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
2
Q
what are the fuels used for cellular respiration?
A
primarily glucose, other sugars, fats, ketone, proteins
3
Q
how much CO2 is formed for each molecule of O2 consumed in carbohydrate respiration?
A
1 CO2 molecule
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
5
Q
what is the respiratory quotient?
A
ratio of CO2 output to O2 usage
6
Q
what is the RQ of carbohydrates?
A
1
7
Q
what is the RQ of fats?
A
0.7
8
Q
what is the RQ of protein?
A
0.8
9
Q
what is the typical RQ assumed in the alveolar gas equation?
A
0.8
10
Q
how can RQ be used in physiological experiments?
A
to give an insight into substrate use in the body
11
Q
what are the functions of the respiratory system?
A
gas exchange, acid base balance, phonation, pulmonary defence, metabolism, handling bioactive materials, thermoregulation
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
13
Q
how does the respiratory system meet the need to match supply and demand?
A
central and peripheral regulation of breathing, ventilation/perfusion
14
Q
how does the respiratory system deliver oxygen to respiring cells?
A
transport of gases in the blood
15
Q
what makes up the upper respiratory tract?
A
nares, nasal passages, pharynx, larynx
16
Q
what makes up the lower respiratory tract?
A
trachea, bronchi, bronchioles
17
Q
how do the branches of the respiratory tract receive blood?
A
from bronchial arteries, and pulmonary circulation
18
Q
what makes up the conducting zone of the respiratory tract?
A
the nares to the terminal bronchioles
19
Q
what is the conducting zone?
A
the conducting airways that aren’t involved in gas exchange
20
Q
what are the secondary bronchi?
A
lobar bronchi
21
Q
what are the tertiary bronchi?
A
segmental bronchi
22
Q
what are the smallest airways without gas exchanging capability?
A
terminal bronchioles
23
Q
what resists thoracic pressure changes in the conducting airways?
A
cartilage support in walls
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
25
what is the cartilage support in the lobar and segmental bronchi and further branches before bronchioles?
cartilaginous plates
26
how are bronchiolar airways kept open?
by elastic connections between the airways and lung parenchyma
27
what is the vascular system of the conducting zone?
bronchial circulation
28
what is the purpose of the bronchial circulation?
to support gas exchange at level of lung tissues making up the conducting zone
29
what are the conducting airways lined with?
pseudostratified columnar ciliated epithelium
30
what do the conducting airways do?
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
31
how do the conducting airways filter and clear particles?
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
32
what is the anatomic dead space?
the conducting airways- because they have no exchange function
33
what is the last gas to be breathed in and first to be breathed out?
dead space gas
34
what is alveolar dead space?
the volume which reaches the alveoli but doesn't participate in gas exchange as the alveolus isn't perfused
35
what is the physiological dead space?
the anatomical and alveolar dead space combined
36
what is the respiratory zone?
airways where gas exchange occurs
37
what are the respiratory airways?
respiratory bronchioles, alveolar ducts, alveoli
38
why is the pulmonary circulation's flow very high?
receives the entire cardiac output
39
how quickly can red blood cells pass through pulmonary circulation?
less than a second
40
what makes up the majority of the lung volume?
the respiratory zone
41
what is the volume of the respiratory zone in humans?
2.5-3 litres
42
what is the volume of the conducting zone in humans?
150 ml
43
why is velocity of flow lower in the respiratory airways than the conducting airways?
respiratory airways have much greater cross-sectional area due to branching
44
what is the movement of gas by predominantly in the respiratory zone?
diffusion
45
why is diffusion very rapid in the respiratory zone?
distances are very short
46
what is an advantage of the dramatic reduction in air velocity in the respiratory zone?
inhaled dust and pollutant frequently settle out prior to the alveoli
47
what is the functional gas exchange unit of the lung?
alveoli
48
how many alveoli are there per human lung?
300-500 million
49
what are alveoli connected by?
septa
50
what are alveoli like?
polyhedral with cup-like openings which fold along septae when lung is deflated
51
how close is blood in pulmonary circulation to the air in alveoli
within 0.5 micrometers
52
what is within alveolar walls?
a dense network of tiny capillaries forming an almost continuous sheet of blood
53
what is the size of the SA for gas exchange between alveoli and the blood in humans?
75-140 m2
54
what is the driving force for diffusion of O2 into blood/CO2 into alveoli?
pressure gradient across the alveoli/blood interface
55
what are alveoli lined by?
type 1 and type 2 cells
56
what are type I cells in alveoli?
flat, branched, very thin cells with few organelles
57
what are type II cells in alveoli?
cells which secrete surfactant, have a role in immune function and are progenitors that can repopulate alveolar lining after injury
58
how thick is the alveolar blood gas barrier?
0.2-2 micrometers
59
what are the 3 layers of the alveolar wall?
surfactant, type 1 cells, capillary endothelium
60
what is the bronchial circulation system?
a high pressure, low flow system fed by bronchial arteries delivering oxygenated blood to the conducting airways and supporting structures of the lungs
61
what % of the left CO does bronchial circulation receive?
less than 2%
62
where does the majority of the bronchial circulation drain into?
pulmonary circulation
63
what does blood draining from the bronchial circulation into the pulmonary circulation cause?
