-40%

351
Q

when do peripheral chemoreceptors start to affect ventilation?

A

when PaO2 drops below normal

352
Q

what is coughing?

A

reflex response which protect airways by acting as defense against foreign materials in the airways

353
Q

stimuli for coughing?

A

can be chemical, biological or mechanical.

354
Q

what are the phases of the process of coughing?

A

sensory phase, inspiratory phase, compressive phase, expulsive phase

355
Q

what happens in the inspiratory phase of coughing?

A

glottis opens and deep breath inhaled

356
Q

what happens in the compressive phase of coughing?

A

glottis closes, expiratory muscles forcibly contract

357
Q

what happens in the expulsive phase of coughing?

A

glottis opens and rapid airflow begins, turbulent flow loosens secretions and dislodges foreign particles

358
Q

role of hyperventilation in elevating alveolar PO2?

A

CSF and cerebral interstitial fluid become alkaline as result of lowing arterial PCO2 by hyperventilation, reduces central chemoreceptor stimulus, after HCO3- levels in CSF lowered to return pH towards normal levels central afferent input to reduce ventilation reduced. sustained arterial hypoxic stimuli on peripheral chemoreceptors become dominant and ventilation rate will increase further

359
Q

effect of generalised alveolar hypoxia?

A

deleterious effects including pulmonary hypertension leading to pulmonary oedema

360
Q

structure of lamellar gills?

A

fine, flat lamellae extend to either side from supporting gill arch forming water channels. in more complex gills secondary lamellae extend to either side of primary lamellae

361
Q

counter current system of gills?

A

flow of water is in opposite direction to flow of blood through lamellae setting up counter current system- so extraction of O2 from water flowing through gills is very efficient

362
Q

how are gills ventilated?

A

pressure differential generated between buccal cavity and opercular cavity- opening controlled by muscles in mouth for buccal cavity and in operculum for opercular cavity

363
Q

respiratory system of birds?

A

lungs are rigid structures, mechanically + functionally linked to system of air sacs spread throughout body- air sacs act like bellow along with movement of body wall, mechanically ventilate lung continuously + unidirectionally across gas exchange surface

364
Q

structure of bird lungs?

A

primary bronchi branch to mesobronchi and dorsobronchi which in turn lead to small parabronchi which make up core of gas exchange units- parabronchi have network of tiny air capillaries

365
Q

advantage of bird respiratory system?

A

much more intricate association between capillaries and air, greater SA for gas exchange between lungs and blood in comparison to mammalian alveolus

366
Q

process of ventilation in birds?

A

during inspiration posterior and anterior air sacs expand, causing negative pressure within them. air from trachea and bronchi moves into posterior air sacs and lungs, simultaneously air from lungs moves into anterior air sacs. during expiration volume of thoracoabdominal cavity reduced, air from posterior sacs moves into lungs and air from anterior sacs moves into trachea and out of body

367
Q

structure of respiratory system in insects?

A

rely on tracheal system- network of air filled tubes that penetrate throughout body punctuated at intervals by small air sacs that enlarge tracheal volum.

368
Q

how do insects ventilate?

A

air enters body through valve-like spiracles in exoskeleton. beyond spiracles= longitudinal tracheal trunks which branch into network of tracheal tubes that subdivide repeatedly. at end of each tracheal branch is very fine tracheole, provides thin moist interface for gas exchange

369
Q

how do aquatic insects get air while underwater?

A

consume air stored in dilated areas of tracheal system

370
Q

what is the diving reflex?

A

vagally mediated increase in parasympathetic nerve activity causes bradycardia- sympathetically mediated vasoconstriction of peripheral vascular beds

371
Q

why do divers hyperventilate before diving?

A

increased oxygen stores- less powerful drive to surface to breathe as peripheral chemoreceptors detect hypoxia and are easily overridden by conscious control

372
Q

what causes ‘shallow water blackout’?

A

when divers descend transient increase in PO2 as at greater pressure PO2 increases as total pressure increases rapidly. while at depth oxygen consumed but partial pressure so high that it may be enough to maintain PO2, as diver ascends total pressure decreases so PO2 does too, resulting in reversed/reduced O2 uptake

373
Q

why do some free divers experience pulmonary oedema or haemorrhage after a dive?

