module 3: respiratory physiology Flashcards
1
Q
o2 is necessary for production of cellular energy which takes the form of…
A
ATP, which creates Co2 that must be expelled from the cells
(this is known as internal respiration)
2
Q
external respiration 4 steps
A
- ventilation: air is moved in and out of the lungs
- exchange of o2 and co2 between air and blood
- transport of o2 and co2
- exchange of o2 and co2 between blood and tissues
3
Q
what does the upper airway include
A
nose, nasal cavities, pharynx, larynx
4
Q
the larynx is the location of the
A
vocal cords
5
Q
what does the lower airway include
A
trachea, left and right bronchi, bronchioles, alveoli
6
Q
what is convective flow
A
requires energy in the form of muscle contraction to maintain air flow
7
Q
what is diffusive flow
A
occurs passively to allow air to flow into the alveoli
8
Q
where does the diffusive zone begin?
A
level of the respiratory bronchioles
9
Q
what are the main inspiratory muscles
A
the diaphragm, and the external intercostal muscles
during inspiration diaphragm descends to enlarge the thoracic cavity. contraction of the external intercostal muscles elevates the ribs to further enlarge the thoracic cavity.
10
Q
what are the main expiratory muscles
A
internal intercostal muscles, and the abdominal muscles (generally inactive, but get recruited in ventilator demand)
11
Q
what is the pleural space (pleura)
A
covers the lung, and the inside wall of the thorax is lined by the parietal pleura
between these 2 membranes is the pleural space, which is relatively small and filled w fluid, the pleural fluid. this fluid allows the membranes to rub against each other during breathing w reduced friction.
12
Q
2 processes for external respiration (the 4 steps broken down even further)
A
- ability of the resp muscles to generate the necessary pressure gradient to move air through the airways (overcoming the resistance to flow) and to inflate the lungs
- the ability of oxygen and carbon dioxide to diffuse across the alveolar-capillary barrier
13
Q
what is the eqtn for external respiration
A
change in pressure / resistance = flow (or diffusion)
14
Q
why is the pressure gradient important in respiratory mechanics
A
pressure gradient is drives the force of air flow
if this pressure gradient is used to overcome the elastance, or stiffness, of the respiratory system, the resistance to flow, and the inertia of the system
15
Q
for air to flow out of the alveoli, the pressure in the alveoli must be _______ than the pressure in the nose
A
greater
16
Q
what is atmospheric pressure (Pa)
A
- aka barometric pressure
- pressure exerted by the weight of the air in the atmosphere on the Earth’s surface
- @ sea level it is 760 mmHg and this value decreases as you gain altitude
17
Q
what alveolar pressure (PA)
A
pressure in the alveoli, aka intrapulmonary pressure
at the end of inspiration, alveolar pressure is the same as atmospheric pressure at 0 cmH2O
18
Q
what is pleural pressure (PPL)
A
- pressure in the pleural space aka intrapleural pressure and closely approximates the intrathoracic pressure
- pleural pressure is negative to atmospheric pressure and is normally around -5cmH2O. It is negative bc the lungs want to collapse yet the chest wall wants to expand
19
Q
transpulmonary pressure (PTP)
A
pressure is the difference between the alveolar pressure and the pleural pressure. also referred to as lung recoil pressure, or transmural pressure
20
Q
what does mmHg describe
A
for the partial pressures of gases when discussing diffusion
21
Q
what does cmH2O describe
A
when discussing bulk flow (convection)
22
Q
what is an important property of the lungs to remember
A
elastic recoil/intrinsic tendency to deflate following inflation
23
Q
what are elastin fibres
A
connective tissues within the lung contain lots of elastin fibres that are arranged in a meshwork that enhances their elastic behaviour. when lung is stretched, this elastic recoil causes the lung to deflate
24
Q
describe surface tension of the lung
A
the force exerted by the liquid lining the inside of the alveoli and accounts for 70% of elastic recoil properties of the lung
25
surface tension has a 2-fold effect on elastic recoil what are they
1. the liquid layer resists any forces that try to increase its surface area. this is due to the water molecules resisting being pulled apart
2. the surface area of the liquid shrinks as much as it possibly can. this is due to the water molecules being so strongly attracted to each other.