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
64
what does the pulmonary artery do?
receives blood from RV and its arterial branches, carries blood to the alveolar capillaries for gas exchange
65
what do the pulmonary veins do?
return the blood to the left atrium to be pumped by the left ventricle through the systemic circulation
66
what sort of system is the pulmonary circulation (pressure and flow)?
low pressure, high flow
67
what is the primary function of the capillary bed that places blood in intimate contact with alveoli?
facilitates rapid gas diffusion
68
what are the secondary functions of the capillary bed that places blood in intimate contact with alveoli?
blood reservoir, filters blood of emboli, metabolises vasoactive hormones
69
how does the capillary bed supplying blood close to alveoli act as a blood reservoir?
40% of its weight is blood, contains 10% of blood volume in humans- approximately equal to stroke volume of right heart under normal conditions
70
how does the capillary bed supplying blood close to alveoli filter blood of emboli?
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
71
what can emboli cause in the lungs?
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
72
how does the capillary bed supplying blood close to alveoli metabolise vasoactive hormones?
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
73
where do lymph vessels in the supportive structures of the lung mainly drain into?
right thoracic lymph duct
74
what is the difference between driving pressure and mean capillary pressure in the pulmonary circulation vs systemic circulation?
much lower in pulmonary circulation
75
what is the difference in the resistance to flow in the pulmonary circulation vs the systemic circulation?
pulmonary is lower
76
what is the difference in the compliance of the pulmonary and systemic blood vessels and why?
pulmonary vessels much more compliant largely due to less muscle in their walls
77
what is the response to hypoxia in pulmonary vessels?
vasoconstriction
78
what is the response to hypoxia in systemic vessels?
vasodilation
79
what is the approx. pressure gradient for the entire CO being driven through the lungs vs through systemic circulation?
10mmHg vs 85-90mmHg
80
why is the resistance of the pulmonary circulation lower than the systemic vascular resistance?
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
81
what 2 local mechanisms are responsible for reducing vascular resistance when CO increases?
capillary recruitment and capillary distension
82
what influences the extra-alveolar vessels?
intra-pleural pressure changes during the breathing cycle
83
why is alveolar vessel diameter not influenced by intrapleural pressures?
the tissue network surrounding the vessels buffers them from the intrapleural influences
84
what is the likely way alveolar hypoxia leads to vasoconstriction in the pulmonary circulation?
probably increases local sensitivity to circulating vasoconstrictive substances/decreases local release of a vasodilator
85
what is the pulmonary response to regional hypoxia?
a localised, regional vasoconstriction which diverts blood away from the affected region with little effect on pulmonary arterial pressure
86
what is the pulmonary response to general hypoxia?
general vasoconstriction which increases pulmonary vascular resistance, increased pulmonary arterial pressure
87
what can the vasoconstriction caused by general hypoxia lead to?
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
88
what is the mean pulmonary arterial pressure at the top of the lung compared to the middle and base?
top is 11mHg less than middle, base is about 11mmHg greater than middle
89
why are blood flow and pressures within alveolar capillaries higher at the base than the top of the lung?
hydrostatic pressure gradient affected by gravity
90
what provides the driving force to push blood through the blood capillaries as they flow past alveoli?
the difference between pulmonary arterial and venous pressure
91
what does low hydrostatic pressure lead to in the lungs?
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)
92
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?
zone 1= upper zone; zone 2= middle zone; zone 3= lower zone
93
what is the relationship between alveolar pressure, pulmonary arterial pressure and pulmonary venous pressure in zone 1?
alveolar pressure is greater than arterial pressure so pulmonary capillaries are collapsed and there is no flow
94
what is the relationship between alveolar pressure, pulmonary arterial pressure and pulmonary venous pressure in zone 2?
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
95
what is the relationship between alveolar, pulmonary arterial and pulmonary venous pressure in zone 3?
arterial and venous pressures greater than alveolar, flow determined by the usual arterial-venous pressure difference
96
which zone conditions don't exist in normal healthy individuals?
zone 1
97
when can zone 1 conditions exist?
if pulmonary arterial pressure falls, as in severe haemorrhage, or if alveolar pressure is increased, as in forced ventilation
98
why are alveoli in the base of the lungs usually better ventilated than at the top?
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
99
when is the ventilation/perfusion (V/Q) ratio at 1?
at approximately the level of the 3rd rib
100
when is the ventilation/perfusion (V/Q) ratio >1?
higher up in thorax. indicates presence of well-ventilated alveoli with poor blood flow so gas exchange can't occur- dead space
101
when is the ventilation/perfusion (V/Q) ratio <1?
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)
102
what does a V/Q of 0 indicate?
complete 'shunt' of blood past gas exchange surface
103
what is venous admixture?
blood that hasn't participated in gas exchange being added to the pulmonary venous (oxygenated) circulation
104
what is a normal % of venous admixture from bronchial circulation?
