1
Q
Q1: What is the composition of the visceral pleura?
A
A1: The visceral pleura is composed of thin epithelial tissue with areolar connective tissue.
2
Q
Q2: What is the function of the pleural cavity?
A
A2: The pleural cavity is a potential space that tethers the visceral pleura to the parietal pleura. It contains pleural fluid, which allows for no friction, prevents inflammation, and is constantly pumped out by lymphatic vessels to maintain a normal volume.
3
Q
Q3: What is pleurisy?
A
A3: Pleurisy is a condition characterized by a lot of friction between the parietal and visceral pleura due to a decreased amount of pleural fluid.
4
Q
Q4: What is parietal pleura?
A
A4: The parietal pleura is a membrane that lines the inner surface of the chest wall, diaphragm, and mediastinum.
5
Q
Q5: In which areas of the respiratory tract are mucus and ciliated epithelium absent?
A
A5: Mucus and ciliated epithelium are absent in the alveoli.
6
Q
Q6: What does internal respiration refer to?
A
A6:
- refers to the intracellular mechanisms that consume oxygen (O2) and produce carbon dioxide (CO2).
- It involves gas exchange between the vascular compartment and cellular compartment.
7
Q
Q7: What is external respiration?
A
AA7:
- External respiration is the sequence of events that lead to the exchange of oxygen (O2) and carbon dioxide (CO2) between the external environment and the cells of the body.
- It includes ventilation, exchange of gases in the alveoli and pulmonary capillaries, transport of gases in the blood, and exchange of gases between the blood and tissues.
8
Q
Q8: What are the pressure changes in the lung?
A
A8: The pressure changes in the lung include:
Intrapulmonary or intra-alveolar pressure (Ppul)
Intrapleural pressure (Pip)
Atmospheric or barometric pressure (Patm)
Transpulmonary pressure (TP) (Ppul - Pip)
Transthoracic pressure (TTP) (Pip - Patm)
Transrespiratory pressure (TRP) (Ppul - Patm)
9
Q
Q9: What factors contribute to the negative intrapleural pressure (Pip)?
A
A9: The negative intrapleural pressure (Pip) is due to:
Elasticity of the lungs
Surface tension
Elasticity of the chest wall
Gravity
10
Q
Q1: What is ventilation?
A
A1: Ventilation is the mechanical process of moving air between the atmosphere and the alveolar sacs in the lungs.
11
Q
Q2: What is Boyle’s Law?
A
A2:
- at any constant temperature, the pressure exerted by a gas varies inversely with the volume of the gas.
- This means that when the pressure of a gas increases, the volume decreases, and vice versa.
12
Q
Q3: What is atmospheric pressure?
A
A3:
* is the pressure caused by the weight of the gas in the atmosphere on the Earth’s surface.
It is typically around 760 mmHg.
13
Q
Q4: What is intra-alveolar pressure?
A
A4:
* Intra-alveolar pressure refers to the pressure within the lung alveoli.
It is usually the same as atmospheric pressure, around 760 mmHg.
14
Q
Q5: What is intrapleural pressure?
A
A5:
* is the pressure exerted outside the lungs within the pleural cavity.
It is typically lower than atmospheric pressure, around -4 mmHg.
15
Q
Q6: How is intrapleural fluid prevented from accumulating?
A
A6: through lymphatic vessels that drain the pleural cavity.
16
Q
Q7: What is the significance of negative intrapleural pressure?
A
A7:
- Negative intrapleural pressure creates a transmural pressure gradient across the lung wall and chest wall.
- This forces the lungs to expand outward while the chest is forced to squeeze inward, contributing to the recoil mechanism.
- It also causes the pleural membranes to stick together.
17
Q
Q1: What are the primary muscles involved in inspiration?
A
A1:
are the diaphragm and the external intercostal muscles.
18
Q
Q2: What activates the diaphragm during inspiration?
A
A2:
the phrenic nerve, which receives input from the cerebral cortex and the ventral respiratory group (VRG) within the medulla.
19
Q
Q3: How do the external intercostal muscles contribute to inspiration?
A
A3:
- lift the ribs and move out the sternum, increasing the volume of the thorax.
BY : - They pull the ribs outwards, increasing the thoracic cavity volume, and
- push the sternum outwards and upwards, increasing the thoracic cavity volume anteroposteriorly.
20
Q
Q4: What happens to the lung size and intra-alveolar pressure during inspiration?
A
A4:
- During inspiration, the lung size increases, and as per Boyle’s Law, the intra-alveolar pressure decreases.
- This creates a pressure gradient that allows air to enter the lungs until the intra-alveolar pressure becomes equal to atmospheric pressure.
21
Q
Q5: What happens to the three types of pressures during inspiration?
A
A5: During inspiration:
(i) The transpulmonary pressure (TP) increases.
(ii) The transthoracic pressure (TTP) decreases.
(iii) The transrespiratory pressure (TRP) decreases.
allwoing the lungs to expand
22
Q
Q6: What are the accessory muscles involved in forced inspiration?
A
A6:
the pectoralis major,
pectoralis minor,
sternocleidomastoid,
scalenus anterior,
scalenus medius, and
scalenus posterior.
23
Q
Q7: What is the pleural pressure during forced inspiration?
A
A7: The pleural pressure is around -6mmHg during forced inspiration.
24
Q
Q1: What muscles are involved during forced expiration?
A
A1:
- Abdominal wall muscles: External oblique, internal oblique, transverse abdominis, rectus abdominis
- Internal intercostal muscles
25
Q2: How do the internal intercostal muscles contribute to forced expiration?
A2:
* The internal intercostal muscles, located between the ribs, pull the upper rib downwards, depressing the rib cage, which decreases the thoracic cavity volume.
* They also push the sternum and ribs inward.
26
Q3: How do the abdominal wall muscles contribute to forced expiration?
A3:
* Contraction of the abdominal wall muscles increases intra-abdominal pressure, which **pushes upwards and backwards on the diaphragm.**
* This decreases the thoracic cavity volume and increases intrapleural pressure.