26
what is pulmonary surfactant
a complex mixture of lipids and proteins secreted by type 2 alveolar cells. these secretions help disperse H2O on surface of the alveoli. by dispersing H2O, the water-water attractions are decreased, which causes alveolar surface tension to be decreased. this reduced surface tension is very important for respiratory mechanics as it decreases the effort needed for inflation and it reduces the surface tension of smaller alveoli more so than it does larger alveoli.
27
what is alveolar interdependence
1. when an alveolus in a group of interconnected alveoli starts to collapse, the surrounding alveoli are stretched by the collapsing alveolus
2. as the neighbouring alveoli recoil, they pull outward on the collapsing alveolus. this helps prevent the alveolus from collapsing.
28
what is the law of LaPlace
states that the magnitude of this collapsing pressure is directly proportional to the surface tension and inversely proportional to the radius of the alveoli
eqtn: 2T (surface tension) / r (alveolar radius) = P (collapsing pressure)
29
in order to prevent alveolar collapse...
small alveoli secrete more surfactant!
30
what is pulmonary surfactant
a compound composed of a mixture of lipids and proteins, and is produced and secreted by alveolar cells onto the surface of the alveoli. the hydrophobicity of surfactant enables it to interfere with the attractive intermolecular forces between the water molecules found lining the alveoli, thus reducing surface tension.
31
what is the equation for alveolar pressure
alveolar pressure (PA) - pleural pressure (PPI) = lung recoil pressure (PI)
32
describe the onset of inhalation
immediately b4 inhalation, alveolar pressure equals atmospheric pressure. Air flows neither in or out. Contraction of the inspiratory muscles causes the pleural pressure to decrease and the thoracic cavity enlarges. this decreases alveolar pressure and air flows down its pressure gradient into the lungs and inflates the alveoli. This continues until the increasing alveolar pressure again equals that of atmospheric pressure. changes in alveolar pressure is relatively small.
33
describe the onset of exhalation
at the end of inspiration, inspiratory muscles relax. this increases pleural pressure and therefore increases alveolar pressure. air flows from lungs until alveolar pressure = atmospheric pressure. activation of expiratory muscles is not necessary for normal expiration due to the strong recoil forces
34
describe active exhalation
in healthy people at rest, expiration is passive. activation of expiratory muscles reduces the end-expiratory lung volume which increases the tidal volume independent of the inspiratory muscles.
during routine exercise: to breath out alveolar pressure must be increased more than is accomplished by decreased excitation of inspiratory muscles and elastic recoil.
forced expiration: activates the expiratory muscles to generate a high pleural pressure for forced expiration. as expiratory flow continues, the pressure decreases because of energy lost due to resistance. at some point along the airways the equal pressure point will be reach.
35
describe active expiration
pleural pressure becomes +'ve due to the increased abdominal pressure, but the lungs do not collapse. this occurs bc the alveolar pressure increases correspondingly. also, any pressure increase in the pleural pressure is offset by a proportionate increase in airway resistance due to the compression of the airways. this blocks further outflow and, as such, active expiration never results in a person exhaling past their psychological residual volume (which would collapse the bronchioles).
36
as lung volume increased its PI increased from _____ cmH2O to residual volume to about ______ cmH2O at total lung capacity
0, 30
37
in opposition the pressure of the chest wall (PW) functions more like a spring about ______ of _________, the compressed spring exerts negative pressure yet ______ total vital capacity, the chest wall now a stretched spring wants to collapse
65%, total vital capacity, 100%
Pw
38
if we combine ____ and ____ we get ______ which rep the pressure-volume relationship of the resp sys
PI and PW we get Prs
39
describe compliance
the pressure-volume curve can derive compliance, which is the slope of the curve. is the greatest at functional residual capacity, which means the amount of work, or pressure needed, to either inhale or exhale is at its minimum
40
describe low compliance
means more pressure is required to move air in or out. compliance is affected by lung diseases, like emphysema.