20%
105
why do airflow and blood flow both increase down the lung?
ventilation and perfusion are gravity dependent
106
why is blood flow proportionately greater at the base and ventilation proportionately greater at the apex?
blood flow shows a 5 fold difference from top to bottom, ventilation shows a 2 fold difference
107
what determines the pulmonary mixed venous gas concentrations?
the relative contribution of the CO exposed to different V/Q rations
108
what region of the lung does TB tend to localise to?
apex, since high V/q ration provides favourable high PO2 environment for the Mycobacterium tuberculosis
109
how is a low V/Q ratio compensated for?
increase in overall ventilation, regional vasoconstriction induced by local hypoxia to shunt blood from poorly ventilated alveoli
110
how is a high V/Q ratio compensated for?
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
111
why does pulmonary fluid accumulation in the interstitial space impair gas exchange?
increases the diffusion distances
112
how is the interstitial pressure in the lungs modulated?
by the surface tension of the alveoli (tends to expand fluid volume) and the alveolar pressure (tends to compress fluid volume)
113
how is net fluid exchange across the capillary determined?
difference in hydrostatic and colloid pressure across capillary wall
114
what counters hydrostatic pressure in the pulmonary circulation?
the colloid osmotic pressure difference across the capillary wall
115
why are there higher concentrations of protein in the interstitial fluid in the lung than the interstitial space in the periphery?
the pulmonary capillaries are more permeant to proteins than capillaries in the systemic circulation
116
where is the colloid osmotic pressure greater, the capillary or the interstitial space?
in the capillary
117
what drains the net flow of fluid into the interstitial space?
lymph system in terminal bronchiole region
118
what is the total outward force of fluid from capillaries into the pulmonary interstitium?
29mmHg
119
what 2 factors serve to ensure interstitial fluid doesn't enter alveoli?
interstitial pressure is negative so pulls water away from alveoli, surfactant acts as barrier to fluid entering alveoli
120
what can lead to filtration of fluid exceeding removal in the pulmonary interstitium?
increased pulmonary capillary pressure, increased pulmonary permeability, decreased capillary colloid osmotic pressure, failure of lymphatic drainage
121
what is the cause of death usually in fresh water drowning?
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
122
what does the rapid diffusion of pure water into pulmonary capillaries in fresh water drowning lead to?
RBC lysis releasing K+, dilution of extracellular Na+, leading to cardiac fibrillation and death
123
what is the result of aspiration of sea water with osmolarity greater than plasma?
net flow of water out of the pulmonary capillaries into the interstitial space and alveoli after overcoming the negative interstitial pressure, death by asphyxiation
124
what is flow?
change in pressure/resistance
125
what would happen if the lungs weren't held partially inflated?
would collapse and expel all air from them completely
126
what is the thoracic cage made up of?
12 pairs of ribs, a sternum and a set of internal and external intercostal muscles that lie between the ribs
127
what encases the lungs?
thin visceral pleura
128
what separates the visceral pleura of the lungs and the parietal viscera of the thoracic cage?
thin layer of fluid (approx 10µm thick)
129
what determines volume of the thoracic cavity at rest?
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
130
what is the transpulmonary pressure?
the difference between alveolar pressure and pleural pressure, outward force that keeps alveoli open
131
what happens if the thoracic cavity is punctured?
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
132
what is Boyle's Law?
P1V1 = P2V2
133
what happens to the thoracic cage during inspiration?
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
134
what happens when inspiratory muscles contract?
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
135
what happens to the thoracic cage during expiration?
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
136
what are transmural pressures?
differences in pressure recorded across organ and tissue walls
137
what are the 3 transmural pressures in the mammalian respiratory system?
transpulmonary, trans chest wall and trans total system
138
how does inspired air flow through the conducting zone?
bulk flow
139
how are transmural pressures calculated?
the pressure differential of the inside compartment minus the outside compartment
140
is the transpulmonary pressure always positive or negative in normal breathing?
positive
141
what is the distending pressure?
the transpulmonary pressure keeping the lungs inflated
142
what determines the volume of the thoracic cavity at end expiration under normal conditions?
the outward elastic recoil tendency of the chest wall and the inward elastic recoil properties of the lungs
143
what is a spirometer used for?
measuring the volume of air breathed in and out of the lungs
144
what is bulk flow?
movement of a mass of fluids down a pressure gradient- active process reliant on pressure gradient
145
what is a fluid?
substance that has no fixed shape and yields easily to external pressure- a liquid or gas
146
what is a gas?
substance or matter in a state with no fixed shape and no fixed volume
147
what is the lung volume at any given pressure like in inflation compared to deflation?
smaller in inflation than deflation
148
what is respiratory compliance?
the change in lung volume per unit change in transpulmonary pressure gradient
149
what is static compliance?
the change in lung volume per unit change in transpulmonary pressure in the absence of flow
150
what is static compliance composed of?
chest wall compliance, lung tissue compliance
151
what is chest wall compliance?
relates to the tendency of the chest wall to expand and exert a negative pressure at all lung volumes
152
what is lung tissue compliance made up of?