27
Q4: What are the pressure changes during forced expiration?
A4:
* During forced expiration, the chest wall pushes inward, and the diaphragm pushes upward, resulting in a decrease in thoracic cavity volume and an increase in intrapleural pressure (Pip).
* This leads to an increase in intra-alveolar pressure (Ppul), causing air to move out of the lungs until the intra-alveolar pressure becomes equal to atmospheric pressure (Patm).
28
Q5: What happens to the diaphragm during forced expiration?
A5: During forced expiration, the diaphragm relaxes and moves superiorly due to the compressed abdominal contents.
29
Q6: Is forced expiration an active or passive process?
A6:
* Forced expiration is an active process because it involves the contraction of muscles, specifically the abdominal wall muscles.
30
Q1: What is surface tension?
A1:
* refers to the attraction between water molecules at the liquid-air interface.
* It is a cohesive intermolecular force interaction between water molecules on the surface.
31
Q2: How does surface tension contribute to the recoil of the lungs during expiration?
A2:
* Surface tension produces a force that resists the stretching of the lungs, helping the lungs recoil during expiration.
* It causes the alveoli to shrink and collapse, leading to the smallest size possible.
32
Q3: What happens if there is an increase in surface tension but no recoil?
A3:
I
* f there is an increase in surface tension but no recoil, the alveoli collapse, leading to unequal ventilation (air flow) to the alveoli.
* It can also pull water into the collapsed alveoli, causing pulmonary edema, thickening of the respiratory membrane, and reduced gas exchange.
33
Q4: What is the respiratory membrane composed of?
A4: The respiratory membrane consists of four structures:
* the alveolar wall (type I and type II alveolar cells and associated alveolar macrophages),
* the epithelial basement membrane,
* the capillary basement membrane, and
* the capillary endothelium.
34
Q5: What are the two types of alveolar cells?
A5:
* Type I alveolar cells: These are simple squamous epithelial cells and are most abundant.
* They are primarily involved in gas exchange, allowing oxygen to move from the alveoli into the blood and carbon dioxide to move from the blood into the alveoli.
* Type II alveolar cells: These are simple cuboidal epithelial cells and are less abundant.
* They play a role in producing a lipid-protein detergent complex called surfactant.
35
Q6: How is surface tension formed?
A6:
* formed due to the intermolecular attraction between water molecules at the water-air interface.
* The water molecules interact with each other through hydrogen bonds, creating a certain amount of force that results in surface tension.
36
Q7: How is air pushed out of the alveoli during expiration?
A7:
* Water molecules on the surface of the alveoli do not want to interact with gas. The water layer gets thinner, causing the alveoli to develop tension and collapse.
* As a result, the alveoli push out the air during expiration.
37
Q8: What is the Law of Laplace?
A8:
* The Law of **Laplace (P = 2T/r)** states that smaller alveoli have a higher tendency to collapse.
* In this equation, P represents the collapsing pressure of the alveoli, T represents surface tension, and r represents the alveolar radius.
38
Q9: What is the significance of alveolar pores (pores of Kohn)?
A9:
* Alveolar pores (pores of Kohn) are connections between adjacent alveoli.
* They allow for the flow of excessive air from hyperventilated alveoli to hypoventilated alveoli, preventing the collapsing of the alveoli.
* This helps maintain proper ventilation and prevents ventilation-perfusion mismatch.
39
Q10: How does an increase in surface tension affect gas exchange in the respiratory membrane?
A10:
* An increase in surface tension can lead to the collapse of alveoli, creating a vacuum-like effect.
* This can pull water from pulmonary capillaries into the alveoli, causing the respiratory membrane to become thicker and resulting in a decrease in gas exchange.
40
Q1: What is surfactant?
A1:
* Surfactant is a complex mixture of lipids and proteins that is secreted by type II alveolar cells.
* It reduces alveolar surface tension and prevents the collapse of the alveoli.
41
Q2: What is the purpose of surfactant?
A2:
* decrease surface tension by reducing the cohesiveness of water molecules in the alveoli.
* This is achieved by pulling the water molecules upward, allowing the alveoli to expand and decreasing the collapsing pressure of the alveoli.
42
Q3: What is the role of the phosphatidylcholine group and dipalmitoyl group in surfactant structure?
A3:
* The phosphatidylcholine group in surfactant is hydrophilic and binds to water molecules.
* The dipalmitoyl group, which is hydrophobic, does not want to be in the water.
* It pulls the surfactant molecule upwards along with the water molecules attached to the phosphatidylcholine group, thereby reducing surface tension and allowing the water layer to expand.
43
Q4: How does surfactant spread in the alveoli?
A4:
* Surfactant is distributed between water molecules in the alveoli, causing breaks in certain points of the water layer.
* When the alveolar radius increases, the distribution of surfactant becomes less dense, resulting in a slight increase in surface tension and a bit of collapsing of the alveoli.
* When the alveolar radius decreases, the distribution of surfactant becomes condensed and concentrated, leading to a decrease in surface tension.
* This allows the alveoli to expand and reduces the collapsing pressure.
44
Q5: What is the pharmacological name for surfactant?
A5:
**amphiphilic phospholipid.**
* It is used to treat respiratory distress syndrome.
45
Q6: What is respiratory distress syndrome of the newborn?
A6:
* Respiratory distress syndrome of the newborn occurs when developing fetal lungs are unable to synthesize surfactant until late in the 36th week of pregnancy.
* Premature babies may not have enough pulmonary surfactant, leading to high surface tension in the lungs.
* At birth, babies make strenuous inspiratory efforts to overcome the high surface tension and inflate the lungs, which can cause physical damage to the lung cells.
46
Q7: What are the opposing forces acting on the lungs?
A7:
include the elasticity of the lung tissue, surface tension, compliance, and airway resistance.
47
Q1: What are the major inspiratory muscles?
A1: The major inspiratory muscles are the diaphragm and the external intercostal muscles.
