1
Q
What is internal respiration?
A
The cellular process where oxygen (O₂) is used to produce ATP, generating carbon dioxide (CO₂) as a byproduct that must be removed.
2
Q
What is external respiration?
A
It involves:
- Bringing O₂ from the atmosphere into the body
- Transporting O₂ to tissues
- Removing CO₂ from tissues and releasing it back into the atmosphere
3
Q
What are the four steps of external respiration (i.e., the primary functions)
A
- Ventilation: Air is moved in and out of the lungs. This is called breathing, or ventilation, and
moves air between the atmosphere and the air sacs (alveoli) in the lungs. - Exchange of O2 and CO2 between Air and Blood: The diffusion of oxygen from the alveoli to the pulmonary capillaries and the movement of carbon dioxide in the opposite direction.
- Transport of O2 and CO2: The transport of oxygen in the blood to the tissues and the movement of carbon dioxide in the opposite direction.
- Exchange of O2 and CO2 between Blood and Tissues: The exchange of oxygen from the blood to the tissues and carbon dioxide from the tissues into the blood via diffusion.
4
Q
What are the other key roles of external respiration in the body?
A
- Enables speech by air passing over the vocal chords.
- Defends against inhaled foreign matter.
- The respiratory muscles play a role in parturition and defecation.
- The lung acts as a blood reservoir to allow for rapid equalization of left and right cardiac outputs.
- Helps to maintain the acid-base balance
5
Q
Upper airway includes?
A
The nose, nasal cavities, pharynx, the digestive system, and the larynx
6
Q
Lower airway includes?
A
Begins with the trachea, bronchi, bronchiole, and alveoli
7
Q
The respiratory system can be divided into which three anatomical parts?
A
The lungs, chest wall, and pleural space
8
Q
The smallest bronchioles are known as?
A
Respiratory bronchioles as their walls are so thin that some gas exchange can occur
9
Q
Where is the majority of gases and exchanged between air and blood?
A
Alveoli
10
Q
Branching airways of the lower tract are often described as?
A
Respiratory tree or tracheobronchial tree
11
Q
How the cross sectional area changes with the branching of the airways? Why is it important?
A
Even though each branch gets smaller and smaller, the overall cross sectional area increases. It’s important as it allows for the transition from connective flow to diffusive flow
12
Q
Connective vs. Diffusive flow
A
Connective flow = requires energy in the form of muscle contraction to maintain air flow (trachea, main bronchus, bronchus, bronchiole, terminal bronchiole)
Diffusive flow = occurs passively to allow air to flow into the alveoli (respiratory bronchioles, alveoli ducts, alveoli sacs)
13
Q
The chest wall includes?
A
Thorax (chest) + abdomen
14
Q
The intercostal muscles are found?
A
Between the ribs and are divided into the inner intercostal muscles and the external intercostal muscles, which lie over the innermost intercostals
15
Q
The thoracic cavity and abdominal cavity are separate by?
A
The diaphragm
16
Q
What are the main muscles of inspiration? What happens during inhalation?
A
The diaphragm + external intercostal muscles. The diaphragm descends to enlarge the thoracic cavity. Contraction of the external intercostal muscles elevates the ribs to further enlarge the thoracic cavity
17
Q
What are the main muscles of expiration?
A
Internal intercostal + internal obliques + diaphragm. They are responsible for decreasing the volume of thoracic cavity.
18
Q
What happens to the muscles of expiration in healthy individuals?
A
They are generally inactive and only get recruited when there is an increase in ventilator demand as during exercise or during coughing, sneezing and vomiting
19
Q
What is the pleural space?
A
The lung is covered by the visceral pleura and the inside wall of the thorax is lined by the parietal pleura. Between these two membranes is the pleural space, it’s small (2 mm) and filled with pleural fluid.
20
Q
What is the role of the pleural fluid?
A
Allows the membranes to rub against each other during breathing with reduced friction
21
Q
External respiration involves the movement of oxygen into the alveoli and the removal of carbon dioxide from the lungs. What are the two key processes that allow external respiration to occur?
A
- The respiratory muscles generating the pressure gradient needed to move air through the airways and inflate the lungs.
- The diffusion of oxygen and carbon dioxide across the alveolar-capillary barrier.
22
Q
The two key processes that allow external respiration to occur can be explained by which equation?
A
delta Pressure / Resistance = Flow (or diffusion) (V)
23
Q
In the respiratory system, airflow (V) is driven by a pressure gradient. What factors must this pressure gradient overcome for air to move into and out of the alveoli?
A
- Elastance (stiffness of the respiratory system)
- Resistance to airflow in the airways
- Inertia of the system
24
Q
How do pressure differences between the alveoli and the nose determine the direction of airflow during breathing?
A
Air flows into the alveoli when alveolar pressure is lower than nasal pressure.
Air flows out of the alveoli when alveolar pressure is higher than nasal pressure.
25
What is PB?
Atmospheric pressure (aka barometric pressure). It's the pressure exerted by the weight of the air in the atmosphere on the Earth's surface. At sea level, it's 760 mmHg and it decreases as you gain altitude. Given that, even when standing, there is not enough difference in height between the lungs and the nose/mouth, PB is the same in both places so we treat it as if it was 0.
26
What is PA?
Alveolar pressure (aka intrapulmonary pressure). At the end of inspiration, alveolar pressure is the same as atmospheric pressure at 0 cm H2O.
27
What is Ppl?
Pleural pressure (aka intrapleural pressure). It closely approximates the intrathoracic pressure. It is negative to atmospheric pressure and is normally around -5 cm H2O. It's negative because the lungs want to collapse yet the chest wall wants to expand.
28
What closely approximates the intrathoracic pressure?
The pleural pressure
29
Why the pleural pressure is negative?
Because the lungs want to collapse yet the chest wall wants to expand.
30
What is Ptp?
Transpulmonary pressure. This pressure is the difference between the alveolar pressure and the pleural pressure. It is also referred to as lung recoil pressure or transmural pressure.
31
The difference between the alveolar pressure and the pleural pressure is?
Transpulmonary pressure
32
What is a manometer?
A device to measure pressures
33
What are the traditional units we use for respiratory physiology?
mmHg for the partial pressures of gases when discussing diffusion
cmH2O when discussing bulk flow (convection)
34
Why cmH2O is used for bulk flow?
Because the pressures needed to generate airflow are small and easier to measure accurately in cmH₂O.
35
How are pressures related to convective airflow expressed relative to atmospheric pressure, and what does a “negative” pressure indicate?
Pressures are expressed relative to atmospheric pressure.
Example: If atmospheric pressure = 1034 cmH₂O, an alveolar pressure of 1029 cmH₂O is written as -5 cmH₂O.