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
153
how is lung compliance normalised to correct for differences in size?
dividing compliance by FRC yielding value called specific compliance
154
why is there a lower pleural pressure at the apex than the base of the lungs?
the 'downward pull' of gravity
155
what does the higher transpulmonary pressure at the apex of the lungs result in?
the alveoli being expanded more than alveoli at the base leading to regional difference in compliance of the lung
156
what does the greater compliance of the base of the lung compared to the apex of the lung lead to?
base of lung undergoes a greater increase in volume for a given pressure change relative to the apex
157
what is the net result of the greater compliance in the base of the lung?
greater proportion of the tidal volume goes to the base of the lung so a greater alveolar ventilation occurs at the base
158
what generates the elastic forces of the lung tissue?
the collagen and elastin fibres within the lung parenchyma
159
why does the compliance curve flatten at greatest lung volumes?
when collagen and elastin fibres stretched towards their limit they exert a greater resistance to expansion
160
what proportion of the elastic recoil of the lungs are the elastic forces generated by surface tension responsible for?
more than 2/3
161
what is the calculation relating pressure and surface tension?
pressure= (2xsurface tension)/radius
162
what is surfactant?
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
what is the principle agent in surfactant?
dipalmitoyl phosphatidyl choline (DPCC)
164
why is surfactant turnover high?
continual renewal of surfactant of alveolar inner surface brough about by each expansion of the lungs
165
how does DPPC reduce surface tension?
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
why is the reduction in surface tension by surfactant greatest when the film is compressed?
molecules of DPPC crowded together so greater repulsion
167
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?
some surfactant is squeezed out of the surface layer at low lung volumes
168
where is surfactant positioned in the alveoli and what does this mean?
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
how does sighing help to maintain compliance?
increases release of surfactant and helps disperse it
170
why is the lung functionally immature prior to 85-90% of the gestation period?
doesn't have adequate surfactant production
171
what causes infant respiratory distress syndrome?
low surfactant production reducing lung compliance
172
how is infant respiratory distress syndrome treated?
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
what is hysteresis?
differences between pressure-volume relationships of inflation and deflation portions of compliance diagram
174
why is the compliance diagram shaped the way it is?
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
what are the functional consequences of a loss of lung compliance?
stiff lung, more work performed to maintain normal alveolar ventilation so energy cost of breathing increased
176
what are the functional consequences of an increase in compliance?
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
what causes the resistance of the respiratory system?
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
what affects airway resistance?
airway diameter (greater resistance in narrower airways) and turbulent or laminar flow (greater with turbulent flow)
179
where does turbulent flow occur in the lungs?
in the large airways such as the trachea and large bronchi
180
what causes the sounds which can be heard when breathing deeply/with a stethoscope when breathing normally?
turbulent air flow
181
what is laminar flow?
streamlined flow of air that runs parallel to the sides of the airways and is silent
182
where does laminar flow occur in the airways?
the small airways where flow is very slow
183
what is transitional flow?
a mix between laminar and turbulent flow
184
what is most of the air flow in the lower airways of the lung?
turbulent flow
185
effect of turbulent flow on resistance to flow?
increases it
186
what type of air flow does the flow equation used by physiologists to describe airflow in the lungs define?
laminar flow
187
what is the most important factor to resistance?
tube diameter- small changes will dramatically change resistance
188
where is the greatest resistance to airflow in the lungs?
upper respiratory tract
189
why is the resistance in the bronchioles low despite the small individual diameters?
very numerous so only tiny amounts of air must flow through each
190
where does most of the pressure drop in the airways occur before?
the 7th generation
191
what can regional bronchiole constriction help to maintain?
a normal ventilation:perfusion ratio
192
what causes dilation of the bronchioles?
sympathetic stimulation of adrenergic fibres by stimulating beta-adrenergic receptors
193
effect of isoproterenol and epinephrine on bronchioles?
cause dilation by stimulating beta2-adrenergic receptors in airways
194
what is the effect of PCO2 on conducting airway dilation/constriction?
increased PCO2 can induce dilation, decreased PCO2 induces airway constriction
195
what is the effect of parasympathetic stimulation of the bronchioles by the vagus nerve?
stimulates cholinergic fibres causing constriction and stimulation of mucus secretion
196
what stimulates parasympathetic nerves in the lungs?
local reflexes, noxious stimuli (gases or infection), CNS
197
what does histamine release by mast cells cause in the bronchioles? what condition is this important in?
bronchoconstriction, asthma
198
why are helium-oxygen mixtures frequently used in underwater breathing situations?
helium reduces resistance of breathing
199
why does resistance in airways decrease as lungs expand?
radius of bronchi and small airways increases
200
what do spirometers measure directly and what value is determined from spirometer data?
directly measure lung volumes, lung capacities are calculated theoretical values
201
what are the lung volumes measured with a spirometer?