48
Q2: Which muscles are considered accessory muscles of inspiration?
A2: The accessory muscles of inspiration, used during forceful inspiration, include the
* sternocleidomastoid, scalenus, and pectoral muscles.
49
Q3: Which muscles are involved in active expiration?
A3:
Active expiration involves the contraction of the abdominal muscles and the internal intercostal muscles.
50
Q4: What is tidal volume (TV)?
A4: Tidal volume refers to the volume of air that enters and leaves the lungs with each normal breath during quiet respiration.
51
Q5: What is inspiratory reserve volume (IRV)?
A5: Inspiratory reserve volume is the additional volume of air that can be forcibly inhaled after a normal tidal volume inhalation.
52
Q6: What is expiratory reserve volume (ERV)?
A6: Expiratory reserve volume is the volume of air that can be forcibly exhaled after exhalation of a normal tidal volume.
53
Q7: What is residual volume (RV)?
A7: Residual volume is the volume of air that remains in the lungs after maximal exhalation. It cannot be measured by spirometry.
54
Q8: What is vital capacity (VC)?
A8: Vital capacity is the total volume of air that can be inhaled and exhaled forcefully, including tidal volume, inspiratory reserve volume, and expiratory reserve volume.
55
Q9: What is functional residual capacity (FRC)?
A9: is the volume of air that remains in the lungs without forceful expiration, including expiratory reserve volume and residual volume.
56
Q10: What is total lung capacity (TLC)?
A10: is the total volume of air that the lungs can hold, including vital capacity and residual volume. It cannot be measured by spirometry.
57
Q1: What is the purpose of a pulmonary function test?
A1:
* Is used to determine if a person has an obstructive or restrictive pulmonary disorder.
* It is performed using a spirometer.
58
Q2: What are examples of obstructive pulmonary disorders?
A2:
emphysema, chronic bronchitis, and asthma. These conditions are characterized by a decreased percentage of pulmonary function test (**<80%) and a decreased forced expiratory volume (FEV).**
59
Q3: What are examples of restrictive pulmonary disorders?
A3:
tuberculosis, interstitial lung diseases, and pulmonary fibrosis.
These conditions are characterized by an increased percentage of pulmonary function test **(>80%) and a decreased forced vital capacity (FVC).**
60
Q4: Is tuberculosis (TB) considered a restrictive or obstructive disorder?
A4:
* Tuberculosis (TB) is typically considered a restrictive lung disorder rather than an obstructive one.
* While TB can cause narrowing of the airways and obstructive symptoms in some cases, it primarily leads to scarring and inflammation in the lungs, resulting in reduced lung volume and restrictive lung disease.
61
Q5: What is the FEV1/FVC ratio?
A5: T
* is the proportion of air that can be exhaled in the first second (FEV1) compared to the total volume of air that can be exhaled (FVC).
* A normal pulmonary function typically has an FEV1/FVC ratio of around 80%.
* In obstructive disorders, such as emphysema and asthma, the FEV1 is significantly lower than the FVC, resulting in a decreased FEV1/FVC ratio.
* In restrictive disorders, such as tuberculosis and pulmonary fibrosis, the FVC is decreased, leading to an increased FEV1/FVC ratio.
62
Q1: What is the primary determinant of airway resistance?
A1:
* The radius of the conducting airway is the primary determinant of airway resistance.
* As the radius decreases, airway resistance increases, and vice versa.
63
Q2: What is the effect of parasympathetic stimulation on the airways?
A2:
leads to bronchoconstriction, causing a decrease in the diameter of the airways and an increase in airway resistance.
64
Q3: What is the effect of sympathetic stimulation on the airways?
A3:
Sympathetic stimulation leads to bronchodilation, causing an increase in the diameter of the airways and a decrease in airway resistance.
65
Q4: What happens in asthma or allergic reactions in terms of airway function?
A4:
* In asthma or allergic reactions, there is an excessive bronchoconstriction response, leading to a significant decrease in the diameter of the airways.
* This limits the amount of air that can flow in and out of the lungs, resulting in labored breathing.
66
Q5: What is dynamic airway compression?
A5:
* Dynamic airway compression refers to the phenomenon observed during active expiration, where the rising pleural pressure compresses the alveoli and airway, decreasing the radius of the airway.
* In normal individuals, the increased airway resistance helps open the airways by increasing the driving pressure between the alveolus and the airway.
* However, in patients with obstructive lung diseases, such as asthma or COPD, the obstructed segment loses the driving pressure, causing a fall in airway pressure along the airway downstream and resulting in airway compression during active expiration.
67
Q6: What is the purpose of a peak flow meter?
A6:
* is used to estimate the peak flow rate (PEFR) and assess airway function.
* It is particularly useful in patients with obstructive lung diseases to monitor changes in airflow and assess the effectiveness of treatment.
68
Q1: What is compliance in the context of respiratory physiology?
A1:
* Compliance refers to the measure of effort required to stretch the lungs.
* It represents the volume change per unit of pressure change across the lungs.
* In other words, compliance indicates how easily the lungs can expand or stretch in response to changes in pressure.
69
Q2: How does compliance change in restrictive lung diseases?
A2:
* Compliance is decreased in restrictive lung diseases.
* These diseases cause stiffness or reduced elasticity of the lung tissues, making it more difficult for the lungs to expand.
* As a result, a greater change in pressure is required to produce inflation, leading to a decreased compliance.
* Patients with restrictive lung diseases often experience shortness of breath, especially on exertion, due to the increased work required to breathe.
70
Q3: Can compliance be abnormally increased? If so, what condition is associated with increased compliance?
A3:
* Yes, compliance can become abnormally increased in certain conditions.
* Emphysema is an example of a condition where compliance is increased.
* In emphysema, the elastic tissues of the lungs are destroyed, causing the lungs to become hyperinflated.
* While the lungs are easy to inflate, they have difficulty deflating, leading to an increased compliance.
71
Q4: What factors can decrease lung compliance other than changes in elasticity?