“Negative” pressure does not mean less than zero; it indicates pressure below atmospheric pressure, which drives airflow into the lungs.
36
Why the lungs have an intrinsic tendency to deflate?
This is due to elastin fibres and surface tension
Elastin fibres: The connective tissues within the lung contain lots of elastin fibres that are arranged in a meshwork that enhances their elastic behaviour. When the lung is stretched, as happens during inhalation, this elastic recoil causes the lung to deflate.
Surface tensions: The force exerted by the liquid lining the inside of the alveoli and accounts for about 70% of the elastic recoil properties of the lung.
37
Of the two reasons, which contributes more to the elastic recoil properties of the lung?
Surface tensions
38
Surface tension has what two-fold effects on elastic recoil?
1. The liquid layer resists any forces that try to increase its surface area. This is due to the water molecules resisting bing 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.
As a result, in the absence of expanding forces, alveoli shrink and expel alveolar gas
39
If surface tension in the alveoli is so strong, why don’t the alveoli collapse during normal breathing?
The alveoli do not collapse because of two key factors:
1. Pulmonary surfactant – reduces surface tension, making it easier to keep alveoli open.
2. Alveolar interdependence – neighboring alveoli support each other structurally, helping maintain openness.
40
What is pulmonary surfactant?
A complex mixture of lipids and proteins secreted by type II alveolar cells.
41
How does pulmonary surfactant affect alveolar surface tension and lung mechanics?
It disperses water molecules on the alveolar surface, reducing water-water attractions.
This decreases alveolar surface tension, which:
1. Reduces the effort needed to inflate the lungs (increases compliance).
2. Reduces surface tension more in smaller alveoli than larger alveoli, helping prevent collapse.
42
What is alveolar interdependence, and how does it help prevent alveoli from collapsing?
Alveolar interdependence refers to the structural connections between each alveolus and its surrounding alveoli via connective tissue.
If one alveolus begins to collapse:
1. Neighbouring alveoli are stretched by the collapsing alveolus.
2. As these neighbouring alveoli recoil, they pull outward on the collapsing alveolus.
This mechanical support helps prevent alveolar collapse.
43
How does the Law of LaPlace explain the relationship between alveolar size, surface tension, and the tendency of alveoli to collapse?
The law of LaPlace states that the collapsing pressure of an alveolus is: P = 2T/r, where P = collapsing pressure, T = surface tension, r = radius of the alveolus
According to this relationship:
- Collapsing pressure is directly proportional to surface tension (T)
- Collapsing pressure is inversely proportional to radius (r)
This means:
- Smaller alveoli (smaller r) have higher collapsing pressure and are more likely to collapse
- Differences in alveolar size can therefore threaten alveolar stability
44
What mechanism helps prevent small alveoli from collapsing into larger alveoli in the lungs?
Small alveoli produce more surfactant. Surfactant reduces surface tension. Because smaller alveoli naturally have higher collapsing pressure (according to the Law of LaPlace), increasing surfactant lowers their surface tension and therefore lowers their collapsing pressure. This helps stabilize alveoli of different sizes and prevents small alveoli from collapsing into larger ones.
45
How pulmonary surfactants lower surface tension?
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.
46
What other factors contribute to the maintenance of alveolar structure other than pulmonary surfactants?
Alveolar interdependence, which is the supportive recoil of neighbouring alveoli, helps to maintain alveolar structure and prevent collapse.
47
How does the ability of each alveolus to regulate its own surfactant secretion contribute to alveolar stability and gas exchange?
Each alveolus can adjust how much surfactant it secretes, allowing it to regulate its surface tension. By lowering surface tension as needed, alveoli of different sizes can equalize their collapsing pressures. This prevents collapse and helps maintain a large surface area for optimal gas exchange.
48
How is transpulmonary pressure calculated?
Alveolar pressure - pleural pressure = lung recoil pressure
Lung recoil pressure + pleural pressure = alveolar pressure
49
How can we change alveolar pressure?
Since lung recoil pressure depends on lung volume, it cannot be directly changed to initiate airflow. Therefore, to change alveolar pressure, pleural pressure must change.
Inspiration: Contraction of inspiratory muscles decreases pleural pressure → decreases alveolar pressure below atmospheric pressure → air flows into the alveoli.
Expiration: Activation of expiratory muscles increases pleural pressure → increases alveolar pressure above atmospheric pressure → air flows out.
50
How do changes in pleural and alveolar pressures produce inspiration and expiration during normal breathing?
Before inspiration (end of expiration), alveolar pressure equals atmospheric pressure, so there is no airflow.
During inspiration, contraction of inspiratory muscles lowers pleural pressure, which lowers alveolar pressure below atmospheric pressure. This creates a pressure gradient from atmosphere to alveoli, causing air to flow in. Inspiration ends when muscle contraction decreases and lung recoil pressure equalizes with pleural pressure.
During expiration, inspiratory muscles relax. Lung recoil pressure becomes greater than pleural pressure, making alveolar pressure positive relative to atmospheric pressure. This causes air to flow out of the lungs.
51
What happens at the onset of inhalation in terms of alveolar and pleural pressures, and how do these changes produce airflow?
Immediately before inhalation, alveolar pressure equals atmospheric pressure, so no air flows.
At the onset of inhalation, contraction of the inspiratory muscles decreases pleural pressure and expands the thoracic cavity. This lowers alveolar pressure (by about 1 cmH₂O), creating a pressure gradient that causes air to flow into the lungs until alveolar pressure again equals atmospheric pressure.
It is also important to note that the change in pleural pressure is not linear, as it must initially overcome increased resistance to airflow at the start of inspiration.
52
What happens at the onset of exhalation, and why are expiratory muscles not needed for normal breathing?
At the end of inspiration, inspiratory muscles relax, which increases pleural pressure and consequently raises alveolar pressure. Air flows out of the lungs until alveolar pressure equals atmospheric pressure.
Expiratory muscles are not needed for normal breathing because lung recoil forces are sufficient to drive passive expiration.
53
What is active exhalation, and how does it differ from passive exhalation?
Active exhalation occurs when expiratory muscles contract, allowing the lungs to empty faster or more forcefully, such as during exercise. This reduces end-expiratory lung volume and increases tidal volume, independent of inspiratory muscles.
In contrast, passive exhalation at rest relies only on lung recoil and does not require expiratory muscle activity.
54
What is the end-expiratory lung volume?
The basal level of inflation that lungs tend to return to during relaxed breathing. This is also called functional residual capacity (FRC)
55
During routine exercise, how do expiratory muscles help increase alveolar pressure to forcefully exhale?