tidal volume, expiratory reserve volume, residual volume
202
what is the tidal volume?
volume of gas inhaled or exhaled during the respiratory cycle
203
what is the expiratory reserve volume?
volume of gas that can be maximally exhaled from the end-inspiratory level during tidal breathing
204
what is the residual volume?
volume of gas remaining in the lung after maximal exhalation
205
what standard capacities can be determined from spirometer data?
functional residual capacity, inspiratory capacity, vital capacity, total lung capacity
206
what is the functional residual capacity?
the volume of gas present in the lung at end expiration during tidal breathing
207
what is the inspiratory capacity?
maximum volume of gas that can be inspired from the FRC
208
what is the vital capacity?
volume change at the mouth between the positions of full inspiration and complete expiration
209
what is the total lung capacity?
volume of gas in the lungs after maximal inspiration
210
why can't RV and FRC be measured directly from spirometry?
the lungs can't be completely emptied following forced expiration
211
why does the descending portion of the flow-volume curve always take the same path regardless of force of expiration?
compression of the airways by intrathoracic pressure during forced expiration
212
what changes occur during the initiation of forced expiration?
pleural pressure rises to above atmospheric, alveolar pressure becomes greater than pleural pressure
213
what causes the added pressure in the alveoli during initiation of forced expiration?
elastic recoil of the lung acting in series with the positive intrapleural pressure
214
what is the equal pressure point (EPP)?
point during maximal forced expiration where the transairway pressure is 0
215
what are the consequences of the large positive intrathoracic pressures produced in forced expiration?
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
why do emphysema patients breath out through pursed lips?
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
why can't peak flow rate be increased by increased expiratory effort?
the increased effort increases the intrapleural and alveolar pressure so transairway pressure remains constant
218
what primarily determines maximal flow rates and why does maximal flow rate fall with decreased lung volume?
elastic recoil of lung which generates the alveolar pressure, decrease in elastic recoil as lung volume decreases
219
what is forced maximal exhalation?
when exhalation performed as forcibly and rapidly as possible
220
what is forced vital capacity?
the measure provided by forced maximal exhalation
221
how can FEV be normalised for lung size?
by expressing it as a percentage of the FVC- approx. 80% under normal conditions
222
what is STPD?
standard temperature and pressure dry
223
what conditions are required for STP?
273.15 K, pressure of 105Pa, dryness of gas mixture
224
how many litres will a mole of gas occupy at STPD?
22.4
225
Ideal gas law?
PV = nRT
226
combined gas law?
(P1V1)/T1 = (P2V2)/T2
227
what is BTPS?
body temperature and pressure saturated- physiological conditions within the body
228
Dalton's Law?
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
calculation for partial pressure of a gas?
the fraction of the mixture occupied by the gas x the total pressure exerted by the mixture
230
231
why is there (very small) variation of partial pressure of O2 and CO2 around the mean in the alveoli?
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
what partial pressure does saturated water vapour exert at atmospheric pressure?
47mmHg
233
what happens to the air inhaled into the lungs (temp, composition, etc)?
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
what is the major respiratory adaptation to increased metabolic rate?
increased ventilation of the respiratory exchange surface- increases delivery of O2 and removal of CO2
235
what is ventilation rate the product of?
tidal volume and respiratory rate
236
what does total lung ventilation refer to?
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
what is the alveolar ventilation?
the ventilatory rate of the gas exchange areas
238
what is a person breathing rapid, shallow breaths doing?
moving air in and out of their dead space with no alveolar ventilation
239
why doe alveoli with reduced blood flow have alveolar ventilation in excess of what's needed?
to maintain appropriate gas exchange for the reduced blood flow
240
what is the expired minute volume?
the volume of air moved out of the lungs in 1 minute- tidal volume x breathing frequency
241
why doesn't the minute ventilation represent the amount of O2 reaching the alveoli?
anatomic dead space
242
issues with correcting tidal volume by dead space volume to estimate alveolar ventilation?
it is difficult to quantify dead space
243
what is the alveolar ventilation equation?
volume CO2 expired per unit time/fractional concentration of CO2 in alveolar gas
244
what observation does the alveolar ventilation rate equation take advantage of?
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
how can the volume of CO2 expired per unit time be measured?
by collecting expired gas over a defined time period and measuring the CO2 concentration within it
246
how is the fractional concentration of CO2 in alveolar gas measured?
by sampling the last portion of the tidal volume during expiration which contains pure alveolar gas
247
what values are needed to calculate alveolar pressure of CO2?
alveolar ventilation and volume of expired CO2
248
effect of high alveolar ventilation?
higher concentration of oxygen, lower concentration of CO2, in alveoli and arteries
249
effect of doubling alveolar ventilation on PCO2?
halves alveolar PCO2
250
what is the main use for the alveolar gas equation?
calculating a theoretical alveolar oxygen partial pressure to determine the A-a gradient
251
what is the A-a gradient?
theoretical alveolar oxygen - actual arterial oxygen
252
what does the alveolar gas equation assume?
healthy lung with no ventilation-perfusion mismatch or diffusion defects
253
what does the alveolar gas equation calculate?
what the arterial PO2 would be when arterial PCO2 is known
254
what is the difference in alveolar and arterial PO2 a result of?
a mixture of factors including venous admixture and ventilation/perfusion mismatching
255
what pathologies can cause ventilation/perfusion mismatch?