41
Poiseuille's Law eqtn
flow rate (Q) = pi(triangle)Pr4/8nL
42
what is the primary determinant of resistance
the radius of the airway
43
bronchoconstriction
occurs under the influence of local chemical control. specificantly, decreased CO2 causes constriction to decrease ventilation and maintain a psychological level of CO2
44
pathological factors of bronchoconstriction
1. histamine release
2. excess mucus
3. airway collapse
4. oedema of the airway walls
5. allergy-induced spasm of the airways caused by slow-reactive substance of anaphylaxis
45
what is bronchodilation
when not at rest, or during periods of sympathetic domination when body O2 demands are increased, sympathetic activity causes bronchodilation to allow max flow rates with minimum resistance
46
what is sympathetic activity mediated by
both direct and indirect innervation
47
what is direct innervation
nerve terminals release NE, which activates B2 receptors on the bronchial smooth muscle cells
48
what is indirect innervation
E released from the adrenal medulla circulates through the pulmonary circulation to the airway smooth muscle
49
true/false
there are no pathological conditions that cause bronchodilation
50
true/false oedema of the airway walls leads to bronchodilation of airways
false
51
true/false NE release activates B2 receptors on bronchial smooth muscle cells
true
52
true/false bronchodilation primarily occurs under the influence of local chemical control
false
53
true/false when body O2 demands are increased, sympathetic activity causes bronchodilation
true
54
what is asthma
chronic inflammatory disease of the airways that causes difficulty breathing.
sympt: SOB, chest tightness, coughing, wheezing
caused from:
1. airway walls are thickened due to histamine-induced oedema
2. thick mucus secretion physically blocks the airways
3. airway hyper-responsiveness causes spasms of smooth muscles in smaller airways, resulting in their constriction
triggers can be allergens, irritants, or infection
55
what is COPD
term used to cover emphysema and chronic bronchitis and is usually caused by long-term smoking
chronic bronchitis: longterm inflammatory condition of lower airways. caused by chronic exposure to smoking, allergens, or air pollution. airways become narrowed due to oedema of the airway walls and secretion of a thick mucus
emphysema: irreversible condition is characterized by the collapse of the smaller airways and breakdown of alveolar tissues. in response to chronic exposure to smoke, alveolar macrophages release substances like trypsin as a defensive mechanism. excess trypsin and other destructive enzymes destroy the lung tissue
56
what is VT
tidal volume - the volume of air entering or leaving the lung during a single breath. at rest, this is typically around 500mL
57
what is IRV
inspiratory reserve volume - the extra volume of air that can be maximally inspired above the resting tidal volume. at rest, this is typically around 3000 mL
58
what is inspiratory capacity (IC)
max volume of air that can be inhaled starting from the end of a normal expiration at rest. this value is typically 3500 mL (VT + IRV)
59
what is ERV
expiratory reserve volume - max volume of air that can be expelled starting at the end of a typical tidal volume. at rest, this is typically around 1000 mL
60
what is RV
residual volume - the volume of air remaining in the lungs after max expiration. at rest, this is typically around 1200 mL. this volume cannot be directly measured by spirometry, but rather indirectly by inspiration of a tracer gas such as helium
61
what is FRC
functional residual capacity - the volume of air in the lungs at the end of normal passive expiration. this value is typically around 2200 mL (FRC = ERV + RV)
62
what is VC
vital capacity - the max volume of air that can be expelled during a single breath following a max inspiration. this value is typically around 4500 mL. (VC = IRV + VT + ERV)
63
what is TLC
total lung capacity - max volume of air the lungs can hold. typically around 5700 mL (TLC = VC + RV)
64
what is FEV1
forced expiratory volume in 1 sec - this is similar to TLC but is derived from only the 1st second of expiratory effort. normally expressed as a ratio (FEV1/FVC) or converted to a %. at rest, this value is typically around 80%.
65
what is obstructive lung disease
a healthy individually has a FEV1 of 80%. w this disease they cannot exhale so much of their FEV1 is lower. the FRC and RV are greater but the VC is smaller. these trends would continue to worsen as the breath stacking continued.