To exhale forcefully, alveolar pressure must rise above what is achieved by passive recoil. Expiratory muscles of the abdominal wall contract, increasing abdominal pressure, which is transmitted to the pleural space and raises pleural pressure. Internal intercostal muscles also contract, pulling the ribs downward and inward, decreasing thoracic cavity size and further increasing alveolar pressure to expel air.
56
What happens during forced expiration when expiratory muscles generate high pleural pressure, and why does increasing effort not always increase airflow?
During forced expiration, expiratory muscles raise pleural pressure to push air out. As air flows, resistance causes pleural pressure to drop, and an equal pressure point is reached along the airways. Beyond this point, transpulmonary pressure becomes negative, compressing the airway.
As a result, trying to exhale harder does not increase airflow because any extra pressure is counteracted by increased airway resistance. At this stage, airflow is mainly driven by lung recoil pressure (PA – Pl) rather than muscular effort.
57
What is the equal pressure point?
The point at which the pressure within the airways equals the pleural pressure
58
Why the lungs do no collapse during active expiration?
During active expiration, pleural pressure becomes positive due to the increased abdominal pressure, but the lungs do not collapse. This occurs because 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 physiological residual volume (which would collapse the bronchioles).
59
How do the pressure-volume relationships of the lung, chest wall, and respiratory system change during the breathing cycle?
Lung (Pl): As lung volume increases from residual volume to total lung capacity, lung recoil pressure (Pl) rises from ~0 cmH₂O to ~30 cmH₂O, reflecting the lung’s increasing tendency to deflate at higher volumes.
Chest wall (Pw): Acts like a spring. Below ~65% of vital capacity, it generates negative (inflating) pressures, helping the lungs expand. At total lung capacity, it is stretched and generates positive (deflating) pressures, tending to collapse.
Respiratory system (Prs): The combination of lung and chest wall pressures (Prs = Pl + Pw) shows the overall pressure-volume relationship. Negative pressures indicate a tendency to inflate, and positive pressures indicate a tendency to deflate.
60
What is compliance?
The ability of the lung to stretch so at functional residual capacity, it is easy to move air in or out of the lungs. Slope of the pressure-volume curve and reflex how easily the lungs can expand when you inhale
61
Compliance is greatest at?
Functional residual capacity (FRC): least work/pressure is needed to inhale or exhale
62
How is compliance affected by different lung diseases?
Low compliance: More pressure is required to move air (e.g., pulmonary fibrosis, pulmonary edema, pneumonia).
High compliance: Lungs expand easily but may not recoil well (e.g., emphysema). Surfactant increases compliance.
63
What is tidal volume?
The amount of air inhaled or exhaled during a normal, relaxed breath. In a healthy adult: ~ 500 mL per breath
64
What is the relationship between compliance of lungs, chest walls, and their combination (i.e., lung-chest wall system)?
The compliance of lung-chest wall is lower than the individual ones.
65
Resistance to flow is determined by using?
The Poiseuille's Law:
Flow rate (Q) = [pai delta Pr^4]/(8 miu L)
66
What is the primary determinant of resistance based on Poiseuille's Law?
The radius of the airway
67
What is bronchoconstriction?
When airway radii become smaller and cause an increase in airway resistance
68
How is airway resistance regulated?
Neural control: Airways receive sympathetic and parasympathetic innervation. At rest, parasympathetic activity dominates, maintaining bronchial smooth muscle tone and causing bronchoconstriction.
Chemical control: Low CO₂ levels cause bronchioles to constrict, helping maintain proper ventilation.
69
What factors can cause bronchoconstriction?
Pathological factors: Bronchoconstriction can also result from:
- Histamine release
- Excess mucus
- Airway collapse
- Oedema of airway walls
- Allergy-induced spasm (slow-reactive substance of anaphylaxis)
70
How does sympathetic activity regulate bronchodilation, and what other factors can cause bronchodilation?
Sympathetic activity during increased O₂ demand causes bronchodilation to maximize airflow and reduce resistance.
1. Direct: Nerve terminals release norepinephrine, activating β₂-receptors on bronchial smooth muscle.
2. Indirect: Epinephrine from the adrenal medulla circulates to the airways, relaxing smooth muscle.
Chemical control: Increased CO₂ also causes bronchodilation to enhance ventilation and remove excess CO₂.
Note: There are no pathological conditions that cause bronchodilation.
71
What is asthma, and how are the airways impaired in individuals with this condition?
Asthma is a chronic inflammatory disease of the airways causing difficulty breathing, with symptoms like shortness of breath, chest tightness, coughing, or wheezing. Airways can be impaired in three ways:
1. Thickened airway walls due to histamine-induced oedema.
2. Thick mucus secretion that physically blocks airflow.
3. Airway hyper-responsiveness, causing smooth muscle spasms and constriction of smaller airways.
72
What is chronic obstructive pulmonary disease (COPD), and how do chronic bronchitis and emphysema contribute to it?
COPD is a term covering emphysema and chronic bronchitis, usually caused by long-term cigarette smoking, and is a leading cause of death.
Chronic bronchitis: Long-term inflammation of the lower airways due to cigarette smoke, allergens, or air pollution. Airways narrow because of oedema and thick mucus secretion.
Emphysema: Irreversible collapse of smaller airways and destruction of alveolar tissue. Chronic smoke exposure triggers alveolar macrophages to release trypsin and other enzymes, which destroy lung tissue.
73
What triggers airway impairments in asthma, and what can happen during severe asthma attacks?
Airway impairments in asthma are often triggered by repeated exposure to allergens, irritants, or infections. During severe asthma attacks, airways can narrow so much that airflow is completely blocked, which can be life-threatening.
74
Long-term inflammatory disease of the airways, characterized by variable/recurring
symptoms.
Asthma
75
Inflammation of the lining of your lower airways (bronchioles), which carry air to and
from your lungs.
Bronchitis
76
An umbrella term used to describe progressive pulmonary diseases.
COPD
77
A progressive disease of the lungs that primarily causes shortness of breath due to
breakdown of alveolar tissue.
Emphysema
78
Why is expiration more difficult than inspiration in pulmonary diseases that increase airway resistance?
During inspiration, larger airways are supported by cartilaginous rings and smaller airways are held open by the positive transpulmonary pressure (negative pleural pressure), allowing air to flow in.
During expiration, intrathoracic pressure rises, adding pressure on already narrowed airways, which reduces airflow out of the lungs, making exhalation more difficult.
79
Why COPD patients complain that they cannot get enough air in?