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
what is Henry's Law?
concentration of gas in liquid= solubility constant x partial pressure of gas in contact with the liquid
257
what is Henry's Law used for?
determining amount of gas in solution where the air meets the layer of liquid in the alveoli
258
what is the amount of gas in solution determined by when a gas and liquid in contact are allowed to equilibrate?
partial pressure of the gas in contact with the solution, chemical properties of the gas and liquid (solubility constant), temperature
259
why is haemoglobin needed?
to increase the O2 carrying capacity of the blood as O2 is much less soluble in blood than CO2
260
what is Fick's law?
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
what determines rate of diffusion across a permeable membrane?
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
in what ways can gas exchange at the alveoli be limited?
can be diffusion limited or perfusion limited
263
which is more common, diffusion or perfusion limited gas exchange?
diffusion limited
264
what is the oxygen cascade?
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
what 2 means is oxygen transported by?
dissolved in blood, mostly bound to haemoglobin
266
what does mammalian type A haemoglobin consist of?
4 subunits, each has 1 haem associated with globin protein, each subunit has 2 pairs of polypeptide chains- 2 alpha and 2 beta
267
what does mammalian type F (foetal) haemoglobin consist of?
4 subunits, each has 1 haem associated with globin protein, each subunit has 2 pairs of polypeptide chains- 2 alpha and 2 gamma
268
differences in haemoglobin S (sickle cell type)?
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
what is the structure of haem?
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
colour of Hb and HbO2?
Hb is blue-ish, HbO2 is bright red
271
why do patients with poor lung function tend to have cyanosis (blue tinge to normally pink tissues)?
gas exchange compromised, less oxygenated Hb (which is red), more regular Hb which is blue-ish
272
what gives haemoglobin sigmoidal properties?
cooperative binding- as each haemoglobin subunit combines with oxygen it increases the affinity for oxygen of the remaining subunits
273
what is anaemia? what effects does it have?
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
why does the spleen contract during exercise?
to increase the RBC fraction of the blood and its Hb concentration to increase its O2 carrying capacity
275
what limits the usefulness of splenic contraction during exercise?
increased blood viscosity that affects perfusion of peripheral capillaries and increases cardiac work
276
how does Hb maintain the partial pressure gradient at the alveolus?
as O2 diffuses into blood it is bound to Hb so doesn't exert a partial pressure
277
why can changes in ventilation be used to regulate arterial PCO2 without affecting O2 supply?
quantity of O2 in arterial blood remains the same over range of high ventilation rates
278
what does a left shift in the haemoglobin O2 dissociation curve signify?
greater O2 affinity- more O2 is bound to Hb at a given PO2
279
why is there a left shift in the oxygen dissociation curve of fetal haemoglobin compared to adult Hb?
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
factors that will shift the O2 dissociation curve to the right?
H+, CO2, temperature, BPG
281
why does greater metabolic rate tend to increase unloading of O2 from Hb at the tissue?
products of metabolism (heat, CO2, H+ in lactic acid) all shift O2 dissociation curve to right
282
what is the Bohr effect?
the effect of CO2 and H+ ions on the affinity of haemoglobin for O2
283
what is 2,3-biphosphoglycerate? how does it interact with Hb?
metabolite present in RBCs. binds and stabilises Hb so that there is right shift in O2-Hb dissociation curve
284
how does the body use B/DPG to cause better unloading of O2 in hypoxic tissues?
conditions that cause low tissue PO2 (e.g. acclimatisation to altitude) stimulate production of B/DPG
285
difference between right shift caused by DPG and right shift caused by pH, CO2 and temperature?
DPG causes permanent right shift that will impair O2 loading at lungs- the others are reversed in the lungs
286
effect of pregnancy on maternal BPG and Hb?
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
effect of CO on Hb-oxygen relationship?
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
complications of CO poisoning diagnosis?
normal pulse oximetry readings of saturation, normal pink colouring, blood stays red when CO binds Hb, CO is odourless, colourless and non-irritating
289
how is CO2 transported in the blood?
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
what 3 forms is CO2 transported into the blood via?
bicarbonate, dissolved and bound to proteins (particularly Hb)
291
how is the majority of CO2 transported into the blood?
as bicarbonate
292
why are chloride levels much higher in RBCs than blood or tissues?
in RBCs carbonic anhydrase catalyses conversion of CO2 to bicarbonate, which is exchanged for Cl- ions to maintain electrical neutrality
293
what is the Haldane effect?
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
what is the sequence of events for CO2 movement out of the tissues?