A4:
postural abnormalities such as hunched-over posture (ankylosing spondylitis, kyphosis, scoliosis),
aging-related changes (ossification of rib cartilage),
injuries to the diaphragm or external intercostal muscles,
and conditions such as chronic bronchitis or cystic fibrosis.
* These factors can impair the ability of the lungs to expand and contribute to decreased compliance.
72
Q5: What is the work of breathing, and how does it relate to pulmonary compliance, airway resistance, and elastic recoil?
A5:
* refers to the energy expenditure required for the respiratory muscles to generate airflow and facilitate breathing.
* During increased work of breathing, pulmonary compliance, airway resistance, and elastic recoil can be affected.
* Decreased compliance makes it more difficult for the lungs to stretch and expand, increased airway resistance hinders airflow, and decreased elastic recoil impairs the ability of the lungs to passively return to their original shape.
* These factors collectively contribute to an increased workload on the respiratory muscles during breathing.
73
Q6: How does parietal pleura injury or atelectasis affect lung compliance?
A6:
* Parietal pleura injury, such as a stab wound through the parietal pleura, can result in air entering the pleural cavity and equalizing the intrapleural pressure with atmospheric pressure.
* This equalization leads to lung collapse and decreased compliance.
* Atelectasis, which refers to the collapse of lung tissue, also results in decreased compliance.
* Injuries causing hemothorax, pneumothorax, or pleural effusion can lead to atelectasis and reduced lung volume, resulting in decreased compliance.
74
Q1: What is the formula for calculating the alveolar ventilation rate?
A1: Alveolar ventilation rate = (Tidal volume - Dead space) x Respiration rate.
75
Q2: What is the normal respiratory rate?
A2: The normal respiratory rate is 12-16 breaths per minute.
76
Q3: Define pulmonary ventilation.
A3: the volume of air breathed in and out per minute.
77
Q4: How is pulmonary ventilation calculated?
A4: is calculated by multiplying the tidal volume by the respiratory rate.
78
Q5: What is alveolar respiration?
A5: the volume of air exchanged between the atmosphere and alveoli per minute.
79
Q6: How is alveolar respiration calculated?
A6: subtracting the dead space volume from the tidal volume and then multiplying by the respiratory rate.
80
Q7: What is anatomical dead space?
A7: the conducting zone of the respiratory system, which includes airways that fill with air but cannot perform gas exchange.
81
Q8: Why is it advantageous to increase the depth of breathing when increasing ventilation?
A8: Increasing the depth of breathing helps to overcome the anatomical dead space and ensure more effective gas exchange.
82
Q9: What are the two types of dead space?
A9:
anatomical dead space (conducting zone) and
physiological dead space.
83
Q1: Define ventilation.
A1: the rate at which gas is passing through the lungs.
84
Q2: Define perfusion.
A2: the rate at which blood is passing through the lungs, which is technically cardiac output.
85
Q3: How does blood flow and ventilation vary from top to bottom of the lung?
A3: Blood flow and ventilation vary from top to bottom of the lung.
* The lung apex has good ventilation but poor blood flow (perfusion),
* while the lung base has poor ventilation but good blood flow.
* This variation is due to gravity.
86
Q4: What is alveolar dead space?
A4:
* Alveolar dead space refers to ventilated alveoli that are not adequately perfused with blood.
* It is typically very small in healthy individuals but can increase in disease.
* Physiological dead space is the sum of anatomical dead space and alveolar dead space.
87
Q5: What is the significance of matching ventilation and perfusion?
A5: The transfer of gases between the body and the atmosphere is most efficient when ventilation and perfusion are matched.
88
Q6: What happens when ventilation is greater than perfusion (good ventilation)?
A6:
* When ventilation is greater than perfusion, there is a decrease in CO2 levels, leading to vasoconstriction of local airways and a decrease in airflow.
* Meanwhile, there is an increase in O2 levels, causing vasodilation of local blood vessels and an increase in blood flow.
* This helps to bring the ventilation/perfusion (V/Q) ratio back to normal.
89
Q7: What happens when perfusion is greater than ventilation (poor ventilation)?
A7:
* When perfusion is greater than ventilation, there is an increase in the partial pressure of CO2, leading to vasodilation of local airways and an increase in airflow.
* At the same time, there is a decrease in O2 levels, resulting in vasoconstriction of local blood vessels and a decrease in blood flow.
* This helps to bring the V/Q ratio back to normal.
90
Q8: What happens when there is an increase in cardiac output (increased perfusion)?
A8:
* An increase in cardiac output leads to an increase in the partial pressure of CO2 in the alveoli.
* This causes bronchial smooth muscle dilation, resulting in bronchial dilation and increased airflow.
91
Q9: What happens when there is a decrease in cardiac output (poor perfusion)?
A9:
* A decrease in cardiac output, such as in the case of pulmonary embolism, leads to vasoconstriction of poorly perfused alveoli and bronchial smooth muscle constriction.
* This decreases flow and results in decreased ventilation.
* The V/Q ratio is brought back to normal in this situation.
92
Q1: What are some non-respiratory functions of the respiratory system?
A1:
serving as a route for water loss and heat elimination,
enhancing venous return (cardiovascular function),
helping maintain normal acid-base balance (respiratory and renal function), and
facilitating speech, singing, etc.
93
Q2: How does the respiratory system enhance venous return?
A2:
* The respiratory system enhances venous return by creating negative pressure during inspiration.
* When the diaphragm contracts and the thoracic cavity expands, it creates a pressure gradient that helps draw venous blood back to the heart.
94
Q3: How does the respiratory system help maintain normal acid-base balance?
A3:
* through the regulation of carbon dioxide (CO2) levels in the blood.
* By controlling the rate and depth of breathing, the respiratory system can adjust the elimination of CO2, which helps regulate the pH of the body fluids in coordination with the kidneys' renal function.
95
Q4: What are some factors affecting the rate of gas exchange?
A4:
* the surface area available for exchange,
* the thickness of the respiratory membrane,
* the concentration gradient of gases,
* the solubility of gases, and
* the ventilation-perfusion matching.
