Topic 7: Chpt 17-18 Flashcards

1
Q

Why do human lungs have such a large surface area?

A

Human lungs have a gas exchange surface area equivalent to about 75 square meters to efficiently supply oxygen to trillions of cells and remove CO2. This large surface area, comparable to a racquetball court, is compressed into a small volume to maximize gas exchange.

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2
Q

How do humans meet the challenge of dehydration in respiration?

A

Humans have internalized lungs within the chest cavity, creating a humid environment protected from external air, which helps maintain the necessary moisture for gas exchange.

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3
Q

What are the main components of a complex respiratory system in humans?

A

The respiratory system in humans consists of a muscular pump (thorax musculoskeletal structure) for moving air and a thin, moist exchange surface (lung epithelium and blood vessels) for gas exchange.

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4
Q

What are the four primary functions of the respiratory system?

A
  1. Gas exchange between the atmosphere and blood. 2. Regulation of body pH by managing CO2 levels. 3. Protection from inhaled pathogens and irritants. 4. Vocalization through air movement across the vocal cords.
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5
Q

How does the respiratory system contribute to homeostasis beyond gas exchange?

A

The respiratory system helps in regulating body temperature and water balance through heat and moisture loss, which must be compensated for by homeostatic mechanisms.

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6
Q

What principles govern the flow of air in the respiratory system?

A

Air flow in the respiratory system follows from regions of higher pressure to lower pressure, driven by a muscular pump, and is primarily influenced by the diameter of the air passages.

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7
Q

What are the different meanings of respiration in physiology?

A

In physiology, respiration refers to cellular respiration, the biochemical process producing ATP by reacting oxygen with organic molecules, and external respiration, which is the exchange of gases between the environment and body cells, involving ventilation and gas transport.

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8
Q

What are the four processes of external respiration?

A
  1. Ventilation (air exchange between the atmosphere and lungs). 2. Gas exchange between lungs and blood. 3. O2 and CO2 transport by the blood. 4. Gas exchange between blood and cells.
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9
Q

What is ventilation and what are its mechanisms?

A

Ventilation, or breathing, involves inspiration (inhalation) to move air into the lungs and expiration (exhalation) to move air out, governed by the mechanics of breathing involving thoracic and abdominal structures.

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10
Q

What are the main components of the respiratory system?

A

he respiratory system includes conducting airways leading to the lungs, alveoli for gas exchange, and thorax and abdomen muscles that assist in breathing.

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11
Q

What is the role of alveoli in the respiratory system?

A

Alveoli are interconnected sacs lined with pulmonary capillaries where oxygen is transferred from inhaled air to the blood, and CO2 is transferred from the blood to air being exhaled.

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12
Q

How is the respiratory system anatomically divided?

A

The upper respiratory tract includes the mouth, nasal cavity, pharynx, and larynx. The lower respiratory tract, or thoracic portion, includes the trachea, primary bronchi, their branches, and the lungs.

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13
Q

How are the respiratory and cardiovascular systems coordinated in external respiration?

A

External respiration requires coordination between the respiratory system (air movement and gas exchange) and the cardiovascular system (transport of gases), ensuring efficient oxygen delivery and CO2 removal.

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14
Q

What are the components of the thoracic cage?

A

The thoracic cage consists of the spine, rib cage, and associated muscles, forming a protective structure around the chest cavity. The ribs and spine form the sides and top, while the diaphragm acts as the floor.

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15
Q

What muscles assist in the movement of the thoracic cage during breathing?

A

Two sets of intercostal muscles (internal and external) connect the ribs. Additional muscles like the sternocleidomastoids and scalenes extend from the head and neck to the sternum and first two ribs, aiding in respiratory movements.

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16
Q

What is the functional role of the thorax?

A

Functionally, the thorax acts as a sealed container with membranous sacs: one pericardial sac for the heart and two pleural sacs, each surrounding a lung. It also allows passage for the esophagus, thoracic blood vessels, and nerves.

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17
Q

Describe the structure and position of the lungs within the thoracic cavity.

A

The lungs are light, spongy organs that nearly fill the thoracic cavity, resting on the diaphragm. They connect to the trachea via semi-rigid bronchi and are encased in double-walled pleural sacs

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18
Q

What is the structure and function of the pleural sacs surrounding the lungs?

A

Each lung is encased in a pleural sac with double-walled membranes lined with elastic connective tissue and capillaries. Pleural fluid between the membranes allows lung movement, holds the lungs tight against the thoracic wall, and keeps them partially inflated.

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19
Q

What is the purpose of pleural fluid in the respiratory system?

A

Pleural fluid lubricates the space between the pleural membranes, allowing them to slide easily during breathing. It also creates a cohesive force that keeps the lungs expanded against the thoracic wall, similar to two wet glass panes sticking together.

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20
Q

How does air enter the respiratory system and what is the role of the pharynx?

A

Air enters through the mouth and nose, passing into the pharynx, which serves as a common pathway for food, liquids, and air, connecting to the larynx and trachea

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21
Q

What are the functions of the larynx and vocal cords in the respiratory system?

A

The larynx directs air into the trachea and houses the vocal cords, which vibrate to create sound when air passes through them.

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22
Q

Describe the structural features of the trachea.

A

The trachea is a semiflexible tube supported by 15 to 20 C-shaped cartilage rings, ensuring it remains open for air passage into the primary bronchi.

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23
Q

Explain the branching pattern of the bronchial tree within the lungs.

A

The trachea divides into primary bronchi, which branch into smaller bronchi and then into bronchioles, ending in respiratory bronchioles that connect to the alveoli.

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24
Q

How does the diameter of airways change from the trachea to the bronchioles, and what is its effect on air flow?

A

Airway diameter decreases from the trachea to the bronchioles, but the total cross-sectional area increases due to the geometric rise in the number of airways, decreasing the velocity of air flow as it progresses deeper into the lungs.

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25
Q

Compare the changes in airway cross-sectional area with changes in the circulatory system.

A

Similar to the increase in cross-sectional area from the aorta to the capillaries in the circulatory system, the respiratory system increases in total cross-sectional area from the trachea to the bronchioles, reducing air flow velocity analogous to blood flow.

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26
Q

What are the three components of air conditioning in the respiratory system?

A

The three components are warming the air to body temperature, adding water vapor to reach 100% humidity, and filtering out foreign material to protect the alveoli.

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27
Q

How are inhaled air warmed and humidified in the respiratory system?

A

Air is warmed by heat from the body and humidified by water evaporating from the mucosal lining of the airways, reaching 100% humidity and 37 °C by the time it enters the trachea.

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28
Q

What is the difference in air conditioning between breathing through the mouth and the nose?

A

Breathing through the nose is more effective in warming and humidifying air than mouth breathing, which can cause chest ache from cold air when exercising in cold weather.

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29
Q

Describe the air filtration mechanism in the trachea and bronchi.

A

Air is filtered through ciliated epithelium, which traps particles in a mucus layer moved by the cilia in an upward motion toward the pharynx, a system known as the mucociliary escalator.

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30
Q

How do mucus and cilia contribute to protecting the respiratory system?

A

Mucus secreted by goblet cells traps particles and pathogens, which are then moved by cilia through the mucociliary escalator toward the pharynx for expulsion or swallowing.

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31
Q

How does cystic fibrosis affect the mucociliary escalator and airway conditioning?

A

Cystic fibrosis leads to inadequate ion secretion, reducing the watery saline layer essential for cilia function. This results in thick, sticky mucus that traps cilia and prevents mucus clearance, increasing the risk of lung infections.

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32
Q

What is the primary function of the alveoli in the lungs?

A

The primary function of the alveoli is the exchange of gases between the air in the lungs and the blood, facilitated by their air-filled structure.

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33
Q

Describe the characteristics and role of Type I alveolar cells.

A

Type I alveolar cells make up about 95% of the alveolar surface area and are very thin, optimizing them for rapid gas diffusion. They are primarily responsible for the gas exchange function of the alveoli.

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34
Q

What is the function of Type II alveolar cells?

A

Type II alveolar cells synthesize and secrete surfactant, which reduces surface tension and aids lung expansion during breathing. They also help minimize fluid in the alveoli by transporting solutes and water out of the alveolar air space.

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35
Q

How is the alveolar structure adapted to facilitate gas exchange with the blood?

A

The alveolar walls are extremely thin and closely associated with an extensive network of capillaries, allowing for efficient gas exchange due to minimal diffusion distances between air and blood.

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36
Q

What is the role of elastic and collagen fibers in the lungs?

A

Elastic and collagen fibers in the connective tissue between alveolar cells provide elastic recoil, helping the lungs return to their original shape after being stretched during inhalation.

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37
Q

Explain the interaction between the respiratory and cardiovascular systems at the alveoli.

A

The alveoli are embedded within a dense network of capillaries. This close proximity ensures that the capillary blood can rapidly exchange gases with the air in the alveoli, demonstrating the tight integration of these two systems for optimal gas exchange.

