Respiratory Physiology II: Guyton Chapter 42 - 45

Question 1

[16-minute video]: Guyton and Hall Medical Physiology (Chapter 26) - Respiratory Insufficiency - Pathophysiology, Diagnosis, Oxygen Therapy

Answer 1

💨

Question 2

Discuss the organisation of the respiratory centre in the brainstem.

Answer 2

The respiratory center is composed of several groups of neurons located bilaterally in the medulla oblongata and pons of the brain stem. It is divided into three major collections of neurons:
(1) a dorsal respiratory group, located in the dorsal portion of the medulla, which mainly causes inspiration
(2) a ventral respiratory group, located in the ventrolateral part of the medulla, which mainly causes expiration
(3) the pneumotaxic center, located dorsally in the superior portion of the pons, which mainly controls rate and depth of breathing.
[Diagram 1] [Diagram 2]

Question 3

Where are most neurons of the dorsal respiratory group located?

Answer 3

Most neurons are located in the nucleus of the tractus solitarius (NTS).

Question 4

Besides the NTS, where else are neurons involved in respiratory control located?

Answer 4

Additional neurons are located in the adjacent reticular substance of the medulla.

Question 5

Explain the inspiratory ramp signal.

Answer 5

💨 The signal originates from the dorsal respiratory group (DRG) in the medulla oblongata.
💨 It generates a rhythmic, ramp-like discharge of nerve signals. This signal starts weakly and increases steadily over about 2 seconds during normal inspiration.
💨 The signal is transmitted to the inspiratory muscles, primarily the diaphragm.
💨 As the signal ramps up, it causes the inspiratory muscles to contract, leading to the expansion of the lungs.
💨 The signal ceases abruptly, allowing the inspiratory muscles to relax and the lungs to recoil, leading to expiration.
[Diagram]

Question 6

What are two qualities of the inspiratory ramp that are controlled?

Answer 6

(1) The rate of increase of the ramp signal [so that during heavy inspiration, the ramp increases rapidly and therefore fills the lungs rapidly]
(2) The point at which the ramp suddenly ceases [That is, the earlier the ramp ceases, the shorter the duration of inspiration. This method also shortens the duration of expiration. Thus, the frequency of respiration is increased.]

Question 7

(a) In which nucleus is the pneumotaxic center located?
(b) What is the function of the pneumotaxic centre?

Answer 7

(a) nucleus parabrachialis
(b) It transmits signals to the inspiratory center, controlling the “switch-off” point of the inspiratory ramp, thereby controlling the duration of inspiration. [This will have the secondary effect of controlling the breathing rate because limitation of inspiration also shortens expiration and the entire period of each respiration.]

Question 8

In which nuclei are the ventral respiratory group of neurons found?

Answer 8

nucleus ambiguus rostrally
nucleus retroambiguus caudally

Question 9

Discuss the activity and function of the ventral respiratory group.

Answer 9

💨 The neurons of the ventral respiratory group remain almost totally inactive during normal quiet respiration. Therefore, normal quiet breathing is caused only by repetitive inspiratory signals from the dorsal respiratory group transmitted mainly to the diaphragm, and expiration results from elastic recoil of the lungs and thoracic cage.

💨 The ventral respiratory neurons do not appear to participate in the basic rhythmical oscillation that controls respiration.

💨 When the respiratory drive for increased pulmonary ventilation becomes greater than normal, respiratory signals spill over into the ventral respiratory neurons from the basic oscillating mechanism of the dorsal respiratory area. As a consequence, the ventral respiratory area also contributes extra respiratory drive.

💨 Electrical stimulation of a few of the neurons in the ventral group causes inspiration, whereas stimulation of others causes expiration. Therefore, these neurons contribute to both inspiration and expiration. They are especially important in providing the powerful expiratory signals to the abdominal muscles during very heavy expiration. Thus, this area operates more or less as an overdrive mechanism when high levels of pulmonary ventilation are required, especially during heavy exercise.,

Question 10

Explain the Hering-Breuer inflation reflex.

Answer 10

(1) Stretch receptors located in the walls of the bronchi and bronchioles detect excessive stretching of the lungs during deep inhalation.