96
Q5: How does the surface area available for gas exchange affect the rate of gas exchange?
A5:
* The surface area available for gas exchange directly influences the rate of gas exchange.
* A larger surface area allows for more contact between the respiratory surfaces and the blood, facilitating a higher rate of diffusion.
97
Q6: How does the thickness of the respiratory membrane affect the rate of gas exchange?
A6:
* The thickness of the respiratory membrane, which includes the alveolar wall and the capillary wall, affects the rate of gas exchange.
* A thinner membrane allows for faster diffusion of gases, while a thicker membrane slows down the rate of gas exchange.
98
Q7: What is the significance of the concentration gradient of gases in gas exchange?
A7:
* The concentration gradient of gases refers to the difference in partial pressures of gases between the alveoli and the blood.
* A steep concentration gradient promotes rapid diffusion of gases across the respiratory membrane, facilitating efficient gas exchange.
99
Q8: How does the solubility of gases affect the rate of gas exchange?
A8:
* The solubility of gases influences the rate of gas exchange.
* Gases that are highly soluble in fluids, such as carbon dioxide, diffuse more easily across the respiratory membrane compared to gases with lower solubility, such as oxygen.
100
Q9: What is the importance of ventilation-perfusion matching in gas exchange?
A9:
* Ventilation-perfusion matching refers to the matching of airflow (ventilation) and blood flow (perfusion) in the lungs.
* It ensures that the areas with well-ventilated alveoli receive adequate blood flow and vice versa, optimizing gas exchange efficiency.
101
Q1: What is Henry's law of partial pressure?
A1:
Henry's law states that the amount of a given gas dissolved in a given type and volume of liquid (e.g., blood) at a constant temperature is proportional to the partial pressure of the gas in equilibrium with the liquid.
* In other words, if the partial pressure of a gas in the gas phase is increased, the concentration of that gas in the liquid phase will increase proportionally.
102
Q2: How does the solubility of gases influence their movement across the respiratory membrane?
A2:
The solubility of gases affects their movement across the respiratory membrane.
Gases with higher solubility, such as carbon dioxide, diffuse more easily across the membrane compared to gases with lower solubility, such as oxygen.
103
Q3: What is the relationship between pressure and solubility according to Henry's law?
A3:
* According to Henry's law, the solubility of a gas in a liquid is directly proportional to the partial pressure of the gas.
* When the pressure of a gas increases, its solubility in the liquid also increases.
104
Q4: Why is carbon dioxide more soluble than oxygen in the blood plasma and alveolar fluid?
A4:
* Carbon dioxide is 20 times more soluble than oxygen in the blood plasma and alveolar fluid.
* This higher solubility allows carbon dioxide to move more easily across the respiratory membrane, despite having a smaller partial pressure gradient compared to oxygen.
105
Q5: How does an increase in the partial pressure of a gas affect its solubility in a fluid?
A5:
* An increase in the partial pressure of a gas will increase its solubility in the fluid, according to Henry's law.
* The solubility of a gas in a given type and volume of liquid is directly proportional to its partial pressure.
106
Q1: How is most of the oxygen in the blood transported?
A1:
* Most of the oxygen in the blood is transported bound to hemoglobin in red blood cells, accounting for 98.5% of oxygen transport.
* The remaining 1.5% is dissolved in the blood.
107
Q2: What is the structure of hemoglobin?
A2:
* Hemoglobin consists of two alpha (⍺) and two beta (β) globin chains, with each chain containing a heme group.
* Each heme group can reversibly bind to one oxygen molecule.
108
Q3: What determines the percentage saturation of hemoglobin with oxygen?
A3: The primary factor is the partial pressure of oxygen (PO2).
109
Q4: What is the oxygen delivery index (DO2I)?
A4:
* The oxygen delivery index is a function of cardiac output (cardiac index) and the oxygen content of arterial blood (CaO2).
* It is calculated as DO2I = CaO2 x CI.
110
Q5: What is the oxygen content of arterial blood (CaO2) determined by?
A5:
The oxygen content of arterial blood is determined by the concentration of hemoglobin in the blood and the percentage saturation of hemoglobin with oxygen.
111
Q6: What does a low partial pressure of oxygen indicate?
A6: A low partial pressure of oxygen indicates a low level of oxygen bound to hemoglobin.
112
Q7: How is the partial pressure of oxygen in the alveolar air determined?
A7:
* The partial pressure of oxygen in the alveolar air depends on the total pressure (e.g., atmospheric pressure) and the proportion of oxygen in the gas mixture.
* It is calculated as PAO2 = PiO2 – [PaCO2/0.8], where PAO2 is the partial pressure of oxygen in alveolar air, PiO2 is the partial pressure of oxygen in inspired air, PaCO2 is the partial pressure of carbon dioxide in arterial blood, and 0.8 is the respiratory exchange ratio.
113
Q8: What are the contents of deoxygenated blood (T state hemoglobin)?
A8:
* oxygen molecules bound to the iron-containing heme group,
* CO2 bound to the amino acids of the globin chains as carbamino hemoglobin,
* protons bound to negatively charged amino acids of the globin chains,
* and 2,3-BPG (bisphosphoglycerate) bound to positively charged pockets within hemoglobin.
114
Q9: How is carbon dioxide distributed in the blood?
A9:
Carbon dioxide is distributed in the blood in different forms.
Approximately 20% is bound to amino acids of the globin chains as carbamino hemoglobin, 70% is in the form of bicarbonate (HCO3-), and 2-10% is dissolved in the blood plasma.
115
Q1: How does oxygen move from the alveoli to the blood and bind to hemoglobin?
A1:
* Oxygen moves from the alveoli, where the concentration is high, to the blood, where the concentration is low.
* It binds to the iron-containing heme groups of hemoglobin.
* The movement of oxygen is driven by the large difference in concentration gradient.
* Initially, it is difficult for the first oxygen molecule to bind to the iron, but as more oxygen molecules bind, it becomes easier.