In COPD, the first problem is usually difficulty breathing out due to airway obstruction. Because patients cannot fully exhale, their lungs start the next breath at a higher volume. While higher lung volumes reduce airway resistance, incomplete exhalation limits the amount of air that can be inhaled in subsequent breaths. This breath stacking can continue, causing dynamic hyperinflation, where the lungs become overinflated. At this point, it becomes difficult to breathe in or out, leading to the sensation of dyspnea (shortness of breath).
80
What is a spirometer?
A device that measures the volume of air breathed in and out, and records the readings as a spirogram.
Spirometry cannot determine all of the lung volumes and capacities (the sum of two or more lung volumes).
81
What is IRV?
Inspiratory reserve volume (I R V ) - the extra volume of air that can be maximally inspired above the
resting tidal volume. At rest, this is typically around 3000 ml.
82
What is IC?
Inspiratory capacity (I C ) - the maximal 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).
83
What is ERV?
Expiratory reserve volume (ERV) - the maximal volume of air that can be expelled starting at the end of
a typical tidal volume. At rest, this is typically around 1000 ml.
84
What is RV?
Residual volume (RV) - the volume of air remaining in the lungs after maximal 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.
85
Can residual volume be measured by spirometry?
No, it can be measured indirectly by inspiration of a tracer gas such as helium.
86
What is FRC?
Functional residual capacity (FRC) - the volume of air in the lungs at the end of normal passive
expiration. This value is typically around 2200 ml (F R C= E R V+ R V).
87
What is VC?
Vital capacity - the maximum volume of air that can be expelled during a single breath following a
maximal inspiration. This value is typically around 4500 ml (V C = I R V+ VT + E R V).
88
What is TLC?
Total lung capacity (TLC) - the maximum volume of air the lungs can hold. This value is typically around
5700 ml (TLC= V C + R V).
89
What is FEV1?
Forced expiratory volume in one second (FEV1) - this is similar to TLC but is derived from only the first second of expiratory effort. This value is normally expressed as a ratio (F E V 1 /F V C ) or converted to a percentage. At rest, this value is typically around 80%.
90
Respiratory dysfunction generally falls into two categories. What are they, and how do they differ in lung function?
1. Obstructive lung disease:
- Patients cannot exhale fully → FEV₁ is reduced, FRC and RV are increased, VC is decreased.
- Worsens with breath stacking.
2. Restrictive lung disease:
- Lungs have reduced volume → FEV₁ is reduced, but FEV₁/FVC ratio is normal because airflow is not obstructed.
- Total lung capacity is decreased.
91
Why is expiratory data more commonly used than inspiratory data in pulmonary function testing, and how do flow-volume curves differ between normal, obstructive, and restrictive lung disease?
- Expiratory data is preferred because it is easier to measure and more reproducible.
- Normal person: Flow peaks around 7 L/s, then decreases linearly.
- Obstructive lung disease: Starts at higher lung volume but cannot reach normal peak flow and ends at a higher residual volume.
- Restrictive lung disease: Starts at lower lung volume, lower peak flow, and ends at a lower residual volume.
92
Why is expiratory flow more informative than inspiratory flow for assessing lung function?
A simple experiment shows that inhalation is very fast (less than 0.5 seconds) while forced exhalation takes much longer (around 5 seconds). This indicates that ventilation is limited during expiration, making expiratory flow more useful for assessing pulmonary function.
93
What is anatomical dead space?
The volume of the airways that represents the inspired gas that is unavailable for exchange with pulmonary capillary blood.
94
What is minute ventilation, how is it calculated, and why does anatomical dead space reduce the effective ventilation for gas exchange?
Minute ventilation (VE) is the total volume of air breathed per minute:
VE=Tidal Volume (VT) × Respiratory Frequency (f)
At rest: VT = 500 mL, f = 12 breaths/min → VE = 6 L/min.
Anatomical dead space (~150 mL) is the portion of each breath that remains in the airways and does not reach the alveoli, so only ~350 mL contributes to effective alveolar ventilation.
With each breath, air in the dead space is re-breathed, reducing the efficiency of gas exchange.
95
Is it better to increase frequency of breathing or tidal volume in order to increase gas exchange in the alveoli?
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 has important consequences for alveolar ventilation. If the volume of gas a person breathes in with each breath (the tidal volume) is the same as the volume of the dead space, then the alveolar ventilation must be zero. In other words, all the inspired gas stays in the anatomic dead space. To have an effective alveolar ventilation (in terms of gas exchange), tidal
volume must exceed dead space volume. It would seem, therefore, that the ideal breathing pattern to
maximize alveolar minute ventilation is one in which an individual uses a slow deep breathing pattern, when tidal volume is much greater than dead space volume.
96
Why is alveolar ventilation more efficient with deeper breaths compared to a faster breathing rate?
Alveolar ventilation requires the tidal volume to exceed anatomical dead space. Deeper breaths deliver more air to the alveoli, making ventilation more efficient, whereas faster, shallow breaths primarily move air in and out of the dead space without effectively exchanging gases.
97
What is work of breathing?
The energy expended to inhale and exhale a breathing gas
98
How do tidal volume and respiratory rate affect the work of breathing during normal quiet respiration?
- During quiet breathing, inspiration overcomes lung elastic recoil and airway resistance, while expiration is passive.
- Energy cost is low (<3% of total body energy) because lungs are compliant and resistance is low.
- Low respiratory rates: Tidal volume must increase to maintain alveolar ventilation → inspiratory muscles work harder, and elastic work of the lung increases.
- High respiratory rates: Tidal volume decreases → elastic work decreases, but flow-resistive work increases due to moving more air.
99
What are the factors affecting the work of breathing?
The work of breathing is increased during four conditions:
1. Decreased compliance:
Lungs are stiff (e.g., pulmonary fibrosis) → tidal volume decreases, respiratory rate increases.
2. Increased airway resistance:
Seen in COPD or asthma → more effort to overcome resistance, respiratory frequency decreases, tidal volume roughly unchanged.
3. Decreased elastic recoil:
Seen in emphysema → passive expiration is insufficient, expiratory muscles recruited → respiratory frequency decreases, tidal volume roughly unchanged.
4. Increased demand for ventilation:
Occurs during exercise → tidal volume and respiratory rate both increase to meet higher oxygen needs.
100
What is gas exchange?
The diffusion of oxygen from the alveoli into the blood, and carbon dioxide from the blood to the alveoli
101
What factors determine gas exchange in the lungs, and how are they related to pressure gradients and resistance to diffusion?
Gas exchange is determined by a pressure gradient and resistance to diffusion. The pressure gradient is the difference in partial pressures between the alveoli (PA) and the pulmonary artery (PV). Diffusion resistance depends on the surface area of the membrane (A), its thickness (T), and the diffusibility (D) of the gas. Since D is constant, gas exchange mainly depends on the pressure difference, membrane surface area, and membrane thickness.