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38
Q

What is the pulmonary circulation and where does it begin?

A

The pulmonary circulation begins with the pulmonary trunk, which receives low-oxygen blood from the right ventricle. It includes the journey of blood through the lungs where it is oxygenated, and back to the heart.

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39
Q

How are the pulmonary arteries and veins structured in relation to the lungs?

A

The pulmonary trunk divides into two pulmonary arteries, one for each lung. Oxygenated blood returns to the left atrium via pulmonary veins, ensuring efficient gas exchange in the lungs.

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40
Q

How much blood is contained within the pulmonary circulation?

A

About 0.5 liters, which is 10% of the total blood volume. Approximately 75 mL is in the capillaries for gas exchange, with the remainder in the pulmonary arteries and veins.

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41
Q

How does the rate of blood flow through the lungs compare to other tissues?

A

The blood flow rate through the lungs is exceptionally high at 5 L/min, equal to the entire cardiac output of the right ventricle, ensuring that as much blood flows through the lungs in one minute as through the rest of the body.

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42
Q

What are the characteristics of pulmonary arterial pressure?

A

Pulmonary arterial pressure averages 25/8 mm Hg, significantly lower than systemic arterial pressure, due to the low resistance in pulmonary circulation.

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43
Q

Why is the resistance in the pulmonary circulation low?

A

The low resistance is due to the shorter total length of the pulmonary vessels and the distensibility and large cross-sectional area of pulmonary arterioles.

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44
Q

How does the lymphatic system affect the pulmonary circulation?

A

The lymphatic system efficiently removes filtered fluid from the lung interstitial space, keeping interstitial fluid volume minimal and ensuring short distances for gas diffusion between alveoli and capillaries.

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45
Q

What is the primary difference between blood and air as fluids in physiological systems?

A

Blood is a noncompressible liquid, whereas air is a compressible mixture of gases. This affects how each behaves under pressure and during flow.

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46
Q

What units are used to measure air and blood pressure in respiratory physiology?

A

Pressure is typically reported in millimeters of mercury (mm Hg), but respiratory physiologists sometimes use centimeters of water (1 mm Hg = 1.36 cm H₂O) or kiloPascals (760 mm Hg = 101.325 kPa).

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47
Q

What convention do respiratory physiologists use for atmospheric pressure?

A

Atmospheric pressure at sea level is conventionally designated as 0 mm Hg in respiratory physiology to simplify comparisons of pressure differences during ventilation, regardless of altitude

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48
Q

How does air flow occur in ventilation?

A

Air flow results from pressure gradients, moving from areas of higher pressure to lower pressure. This bulk flow is facilitated by changes in thoracic cavity volume during breathing.

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49
Q

How does Boyle’s law relate to respiratory physiology?

A

Boyle’s law states that the pressure of a gas is inversely proportional to its volume (P₁V₁ = P₂V₂). In respiration, increasing chest volume decreases alveolar pressure (drawing air in), and decreasing it increases pressure (pushing air out).

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50
Q

What are the mechanisms by which gases move in and out of the lungs?

A

Gases move by bulk flow and diffusion. Bulk flow moves the entire gas mixture due to pressure changes, while diffusion moves individual gases down their partial pressure gradients.

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51
Q

How are the gas laws applied in respiratory physiology?

A

Gas laws govern the behavior of gases in the lungs and airways, explaining phenomena like the exchange of oxygen and carbon dioxide between alveoli and blood, based on pressure and volume changes.

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52
Q

What is Tidal Volume (V T)?

A

Tidal Volume is the amount of air moved during a single inspiration or expiration during quiet breathing, typically about 500 mL in a healthy adult.

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53
Q

How do you measure Inspiratory Reserve Volume and what does it represent?

A

Inspiratory Reserve Volume is the additional air inhaled after a normal inhalation. Measured by inhaling as much air as possible after a normal inhalation, averaging about 3000 mL in a 70-kg man.

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54
Q

What is Expiratory Reserve Volume and how is it measured?

A

Expiratory Reserve Volume is the amount of air that can be forcefully exhaled after the end of a normal expiration, averaging about 1100 mL in a healthy adult.

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55
Q

What is Residual Volume and why can’t it be directly measured?

A

Residual Volume is the air remaining in the lungs after maximal exhalation, about 1200 mL, which helps keep the lungs inflated against the chest wall. It cannot be measured directly by spirometry because it involves air that remains in the lungs after forceful exhalation.

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56
Q

Define Vital Capacity and how is it calculated?

A

Vital Capacity is the total amount of air that can be voluntarily moved in or out of the respiratory system with one breath. It is the sum of Inspiratory Reserve Volume, Tidal Volume, and Expiratory Reserve Volume.

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57
Q

What does Total Lung Capacity comprise?

A

Total Lung Capacity is the sum of Vital Capacity and Residual Volume. It represents the total volume of air the lungs can hold.

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58
Q

What are Inspiratory Capacity and Functional Residual Capacity?

A

Inspiratory Capacity is the total amount of air a person can inspire from a resting expiratory level, calculated as Tidal Volume plus Inspiratory Reserve Volume. Functional Residual Capacity is the volume of air remaining in the lungs after a normal exhalation, calculated as Expiratory Reserve Volume plus Residual Volume.

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59
Q

What creates the pressure gradient necessary for breathing?

A

Muscle contraction in the thoracic cage and diaphragm expands the lungs, creating a negative pressure inside the chest relative to atmospheric pressure, which draws air into the lungs.

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60
Q

How does Boyle’s Law explain the movement of air in and out of the lungs?

A

Boyle’s Law states that the pressure of a gas is inversely proportional to its volume. During inhalation, lung volume increases, decreasing internal pressure below atmospheric pressure, drawing air in. During exhalation, lung volume decreases, increasing pressure, and pushing air out.

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61
Q

Which muscles are primarily involved in quiet breathing?

A

The diaphragm, external intercostals, and scalene muscles are the primary muscles involved in quiet breathing, contracting to increase the thoracic cavity’s volume and decrease its internal pressure.

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62
Q

What happens during forced breathing?

A

During forced breathing, such as during intense exercise or blowing a balloon, additional chest and abdominal muscles are recruited to increase the volume change and pressure gradient for greater air movement.

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63
Q

What is the formula that describes airflow in the respiratory system?

A

Airflow (∆P/R) is directly proportional to the pressure gradient (∆P) and inversely proportional to the resistance (R) in the respiratory pathways.

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64
Q

What factors can increase resistance in the respiratory system?

A

Resistance can increase due to narrowed or obstructed airways, such as from inflammation, mucus buildup, or structural changes, which impedes airflow and requires greater pressure gradients to maintain air movement.

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65
Q

Describe the diaphragm’s mechanical action and its impact on thoracic volume during quiet breathing.

A

In quiet breathing, the diaphragm contracts, moving downwards approximately 1.5 cm towards the abdomen, thus increasing the thoracic volume significantly. This diaphragmatic movement is responsible for 60% to 75% of the volume change during inspiration, making it the primary driver of air intake

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66
Q

How do the external intercostal and scalene muscles contribute to thoracic expansion during inspiration?

A

The external intercostal and scalene muscles contract to elevate the ribs upwards and outwards. This action enlarges the thoracic cavity in both the vertical and lateral dimensions, accounting for 25-40% of the volume change during inspiration, complementing the diaphragm’s function.

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67
Q

What is the revised understanding of the scalene muscles’ role in quiet breathing?

A

Recent studies have revealed that scalene muscles actively participate in quiet breathing by lifting the sternum and the upper ribs. This action prevents the lower ribs from moving inward during diaphragmatic contraction, ensuring an efficient increase in thoracic volume.

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68
Q

What is the current understanding of the role of external intercostal muscles in breathing?

A

The external intercostal muscles are now understood to play a minor role in quiet breathing but become increasingly important in elevating rib cage expansion during more forceful respiratory activities like deep breathing or physical exertion.

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69
Q

What is the alveolar pressure just before inspiration begins?

A

Just before inspiration starts, alveolar pressure is at atmospheric level, assigned a value of 0 mm Hg. This equilibrium state where alveolar and atmospheric pressures are equal ensures that there is no air flow into the lungs at this moment.

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70
Q

Describe the changes in alveolar pressure at the onset of inspiratory muscle contraction.

A

As inspiratory muscles contract, thoracic volume begins to increase around Time 0 to 2 seconds. This volume increase causes alveolar pressure to decrease to about -1 mm Hg below atmospheric pressure (point A2), initiating the flow of air into the lungs.

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71
Q

When does alveolar pressure reach its minimum during inspiration, and what is this pressure?

A

Midway through the inspiration phase, approximately 1 second after the onset, alveolar pressure reaches its lowest point, slightly more negative than -1 mm Hg. This lowest pressure corresponds with the maximum rate of air entering the lungs.

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72
Q

What happens to alveolar pressure at the end of the inspiratory phase?

A

By the end of inspiration, as the thoracic volume expansion ceases (around 2 seconds), alveolar pressure rises back to equal atmospheric pressure (0 mm Hg). Airflow stops because the pressure gradient between the atmosphere and the alveoli has been neutralized.