66
what is restrictive lung disease
is characterized by low lung volumes. the absolute amount of air that can be exhaled in 1 sec (FEV1) is reduced bc lungs are smaller. the proportion of the FVC that can be exhaled (FEV1/FVC) is normal since there is no obstruction to airflow.
67
look at section 4, side 4 at the chart
68
during pulmonary function testing it is more common to use what data
expiratory data>inspiratory data
69
what is the equation for ventilation
tidal volume (VT) x respiratory frequency (f) = minute ventilation (VE)
the amount of gas breather in 1 min is called the min ventilation
70
describe ventilation
during inspiration, some of the inspired air remains in the airways and never reaches the alveoli due to the anatomic dead space. the dead space volume had important consequences for alveolar ventilation. if the V of gas a person breathes in w each breath is the same as the volume of the dead space, then the alveolar ventilation must be zero. all the inspired gas stays in the anatomic dead space. to have an effective alveolar ventilation, tidal volume must exceed dead space volume.
71
learn the chart on section 4, slide 9
72
what happens at low resp rates
in order to maintain alveolar ventilation, the tidal volume must increase. increasing the tidal volume means the inspiratory muscles are working harder, the elastic work of the lung is higher.
73
what happens in high respiratory rates
when we increase respiratory rates, the tidal volume can decrease, which reduces the elastic work of the lung, but bc you are now moving more air, the flow-resistive work of the lung increases.
74
what 4 conditions increase the work of breathing
- decreased compliance
- increased resistance
- decreased elastic recoil
- increased demand for ventilation
75
what is gas exchange
the diffusion of o2 from the alveoli into the blood, and carbon dioxide from the blood to the alveoli
76
what are the factors that determine gas exchange
are the same as those for convective flow through the airways (Flow = change in P/R)
77
does alveolar air have the same composition of inspired air
no
78
alveolar gas equation
PIO2 - PACO2/R = PAO2
PIO2 = is the partial pressure of inspired oxygen (150 mmHg)
PACO2 is the partial pressure of alveolar carbon dioxide (about 40 mmHg), and R is the respiratory quotient or ratio of metabolic carbon dioxide formation to oxide consumption, roughly 0.8 in healthy people
79
describe gas exchange at the pulmonary capillaries
as blood passes through the lungs, carbon dioxide moves from the blood to the alveoli and oxygen moves from the alveoli to the blood. the movement of gases is by diffusion and is driven by partial pressure gradients. the process of ventilation is constantly replenishing alveolar oxygen and removing carbon dioxide.
80
concentrated of oxygen
blood leaving the lungs has an oxygen partial pressure of 100 mmHg, which is about 200 mL O2/L. blood returning to the lungs has a partial pressure of 40 mmHg, which is about 150 mL O2/L. from this, you can calculate that at rest, 50 mL O2/L was removed by the tissues. the remaining 150 mL O2/L represents the functional reserve for when there is an increased tissue demand.
81
concentration of carbon dioxide
blood leaving the lungs has a carbon dioxide partial pressure of 40 mmHg which is about 480 mL Co2/L. blood returning to the lungs has a partial pressure of 46 mmHg, which is about 520 mL CO2/L. this is because of the essential role that CO2 have in acid-base balance.
82
factors affecting gas exchange (3)
1. surface area (greatre the SA, greater amount of gas exchange)
2. capillary transit time (bc gases can only be exchanged between blood and alveoli the flow rate of blood can influence gas exchange)
3. membrane thickness (thickness of the barrier separating the blood and the alveoli can be increased due to inflammation)
83
PO2 of arterial blood is ___________ mmHg, which is around _____ mL O2/L
100, 200
84
is oxygen poorly soluble in liquids such as plasma
yes
85
what is hemoglobin
once bound to hemoglobin, o2 no longer contributes to the PO2 meaning that the PO2 only represents the freely dissolved O2 in the plasma and the Hb-bound oxygen acts as a reserve.