102
What is partial pressure?
The pressure that would be exerted by one of the gases in a mixture of gases, if it occupied the same volume on its own
103
According to Dalton’s law, how are the partial pressures of gases in atmospheric air determined, and what are the approximate partial pressures of nitrogen, oxygen, and carbon dioxide at sea level?
Dalton’s law states that the partial pressure of a gas in a mixture is proportional to its percentage in the mixture. At sea level (760 mmHg):
Nitrogen (79%) ≈ 600 mmHg
Oxygen (21%) ≈ 160 mmHg
Carbon dioxide (very small percentage) ≈ 0.23 mmHg
104
What are the two key factors that determine the amount of gas that can dissolve in a liquid?
1. Partial pressure in air: The greater its partial pressure, the more gas will be driven into the liquid
2. Solubility in the liquid: The more soluble a gas is in a liquid, the more will dissolve
105
Why does alveolar air differ in composition from inspired atmospheric air, and how does water vapour affect the partial pressures of gases in the alveoli?
Alveolar air differs from inspired air because inhaled air becomes fully saturated with water vapour in the airways. At body temperature, water vapour exerts a partial pressure of 47 mmHg, reducing the pressure available for other gases from 760 mmHg to 713 mmHg. As a result:
Inspired nitrogen (79%) ≈ 563 mmHg
Inspired oxygen (21%) ≈ 150 mmHg
Thus, humidification lowers the partial pressures of oxygen and nitrogen compared to dry atmospheric air.
106
Why is the partial pressure of oxygen in the alveoli (PAO₂) lower than inspired oxygen, and how does the alveolar gas equation explain this?
With a tidal volume of 500 mL, only about 350 mL reaches the alveoli, and at the end of inspiration only ~15% of alveolar gas is fresh air. This lowers PAO₂ to about 100 mmHg.
The alveolar gas equation explains this:
PAO₂ = PIO₂ − (PACO₂ / R)
Where:
PIO₂ ≈ 150 mmHg
PACO₂ ≈ 40 mmHg
R ≈ 0.8
So:
150 − (40 / 0.8) = 150 − 50 = 100 mmHg
PAO₂ and PACO₂ remain relatively constant because only a small amount of fresh air enters the alveoli each breath and gas exchange rapidly adjusts to maintain stable partial pressures.
107
How do oxygen and carbon dioxide move between the alveoli and the blood, and what maintains this gas exchange process?
Oxygen diffuses from the alveoli into the blood, and carbon dioxide diffuses from the blood into the alveoli. This movement occurs by diffusion and is driven by partial pressure gradients. Ventilation continuously replenishes alveolar oxygen and removes carbon dioxide, maintaining these gradients.
108
What are the partial pressures of oxygen and carbon dioxide in the alveoli compared to those in mixed venous blood entering the lungs?
In the alveoli, the partial pressure of oxygen (PAO₂) is about 100 mmHg and carbon dioxide (PACO₂) is about 40 mmHg.
In mixed venous blood entering the lungs, the partial pressure of oxygen (PvO₂) is lower, about 40 mmHg, and the partial pressure of carbon dioxide (PvCO₂) is higher, about 46 mmHg.
109
Based on the partial pressure gradients between the alveoli and mixed venous blood, what will happen to oxygen and carbon dioxide as blood passes through the lungs, and why?
Oxygen will diffuse from the alveoli (PAO₂ ≈ 100 mmHg) into the blood (PvO₂ ≈ 40 mmHg) because gases move from areas of higher to lower partial pressure.
Carbon dioxide will diffuse from the blood (PvCO₂ ≈ 46 mmHg) into the alveoli (PACO₂ ≈ 40 mmHg) for the same reason.
Ventilation continuously maintains alveolar PO₂ at about 100 mmHg and PCO₂ at about 40 mmHg, so the blood leaving the lungs equilibrates to these values.
110
How do partial pressures of gases relate to the actual amount of oxygen and carbon dioxide dissolved in the blood, and why is there a difference between the two?
The amount of gas dissolved in blood depends on both its partial pressure and solubility.
Carbon dioxide is ~20 times more soluble than oxygen, so even at similar partial pressures, more CO₂ is dissolved in the blood.
- Blood leaving the lungs: PvCO₂ ≈ 40 mmHg → ~480 mL CO₂/L
- Blood returning to lungs: PvCO₂ ≈ 46 mmHg → ~520 mL CO₂/L
- Small change in dissolved CO₂ because CO₂ plays a key role in acid-base balance.
Oxygen is less soluble, so changes in partial pressure have a larger effect on dissolved O₂.
- Blood leaving the lungs: PaO₂ ≈ 100 mmHg → ~200 mL O₂/L
- Blood returning to lungs: PvO₂ ≈ 40 mmHg → ~150 mL O₂/L
- ~50 mL O₂/L is delivered to tissues, with 150 mL O₂/L remaining as a reserve.
111
What is capillary transit time?
The duration of exposure of capillary blood to alveolar gas
112
What factors affect the efficiency of gas exchange in the lungs, and how do changes in these factors influence oxygen and carbon dioxide transfer?
Gas exchange is influenced by surface area, capillary transit time, and membrane thickness:
1. Surface Area:
- Greater alveolar-capillary surface area increases gas exchange.
- Exercise opens more pulmonary capillaries, increasing surface area.
- Diseases like emphysema destroy alveolar walls, reducing surface area and impairing gas exchange.
2. Capillary Transit Time:
- Blood must remain in pulmonary capillaries long enough for gases to diffuse.
- At rest: ~0.75 s, sufficient for complete exchange; during exercise: ~0.4 s.
- If diffusion is impaired, faster blood flow can reduce oxygenation, especially in diseased lungs.
3. Membrane Thickness:
- Thicker alveolar-capillary barriers (due to inflammation or mucus, e.g., in asthma) reduce gas exchange.
- If thickening is severe, diffusion may not complete before blood leaves the capillary, lowering arterial PO₂.
113
How does gas exchange occur across the systemic capillaries, and how does tissue metabolism influence this process?
Gas exchange in systemic capillaries follows the same principles as in the lungs.
Partial pressures drive diffusion:
- Arterial blood: PO₂ ≈ 100 mmHg, PCO₂ ≈ 40 mmHg
- Tissue cells: PO₂ ≈ 40 mmHg, PCO₂ ≈ 46 mmHg
→ Oxygen diffuses into the tissues, and carbon dioxide diffuses into the blood.
Equilibration: By the time blood leaves the systemic capillaries, its PO₂ and PCO₂ match tissue values (≈40 mmHg O₂, 46 mmHg CO₂).