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
what is Hamburger's phenomena/the Cl- shift?
most HCO3- leaves the RBC down its concentration gradient in exchange for Cl-
296
effect of extra intracellular HCO3- and Cl-?
increase the intracellular osmolarity and osmotic pressure resulting in water influx and cell swelling
297
what maintains the concentration gradient for CO2 diffusion into the RBC?
efflux of HCO3-, production of carbamino compounds, H+ buffering by Hb
298
what are the 4 general categories of hypoxia?
hypoxic hypoxia, anaemic hypoxia, circulatory hypoxia, histotoxic hypoxia
299
what is hypoxic hypoxia?
low arterial blood PO2 accompanied by inadequate Hb saturation
300
what is anaemic hypoxia?
reduced O2 carrying capacity of the blood
301
what is circulatory hypoxia?
when too little oxygenated blood is delivered to the tissues
302
what is histotoxic hypoxia?
normal O2 delivery to tissue but cells unable to use the oxygen available to them (e.g. cyanide poisoning)
303
what is hyperoxia?
when an above normal arterial PO2 occurs
304
what is hypercapnia?
excess CO2 in arterial blood, caused by hypoventilation
305
what is hypocapnia?
below normal arterial pCO2 levels brought about by hyperventilation
306
what can override central pattern generator in breathing?
cerebrum
307
what monitor movements of the chest wall?
proprioceptive receptors
308
what is 'system control theory'?
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
what are the 3 regions of the medulla oblongata and pons that make up the central pattern generator?
medullary centre, apneustic centre, pneumotaxic centre
310
what are the 3 major groups of neurons involved in the central pattern generator?
dorsal respiratory group, ventral respiratory group, pneumotaxic centre
311
location and role of dorsal respiratory group of neurons?
dorsal medulla, primarily nucleus of solitary tract. mainly causes inspiration
312
location and role of ventral respiratory group of neurons?
ventral medulla, mainly causes expiration
313
location and role of pneumotaxic centre neurons?
dorsal pons, mainly controls rate and depth of respiration
314
what does the nucleus of the solitary tract contain?
dorsal respiratory group of neurons, termination of vagal and glossopharyngeal nerves
315
what are the 2 groups in the medullary respiratory centre?
dorsal and ventral
316
what group in the medullary respiratory centre is most important in normal inspiration?
dorsal respiratory group
317
pattern of firing of dorsal respiratory group?
rhythmic pattern independent of other inputs, which ramps up over time then abruptly stops for approx. 3 seconds
318
where are APs from the dorsal respiratory group transmitted to? what is their effect?
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
what is responsible for the entirety of exhalation in quiet breathing?
passive exhalation
320
when does the ventral respiratory group become active?
only when there is greater demand on respiratory system such as in intense exercise
321
what is the effect of the neurons in the ventral respiratory group?
some cause inspiration, some cause expiration
322
what do the neurons in the ventral respiratory group appear to be particularly important in?
increasing the depth of inspiration and force of exhalation by activating the contraction of abdominal muscles to cause rapid, active exhalation
323
function of the pontine respiratory group of pneumotaxic centre?
appears to switch off inspiration thereby regulating tidal volume and breathing frequency
324
what are the neurons in the pneumotaxic centre called?
pontine respiratory group
325
effect of a strong or weak pneumotaxic signal?
strong can increase respiratory rate to 40 breaths pm, weak may be associated with very slow breathing rate
326
effect of direct electrical stimulation of the pneumotaxic centre?
attenuates the inspiratory ramp-may play roles in fine-tuning/controlling period of respiratory rhythm
327
possible role of neurons in the apneustic centre?
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
why is positioning the central pattern generator in the brain stem ideal?
it is under autonomic neural control and requires no consciuous input
329
interaction of voluntary and automatic use of respiratory muscles?
can override automatic control of breathing by breath holding but automatic system will eventually override voluntary one
330
evidence that the central pattern generator is located within the medullary centre?
transection below the medulla results in complete cessation of breathing, sectioning above pons (with vagus nerve intact) leaves breathing unaffected
331
evidence that vagal afferent input is important in terminating inspiration?
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
evidence that the pneumotaxic centre inhibits the inspiratory phase?
transection at level of upper pons leads to slowing of respiration and increase in tidal volume
333
effect of sectioning above the medulla + then of vagotomy?
rhyhmic but irregular breathing, vagotomy slows irregular pattern
334
role of stretch receptors in influencing ventilation?
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
roles of irritant receptors and mechanoreceptors in influencing ventilation?
detect chemicals or particulates in airways, can trigger sneezing and coughing reflexes aimed at dislodging foreign material from airway
336
role of proprioceptive receptors in influencing ventilation?
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
effect of anaesthetic drugs on respiration?
depress the function respiratory centre, hypoventilation common without mechanical ventilation
338
why do opioids cause respiratory arrest?
medulla is rich in opioid receptors
339
why can raised intracranial pressure impair ventilation?
caudal position of pons/medulla makes it susceptible to compression by back of skull
340
coupling of respiratory rhythm to movement in galloping horses and dogs?