86
how many iron atoms are in a Hb molecule
4
87
the most important factor for determining % of Hb saturation is
PO2
88
the relationship between PO2 and % of Hb saturation is described as...
the oxygen dissociation curve
89
what is the significance of the steep portion of the O2-Hb curve
the steep portion between 0-60 mmHg corresponds to the range of PO2 that is found in the systemic capillaries. in metabolically active tissues where more o2 is needed, a drop in PO2 to 20 mmHg can release an additional 45% of the total oxygen. the steep portion of the curve allows for larger amounts of O2 dissociation for small decreases in PO2.
90
why is the steep portion of the curve is also beneficial for persons breathing at altitude
w a decreased atmospheric pressure, there is a decrease in alveolar PO2 and therefore a decrease in arterial PO2. the decrease in arterial PO2 activates carotid chemoreceptors that causes an increase in ventilation. if the person is still at rest (no increase in metabolic activity) then this increased ventilation will result small decrease in arterial PCO2, which according to the arterial gas eqtn, means there will be a small increase in alveolar PO2. on the steep portion of the curve, this small increase in alveolar PO2 can greatly increase % Hb saturation.
91
what is the significance of the plateau portion of the O2-Hb curve
from 60 mmHg to 100 mmHg, represents the PO1 range found in the pulmonary capillaries
92
the plateau phase of the curve represents a margin of safety, important to know for people w pulmonary disease but also healthy people under which 2 circumstances
1. high altitude where PO2 of inspired air is reduced
2. in oxygen-deprived environments at sea level. say you were locked into an airtight room for a period of time, the plateau phase of the
93
if no Hb was present what would happen
the alveolar PO2 and the pulmonary capillary blood PO2 are at equilibrium
94
if HB partially saturated what happens
as Hb starts to bind w O2, it removes O2 from solution. Bc only dissolved o2 contributes to blood PO2, the blood PO2 remains below that of the alveoli, even tho the # of o2 molecules are present in the blood. by binding some of the dissolved o2, Hb favours the net diffusion of more o2 down its partial pressure gradient from the alveoli to the blood.
95
what happens when Hb is fully saturated
the alveolar and blood PO2 are at equilibrium again. the blood PO2 resulting from dissolved o2 is equal to the alveolar PO2 despite the fact that the total o2 content in the blood is much greater than in the case of no Hb
96
4 factors affecting the dissociation curve
1. pH
2. BPG
3. CO2
4. Hb and CO
97
describe pH
pH: primary form that Co2 is carried in the blood as HCO3. combo of H+ and lactic acid can cause pH to decrease, enhancing the dissociation of oxygen from hemoglobin (Bohr effect)
98
describe BPG
when o2 saturation in arterial blood is below normal, BPG production is increased. acts like an o2 sensor such than in conditions of lower PO2, BPG enhances the unloading of oxygen. unlike H+ and CO2 the effects of which are reversed in the lungs, BPG produced is not eliminated in the lungs so it persists in limiting o2 binding to Hb resulting in arterial blood to have a decreased % saturation.
99
describe CO2
CO2 can also bind to Hb. when there is an icnrease in PCO2, the O2 dissociation curve shifts to the right. this is another mechanism to increase o2 unloading in metabolically active tissues where PCO2 is increasing such as the systemic capillaries. called the Haldane effect, and leads to more o2 unloading than a decrease in PO2 alone could accomplish.
100
describe Hb and CO
CO is a toxic gas produced from incomplete combustion of carbon-based products. CO competes with O2 for the same binding sit on Hb and forms HbCO, meaning low levels of CO can make a larger number of oxygen-binding sites unavailable and the % saturation is decreased. CO also shifts the o2 dissociation curve to the left, requiring larger drops in PO2 to unload o2 into the tissues.
101
how is CO2 physically dissolved
CO2 is 20x more soluble than O2 so it makes sens more CO2 is transported physically dissolved in plasma. only about 5-10% of total blood CO2 is freely dissolved but this small fraction accounts for 46 mmHg partial pressure of CO2 when blood leaves the systemic capillaries.