Effect of increased metabolism: Exercise or higher metabolic activity lowers tissue PO₂ and raises PCO₂, increasing the pressure gradients and enhancing oxygen delivery and CO₂ removal.
Tissue metabolism is the driving force for gas exchange in both systemic and pulmonary capillaries.
114
What are the key steps of O2 and CO2 gas exchange within the pulmonary and systemic capillaries?
1. The venous blood entering the lungs is low in O2 (40 m m H g ; this value decreases during
exercise) and high C O 2 (46 m m H g ), due to the consumption of O2 and production of C O 2 by the
tissues.
2. Alveolar PO2 remains high (100 m m H g ) and alveolar PCO2 low (40 m m H g ) because only a portion of the alveolar air is replaced with fresh atmospheric air during each breath.
3. The partial pressure gradients for O2 (100 - 40 = 60 m m H g ) and CO2 (46 - 40 = 6 m m H g )
between the alveoli and pulmonary capillary blood cause O2 to diffuse into the blood and CO2 to diffuse into the alveoli. Diffusion continues into the blood and alveolar partial pressures
become equal.
4. Blood leaving the lungs has, compared to the lungs, a high partial pressure and content of O2
and a low partial pressure and content of CO2. These partial pressures and contents are
identical to those delivered to the tissues.
5. The partial pressures of O2 and CO2 are, compared to those in arterial blood, lower and higher,
respectively, in the O2- consuming, CO2-producing tissue cells.
6. O2 diffuses from the arterial blood into cells to support their metabolic requirements, and metabolically produced CO2 diffuses into the blood.
7. Having equilibrated with the tissue cells, the blood leaving the tissues is relatively low in O2
and high in CO2. The blood then returns to the lungs to once again replenish on O2 and release
CO2.
115
What is haemoglobin (Hb)?
Hb is an iron-bearing protein within RBCs that can carry oxygen. 98.5% of circulating oxygen is bound to Hb.
116
Why is hemoglobin necessary for oxygen transport in the blood, and how does it help meet the body’s metabolic needs?
Oxygen is poorly soluble in plasma—only about 3 mL O₂/L can dissolve—so dissolved O₂ alone cannot meet metabolic demands.
Hemoglobin (Hb) binds oxygen, greatly increasing the blood’s O₂-carrying capacity.
Hb-bound O₂ does not contribute to PO₂, so PO₂ reflects only the dissolved oxygen.
Each hemoglobin molecule has four subunits, each with a heme group containing iron, which binds O₂, acting as a reserve for tissues.
117
What is the most important factor for determining %Hb saturation?
PO2
118
How does hemoglobin bind oxygen, and what determines its saturation level?
Each hemoglobin (Hb) molecule has four iron atoms, each capable of binding one O₂ molecule:
H b + O₂ ⇌ HbO₂ ⇌ Hb(O₂)₂ ⇌ Hb(O₂)₃ ⇌ Hb(O₂)₄
The binding is fully reversible, allowing oxygen transport to tissues.
Hb saturation (% of Hb carrying oxygen) depends mainly on PO₂: higher PO₂ drives binding, lower PO₂ drives release, following the law of mass action.
119
What does the oxygen dissociation curve show, and what is the significance of its shape?
The oxygen dissociation curve shows the relationship between PO₂ and % hemoglobin (Hb) saturation.
It is sigmoidal:
Steep slope between 0–60 mmHg → small changes in PO₂ cause large changes in Hb saturation.
Plateau above 60 mmHg → Hb saturation approaches 100%, so changes in PO₂ have little effect.
This shape allows efficient oxygen loading in the lungs and unloading in the tissues.
120
What is the significance of the plateau region of the oxygen dissociation curve?
The plateau region (PO₂ 60–100 mmHg) corresponds to the pulmonary capillaries, where hemoglobin collects O₂.
At PO₂ of 100 mmHg, Hb is ~97.5% saturated, ensuring blood leaving the lungs is normally fully saturated.
Even if PO₂ drops to 60 mmHg, Hb remains ~90% saturated, providing a margin of safety.
This safety is important for:
1. High-altitude conditions where inspired PO₂ is lower.
2. Oxygen-deprived environments at sea level, allowing near-normal O₂ transport until PO₂ falls below 60 mmHg.
121
Which two situations make the plateau phase of the oxygen dissociation curve particularly important for maintaining near-normal oxygen transport?
1. High-altitude conditions, where inspired PO₂ is reduced.
2. Oxygen-deprived environments at sea level, such as being in an airtight room.
122
What is the significance of the steep portion of the oxygen dissociation curve (0–60 mmHg PO₂) for oxygen delivery to tissues and adaptation to altitude?
In systemic capillaries at rest, the steep portion allows a large amount of O₂ (25%) to be unloaded when PO₂ drops from 100 to 40 mmHg.
In metabolically active tissues, a further drop to 20 mmHg releases an additional 45% of O₂.
At altitude, a small increase in alveolar PO₂ on the steep portion can greatly increase Hb saturation, improving oxygen delivery even with lower atmospheric PO₂.
123
How does haemoglobin facilitate oxygen transfer from the alveoli to the blood, and what happens when it is partially or fully saturated?
No Hb present: Alveolar PO₂ and blood PO₂ quickly equilibrate, limiting oxygen transfer.
Hb partially saturated: Hb binds oxygen, removing it from solution, keeping blood PO₂ below alveolar PO₂ and favoring continued diffusion from alveoli.
Hb fully saturated: Alveolar and blood PO₂ equilibrate again, but total oxygen content in blood is much higher than without Hb.
124
What factors can shift the oxygen dissociation curve, and how do they affect oxygen unloading from haemoglobin?
The oxygen dissociation curve can be shifted by several factors that affect how readily haemoglobin releases oxygen to the tissues:
1. pH (Bohr effect):
During exercise or high metabolism, H⁺ ions are released from carbonic acid formation (from CO₂) and from lactic acid.
A decrease in pH shifts the curve to the right, enhancing oxygen unloading in metabolically active tissues.
2. 2,3-Bisphosphoglycerate (BPG):
BPG is produced inside red blood cells, especially when arterial PO₂ is below normal.
It shifts the curve to the right, promoting oxygen release in low-oxygen conditions. Unlike H⁺ and CO₂, BPG is not eliminated in the lungs, so it persistently reduces haemoglobin saturation.
3. Carbon dioxide (CO₂) – Haldane effect:
Increased PCO₂ shifts the curve to the right, decreasing haemoglobin saturation for a given PO₂.
This facilitates more oxygen unloading in tissues where CO₂ is high, such as systemic capillaries.
4. Carbon monoxide (CO):
CO binds to haemoglobin 240 times more strongly than oxygen, forming carboxyhaemoglobin (HbCO).