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73
Q

Explain the significance of alveolar pressure equilibration at the end of inspiration.

A

The equilibration of alveolar pressure with atmospheric pressure marks the completion of the inspiratory phase. It ensures that no more air enters the lungs until the next cycle of inspiration begins, maintaining the rhythmic pattern of breathing.

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74
Q

How can you practically demonstrate that alveolar pressure equilibrates with atmospheric pressure at the end of inspiration?

A

By inhaling deeply and then abruptly stopping any further chest or diaphragm movement without holding the breath, you will notice that air flow ceases almost instantly. This cessation demonstrates that alveolar pressure has reached atmospheric level, stopping the airflow.

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75
Q

What initiates passive expiration in the respiratory system?

A

Passive expiration begins when impulses from somatic motor neurons to the inspiratory muscles cease, allowing these muscles to relax. This relaxation triggers the elastic recoil of the lungs and thoracic cage, returning the diaphragm and rib cage to their pre-inspiration positions.

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76
Q

How does the volume and pressure of the lungs change during passive expiration?

A

During passive expiration, the volume of the lungs and thoracic cage decreases due to elastic recoil. This decrease in volume leads to an increase in air pressure inside the lungs. When alveolar pressure surpasses atmospheric pressure, air flows out of the lungs.

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77
Q

What are the specific changes in alveolar pressure during passive expiration, and how long does this phase last?

A

Passive expiration typically occurs from 2 seconds to 4 seconds. Alveolar pressure rises to about 1 mm Hg above atmospheric pressure, facilitating the reversal of air flow out of the lungs. By 4 seconds, alveolar pressure equalizes with atmospheric pressure, halting air movement and marking the end of the respiratory cycle.

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78
Q

Which muscles are involved in active expiration, and what actions do they perform?

A

Active expiration, necessary during vigorous activities or forced breathing, involves the internal intercostal muscles and the abdominal muscles. The internal intercostals help decrease thoracic volume by pulling the ribs inward. Abdominal muscles contract to compress the abdominal cavity, pushing the diaphragm upwards and further reducing lung volume.

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79
Q

How can neuromuscular diseases affect respiratory ventilation?

A

Neuromuscular diseases like myasthenia gravis and poliomyelitis can weaken or paralyze the respiratory muscles, reducing ventilation efficiency. This leads to diminished air exchange, impaired cough reflex, and increased risk of respiratory infections.

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80
Q

What is ventilation, and how is it facilitated in the human body?

A

Ventilation, or breathing, involves the bulk flow exchange of air between the atmosphere and the alveoli. It requires movement of the lungs in association with the thoracic cage. The lungs, encased in fluid-filled pleural sacs, adhere to the thoracic cage due to cohesive forces in the intrapleural fluid. This adhesion allows the lungs to move with the thoracic expansions and contractions during breathing.

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81
Q

What creates subatmospheric intrapleural pressure, and what is its significance?

A

Subatmospheric intrapleural pressure is created during fetal development when the thoracic cage grows more rapidly than the lungs, stretching the lungs to conform to the thoracic volume. This pressure, typically around -3 mm Hg, is crucial as it helps the lungs to adhere tightly to the thoracic wall, facilitating their expansion during inspiration.

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82
Q

What is pneumothorax, and how can it affect lung function?

A

Pneumothorax occurs when air enters the pleural cavity due to trauma or spontaneous events like a ruptured congenital bleb. This disrupts the fluid bond between the lung and chest wall, causing the lung to collapse (like a deflated balloon) and fail to function properly. Treatment involves removing air from the pleural cavity and sealing any openings

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83
Q

How does intrapleural pressure change throughout the respiratory cycle?

A

Intrapleural pressure starts around -3 mm Hg and becomes more negative during inspiration (down to -6 mm Hg or lower during deep breaths) as the lungs expand against the elastic recoil. During expiration, as the lungs recoil to a resting state, the pressure returns to approximately -3 mm Hg, maintaining a subatmospheric level to keep the lungs inflated.

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84
Q

How does the syringe analogy explain the mechanics of intrapleural pressure?

A

A syringe filled with water and sealed can mimic the thoracic cavity’s mechanics. Pulling the plunger (like the diaphragm during inspiration) creates a negative pressure that resists further pulling, similar to lung expansion against elastic recoil. Releasing the plunger mimics expiration, showing how lung volume and pressure return to baseline.

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85
Q

How much energy does the body normally use for quiet breathing, and how does this change during exercise?

A

Normally, about 3–5% of the body’s total energy expenditure is dedicated to quiet breathing. This percentage increases substantially during exercise, reflecting the greater demand for oxygen and the increased effort required to move larger volumes of air.

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86
Q

What are the two main factors that influence the work required for breathing?

A

The work of breathing is primarily influenced by the stretchability (compliance) of the lungs and the resistance of the airways to airflow. These factors determine how much force the respiratory muscles need to exert during the breathing process.

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87
Q

What is lung compliance, and how is it clinically relevant?

A

Lung compliance measures the ease with which the lungs can be expanded, calculated as the change in lung volume (∆V) per unit of pressure change (∆P). High compliance indicates that the lungs stretch easily, requiring less force to expand. Low compliance, conversely, means the lungs are stiff and more force is needed for expansion. Compliance is critical in diagnosing and managing respiratory conditions.

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88
Q

What is elastance, and how does it affect expiration?

A

Elastance is the ability of the lungs to resist deformation and return to their original shape after being stretched. It’s the reciprocal of compliance. High elastance means the lung effectively returns to its resting state after expansion, aiding passive expiration. Low elastance, as seen in conditions like emphysema, results in ineffective passive expiration, requiring active effort to expel air.

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89
Q

How does emphysema affect lung compliance and elastance?

A

Emphysema destroys the elastin fibers in lung tissue, leading to high compliance (easy to stretch lungs) but low elastance (poor recoil). This alteration means that although lungs can inflate easily, they don’t effectively recoil during expiration. Patients often need to actively use their expiratory muscles to force air out, similar to squeezing air out of an inflated plastic bag.

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90
Q

What role does surface tension play in the mechanics of lung expansion?

A

Surface tension in the lungs is created by the thin fluid layer between alveolar cells and the air, and contributes significantly to the resistance to lung stretch. It acts like a thin membrane being stretched at the air-fluid interface, increasing the work needed to expand the lungs.

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91
Q

How does the law of LaPlace relate to alveolar pressure?

A

The law of LaPlace describes how the pressure inside a fluid-lined sphere (like an alveolus) is influenced by surface tension and radius, with the equation
𝑃 = 2𝑇 / 𝑟 . It predicts that smaller alveoli would have higher inward pressure and thus require more force to expand, compared to larger alveoli, if all else is equal.

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92
Q

What is surfactant and how does it affect lung function?

A

Surfactant is a mixture of proteins and phospholipids that reduces the surface tension of alveolar fluid, decreasing the lung’s resistance to stretch and equalizing pressure among alveoli of different sizes. This reduction in surface tension facilitates easier and less energy-intensive lung expansion during breathing.

93
Q

What is the clinical significance of surfactant in newborns?

A

Adequate surfactant production is crucial for normal lung function at birth. Premature babies may lack sufficient surfactant and develop newborn respiratory distress syndrome (NRDS), characterized by stiff lungs and difficulty breathing due to alveolar collapse during exhalation. Treatment can involve artificial surfactant administration and positive-pressure ventilation.

94
Q

How is the production of surfactant stimulated in fetuses at risk of premature birth?

A

If there is a risk of premature birth and the fetus has insufficient surfactant, a mother may be administered glucocorticoids to stimulate the maturation of the fetal alveolar type II cells, which are responsible for surfactant production. This treatment enhances the chances of adequate surfactant levels at birth.

95
Q

What are the main parameters that contribute to resistance in the respiratory system?

A

The main parameters influencing resistance in the respiratory system, as per Poiseuille’s law, are the length of the respiratory system (L), the viscosity of air (η), and the radius of the airways (r). However, length and viscosity are relatively constant, making the airway radius the primary determinant of airway resistance.

96
Q

How does the radius of airways influence resistance to air flow?

A

The radius of airways significantly impacts resistance; narrower airways increase resistance and vice versa. Nearly 90% of airway resistance is attributed to the trachea and bronchi due to their smaller total cross-sectional area compared to other parts of the airway like the bronchioles.

97
Q

What roles do bronchioles play in airway resistance?

A

Bronchioles normally do not contribute significantly to airway resistance because of their large total cross-sectional area. However, their collapsibility can cause a significant increase in resistance if their diameter decreases, particularly during bronchoconstriction.

98
Q

How do paracrine signals affect bronchiolar diameter?

A

Paracrine signals like carbon dioxide and histamine significantly affect bronchiolar diameter. CO2 relaxes bronchiolar smooth muscle, causing bronchodilation. Histamine, released during allergic reactions, acts as a powerful bronchoconstrictor, increasing resistance and potentially leading to breathing difficulties.