* This is known as positive cooperativity.
116
Q2: What happens to the hemoglobin when it is oxygenated (in the R state)?
A2:
* When hemoglobin is oxygenated (in the R state), it undergoes a conformational change.
* The contents of the oxyhemoglobin include the release of 2,3-BPG, the exhalation of CO2 (both carbamino hemoglobin and bicarbonate), the release of protons (which bind with bicarbonate to form carbonic acid), and the binding of oxygen molecules to the iron-containing heme groups.
117
Q3: How does the release of CO2 occur in oxygenated blood?
A3:
* In oxygenated blood, the release of CO2 occurs through several mechanisms.
* Approximately 20% of CO2, which is in the form of carbamino hemoglobin, is released by simple diffusion into the alveoli.
* The 70% of CO2 that is in the form of bicarbonate also moves into the alveoli.
* Additionally, 2-10% of dissolved CO2 in the blood also moves into the alveoli.
118
Q4: What happens to bicarbonate in oxygenated blood?
A4:
* Bicarbonate (HCO3-) enters the red blood cells and binds with protons, producing carbonic acid (H2CO3).
* Carbonic acid is unstable and dissociates quickly into CO2 and water, which is then exhaled.
* This process is facilitated by the presence of the enzyme carbonic anhydrase.
* Bicarbonate in the plasma may also bind with protons and undergo the same process, but it occurs more slowly in the absence of carbonic anhydrase in the plasma.
119
Q5: What are the affinities of hemoglobin in the R state?
A5:
Hemoglobin in the R state (oxygenated state) has a high affinity for oxygen but a low affinity for CO2, protons, and 2,3-BPG.
120
Q1: How does a decreased partial pressure of inspired oxygen (e.g., at altitude) impair oxygen delivery to tissues?
A1:
* A decreased partial pressure of inspired oxygen at altitude leads to a lower concentration of oxygen in the inspired air.
* This, in turn, results in a decreased partial pressure of oxygen in the alveoli and arterial blood.
* As a result, there is a reduced saturation of hemoglobin with oxygen and a decreased oxygen concentration in the blood, impairing oxygen delivery to tissues.
121
Q2: How does respiratory disease impair oxygen delivery to tissues?
A2:
* Respiratory diseases can decrease the arterial partial pressure of oxygen (PO2).
* This reduction in PO2 leads to a decrease in hemoglobin saturation with oxygen and a decrease in the oxygen concentration of the blood.
* Consequently, oxygen delivery to tissues is impaired.
122
Q3: How does anemia impair oxygen delivery to tissues?
A3:
* Anemia is characterized by a decrease in hemoglobin concentration, which results in a lower oxygen-carrying capacity of the blood.
* With reduced hemoglobin, the oxygen concentration in the blood is decreased, leading to impaired oxygen delivery to tissues.
123
Q4: How does heart failure impair oxygen delivery to tissues?
A4:
* Heart failure decreases cardiac output, which is the amount of blood pumped by the heart per minute.
* As a result, there is reduced blood flow to tissues, including the delivery of oxygen.
* This impaired circulation hinders the efficient delivery of oxygen to tissues, affecting their oxygenation and function.
124
Q1: How is carbon dioxide carried in the blood as a solution?
A1:
* Approximately 10% of carbon dioxide is dissolved in the blood as a solution.
* The amount of carbon dioxide dissolved is proportional to its partial pressure, according to Henry's Law.
* Carbon dioxide is about 20 times more soluble in blood than oxygen.
125
Q2: What are carbamino compounds and how do they contribute to carbon dioxide carriage in the blood?
A2:
* Carbamino compounds are formed when carbon dioxide combines with terminal amine groups in blood proteins, particularly hemoglobin.
* This binding of carbon dioxide to hemoglobin forms carbamino-hemoglobin. Around 30% of carbon dioxide is carried in the blood in this manner.
* The combination occurs rapidly even without the presence of an enzyme, and reduced hemoglobin can bind more carbon dioxide than oxygenated hemoglobin.
126
Q3: How is carbon dioxide buffered in the blood as bicarbonate?
A3:
* Approximately 60% of carbon dioxide is buffered with water as carbonic acid (H2CO3).
* Carbonic anhydrase, an enzyme found within red blood cells, converts carbon dioxide into carbonic acid.
* Carbonic acid then dissociates into bicarbonate ions (HCO3-) and hydrogen ions (H+).
* The bicarbonate ions are transported out of the red blood cells into the plasma in exchange for chloride ions, a process known as the chloride shift.
127
Q5: How is carbon dioxide liberated in the lungs?
A5:
* In the lungs, bicarbonate ions are transported back into the red blood cells in exchange for chloride ions.
* Hydrogen ions dissociate from hemoglobin and bind to the bicarbonate ions, forming carbonic acid.
* Carbonic anhydrase then converts carbonic acid back into carbon dioxide, which is expelled through the lungs during exhalation.
* In the lungs, as hemoglobin picks up oxygen, its ability to bind to carbon dioxide and H+ weakens (Haldane effect).
128
Q1: What are chemoreceptors and what types of chemoreceptors are there?
A1:
* Chemoreceptors are cells that respond to chemical compounds and generate impulses to sensory nerves.
There are two sets of chemoreceptors:
* O2 receptors found in the peripheral nervous system, and
* CO2 receptors found in both the peripheral and central nervous systems.
129
Q2: What do stretch receptors respond to and what role do they play?
A2:
* Stretch receptors respond to the stretching of muscles and transmit impulses to the central nervous system.
* They are important for proprioception, which coordinates muscle activity.
130
Q3: What are proprioceptors and what is their function?
A3:
Proprioceptors are cells that monitor body changes brought about by muscular movement and transmit impulses to the central nervous system to coordinate movement.
131
Q4: What are juxtacapillary receptors (J-receptors) and what is their role?
A4:
* Juxtacapillary receptors, also known as J-receptors or pulmonary C-fiber receptors, are cells that cause an increase in breathing rate as a reflex response.