This reduces the number of oxygen-binding sites and shifts the curve to the left, meaning more significant drops in PO₂ are needed to unload oxygen.
Even low levels of CO can severely impair oxygen delivery and be life-threatening.
In summary, rightward shifts (low pH, high CO₂, BPG) enhance oxygen unloading in tissues, while leftward shifts (CO exposure) reduce oxygen delivery, even if PO₂ is normal.
125
How is carbon dioxide transported in the blood?
Carbon dioxide is transported in three main ways:
1. Physically dissolved: About 5–10% of CO₂ is dissolved directly in plasma. This small fraction accounts for the blood’s CO₂ partial pressure (~46 mmHg) leaving the systemic capillaries.
2. Bound to haemoglobin: CO₂ binds to the globin portion of haemoglobin, not the oxygen-binding sites. Deoxygenated Hb has a higher affinity for CO₂, so O₂ unloading in the tissues enhances CO₂ uptake. This also accounts for roughly 5–10% of total CO₂ transport.
3. As bicarbonate (HCO₃⁻): The majority (80–90%) of CO₂ is transported as bicarbonate. CO₂ reacts with water to form carbonic acid, which then dissociates into hydrogen ions and bicarbonate. The reaction is accelerated in red blood cells by the enzyme carbonic anhydrase.
Equation:
CO₂ + H₂O ⇌ H₂CO₃ ⇌ H⁺ + HCO₃⁻
126
How does the chloride (Hamburger) shift facilitate CO₂ transport in the systemic capillaries?
In the systemic capillaries, as CO₂ enters red blood cells, it reacts with water to form carbonic acid, which dissociates into bicarbonate (HCO₃⁻) and hydrogen ions (H⁺). To maintain electrochemical balance, red blood cells use a bicarbonate-chloride carrier to exchange ions across the cell membrane.
Bicarbonate (HCO₃⁻) leaves the red blood cells.
Chloride (Cl⁻) enters the red blood cells down its electrochemical gradient.
This inward movement of chloride in exchange for bicarbonate is called the chloride (Hamburger) shift. This shift helps move CO₂ from the tissues into the blood efficiently, allowing it to be transported to the lungs for exhalation.
127
What is the reverse Haldane effect and how does it influence CO₂ transport when arterial PO₂ increases?
The reverse Haldane effect occurs when arterial PO₂ increases, such as during breathing supplemental oxygen. The higher PO₂ prevents hemoglobin (Hb) from binding carbon dioxide (CO₂). As a result, CO₂ cannot bind to Hb and must instead be transported back to the lungs either:
- Dissolved in plasma, or
- As bicarbonate (HCO₃⁻).
This shift increases the amount of CO₂ in dissolved form, which can raise blood acidity and may explain the increased ventilation rates sometimes observed during supplemental oxygen therapy. Essentially, higher PO₂ reduces Hb’s capacity to carry CO₂, altering CO₂ transport back to the lungs.
128
What are the two forms of arterial PO₂ and what conditions are associated with each?
The two forms of arterial PO₂ are hypoxia and hyperoxia:
1. Hypoxia – insufficient oxygen at the cellular level. There are four main types:
Hypoxic hypoxia: Low arterial PO₂ with inadequate Hb saturation, caused by poor gas exchange or low atmospheric PO₂ (e.g., high altitude).
Circulatory hypoxia: Oxygenated blood is not delivered properly to tissues due to blockages or vascular spasms; arterial PO₂ is usually normal.
Anemic hypoxia: Reduced oxygen-carrying capacity of blood due to fewer red blood cells, low Hb content, or carbon monoxide poisoning; PO₂ is normal but oxygen content is reduced.
Histotoxic hypoxia: Oxygen delivery to tissues is normal, but tissues cannot use it, such as with cyanide poisoning that disrupts cellular respiration.
2. Hyperoxia – abnormally high arterial PO₂, which occurs when breathing supplemental oxygen. Hemoglobin is already saturated at normal air levels, so the extra oxygen mostly dissolves in plasma. Excess dissolved oxygen can be harmful, forming reactive oxygen species that may damage tissues like the brain and retina, potentially causing oxygen toxicity and blindness.
129
How is alveolar PCO₂ regulated, and what are the two types of abnormalities in arterial PCO₂?
Regulation of alveolar PCO₂: Alveolar PCO₂ is directly related to the metabolic production of CO₂ and inversely related to alveolar ventilation. At a constant metabolic rate, increasing ventilation lowers alveolar PCO₂, while decreasing ventilation raises alveolar PCO₂.
Abnormalities in arterial PCO₂:
1. Hypercapnia: Excess CO₂ in the blood, caused by hypoventilation. Since both CO₂ and O₂ are affected by reduced ventilation, hypercapnia can also lead to decreased PO₂.
2. Hypocapnia: Below-normal arterial PCO₂, caused by hyperventilation. This can occur due to anxiety, fever, aspirin poisoning, or exercise (especially with anaerobic metabolism). Hyperventilation increases alveolar PO₂, but this adds very little extra oxygen to the blood because both the dissolved oxygen and Hb saturation are already near maximal.
130
When oxygen dissociation curve shifts left (i.e. increased affinity for O2)?
Decreased temperature, increased pH, decreased pCO2, decreased BPG
131
When oxygen dissociation curve shift right (decreased affinity for O2)?
Increased temperature, decreased pH, increased pCO2, increased BPG
132
How is neural control of respiration organized, and what are its three main components?
The lungs cannot generate their own rhythmic breathing like the heart; instead, they rely on external neural control from the respiratory control centre in the medulla and brainstem. Neural control of respiration involves three main components:
1. Generation of the alternating inspiration/expiration rhythm:
- Occurs in the medullary respiratory centre, which sends signals to the respiratory muscles.
- Dorsal respiratory group (DRG): Inspiratory neurons; their firing causes inspiration, and stopping firing allows expiration.
- Ventral respiratory group (VRG): Contains both inspiratory and expiratory neurons; interneurons connect DRG and VRG to recruit additional neurons when ventilatory demand increases.
2. Regulation of the level of respiration (rate and depth) to match metabolism:
- Controlled by the brainstem and influenced by sensory receptors that monitor blood gases and other factors.
3. Modulation of respiratory activity for other purposes:
- Can be voluntary, such as during speech.
- Can be involuntary, such as during coughing or sneezing.
133
What types of receptors contribute to the control of the rate and depth of ventilation, and what are their roles?
The rate and depth of ventilation are controlled by mechanical and chemical receptors. Mechanical receptors are located in the lungs, diaphragm, and chest wall, and they contribute to the respiratory pattern. The main mechanical receptors include:
1. Pulmonary Receptors:
- Slowly adapting receptors: Located in airway smooth muscle; respond to lung volume changes. Firing rate increases as the lungs inflate.