(2) When these receptors are activated, they send nerve impulses via the vagus nerve to the brainstem, specifically to the medulla and the apneustic center in the pons.

(3) The brainstem responds by inhibiting the inspiratory neurons, which stops further inhalation and initiates exhalation.

Question 11

What is the function of the Hering Breuer reflex?

Answer 11

It acts as a protective mechanism to prevent over-inflation, thus protecting the lungs from potential damage due to over expansion.

Question 12

Discuss the mechanism of direct control of the respiratory center activity by CO₂ and H⁺.

Answer 12

💨 Within the medulla oblongata is a neuronal area known as the chemosensitive area. This area is highly sensitive to changes in either blood PCO₂ or H⁺ concentration, and it in turn excites the other portions of the respiratory center.
💨 CO₂ from the blood diffuses into the CSF because it is lipid soluble.
💨 In the CSF, CO₂ reacts with water to form carbonic acid, which dissociates into bicarbonate and hydrogen ions (H⁺). This reaction is catalyzed by the enzyme carbonic anhydrase.
💨 The increase in H⁺ concentration lowers the pH of the CSF. The chemosensitive area detects this change in pH.
💨 The chemosensitive area sends signals to the dorsal and ventral respiratory groups to increase the rate and depth of breathing.

Question 13

Briefly discuss the attenuated stimulatory effect of CO₂ on the respiratory centers after 1-2 days.

Answer 13

💨 This decline is partly as a result of renal readjustment of the H⁺ concentration in the circulating blood back toward normal after the CO₂ first increases the H⁺ concentration. The kidneys achieve this readjustment by increasing the blood HCO₃⁻, which binds with H⁺ in the blood and cerebrospinal fluid to reduce their concentrations.
💨 But, even more importantly, over a period of hours, the HCO₃⁻ also slowly diffuses through the blood–brain and blood–cerebrospinal fluid barriers and combine directly with H⁺ adjacent to the respiratory neurons as well, thus reducing the H⁺ back to near normal.

Question 14

What is the peripheral chemoreceptor system important for?

Answer 14

It detects changes in O₂ in the blood and, to a lesser extent, changes in CO₂ and H⁺ concentrations.

Question 15

Where are most chemoreceptors located?

Answer 15

In the carotid bodies

Question 16

Where are the carotid bodies located?

Answer 16

Bilaterally in the bifurcations of the common carotid arteries.

Question 17

Through which nerves do the afferent fibers from the carotid bodies pass?

Answer 17

Through Hering’s nerves to the glossopharyngeal nerves and then to the dorsal respiratory area of the medulla.

Question 18

Where are the aortic bodies located?

Answer 18

along the arch of the aorta

Question 19

What are glomus cells and where are they found?

Answer 19

Glomus cells are gluandular-like cells found in the carotid and aortic bodies. They synapse directly or indirectly with nerve endings.

Question 20

How do glomus cells respond to low PO₂ levels?

Answer 20

💨 Glomus cells have O₂-sensitive potassium channels that inactivate when blood PO₂ decreases markedly. This inactivation causes the cell to depolarize, opening voltage-gated calcium channels and increasing intracellular calcium ion concentration.

💨 The increased calcium ion concentration stimulates the release of a neurotransmitter that activates afferent neurons, sending signals to the central nervous system and stimulating respiration.

[Diagram 1] [Diagram 2]

Question 21

How do increased CO₂ and H⁺ concentrations affect respiratory activity, and what is the difference between their direct effects on the respiratory center and their effects through chemoreceptors?

Answer 21

Increased CO₂ and H⁺ concentrations stimulate respiratory activity, with their direct effects on the respiratory center being significantly stronger (about seven times) than their effects through chemoreceptors. However, peripheral chemoreceptors respond much faster, making them crucial for the rapid respiratory response to CO₂, especially at the onset of exercise.

Question 22

How does low arterial oxygen pressure (PO₂) affect alveolar ventilation, and what primarily regulates ventilation in healthy humans at sea level?