102
how does CO2 bound to hemoglobin
CO2 binds to the globin part of the molecule. Hb w/o o2 has a greater affinity for CO2 so the unloading of O2 in the systemic capillaries enhances the uptake of CO2. only 5-10% of total CO2 is transported in this manner.
103
CO2 as bicarbonate
bicarbonate makes up 80-90% of circulating CO2. CO2 combines w water to form carbonic acid. this reaction occurs slowly in the plasma but RBC have the enzyme carbonic anhydrase (CA) which accelerates this reaction. carbonic acid spontaneously dissociates into hydrogen ions and bicarbonate.
104
what is the chloride (hamburger) shift
in systemic capillaries as more CO2 enters the RBC's, bicarbonate, and hydrogen ions accumulate. RBC's have a bicarbonate-chloride carrier that allows the exchange of these ions across the cell membrane. Consequently, bicarbonate leaves the cells and chloride enters the cell down its electrochemical gradient.
105
what is the reverse haldane effect
occurs when there are increases in arterial PO2, such as when breathing supplemental o2. the increased PO2 prevents the hemoglobin from binding CO2. this forces the CO2 to travel back to the lungs either dissolved in the plasma, or as bicarbonate. blood acidity may rise, which might be the explanation for the increased ventilation rates associated w breathing supplemental o2.
106
hypoxia
described as insufficient o2 at the cellular level
107
hypoxic hypoxia
characterized by low arterial PO2 w inadequate Hb sat. caused by inadequate gas exchange or exposure to high altitude.
108
circulating hypoxia
occurs when too little oxygenated blood is delivered to the tissues. caused by something that blocks the delivery of blood, like vascular spasms or a blockage. arterial PO2 and o2 content are usually normal.
109
anemic hypoxia
reduced o2 carrying capacity of the blood and can result from a decrease Hb within the RBC or carbon monoxide poisoning. PO2 is always normal but the o2 content of arterial blood is decreased.
110
histotoxic hypoxia
o2 delivery to the tissues is completely normal but something within the tissues prevents o2 usage. ex: cyanide poisoning.
111
hyperoxia
characterized by an abnormally high arterial PO2. can never happen to a person breathing air at sea level but it can happen in someone breathing supplemental o2. the high o2 content of inspired gas raises arterial PO2 but the total o2 content does not as Hb is essentially saturated w breathing normal air. this is not always good tho as it can raise arterial PO2 to dangerous levels and cause o2 toxicity. in some tissues, the increased dissolved o2 can cause the formation of reactive o2 species that can damage cells. this can cause brain and retina damage, causing blindness.
112
hypercapnia
excess of carbon dioxide in the blood caused by hypoventilation. both CO2 and o2 are equally affected by decreased ventilation, hypercapnia can result in decreased PO2
113
hypocapnia
below-normal arterial PCO2 and is caused by hyperventilation. can be caused by anxiety, fever, aspirin poisoning, and even exercise if there is a shift to anaerobic metabolism. hyperventilation causes an increased alveolar PO2 but very extra O2 is added to the blood bc both the partial pressure of dissolved o2 and the % sat of Hb are near maximal w normal alveolar PO2
114
describe left shift of the o2 dissociation curve
- increased affinity for o2
- decreased temp
- increased pH
- decreased pCO2
- decreased BPG
115
describe right shift of the o2 dissociation curve
decreased affinity for o2
- increased temp
- decreased pH
- increased pCO2
- increased BPG
116
describe neural control of respiration 3 distinct components
1. generation of alternating inspiration/expiration rhythm: occurs in the medullary resp centre that sends its output to the resp muscles. 2 clusters of neurons.
- dorsal resp group neurons are the inspiratory neurons whose firing causes inspiration, and cessation of firing causes expiration
- ventral resp group neurons are both inspiratory and expiratory. there are interneurons between the DRG and VRG to allow for recruitment when there is increased output from the DRG during increased ventilator demand.