- Rapidly adapting receptors: Found in the epithelia of larger airways; respond to mechanical and chemical stimuli. Activation can cause bronchoconstriction, cough, and increased mucus production to protect against inhaled irritants.
- C-fibres: Endings near pulmonary capillaries; detect increases in pulmonary arterial pressure, pulmonary edema, and chemical stimuli like capsaicin. Activation causes bronchoconstriction and rapid shallow breathing.
2. Rib Cage Receptors:
- Muscles of the chest wall contain muscle spindles (and some Golgi tendon organs). They detect differences between expected and actual chest wall distention and may “unload” spindles to allow greater distention.
- Their primary physiological function may relate more to posture regulation, with a secondary role in respiration.
3. Diaphragm Receptors:
- Contains few mechanical receptors, likely because of its primary role in respiration.
- Has many small myelinated and unmyelinated afferents that respond to local metabolic conditions, helping fine-tune respiratory activity.
134
How are arterial PO2 and PCO2 maintained constant despite changes in tissue oxygen consumption and carbon dioxide production?
Arterial PO2 and PCO2 remain remarkably constant because the rate and depth of breathing adjust to match metabolic demand.
- When tissue metabolism increases, oxygen consumption rises and carbon dioxide production increases.
- This change is detected by chemical receptors that monitor the composition of the blood.
- These receptors send information to the medullary respiratory control center, which then increases ventilation (both rate and depth) to maintain arterial PO2 and PCO2 within normal ranges, ensuring stable blood gas levels regardless of metabolic changes.
135
How is arterial PO2 monitored, and what is the role of peripheral chemoreceptors in regulating ventilation and oxygen delivery?
Arterial PO2 is monitored by peripheral chemoreceptors located in the carotid bodies and aortic bodies.
Carotid chemoreceptors respond to changes in arterial PO2, but they are relatively insensitive to small changes until PO2 drops below 60 mmHg, the level at which oxygen desaturation could impair tissue function.
- When activated, they increase ventilation to raise arterial PO2.
- Above 60 mmHg, these receptors are not activated because blood is nearly saturated, so increasing alveolar PO2 has minimal effect.
Aortic chemoreceptors respond to changes in oxygen content rather than PO2.
- When oxygen content decreases, they do not affect ventilation.
- Instead, they increase cardiac output to enhance systemic oxygen delivery.
This dual system ensures that both oxygen levels in the blood and oxygen delivery to tissues are maintained appropriately.
136
How does an increase in arterial PCO2 affect central chemoreceptors and ventilation?
Carbon dioxide (CO2) is the primary regulator of minute-to-minute ventilation at rest because changes in ventilation quickly affect arterial PCO2.
- Slight increases in PCO2 stimulate the central chemoreceptors in the medulla to increase ventilation, helping remove the excess CO2.
- Conversely, a fall in PCO2 reduces ventilation, allowing CO2 to accumulate until PCO2 is normalized.
Key point: Central chemoreceptors do not monitor CO2 directly; they detect CO2-induced changes in hydrogen ion (H⁺) concentration in the brain’s extracellular fluid. Peripheral chemoreceptors play no significant role in this regulation.
137
How does an increase in CO2 lead to changes in ventilation via central chemoreceptors?
1. CO2 crosses the blood-brain barrier easily. An increase in arterial PCO2 raises the PCO2 of the brain extracellular fluid.
2. CO2 reacts with water to form carbonic acid, which dissociates into bicarbonate (HCO3⁻) and hydrogen ions (H⁺). According to the law of mass action, more CO2 means more H⁺.
3. Increased H⁺ stimulates the central chemoreceptors in the medulla, triggering an increase in ventilation to remove excess CO2.
4. As CO2 is exhaled, the reaction reverses, reducing H⁺ concentration. Plasma H⁺ cannot significantly influence breathing because it does not cross the blood-brain barrier easily.
5. The effect of H⁺ is so strong it can override voluntary breath-holding, making it a major determinant of breath-hold duration. Techniques like blowing air out through the mouth or nostrils can prolong breath-hold without affecting arterial PCO2.
138
What are the mechanical control of breathing?
Diaphragm receptors, pulmonary receptors, and rib cage receptors
139
What are the chemical control of breathing?
Aortic bodies, carotid bodies, increase in arterial PCO2, increase in brain ECFH+
140
What are neither mechanical or chemical control of breathing?
Cardiac receptors, increase in arterial PO2, decrease in H-, increase in brain Na2+
141
Why ventilation increases during exercise?
Ventilation increases during exercise to match the higher metabolic demands of the tissues. As muscles work harder, they consume more oxygen and produce more carbon dioxide. This creates:
1. Lower PO2 and higher PCO2 at the tissue level, increasing the gradients for oxygen to enter the blood and carbon dioxide to leave the blood.
2. Central chemoreceptor stimulation: The rise in arterial PCO2 leads to more CO2 in the brain extracellular fluid, which forms H⁺ ions. These H⁺ ions stimulate the central chemoreceptors in the medulla, triggering increased ventilation.
3. Peripheral chemoreceptor input: Carotid chemoreceptors detect changes in PO2, especially if it drops toward 60 mmHg, and contribute to the increased breathing rate.
4. Muscle and joint feedback: Mechanoreceptors in muscles and joints also signal increased activity, further increasing ventilation.
Overall, ventilation increases to supply more oxygen to the active muscles and to remove the extra carbon dioxide produced, maintaining arterial blood gas homeostasis.
142
What causes the rapid increase in ventilation during exercise, given that arterial PO2, PCO2, and H⁺ remain relatively constant?
The increase in ventilation during exercise is driven by several non-metabolic factors, since arterial PO2, PCO2, and brain extracellular fluid H⁺ remain largely unchanged:
1. Reflexes from body movements: Muscle mechanoreceptors are stimulated during contractions, reflexively activating the respiratory center to increase breathing. Even minor movements can significantly increase ventilation.
2. Epinephrine release: Exercise triggers the adrenal medulla to release epinephrine, which stimulates ventilation.
3. Increased body temperature: Exercise raises body temperature slightly, and higher temperature directly increases ventilation, similar to the effect of fever.
4. Cerebral cortex impulses: At exercise onset, the motor areas of the cortex simultaneously activate medullary respiratory neurons and the motor neurons of muscles. This feedforward mechanism increases ventilation immediately, before any metabolic changes occur.
These mechanisms allow ventilation to increase rapidly to meet the anticipated demands of exercise, even before significant changes in blood gases occur.
PHGY 216
flashcards
Decks in class (6)
# Cards