99
Q

What is the primary neural control of the bronchioles and how does it influence airway resistance?

A

The primary neural control of bronchioles comes from parasympathetic neurons, which cause bronchoconstriction to protect against inhaled irritants. Although there is no significant sympathetic innervation, the smooth muscles in bronchioles have beta-2 adrenergic receptors that respond to epinephrine, causing bronchodilation, which is used therapeutically in asthma treatments.

100
Q

What is total pulmonary ventilation and how is it calculated?

A

Total pulmonary ventilation, also known as minute volume, is the volume of air moved into and out of the lungs each minute. It is calculated by multiplying the ventilation rate by the tidal volume. For an adult at a slow ventilation rate of 12 breaths per minute with a typical tidal volume of 500 mL, the total pulmonary ventilation equals 6 L/min (12 br/min * 500 mL/br).

101
Q

What is the anatomical dead space in the respiratory system?

A

Anatomical dead space is the part of each breath that remains in the conducting airways (like the trachea and bronchi) and does not participate in gas exchange with the blood. It averages about 150 mL in adults.

102
Q

How does anatomical dead space affect the efficiency of ventilation?

A

Anatomical dead space reduces the efficiency of ventilation because the air that fills this space does not reach the alveoli and therefore doesn’t participate in gas exchange. During a typical respiratory cycle, only 350 mL of the 500 mL tidal volume effectively participates in gas exchange after accounting for the 150 mL dead space.

103
Q

What is alveolar ventilation and how is it calculated?

A

Alveolar ventilation is the volume of fresh air that reaches the alveoli each minute, providing a more accurate measure of ventilation efficiency. It is calculated by subtracting the dead space volume from the tidal volume and then multiplying by the ventilation rate. Using a dead space of 150 mL, alveolar ventilation is 4.2 L/min (12 br/min * (500 mL - 150 mL)).

104
Q

How can changes in breathing rate and depth affect alveolar ventilation?

A

Changes in breathing rate and depth significantly affect alveolar ventilation. Increasing either rate or depth will increase the volume of fresh air reaching the alveoli, enhancing the efficiency of gas exchange. For example, during maximum voluntary ventilation, total pulmonary ventilation can increase to as much as 170 L/min.

105
Q

What maintains the stability of alveolar P_O2 and P_CO2 during normal quiet breathing?

A

During normal quiet breathing, alveolar P_O2 remains around 100 mm Hg and P_CO2 stays near 40 mm Hg. This stability is maintained because the amount of oxygen entering the alveoli with each breath is approximately equal to the amount of oxygen taken up by the blood. Additionally, the volume of fresh air entering the lungs with each breath is only about 10% of the total lung volume, minimizing swings in gas concentrations

106
Q

How does hyperventilation affect alveolar P_O2 and P_CO2?

A

During hyperventilation, alveolar ventilation increases, which leads to an increase in alveolar P_O2 and a decrease in alveolar P_CO2. This is because more fresh air containing higher concentrations of oxygen is brought into the alveoli, and more carbon dioxide is expelled from the alveoli than is produced by the body, lowering its partial pressure.

107
Q

How does hypoventilation affect alveolar P_O2 and P_CO2?

A

Hypoventilation reduces alveolar ventilation, causing alveolar P_O2 to decrease and P_CO2 to increase. This occurs because less fresh air reaches the alveoli, reducing the input of oxygen and slowing the removal of carbon dioxide, which accumulates as less is expelled with each breath.

108
Q

Why are changes in alveolar ventilation important for pH homeostasis?

A

Changes in alveolar ventilation significantly impact blood pH by altering P_CO2 levels. Increased P_CO2 in the blood due to hypoventilation leads to higher carbonic acid concentrations, decreasing pH (acidosis). Conversely, hyperventilation reduces P_CO2, lowering carbonic acid levels and increasing pH (alkalosis). The body can adjust ventilation rates to help regulate pH in response to varying metabolic demands.

109
Q

What is the primary purpose of pulmonary blood flow (perfusion) in the context of external respiration?

A

Pulmonary blood flow, or perfusion, is crucial for transporting blood past the alveoli to pick up available oxygen after it has been moved from the atmosphere to the alveolar exchange surface. Effective gas exchange across the alveolar-capillary interface requires not just adequate ventilation but also sufficient perfusion to carry the oxygen into the systemic circulation.

110
Q

How does the body match ventilation with perfusion in the lungs?

A

The body matches ventilation (air flow) and perfusion (blood flow) through local regulation of both arterioles and bronchioles in each lung section. Bronchiolar diameter adjusts based on CO2 levels in exhaled air, with higher P_CO2 causing dilation and lower P_CO2 causing constriction. Pulmonary arteriolar resistance is primarily influenced by the oxygen content in the surrounding interstitial fluid, with low P_O2 causing arteriolar constriction.

111
Q

How do pulmonary capillaries respond to changes in blood pressure?

A

Pulmonary capillaries are unique in that they are collapsible. If blood pressure within these capillaries drops below a certain threshold, they close off, diverting blood to capillary beds with higher pressure. This feature is crucial during activities like exercise, when closed capillary beds in the lung’s apex can open to accommodate increased blood flow, enhancing oxygenation.

112
Q

How does local vasoconstriction in the lungs differ in response to low P_O2 compared to systemic circulation?

A

Unlike systemic circulation, where a decrease in tissue P_O2 causes arterioles to dilate to increase oxygen delivery, in the lungs, a decrease in P_O2 due to poor alveolar ventilation causes pulmonary arterioles to constrict. This vasoconstriction diverts blood away from poorly ventilated alveoli to areas with better ventilation, optimizing oxygen uptake.

113
Q

What limits the effectiveness of local control mechanisms in regulating lung air and blood flow?

A

Local control mechanisms in the lungs can be ineffective if there are significant obstructions that affect large portions of the lung. For example, if a pulmonary artery is blocked or if there’s a large airway obstruction, local responses cannot adequately compensate by redirecting air or blood flow, leading to significant impairments in gas exchange.

114
Q

What is the purpose of auscultation in pulmonary diagnostics?

A

Auscultation of breath sounds is a crucial non-invasive diagnostic tool in pulmonary medicine, used to assess lung function by listening to the sounds of breathing. Normal breath sounds are even and resemble a quiet “whoosh.” Abnormal sounds, such as wheezes, crackles, and pops, indicate disturbances like fluid in the lungs or inflammation of the pleural membranes.

115
Q

What distinguishes obstructive lung diseases in terms of airflow and respiratory sounds?

A

Obstructive lung diseases are characterized by reduced airflow due to increased airway resistance. Common symptoms include wheezing and difficulty exhaling fully. Conditions such as asthma, COPD (chronic bronchitis and emphysema), and obstructive sleep apnea fall under this category, where narrowed airways increase resistance and potentially lead to airway collapse during forced expiration.

116
Q

How does restrictive lung disease affect lung function differently than obstructive lung disease?

A

Restrictive lung diseases decrease lung compliance, making the lungs stiffer and harder to inflate. This requires greater effort from respiratory muscles, increasing the energy needed for breathing. Common causes include fibrotic tissue formation and reduced surfactant. Diseases like pulmonary fibrosis lead to stiff lung tissue, significantly hindering lung expansion.

117
Q

How is the Forced Vital Capacity (FVC) test used to differentiate between obstructive and restrictive lung diseases?

A

The FVC test measures the total volume of air exhaled during a forced breath and the speed of exhalation (FEV1, or forced expiratory volume in 1 second). In obstructive lung disease, FEV1 decreases more than FVC, lowering the FEV1/FVC ratio. In restrictive lung disease, both FEV1 and FVC decrease proportionally, so the FEV1/FVC ratio remains unchanged. Normally, the FEV1/FVC ratio is 80% or more.

118
Q

What are the typical changes in breath sounds that indicate pulmonary abnormalities?

A

Changes in breath sounds can indicate various pulmonary issues. Diminished or absent breath sounds may suggest pneumothorax. Squeaks and wheezes indicate narrowed airways typical of asthma or COPD. Bubbling sounds suggest fluid in the airways or alveoli, while a friction rub indicates inflamed pleural surfaces rubbing against each other.

119
Q

What are the key mechanisms of acclimatization to high altitudes like Mt. Everest?

A

Acclimatization to high altitudes involves several physiological adjustments to cope with decreased oxygen availability:

  1. Increased Ventilation: Breathing rate and depth increase to boost oxygen intake and carbon dioxide expulsion.
  2. Hematologic Changes: The body produces more red blood cells to improve oxygen delivery to tissues.
  3. Cellular Adaptations: Cells enhance their ability to use oxygen more efficiently and increase the capacity for anaerobic metabolism.
  4. Increased Capillary Density: The body may develop additional capillaries to facilitate oxygen delivery to tissues.
120
Q

How are plasma gas concentrations commonly expressed by respiratory physiologists and why?