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
what variable is under closest control in the respiratory control system?
arterial pCO2
342
relation of breathing to arterial blood PO2, PCO2 and [H+]
inversely related to pO2, directly related to PCO2 and [H+]
343
proof that breathing is more related to pCO2 than PO2?
if PaCO2 rises without accompanying hypoxia then pulmonary ventilation rises
344
what lies directly below respiratory centre on ventral aspect of medulla?
chemosensitive area important in regulation of respiration
345
what is the blood brain barrier?
highly selective semipermeable border of endothelial cells that regulates the transfer of solutes and chemicals between the circulatory system and CNS
346
effect of CO2 crossing the blood brain barrier?
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
role of peripheral chemoreceptors?
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
where are peripheral chemoreceptors located?
aortic bodies located in aortic arch, carotid bodies located bilaterally in bifurcations of carotid arteries
349
what performs sensing in peripheral chemoreceptors?
glomus cells have O2 sensitive potassium channels inactivated when PaO2 decreases causing depolarisation of the glomus cell
350
how much of the ventilatory response to hypercapnia can be attributed to peripheral chemoreceptors?
20-40%
351
when do peripheral chemoreceptors start to affect ventilation?
when PaO2 drops below normal
352
what is coughing?
reflex response which protect airways by acting as defense against foreign materials in the airways
353
stimuli for coughing?
can be chemical, biological or mechanical.
354
what are the phases of the process of coughing?
sensory phase, inspiratory phase, compressive phase, expulsive phase
355
what happens in the inspiratory phase of coughing?
glottis opens and deep breath inhaled
356
what happens in the compressive phase of coughing?
glottis closes, expiratory muscles forcibly contract
357
what happens in the expulsive phase of coughing?
glottis opens and rapid airflow begins, turbulent flow loosens secretions and dislodges foreign particles
358
role of hyperventilation in elevating alveolar PO2?
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
effect of generalised alveolar hypoxia?
deleterious effects including pulmonary hypertension leading to pulmonary oedema
360
structure of lamellar gills?
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
counter current system of gills?
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
how are gills ventilated?
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
respiratory system of birds?
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
structure of bird lungs?
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
advantage of bird respiratory system?
much more intricate association between capillaries and air, greater SA for gas exchange between lungs and blood in comparison to mammalian alveolus
366
process of ventilation in birds?
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
structure of respiratory system in insects?
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
how do insects ventilate?
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
how do aquatic insects get air while underwater?
consume air stored in dilated areas of tracheal system
370
what is the diving reflex?
vagally mediated increase in parasympathetic nerve activity causes bradycardia- sympathetically mediated vasoconstriction of peripheral vascular beds
371
why do divers hyperventilate before diving?
increased oxygen stores- less powerful drive to surface to breathe as peripheral chemoreceptors detect hypoxia and are easily overridden by conscious control
372
what causes 'shallow water blackout'?
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
why do some free divers experience pulmonary oedema or haemorrhage after a dive?
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
what causes 'the bends'?
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
how can 'the bends' be fatal?
if large numbers of N bubbles make their way to brain and occlude cerebral vessels or the heart and occlude coronary vessels
376
treatment for decompression sickness/'the bends'?
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
what causes the respiratory response to exercise?
decreased O2 causes fastest response, increased CO2 has greatest effect on ventilation rate
378
why does ventilation increase to meet demand in moderate exercise without significant change in O2, CO2, or H+?
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
how does surpassing the anaerobic threshold stimulate further increase in ventilation in exercise?
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
average pH of human body?
7.4, ranges between 7.35 and 7.45
381
what are the 4 main types of acid-base disorders?
metabolic acidosis, metabolic alkalosis, respiratory acidosis, respiratory alkalosis
382
what causes metabolic acidosis?
failure to excrete excess acid normally, such as in renal failure, or accumulation of excess acid, such as in exercise
383
what causes metabolic alkalosis?
loss of acid from body (e.g. vomiting)
384
what causes respiratory acidosis?
if hypoventilation causes CO2 accumulation
385
what causes respiratory alkalosis?
hyperventilation causing reduction in CO2
386
how does the body try to correct metabolic acid-base disorders?
respiratory compensation- changing ventilation to alter CO2 production
387
how does the body try to correct respiratory acid-base disorders?
metabolic compensation- changing excretion of HCO3-/H+ in the kidneys
388
what blunts the effects when climbers first ascend to altitude and experience hypoxia? what is the effect of this?
increased alveolar ventilation lowering PaCO2 blunts effect of increased ventilation driven by peripheral chemoreceptors. this increases pH
389
changes over a few days in response to ascending to altitude?
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
what is pulmonary emphysema?
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
effects of emphysema?
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
what is pulmonary fibrosis?
when scar tissue disrupts the normal delicate alveolar wall leading it to become stiff and thickened
393
key consequences of pulmonary fibrosis?
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
effects of obesity on respiratory function?
decreases lung volumes as less space for expansion, reduces chest wall compliance, increases airway resistance, increases airway hyper-responsiveness so increases risk of asthma