A

as they descend pressure in pulmonary vasculature increases due to peripheral vasoconstriction in diving reflex. plus barotrauma and shear forces on compressed lung disturbing alveolar barrier can cause haemorrhage and oedema

374
Q

what causes ‘the bends’?

A

under hyperbaric conditions increased pressure forces poorly soluble N gas into solution in tissues particularly fat where N2 solubility is higher. equilibration of N2 between fat and environment is slow as blood supply to adipose tissue is poor and blood can carry little N2. during ascent N removed from tissues, if reduction in pressure is rapid bubbles on N can form in the blood- causes N embolism in the joints which is the bends

375
Q

how can ‘the bends’ be fatal?

A

if large numbers of N bubbles make their way to brain and occlude cerebral vessels or the heart and occlude coronary vessels

376
Q

treatment for decompression sickness/’the bends’?

A

immediate compression, controlled slow decompression, or breathing a helium oxygen mixture as helium diffuses more rapidly through tissue than N and has lower resistance to flow

377
Q

what causes the respiratory response to exercise?

A

decreased O2 causes fastest response, increased CO2 has greatest effect on ventilation rate

378
Q

why does ventilation increase to meet demand in moderate exercise without significant change in O2, CO2, or H+?

A

brain signals to exercising muscles to stimulate respiratory centre- mechanism unclear, reflexes from motion of limbs, response to increased CO, response to increased heat production

379
Q

how does surpassing the anaerobic threshold stimulate further increase in ventilation in exercise?

A

lots of lactic acid produced, increased H+ stimulates ventilation as it produces CO2 when buffered by HCO3-. also as H+ accumulates metabolic acidosis produced which stimulates peripheral chemoreceptors to stimulate ventilation further- CO2 response starts at lower than normal PCO2

380
Q

average pH of human body?

A

7.4, ranges between 7.35 and 7.45

381
Q

what are the 4 main types of acid-base disorders?

A

metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis

382
Q

what causes metabolic acidosis?

A

failure to excrete excess acid normally, such as in renal failure, or accumulation of excess acid, such as in exercise

383
Q

what causes metabolic alkalosis?

A

loss of acid from body (e.g. vomiting)

384
Q

what causes respiratory acidosis?

A

if hypoventilation causes CO2 accumulation

385
Q

what causes respiratory alkalosis?

A

hyperventilation causing reduction in CO2

386
Q

how does the body try to correct metabolic acid-base disorders?

A

respiratory compensation- changing ventilation to alter CO2 production

387
Q

how does the body try to correct respiratory acid-base disorders?

A

metabolic compensation- changing excretion of HCO3-/H+ in the kidneys

388
Q

what blunts the effects when climbers first ascend to altitude and experience hypoxia? what is the effect of this?

A

increased alveolar ventilation lowering PaCO2 blunts effect of increased ventilation driven by peripheral chemoreceptors. this increases pH

389
Q

changes over a few days in response to ascending to altitude?

A

kidneys excrete HCO3- to restore increased pH caused initially, removes blunting effect so ventilation increases improving PaO2. BPG and tissue hypoxia promote offloading of O2 in respiring tissues. hypoxia stimulates RBC production to increase O2 carrying capacity.

390
Q

what is pulmonary emphysema?

A

common human disease, usually caused by exposure to noxious particles/gases causing inflammation which leads to the breakdown of elastin in the lung parenchyma leading to breakdown of alveolar walls and airway inflammation

391
Q

effects of emphysema?

A

reduced SA for gas exchange, more compliant lung (means trapping of air and increased EEV so reduced alveolar ventilation), predisposes to bronchoconstriction, ventilation perfusion mismatching, capillary destruction -> pulmonary hypertension and right sided heart failure. florid complexion due to erythrocytosis

392
Q

what is pulmonary fibrosis?

A

when scar tissue disrupts the normal delicate alveolar wall leading it to become stiff and thickened

393
Q

key consequences of pulmonary fibrosis?

A

lung tissue becomes less compliant, alveolar membrane thickened impairing gas exchange- compounded in inflammatory disease by increased airway secretions impairing diffusion and increasing airway resistance

394
Q

effects of obesity on respiratory function?

A

decreases lung volumes as less space for expansion, reduces chest wall compliance, increases airway resistance, increases airway hyper-responsiveness so increases risk of asthma

HOM (9 decks)

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