A

Respiratory physiologists commonly express plasma gas concentrations in partial pressures to indicate concentration gradients between the alveoli and the blood, facilitating understanding of gas movement based on differential pressures.

121
Q

What is the normal partial pressure of oxygen (P O2) in the alveoli at sea level, and how does it compare to venous blood?

A

At sea level, the normal partial pressure of oxygen in the alveoli (P O2) is about 100 mm Hg. This is higher than in “deoxygenated” venous blood arriving at the lungs, which has a P O2 of about 40 mm Hg, creating a gradient that drives oxygen into the blood.

122
Q

How does oxygen move from the alveoli into the blood?

A

Oxygen diffuses from the alveoli into the blood down its partial pressure gradient, moving from a higher P O2 in the alveoli (100 mm Hg) to a lower P O2 in the capillary blood (40 mm Hg) until equilibrium is reached.

123
Q

Describe the partial pressure gradient for oxygen between arterial blood and body cells.

A

Oxygen diffuses from arterial blood (P O2 of 100 mm Hg) into body cells (P O2 of 40 mm Hg) where it is used for metabolic processes. This diffusion continues until the oxygen partial pressures equilibrate.

124
Q

How is CO2 exchanged between body tissues and the blood?

A

CO2 diffuses from body cells (higher P CO2 of 46 mm Hg) into capillary blood (lower P CO2 of 40 mm Hg) due to metabolic production of CO2. The diffusion equalizes the P CO2 across the systemic capillaries and tissues.

125
Q

What happens to CO2 levels in the blood as it moves through pulmonary capillaries?

A

In pulmonary capillaries, CO2 diffuses from venous blood (higher P CO2 of 46 mm Hg) into the alveoli (lower P CO2 of 40 mm Hg) due to a favorable gradient. This process reduces the blood’s P CO2 to match that of the alveolar P CO2 by the time blood leaves the lungs.

126
Q

What factors influence the efficiency of alveolar gas exchange?

A

The efficiency of alveolar gas exchange depends on: 1) Adequate oxygen reaching the alveoli, 2) effective gas transfer between alveoli and pulmonary capillaries, and 3) sufficient blood flow or perfusion of the alveoli.

127
Q

What are possible causes of low alveolar P O2?

A

Low alveolar P O2 can result from either: 1) Inspired air having low oxygen content, often due to high altitude, or 2) inadequate alveolar ventilation (hypoventilation) due to physiological or pathological factors.

128
Q

How does altitude affect the partial pressure of oxygen in the air?

A

Altitude decreases atmospheric pressure, which in turn lowers the partial pressure of oxygen in the air. For example, at higher altitudes such as in Denver, the P O2 of atmospheric air is significantly lower than at sea level.

129
Q

What is alveolar ventilation and how can it affect alveolar P O2?

A

Alveolar ventilation refers to the volume of fresh air entering the alveoli. Inadequate alveolar ventilation, or hypoventilation, reduces the amount of oxygen available in the alveoli, leading to lower alveolar P O2.

130
Q

What are common causes of hypoventilation?

A

Hypoventilation can be caused by decreased lung compliance, increased airway resistance, or CNS depression affecting the respiratory rate and depth. In young people, CNS depression is often caused by alcohol poisoning or drug overdoses.

131
Q

Describe how water vapor pressure affects P O2 at high altitudes.

A

Water vapor pressure remains constant at different altitudes; however, because it constitutes a larger proportion of the total atmospheric pressure at higher altitudes, its effect on reducing the partial pressure of oxygen in the lungs is more pronounced.

132
Q

What factors determine the efficiency of gas exchange between the alveoli and blood?

A

Gas exchange efficiency is primarily determined by the available surface area, the concentration gradient of gases, barrier permeability, and the diffusion distance across the alveolar-capillary membrane.

133
Q

What are the primary pathological changes that can impair gas exchange in the lungs?

A

: Pathological changes that impair gas exchange include a reduction in alveolar surface area, thickening of the alveolar-capillary diffusion barrier, and an increase in the diffusion distance due to fluid accumulation.

134
Q

How does emphysema affect alveolar gas exchange?

A

In emphysema, alveolar surface area is reduced due to the destruction of elastic fibers and apoptosis of cells in the lungs, leading to fewer and larger alveoli, thus diminishing the surface available for gas exchange.

135
Q

What role does diffusion barrier permeability play in respiratory diseases?

A

In diseases like pulmonary fibrosis, scar tissue thickens the alveolar wall, reducing the permeability of the diffusion barrier and slowing the exchange of gases between the alveoli and blood.

136
Q

Explain how pulmonary edema affects gas exchange.

A

Pulmonary edema increases the diffusion distance by accumulating fluid in the interstitial space or alveoli, which hinders the efficient diffusion of gases and slows gas exchange.

137
Q

What are the consequences of severe pulmonary edema?

A

Severe pulmonary edema can lead to alveolar flooding, where fluid leaks into the alveoli, greatly thickening the fluid layer and impairing gas exchange, potentially leading to conditions like adult respiratory distress syndrome (ARDS).

138
Q

How does increased pulmonary blood pressure contribute to pulmonary edema?

A

Elevated pulmonary blood pressure can disrupt the normal filtration/reabsorption balance at the capillaries, leading to increased fluid filtration. If lymphatics cannot remove this excess fluid efficiently, it accumulates in the pulmonary interstitial space, contributing to pulmonary edema.

139
Q

What factors influence the movement of gas molecules between air and a liquid?

A

The movement of gas molecules is directly proportional to the pressure gradient of the gas, the solubility of the gas in the liquid, and the temperature. Since temperature is relatively constant in mammals, the focus is primarily on pressure gradients and solubility.

140
Q

How does gas solubility affect the equilibrium of gas between air and water?

A

Gas solubility determines how much gas dissolves in water at a given partial pressure. If a gas has high solubility, it dissolves more readily at lower pressures; conversely, gases with low solubility require higher pressures to dissolve in significant amounts.

141
Q

Compare the solubility of oxygen and carbon dioxide in water.

A

Oxygen has low solubility in water, requiring high partial pressures to achieve significant dissolution. Carbon dioxide is about 20 times more soluble than oxygen, allowing more CO2 to dissolve in water at the same partial pressure.

142
Q

Why is oxygen’s low solubility significant in physiological contexts?

A

Oxygen’s low solubility means that very little can be carried dissolved in plasma and it crosses diffusion barriers more slowly. This is particularly evident in conditions like pulmonary edema, where the increased diffusion distance further slows oxygen transfer to blood, potentially leading to decreased arterial P O2 even if alveolar P O2 is normal.

143
Q

How does the solubility of carbon dioxide affect its exchange in the lungs compared to oxygen?

A

Due to its higher solubility, carbon dioxide can diffuse more easily and rapidly into body fluids, making its exchange less susceptible to increased diffusion distances. This is why, in cases of pulmonary edema, arterial P CO2 might remain normal while P O2 decreases.

144
Q

What is the impact of gas solubility on the treatment of pulmonary conditions?

A

Understanding gas solubility helps in managing conditions that affect gas exchange, such as pulmonary edema, by highlighting the need for interventions that consider the different behaviors of oxygen and carbon dioxide under various physiological conditions.

145
Q

How is oxygen transported from the lungs to the cells?

A

Oxygen is transported from the lungs to the cells primarily bound to hemoglobin in red blood cells. Although oxygen first dissolves in the plasma, the majority is carried in the blood via hemoglobin, which greatly increases the blood’s oxygen-carrying capacity.

146
Q

What is the role of erythrocytes in oxygen transport?

A

Erythrocytes, or red blood cells, contain hemoglobin, a protein that binds oxygen. Hemoglobin enables the transport of far more oxygen than could be dissolved in the plasma alone, making erythrocytes essential for efficient oxygen delivery to tissues.

147
Q

Define mass flow and its relevance to oxygen transport in the bloodstream.

A

Mass flow is the movement of a substance per unit time and is calculated as concentration times volume flow. For oxygen, this involves multiplying the oxygen content of arterial blood by the cardiac output to determine how much oxygen is transported to the cells per minute.

148
Q

How can oxygen consumption by the cells be calculated?

A

Oxygen consumption by the cells can be calculated using the principle of mass balance, which involves subtracting the oxygen content in venous blood leaving the cells from the oxygen content in arterial blood entering the cells.

149
Q

What is the Fick equation and what does it calculate?

A

The Fick equation, derived from the principles of mass flow and mass balance, calculates oxygen consumption (QO2) as: QO2 = CO * (arterial O2 content - venous O2 content). This equation can also be used to estimate cardiac output or oxygen consumption based on measurements of arterial and venous blood gases.

150
Q

Why is the transport of carbon dioxide different from oxygen in terms of solubility and movement?

A

Carbon dioxide is more soluble in blood than oxygen, which facilitates its movement from the tissues where it is produced into the plasma and red blood cells, allowing it to be efficiently expelled via the lungs. This difference in solubility affects the transport mechanisms and efficiency for each gas.

151
Q

What are the two components of oxygen transport in the blood?