* They are thought to be involved in the sensation of dyspnea.
132
Q5: What are nociceptors and what is their function?
A5: Nociceptors are cells that respond to pain stimuli by transmitting impulses to the central nervous system.
133
Q6: What happens during chronic hypercapnia?
A6:
* In chronic hypercapnia, chemoreceptors in the carotid bodies detect low oxygen levels in the blood.
* They send signals via cranial nerves to the dorsal respiratory group in the medulla.
* Motor output is then sent via the phrenic nerve to stimulate the contraction of the diaphragm, leading to an increase in respiratory rate
134
Q7: What is the Pre-Botzinger complex and its role in the neural control of respiration?
A7:
* The Pre-Botzinger complex is a network of neurons in the medulla believed to generate the breathing rhythm.
* It displays pacemaker activity and is located near the upper end of the medulla respiratory center.
* Neurons in this complex excite the dorsal respiratory group neurons, leading to the contraction of inspiratory muscles and inspiration.
135
Q8: What is the role of the pons in the neural control of respiration?
A8:
* The pons modifies the rhythm generated by the medulla.
* It contains the pneumotaxic center, which terminates inspiration when stimulated, and the apneustic center, which prolongs inspiration when excited.
* Damage to the pneumotaxic center can lead to prolonged inspiration known as apneustic breathing.
136
Q1: What are the higher brain centers involved in respiratory control?
A1:
* The higher brain centers involved in respiratory control include the cerebral cortex and hypothalamus.
* These centers sense changes in pH in the cerebral spinal fluid and some interstitial fluid in the Central Nervous System (CNS).
137
Q2: What are the three types of receptors in the lungs?
A2:
stretch receptors, irritant receptors, and juxta capillary receptors.
138
Q3: Where are stretch receptors located and what is their function?
A3:
* located in the walls of bronchi and bronchioles and within the visceral pleura.
* They are stimulated when the tidal volume exceeds 800 ml.
* Activation of stretch receptors triggers the Hering-Breuer reflex, which guards against hyperinflation of the lungs.
* Stretch receptors send signals via the vagus nerve (cranial nerve X) to the pons and medulla, inhibiting inspiration and stimulating expiration.
139
Q4: What are juxtapulmonary receptors and where are they found?
A4:
* are found in the lung parenchyma (alveoli and respiratory bronchioles) and within the interstitial fluid between pulmonary capillaries and alveoli.
* These receptors are sensitive to increased pulmonary capillary pressure, such as in pulmonary capillary congestion, pulmonary edema, and pulmonary emboli.
* Stimulation of juxtapulmonary receptors triggers rapid shallow breathing.
* Thickening of the respiratory exchange membrane and fluid accumulation in the interstitial space can activate these receptors and cause dyspnea (shortness of breath).
140
Q5: Will pulmonary edema stimulate rapid shallow breathing?
A5:
Yes, pulmonary edema can stimulate rapid shallow breathing, also known as tachypnea.
* Pulmonary edema is characterized by excessive fluid buildup in the lungs, which can impair breathing and decrease oxygenation.
* In response to decreased oxygenation, the body may initiate rapid shallow breathing to increase air exchange in the lungs and improve oxygenation.
* This can manifest as tachypnea, which is characterized by a rapid breathing rate and shallow breaths.
* However, it is important to consult with a healthcare professional for proper evaluation and treatment if experiencing symptoms of pulmonary edema or rapid shallow breathing.
141
Q1: What are irritant receptors and what stimulates them?
A1:
* are located underneath the epithelial layer in the subepithelial tissue of the conducting zone mucosa.
* They respond to irritants present in the mucosal layer, such as debris, harmful chemicals, allergens, pollens, and floating matter.
142
Q2: What is the mechanism of irritant receptor stimulation?
A2:
* When irritant receptors are stimulated, impulses are sent through the sensory afferent fibers of the vagus nerve (cranial nerve X).
* This stimulation can trigger various reflexes, including the cough reflex, sneeze reflex, narrowing of the glottis, and tachypnea (accelerated respiration).
143
Q3: What are joint receptors and how do they influence breathing?
A3:
* Joint receptors are proprioceptors found in skeletal muscles.
* When they are stimulated by impulses from moving limbs, they can lead to an increased breathing response, resulting in increased ventilation during exercise.
* Joint receptors play a role in determining the position within space and contribute to appropriate increases in respiratory rate and depth during physical activity.
144
Q4: How does the hypothalamus influence respiration?
A4:
* Stimulation of thermoreceptors sends impulses to the hypothalamus, which can cause prolonged or increased inspiration.
* For example, jumping into freezing cold water (such as in the polar bear plunge) stimulates thermoreceptors, leading to impulses sent to the hypothalamus and affecting the respiratory centers, resulting in increased or prolonged inspiration.
145
Q5: How do emotions and the cerebral cortex influence respiration?
A5:
* Emotions can stimulate the limbic nuclei, which then send impulses to the respiratory centers,
* potentially increasing or decreasing respiratory rate and depth depending on the emotions experienced.
* The cerebral cortex is responsible for voluntary or volitional control of breathing.
* It can bypass the respiratory centers in the pons and medulla through corticospinal tracts, allowing for voluntary breathing actions such as holding breath or deep breathing.
However, this control is limited. Prolonged breath-holding can lead to an increase in CO2 levels and carbonic acid in the cerebrospinal fluid, stimulating peripheral and central chemoreceptors, and ultimately resulting in increased action potentials in the dorsal respiratory group (DRG) and ventral respiratory group (VRG), leading to inspiration.
146
Q1: What are the stimuli that influence respiration during exercise?
A1:
During exercise, there are various stimuli that influence respiration, including
reflexes originating from body movement,
the release of adrenaline,
impulses from the cerebral cortex,
an increase in body temperature,
and the accumulation of CO2 and H+ generated by active muscles.
147
Q2: What is hyperpnea and how does it relate to exercise?
A2:
Hyperpnea refers to an increase in alveolar ventilation, which is achieved through an increase in both respiratory rate and depth.