2. regulation of the level of respiration (rate and depth) to match metabolism
- controlled by the brain stem under the influence of receptors involved in respiration
3. modulation of respiratory activity for other purposes
- may be voluntary like speech or involuntary like coughing
117
3 classes of pulmonary receptors
1. slowly adapting receptors
2. rapidly adapting receptors
3. c-fibres
118
what do slowly adapting pulmonary receptors do
have endings in the airway smooth muscle and respond to changes in lung volume. their rate of discharge increases as the lungs inflate.
119
what do rapidly adapting pulmonary receptors do
have endings in the epithelia of larger airways and respond to both mechanical and chemical stimuli. their activation can cause the airways to narrow and cough, this is a protective reflex to prevent inhalation of irritants. their activation can also cause mucus production to further trap inhaled particles.
120
what do c-fibre pulmonary receptors do
have ending close to the pulmonary capillaries and detect increases in pulmonary arterial pressure and pulmonary oedema. they also respond to chemical stimuli such as capsaicin, that signal inflammation. activation causes bronchoconstriction and rapid shallow breathing.
121
describe rib cage receptors
muscles of the chest wall are highly innervated w muscle spindles w a few Golgi tendon organs. thei role is unclear. spindles detect discrepancies in actual chest wall distention from the distention that was expected. if there was a smaller distention than expected then the spindles receptors would discharge to "unload" the spindle and permit greater distention. the intercostal muscles play a role in posture.
122
describe diaphragm receptors
contains very few mechanical receptors. likely that the key roles in respiration has limited these types of receptors within it. diaphragm has many small myelinated and unmyelinated afferents that respond to local metabolic conditions.
123
if metabolism ____________, then ventilation also ______________
increases
124
how is arterial PO2 monitored
by peripheral chemoreceptors located in the carotid bodies and the aortic bodies
125
what do the carotid chemoreceptors respond to
changes in arterial PO2
126
what do aortic chemoreceptors respond to
changes in o2 content
127
when do the carotid chemoreceptors pick up change in PO2
insensitive until the PO2 drops below 60 mmHg, the level at which o2 desaturation could impair peripheral tissue functioning. their activation causes increase in ventilation to increase arterial PO2.
128
why are carotid chemoreceptors not activated above PO2 of 60 mmHg
above this level, increasing alveolar PO2 has little effect on o2 content as the blood is near saturated already.
129
does activation of aortic chemoreceptors when o2 content decreases affect ventilation
does not affect ventilation, but increases cardiac output to increase systemic oxygen delivery
130
what is the most important factor when regulating minute-to-minute ventilation when at rest
CO2, but there are no peripheral chemoreceptors that play any significant role
131
where are the central chemoreceptors located
located in the medulla near the respiratory centres. these chemoreceptors monitor CO2-induced changes in H+ concentration in the brain extracellular fluid
132
2 factors about how CO2 causes changes in ventilation
1. CO2 crosses the blood-brain barrier so any increase in arterial PCO2 will cause an increase in brain extracellular fluid PCO2. CO2 is converted to bicarbonate, which raises H+. this increase in H+ stim the central chemoreceptors to increase ventilation.
133
whats under mechanical control
- diaphragm receptors
- pulmonary receptors
- rib cage receptors
134
whats under chemical control
- aortic bodies
- carotid bodies
- increase in arterial PCO2
- increase in brain-ECF H+
135
under neither chem or mech control
- cardiac receptors
- increase in arterial PO2
- decrease in H+
- increase in brain Na2+
136
during exercise alveolar ventilation can increase up to ________ fold
20
PO2, PCO2, and H+ play little role in this effect
137
describe how exercise effects ventilation (PO2, PCO2, H+)
arterial PO2 generally remains normal or may even be slightly elevated, PCO2 also remains normal or may even be slightly elevated, PCO2 qalso remains normal or slightly decreased, H+ stays constant.
138
describe factors (4) that play a role in exercise-induced increases in ventilation
1. reflexes originating from body movements (muscle mechanoreceptors get excited during muscle contraction stim the resp centre)
2. increased body temperature
3. E release
4. impulses from the cerebral cortex
139
what are 7 important module 3 formulas
flow eqtn, law of LaPlace, alveolar pressure, poiseuille's law, minute ventilation eqtn, gas diffusion, alveolar gas eqtn