A

Oxygen transport in the blood consists of oxygen that is dissolved in the plasma (P O2) and oxygen that is bound to hemoglobin (Hb). Dissolved oxygen accounts for less than 2% of total oxygen, while over 98% is carried by hemoglobin.

152
Q

Why is hemoglobin considered an effective oxygen carrier?

A

Hemoglobin is effective because it can reversibly bind oxygen through its iron-containing heme groups. Each hemoglobin molecule can bind up to four oxygen molecules, facilitating efficient oxygen transport and release as needed by body tissues.

153
Q

What is the molecular structure of hemoglobin?

A

Hemoglobin is a tetramer composed of four globular protein chains, each centered around a heme group that contains an iron atom. The iron atom in each heme group can bind one oxygen molecule, allowing a single hemoglobin molecule to carry up to four oxygen molecules.

154
Q

How does the bonding between hemoglobin and oxygen work?

A

The bond between hemoglobin and oxygen is weak and reversible, which allows oxygen to be easily picked up in the lungs and then released to tissues where it is needed without altering the structure of either hemoglobin or oxygen.

155
Q

What is oxyhemoglobin?

A

Oxyhemoglobin (HbO2) is the form of hemoglobin that has oxygen bound to it. It forms when oxygen molecules interact with the iron atoms in the heme groups of hemoglobin. Oxyhemoglobin transports oxygen from the lungs to the tissues.

156
Q

How is the binding capacity of hemoglobin represented, and why is this significant?

A

The binding capacity of hemoglobin is often represented as HbO2, although it can vary from one to four oxygen molecules per hemoglobin molecule (Hb(O2)1-4). This variability allows for flexibility in oxygen delivery depending on the body’s metabolic demands.

157
Q

How does the hemoglobin-oxygen binding reaction obey the law of mass action?

A

According to the law of mass action, as the concentration of free oxygen (O2) increases, more oxygen binds to hemoglobin, shifting the equation
𝐻𝑏 + 𝑂2 ⇌ 𝐻𝑏𝑂2 to the right to form more oxyhemoglobin (HbO2). Conversely, if the concentration of O2 decreases, the reaction shifts to the left, and hemoglobin releases oxygen.

158
Q

What role does dissolved oxygen in plasma play in oxygen transport?

A

Dissolved oxygen in plasma serves as the immediate source of oxygen for hemoglobin binding inside red blood cells. It reflects the partial pressure of oxygen (PO2) in the plasma, facilitating the rapid transfer of oxygen from alveoli to hemoglobin.

159
Q

Describe the process of oxygen transfer from the alveoli to hemoglobin.

A

Oxygen first dissolves in the plasma of the pulmonary capillaries after diffusing from the alveoli. It then diffuses into red blood cells and binds to hemoglobin. This process occurs so rapidly that equilibrium is normally reached, allowing maximal oxygen uptake based on plasma PO2 and red blood cell availability.

160
Q

How does oxygen unloading from hemoglobin occur at the tissues?

A

In systemic capillaries, dissolved oxygen diffuses out into body cells, which generally have a lower PO2. This reduction in plasma PO2 shifts the
𝐻𝑏 + 𝑂2 ⇌ 𝐻𝑏𝑂2 equilibrium to the left, causing hemoglobin to release oxygen.

161
Q

How does cellular activity affect hemoglobin’s oxygen release?

A

Increased cellular activity lowers the PO2 of cells due to higher oxygen consumption. This decrease in PO2 enhances the unloading of oxygen from hemoglobin, as it shifts the hemoglobin binding equilibrium to favor oxygen release.

162
Q

What determines the efficiency of oxygen loading and unloading in the blood?

A

The efficiency of oxygen loading and unloading is determined by the PO2 in the environment (alveoli for loading, tissue for unloading) and the concentration of hemoglobin. The law of mass action dictates the dynamic balance between hemoglobin’s oxygenated and deoxygenated forms, ensuring adequate oxygen supply and release as needed.

163
Q

What is the role of hemoglobin in meeting the oxygen demands of tissues?

A

Hemoglobin greatly enhances the oxygen-carrying capacity of blood. It binds oxygen in red blood cells and carries about 197 mL O2 per liter of blood, far surpassing the amount that could be carried by plasma alone

164
Q

Calculate the total oxygen delivery to tissues with normal hemoglobin levels.

A

With normal hemoglobin levels (197 mL O2/L blood) and a cardiac output of 5 L/min, the total oxygen delivery is 200 mL O2/L blood × 5 L blood/min = 1000 mL O2/min. This exceeds the resting oxygen consumption demand of 250 mL O2/min, providing a significant reserve.

165
Q

How much oxygen can dissolve in plasma, and what fraction of oxygen needs does this meet?

A

Only about 3 mL of O2 can dissolve in plasma per liter of arterial blood. With a cardiac output of 5 L/min, this equates to 15 mL O2/min delivered to tissues, which is insufficient alone, as it meets only a small fraction (6%) of the resting oxygen demand.

166
Q

Why is hemoglobin essential for survival given the low solubility of oxygen in plasma?

A

Hemoglobin is essential because it carries the bulk of oxygen—about 197 mL per liter of blood compared to only 3 mL dissolved in plasma. Without hemoglobin, the blood would not carry sufficient oxygen to sustain body functions, especially under conditions of increased oxygen demand like during exercise.

167
Q

How does the presence of hemoglobin in red blood cells affect oxygen reserves for increased demand?

A

Hemoglobin provides a buffer or reserve of oxygen, ensuring that even at rest, the blood carries four times the amount of oxygen needed by the tissues. This reserve is crucial for meeting increased oxygen demands during activities such as exercise.

168
Q

What factors determine the amount of oxygen that binds to hemoglobin?

A

The amount of oxygen that binds to hemoglobin depends primarily on the plasma PO2 surrounding the red blood cells and the number of available hemoglobin binding sites within those cells.

169
Q

How is the percent saturation of hemoglobin determined?

A

Percent saturation of hemoglobin, which indicates what percentage of hemoglobin binding sites are occupied by oxygen, is primarily determined by the plasma PO2. This reflects how effectively oxygen is being transported and utilized.

170
Q

What factors influence arterial PO2?

A

Arterial PO2 is influenced by the composition of inspired air, alveolar ventilation rate, and the efficiency of gas exchange from the alveoli to the blood.

171
Q

How can hemoglobin levels be clinically assessed?

A

Hemoglobin levels can be assessed by counting red blood cells and measuring the mean corpuscular hemoglobin (average amount of hemoglobin per red blood cell) or by measuring the total hemoglobin content in grams per deciliter of whole blood.

172
Q

What impact do pathological conditions have on oxygen transport?

A

Pathological conditions that decrease the amount of hemoglobin or the number of red blood cells can significantly impair the blood’s capacity to transport oxygen, affecting overall oxygen delivery to tissues.

173
Q

What are the limitations of saline infusions in treating severe blood loss?

A

While saline infusions can replace lost blood volume, they do not carry oxygen. Therefore, they cannot support cellular respiration adequately, unlike blood transfusions which restore both volume and oxygen-carrying capacity.

174
Q

What are artificial oxygen carriers and why are they significant?

A

Artificial oxygen carriers are being developed to replace hemoglobin and can be crucial in emergencies, such as large-scale disasters, where immediate blood type matching isn’t possible. These substitutes could potentially save lives by providing essential oxygen transport without the need for type-matched human blood.

175
Q

How does plasma P O2 influence the percent saturation of hemoglobin with oxygen?

A

Plasma P O2 is the primary factor that determines the percent saturation of hemoglobin. As P O2 increases, more oxygen binds to hemoglobin, increasing the percent saturation. Conversely, a decrease in P O2 causes hemoglobin to release oxygen, decreasing saturation.

176
Q

What analogy is used to explain hemoglobin’s oxygen-binding capacity?

A

Hemoglobin molecules are likened to students carrying books from an old library to a new one. Each student (hemoglobin molecule) can carry up to four books (oxygen molecules). The number of books a student carries (oxygen bound) depends on the librarian’s instructions (plasma P O2).

177
Q

What is the significance of the oxyhemoglobin saturation curve?

A

The oxyhemoglobin saturation curve, or dissociation curve, illustrates how hemoglobin’s oxygen binding changes with varying P O2 levels. It shows that hemoglobin is nearly saturated at normal alveolar P O2 (about 100 mm Hg) and remains highly saturated until P O2 significantly drops below 60 mm Hg.

178
Q

How does the shape of the saturation curve relate to oxygen delivery in the body?

A

The saturation curve is flat at higher P O2 levels, indicating that large changes in P O2 result in minor changes in saturation. The curve steepens as P O2 falls below 60 mm Hg, meaning small decreases in P O2 cause significant oxygen release, facilitating oxygen delivery where it’s needed most.

179
Q

How does the saturation curve behavior affect oxygen availability during exercise?

A

The steep portion of the curve between 60 mm Hg and 20 mm Hg P O2 is crucial during exercise. As muscular P O2 drops (due to increased consumption), hemoglobin releases a significant amount of oxygen, thus supporting higher metabolic activity.