During exercise, hyperpnea occurs to meet the increased oxygen demand of the body, **but there is no significant change in blood gas chemistry**, including arterial PO2 and PCO2.
148
Q3: What are the sensory receptors activated during exercise?
A3:
* During exercise, different sensory receptors called proprioceptors are activated.
* These include muscle spindles, Golgi tendon organs, and joint kinesthetic receptors.
* These receptors provide feedback on body movement and position, contributing to the coordination of muscle activity during exercise.
149
Q4: How does exercise affect heart rate and cardiac output?
A4:
During exercise, both heart rate (HR) and cardiac output (CO) increase.
* The cardiac output of both ventricles is increased, with the normal CO of 5 L/min rising to approximately 6 times the normal CO (30 L/min) due to increased contractility of the right and left ventricles.
150
Q5: What is the role of baroreceptors, chemoreceptors, and the cough reflex in respiration during exercise?
A5:
* Baroreceptors sense changes in blood pressure and can trigger an increased ventilatory rate in response to decreased blood pressure.
* Chemoreceptors, both central and peripheral, monitor chemical changes in the blood and can influence respiration accordingly.
* The cough reflex, activated by irritation or tightness in the airways, helps to clear the airways of dust, dirt, or excessive secretions.
* The cough reflex has a center located in the medulla, which is involved in regulating respiration.
151
Q1: What is the role of central chemoreceptors in the chemical control of respiration?
A1:
Central chemoreceptors, located near the surface of the medulla, detect changes in pCO2 by responding to the H+ concentration of the cerebrospinal fluid (CSF).
* An increase in pCO2 leads to an increase in ventilation, while a decrease in pCO2 leads to a decrease in ventilation, helping to maintain normal levels of pCO2 in the blood.
152
Q2: Where are the peripheral chemoreceptors located and what do they respond to?
A2:
* The peripheral chemoreceptors are located in the carotid body and aortic body.
* They detect large changes in the partial pressure of oxygen (pO2) in the arterial blood supply as it leaves the heart.
153
Q3: What is the hypoxic drive and when does it become important?
A3:
* The hypoxic drive refers to the stimulation of respiration by low arterial pO2 levels (<8.0 kPa).
* In normal respiration, pCO2 is the primary drive for respiration.
* However, in conditions of chronic CO2 retention or at high altitudes, where pO2 is significantly reduced, hypoxic drive becomes more important in regulating respiration.
154
Q4: What are the acute and chronic adaptations to hypoxia?
A4:
The acute response to hypoxia includes hyperventilation and increased cardiac output.
Chronic adaptations to hypoxia include
* increased red blood cell production,
* increased production of 2,3 BPG within red blood cells,
* increased number of capillaries,
* increased number of mitochondria, and
* the conservation of acid by the kidneys.
155
Q5: How does the H+ drive of respiration control acidosis during exercise?
A5:
* During exercise, the stimulation of peripheral chemoreceptors by non-carbonic H+ (e.g., lactic acid) leads to hyperventilation and increased elimination of CO2 from the body.
* This helps to control acidosis and maintain acid-base balance during periods of increased metabolic activity.
156
Q1: What are some examples of airflow obstruction conditions that can contribute to shortness of breath?
A1: Asthma, chronic bronchitis, and tracheal obstruction are examples of airflow obstruction conditions that can contribute to shortness of breath.
157
Q2: What can cause decreased pulmonary compliance, leading to shortness of breath?
A2: Pulmonary edema and fibrosis are factors that can cause decreased pulmonary compliance, contributing to shortness of breath.
158
Q3: What can cause restricted chest expansion, leading to shortness of breath?
A3: Respiratory muscle paralysis can restrict chest expansion and contribute to shortness of breath.
159
Q4: What can lead to an increased ventilatory drive and contribute to shortness of breath?
A4:
* Increased physiological dead space, ventilation-perfusion mismatch (e.g., infection, pulmonary embolism),
* increased hydrogen ion concentration (metabolic acidosis),
* increased arterial carbon dioxide levels (respiratory acidosis),
* decreased arterial oxygen levels (pneumonia, anemia),
* increased central arousal (anxiety, thyrotoxicosis), and
* pulmonary receptor discharge can all increase the ventilatory drive and contribute to shortness of breath.
160
Q5: What are some examples of cardiac causes of shortness of breath?
A5:
* Myocardial infarction is the most common cardiac cause of shortness of breath.
* Other causes include hypertension, arrhythmias, valvular disease, and cardiomyopathies.
161
Q: What is the first step in the physiology of coughing?
A:
the stimulation of sensory receptors in the mucosa of the upper respiratory tract (URT) or respiratory tree.
This can be triggered by various factors such as irritants or foreign particles.
162
Q: How are the sensory receptors in the URT and respiratory tree stimulated during coughing?
A:
* In the URT, sensory receptors are stimulated by the glossopharyngeal nerve (CN IX) or vagus nerve (CN X).
* In the respiratory tree, motor axons travel along the branches of the respiratory tree, supplying the mucous glands and bronchial smooth muscles.
163
Q: What happens after the sensory receptors are stimulated?
A: The pulmonary visceral afferents transmit signals from the visceral pleura and respiratory tree to the medulla via the vagus nerve.
This connection to the central nervous system (CNS) allows for a rapid response.
164
Q: How does the CNS coordinate the process of coughing?
A:
* The CNS coordinates several actions during coughing.
* It initiates deep expiration by activating the diaphragm, intercostal muscles, and accessory muscles.
* The vocal cords adduct to close the rima glottidis, preventing the entry of air into the lower airways.
* The anterolateral abdominal walls contract, increasing intra-abdominal pressure and pushing the diaphragm upward, which further helps in building up pressure in the chest.
* The vocal cords subsequently abduct to open the rima glottidis, allowing the expelled air to pass through.
* Additionally, the soft palate tenses and elevates, closing off the entrance to the nasopharynx and directing the airflow through the oral cavity.
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