180
Q

What is the physiological implication of hemoglobin remaining 75% saturated at a P O2 of 40 mm Hg?

A

At a P O2 of 40 mm Hg, typical of venous blood at rest, hemoglobin is still 75% saturated. This means that blood can release a significant amount of oxygen if required without depleting its reserve, ensuring that tissues have access to oxygen even under increased metabolic demands.

181
Q

What physiological changes can affect hemoglobin’s oxygen-binding affinity?

A

Changes in plasma pH, temperature, and PCO2 can significantly alter hemoglobin’s oxygen-binding affinity. Decreased pH, increased temperature, or increased PCO2 lower the affinity, shifting the oxygen-hemoglobin saturation curve to the right. Conversely, increases in pH or decreases in temperature and PCO2 shift the curve to the left.

182
Q

How does a shift in the oxygen-hemoglobin saturation curve affect oxygen delivery?

A

Shifts in the saturation curve affect oxygen delivery at the tissue level, particularly in the 20–40 mm Hg PO2 range. Such shifts ensure that oxygen binding at the lungs remains stable, while oxygen delivery to tissues is adjusted according to physiological needs.

183
Q

What is the Bohr effect and how does it relate to exercise?

A

The Bohr effect describes the shift in the hemoglobin saturation curve due to changes in pH. During intense exercise, increased anaerobic metabolism produces more H+, lowering blood pH and shifting the curve to the right. This facilitates greater oxygen release to active muscles.

184
Q

How does 2,3-bisphosphoglycerate (2,3-BPG) influence hemoglobin’s oxygen-binding affinity?

A

2,3-BPG decreases hemoglobin’s oxygen-binding affinity, shifting the saturation curve to the right. This shift is beneficial under conditions like high altitude or anemia, where oxygen availability is compromised.

185
Q

How does fetal hemoglobin differ from adult hemoglobin in terms of oxygen-binding affinity?

A

Fetal hemoglobin (HbF) has a higher oxygen-binding affinity compared to adult hemoglobin due to its gamma protein chains. This allows HbF to effectively pick up oxygen from maternal hemoglobin across the placenta, supporting fetal development.

186
Q

Why is understanding the factors that shift the hemoglobin saturation curve important in medicine?

A

Knowledge of what shifts the hemoglobin saturation curve is crucial for managing conditions that affect oxygen delivery, such as respiratory disorders, anemia, and during physiological stress like high-altitude exposure or intense physical activity.

187
Q

What percentage of CO2 in venous blood is dissolved directly in plasma, and what are the primary forms of CO2 transport?

A

Approximately 7% of the CO2 in venous blood is dissolved directly in plasma. The majority of CO2 is transported in two other forms: 23% binds to hemoglobin forming carbaminohemoglobin, and about 70% is converted into bicarbonate ions (HCO3-) within red blood cells.

188
Q

How is CO2 converted to bicarbonate ions in red blood cells?

A

CO2 diffuses into red blood cells and reacts with water in the presence of the enzyme carbonic anhydrase to form bicarbonate ions (HCO3-) and hydrogen ions (H+). This reaction helps transport CO2 to the lungs and buffers the blood against pH changes.

189
Q

What is the “chloride shift” in the context of CO2 transport?

A

The chloride shift is a mechanism where bicarbonate ions (HCO3-) are exchanged for chloride ions (Cl-) across the red blood cell membrane. This anion exchange helps maintain electrical neutrality within the red blood cells and facilitates the movement of HCO3- into plasma.

190
Q

How does hemoglobin contribute to CO2 removal and pH regulation in the blood?

A

Hemoglobin in red blood cells acts as a buffer by binding free hydrogen ions (H+). This buffering action is crucial in preventing large pH changes in the body, particularly under conditions of elevated blood PCO2, which can lead to respiratory acidosis.

191
Q

Describe the role of hemoglobin in the formation of carbaminohemoglobin

A

At the tissues, when oxygen dissociates from hemoglobin, CO2 binds to the exposed amino groups on the hemoglobin molecule to form carbaminohemoglobin (HbCO2). This process is enhanced by the presence of CO2 and H+, which decrease hemoglobin’s affinity for oxygen.

192
Q

What occurs during CO2 removal at the lungs?

A

In the lungs, CO2 diffuses from the blood into the alveoli due to a lower PCO2 in the alveoli. This causes the bicarbonate reaction in the red blood cells to shift, converting bicarbonate ions back to CO2, which then diffuses out of the red blood cells, helping to expel CO2 from the body.

193
Q

What initiates the contraction of skeletal muscles involved in breathing?

A

Skeletal muscle contraction for breathing is initiated by somatic motor neurons, which are controlled by a spontaneously firing network of neurons in the brain stem. Unlike autorhythmic cardiac muscles, skeletal muscles require external neural input to contract.

194
Q

What is the role of the respiratory network in the brain stem?

A

The respiratory network in the brain stem, acting as a central pattern generator, creates the rhythmic cycles of inspiration and expiration. This network includes spontaneously discharging neurons that likely function as pacemakers due to their unstable membrane potentials.

195
Q

How is the breathing pattern influenced?

A

Breathing pattern is largely dependent on the levels of CO2, O2, and H+ in arterial blood and extracellular fluid, monitored by chemoreceptors. These sensory inputs continuously influence the respiratory pattern.

196
Q

What does the contemporary model for the control of ventilation propose?

A

The contemporary model suggests that respiratory neurons in the medulla control inspiratory and expiratory muscles; neurons in the pons integrate sensory information and modulate medullary function; and the intrinsic rhythmic activity of a brainstem neural network dictates the rhythmic breathing pattern. Ventilation is also modulated by chemoreceptor- and mechanoreceptor-linked reflexes and higher brain centers.

197
Q

What are the main areas in the medulla oblongata involved in respiratory control, and what are their functions?

A

The main areas are the nucleus tractus solitarius (NTS), which houses the dorsal respiratory group (DRG) controlling inspiration, and the ventral respiratory group (VRG) with multiple regions managing different respiratory functions. The DRG directs muscles of inspiration via the phrenic and intercostal nerves, while VRG regions include the pre-Bötzinger complex, a potential respiratory rhythm pacemaker, and areas controlling active expiration and upper airway muscle tone.

198
Q

How does the pontine respiratory group influence respiratory rhythm?

A

The pontine respiratory groups, previously called the pneumotaxic center, receive sensory information from the DRG and provide tonic input to medullary networks. They play a crucial role in smoothing the respiratory rhythm by influencing the initiation and termination of inspiration.

199
Q

Describe the interaction between the dorsal and ventral respiratory groups in the medulla.

A

The dorsal respiratory group (DRG) primarily controls inspiration, sending signals to inspiratory muscles. The ventral respiratory group (VRG) contains neurons that are mostly inactive during quiet breathing but become crucial during forced breathing and active expiration, controlling accessory inspiratory muscles and muscles for active expiration.

200
Q

What role do sensory inputs from peripheral chemoreceptors and mechanoreceptors play in respiratory control?

A

Sensory information from peripheral chemoreceptors and mechanoreceptors is relayed to the nucleus tractus solitarius (NTS) via the vagus and glossopharyngeal nerves. This input helps modulate the respiratory pattern based on the body’s needs, adjusting for changes in CO2, O2, and pH levels.

201
Q

How does the pre-Bötzinger complex function in the respiratory system?

A

Located within the VRG, the pre-Bötzinger complex contains spontaneously firing neurons that are thought to serve as the primary pacemaker for the respiratory rhythm, initiating each breathing cycle.

202
Q

What happens during forced breathing and active expiration in terms of neuronal activity?

A

During forced breathing, increased activity in the VRG stimulates accessory muscles for enhanced thoracic expansion. Active expiration involves VRG neurons activating internal intercostal and abdominal muscles. Inspiratory neurons are inhibited during active expiration, indicating communication between inspiratory and expiratory neurons to coordinate breathing.

203
Q

What are the primary roles of peripheral chemoreceptors in respiratory control?

A

Peripheral chemoreceptors, located in carotid bodies, are primarily activated by changes in arterial blood gases and pH. They are most sensitive to decreases in P_O2 (below 60 mm Hg), increases in P_CO2, and decreases in pH. These changes trigger reflex increases in ventilation to maintain homeostasis.

204
Q

How do central chemoreceptors regulate ventilation?

A

Central chemoreceptors, located on the ventral surface of the medulla, primarily respond to changes in CO2 concentration (as reflected by changes in pH) in cerebrospinal fluid (CSF). An increase in CO2 leads to an increase in H+ concentration in CSF, which stimulates these receptors to increase the depth and rate of ventilation.

205
Q

Describe the molecular mechanism of action in peripheral chemoreceptors.

A

In peripheral chemoreceptors like the carotid bodies, hypoxia closes oxygen-sensitive K+ channels, leading to cell depolarization. This opens voltage-gated Ca2+ channels, leading to neurotransmitter release and activation of sensory neurons that signal the brainstem to increase ventilation.

206
Q

What is the significance of the carotid bodies’ response to oxygen levels under normal conditions and in pathological states?

A

Under normal conditions, the carotid bodies respond to significant drops in oxygen levels (e.g., high altitude). In pathological states like COPD, heart failure, and sleep apnea, altered carotid body function can lead to maladaptive ventilation responses, highlighting their role in disease.

207
Q

How do central chemoreceptors adapt to chronic changes in CO2 levels?

A

When arterial P_CO2 remains elevated over several days, the initial strong ventilatory response by central chemoreceptors adapts, and ventilation rates return towards normal due to increased bicarbonate in the CSF, which buffers the excess H+.

208
Q

Explain the interaction between hypoxia and hypercapnia in patients with chronic lung diseases.

A

In chronic lung diseases like COPD, prolonged hypercapnia can lead to an adapted chemoreceptor response, making low arterial P_O2 the primary drive for ventilation. Over-oxygenating these patients can suppress this drive and potentially stop their breathing.

209
Q

What initiates the respiratory pattern in the brainstem?

A

Respiratory patterns are initiated by a network of spontaneously firing neurons located in the brainstem, particularly in the medulla and pons. This network acts as a central pattern generator with intrinsic rhythmic activity, which is influenced by sensory input from chemoreceptors.

210
Q

How does the chloride shift facilitate CO₂ transport in blood?

A

The chloride shift involves the exchange of bicarbonate ions (HCO₃⁻) for chloride ions (Cl⁻) across the red blood cell membrane. This process helps maintain electrical neutrality within the red blood cells while facilitating the transport of CO₂ in the form of bicarbonate in the plasma.

211
Q

What is the role of carbonic anhydrase in CO₂ transport?

A

Carbonic anhydrase, an enzyme located primarily in red blood cells, catalyzes the conversion of CO₂ and water into carbonic acid, which quickly dissociates into hydrogen ions (H⁺) and bicarbonate ions (HCO₃⁻). This reaction is crucial for efficiently converting CO₂ into a transportable form in the blood.

212
Q

How do changes in blood pH affect hemoglobin’s oxygen-binding affinity?

A

Changes in blood pH affect hemoglobin’s oxygen-binding affinity through the Bohr effect. A decrease in pH (more acidic blood) reduces the affinity of hemoglobin for oxygen, causing a rightward shift in the oxygen-hemoglobin dissociation curve. This facilitates oxygen release to tissues.

213
Q

Describe the physiological importance of the steep and flat portions of the oxygen-hemoglobin dissociation curve.

A

The steep part of the curve (around 20-40 mm Hg P_O₂) allows for significant oxygen unloading from hemoglobin to tissues with small changes in P_O₂, which is crucial during increased metabolic activity. The flat portion (above 60 mm Hg P_O₂) provides a buffer effect, maintaining high oxygen saturation in the lungs even if alveolar P_O₂ varies within a certain range.

214
Q

What mechanisms ensure the continuity of CO₂ removal from the body?

A

CO₂ removal is ensured by its high solubility in blood, conversion to bicarbonate ions for transport, binding to hemoglobin as carbaminohemoglobin, and the efficient ventilation facilitated by chemoreceptor feedback that adjusts breathing based on CO₂ levels in the blood and cerebrospinal fluid.

215
Q

What is the role of peripheral chemoreceptors in respiratory control?

A

Peripheral chemoreceptors, particularly located in the carotid bodies and aortic bodies, monitor the arterial levels of O₂, CO₂, and pH. They are highly sensitive to changes in arterial blood gas compositions, triggering reflex adjustments in ventilation to maintain homeostasis.

216
Q

How does the central chemoreceptor system influence ventilation?

A

Central chemoreceptors, located on the ventral surface of the medulla, respond primarily to changes in pH of the cerebrospinal fluid, which reflects CO₂ levels in the blood. An increase in CO₂ leads to a lower pH, stimulating these receptors to increase the rate and depth of ventilation.

217
Q

What triggers the chloride shift during CO₂ transport in blood?

A

The chloride shift is triggered by the rapid conversion of CO₂ to bicarbonate ions (HCO₃⁻) inside red blood cells. This process involves the enzyme carbonic anhydrase and results in the movement of bicarbonate out of the cells in exchange for chloride ions, maintaining ionic balance.

218
Q

Explain the significance of the Bohr effect in oxygen delivery to tissues.

A

The Bohr effect describes how decreases in pH (increased acidity) and increases in CO₂ concentration reduce hemoglobin’s affinity for oxygen. This physiological mechanism facilitates more oxygen being released to active tissues, particularly during states of high metabolic demand.

219
Q

How does 2,3-bisphosphoglycerate (2,3-BPG) influence oxygen release from hemoglobin?

A

2,3-BPG binds to hemoglobin, reducing its affinity for oxygen and enhancing oxygen release. This effect is crucial at high altitudes or under conditions like anemia, where oxygen delivery needs to be optimized despite lower environmental oxygen levels.

220
Q

What factors can cause a leftward shift in the oxygen-hemoglobin dissociation curve?

A

A leftward shift in the dissociation curve, indicating increased oxygen affinity, can occur due to lower temperatures, decreased P_CO₂, increased pH, or structural changes in hemoglobin, such as those seen with fetal hemoglobin (HbF).

221
Q

What is the Hering-Breuer inflation reflex, and when is it observed?

A

The Hering-Breuer inflation reflex is a protective mechanism that prevents overinflation of the lungs by terminating inspiration when lung volume exceeds a certain threshold. It was first described in anesthetized dogs in the late 1800s. Stretch receptors in the lung signal the brain stem to end inspiration when tidal volume is too high. This reflex is less evident in adult humans during normal activities but may be more significant in human infants, helping to limit their ventilation volumes.

222
Q

How do conscious and unconscious thought processes affect respiratory activities?

A

Conscious and unconscious thoughts can influence respiratory functions via higher brain centers like the hypothalamus and cerebrum, which can alter the activity of the brain stem’s respiratory control network, adjusting the rate and depth of breathing. This includes voluntary control of breathing as well as involuntary responses to emotional states such as fear or excitement, which can also impact respiration.

223
Q

What happens when an individual attempts to hold their breath, especially in response to elevated P CO₂ levels?

A

Attempting to hold breath voluntarily is limited by chemoreceptor reflexes, which respond to elevated levels of CO₂ in the blood and cerebrospinal fluid. These reflexes eventually override voluntary efforts, forcing the individual to inhale. In extreme cases, such as with determined children during temper tantrums, they might hold their breath until they pass out from hypoxia; however, normal breathing automatically resumes once unconscious.

224
Q

How are breathing and cardiovascular functions interconnected?

A

Breathing is closely linked to cardiovascular function, with integrating centers for both located in the brain stem. Interneurons project between the respiratory and cardiovascular networks, facilitating communication and coordination between these systems. This integration helps maintain fluid and acid-base homeostasis, involving not just the respiratory and cardiovascular systems, but also the renal system.

225
Q

What are the main components and roles of the brain stem in respiratory control?

A

The brain stem contains critical networks for respiratory control, particularly within the medulla oblongata and pons. The medulla houses the dorsal respiratory group (DRG) and the ventral respiratory group (VRG), which manage inspiration and expiration respectively. The DRG primarily controls inspiratory muscles via signals through phrenic and intercostal nerves, while the VRG manages muscles for active expiration and non-routine inspiratory actions. The pons modulates these activities, smoothing the respiratory rhythm.

226
Q

What role do peripheral chemoreceptors play in respiratory control?

A

Peripheral chemoreceptors, particularly those in the carotid bodies, respond to changes in blood gases—specifically decreases in oxygen (P O₂), increases in carbon dioxide (P CO₂), and decreases in pH. These receptors activate in severe conditions, such as significant hypoxemia or hypercapnia, to increase ventilation and maintain homeostasis. The response mechanism involves the closure of K⁺ channels in glomus cells, leading to cell depolarization and subsequent neurotransmitter release that stimulates increased ventilation.

227
Q

How do central chemoreceptors influence respiration?

A

Central chemoreceptors, located in the medulla, primarily respond to changes in carbon dioxide levels by detecting pH changes in cerebrospinal fluid (CSF). When CO₂ levels rise, it diffuses into the CSF and lowers pH, triggering these receptors to increase ventilation. This helps to expel CO₂ and restore normal pH levels. If CO₂ levels remain high chronically, these receptors adapt by increasing CSF bicarbonate, which buffers the increased acidity and gradually reduces the ventilatory response.

228
Q

How do emotional states influence respiration?

A

Emotional states can significantly influence respiration through connections between the limbic system and respiratory control centers in the brain stem. Fear, excitement, or stress can lead to changes in the rate and depth of breathing, which are mediated by the limbic system’s direct influence on motor pathways controlling respiratory muscles. These adjustments are typically automatic and ensure that oxygen supply meets the body’s changing metabolic demands during emotional experiences.