Answer 22

Low arterial oxygen pressure (PO) significantly increases alveolar ventilation when PO₂ drops below 100 mm Hg, with a dramatic increase at very low PO₂ levels [60 mm Hg and lower]. However, in healthy humans at sea level, the regulation of ventilation is primarily driven by carbon dioxide (PCO₂) and hydrogen ion (H+) concentrations rather than oxygen levels.

Question 23

What is acclimatization?

Answer 23

Acclimatization is the process by which the body adjusts to low atmospheric oxygen concentrations over a period of days to weeks.

Question 24

During strenuous exercise, O₂ consumption and CO₂ formation can increase as much as 20-fold. Yet, in the healthy athlete, alveolar ventilation ordinarily increases almost exactly in step with the increased level of oxygen metabolism. The arterial PO₂, PCO₂, and pH remain almost exactly normal. Therefore, what causes intense ventilation during exercise?

Answer 24

The brain, on transmitting motor impulses to the exercising muscles, is believed to transmit collateral impulses into the brainstem at the same time to excite the respiratory centre.

Question 25

What is maximum expiratory flow?

Answer 25

Maximum expiratory flow is the highest flow rate achieved during forced expiration, beyond which the flow cannot be increased even with additional force.

Question 26

How does increased pressure applied to the outsides of the alveoli and bronchioles affect maximum expiratory flow?

Answer 26

Increased pressure compresses the outsides of the alveoli and bronchioles, forcing air out but also collapsing the bronchioles, which opposes air movement. Beyond a critical degree of expiratory force, further increases in alveolar pressure also increase bronchiolar collapse and airway resistance, preventing further increase in flow.

Further notes:
Maximum respiratory flow curve: [Diagram]

Question 27

Why does maximum expiratory flow rate decrease as lung volume becomes smaller?

Answer 27

As lung volume decreases, the elastic pull on the bronchi and bronchioles by lung structural elements is reduced, making them more easily collapsed by external chest pressure. This progressively reduces the maximum expiratory flow rate.

Further notes:
Maximum respiratory flow curve: [Diagram]

Question 28

What are the characteristics of constricted lungs in the maximum expiratory flow-volume curve?

Answer 28

Constricted lungs have reduced total lung capacity (TLC) and reduced residual volume (RV). The lung cannot expand to a normal maximum volume, resulting in a lower maximal expiratory flow compared to the normal curve. Constricted lung diseases include fibrotic diseases like tuberculosis and silicosis, and conditions that constrict the chest cage such as kyphosis, scoliosis, and fibrotic pleurisy.

[Diagram 1] [Diagram 2]

Question 29

Why is it more difficult to expire than to inspire in diseases with airway obstruction?

Answer 29

In airway obstruction diseases, the closing tendency of the airways is increased by the extra positive pressure required for expiration. During inspiration, the negative pleural pressure pulls the airways open, allowing air to enter easily but trapping it in the lungs. This effect increases both the total lung capacity (TLC) and residual volume (RV) over time, and the maximum expiratory flow rate is greatly reduced.

Question 30

What are some diseases that cause severe airway obstruction and affect the maximum expiratory flow rate?

Answer 30

Answer: Asthma is a classic disease that causes severe airway obstruction. Serious airway obstruction also occurs in some stages of emphysema. These conditions lead to a significant reduction in the maximum expiratory flow rate due to the increased tendency of the airways to collapse during expiration.

Question 31

What is the FVC test and how is it performed?

Answer 31

The Forced Expiratory Vital Capacity (FVC) test is a clinical pulmonary test that records the forced expiratory vital capacity on a spirometer. The person inspires maximally to the total lung capacity (TLC) and then exhales into the spirometer with maximum expiratory effort as rapidly and completely as possible.

Question 32

Distinguish between Vital Capacity and Forced Vital Capacity.

Answer 32

Vital Capacity is the maximum amount of air a person can exhale after a maximum inhalation, whereas the Forced Vital Capacity is the maximum amount of air a person can exhale forcefully and rapidly after a maximum inhalation.

Vital capacity is measured without any time constraint, meaning that the person can exhale slowly and completely.
Foced Vital Capacity is measured with a time constraint, requiring the person to exhale as quickly and forcefully as possible.

Question 33

What is the difference in FVC between normal lungs and partial airway obstruction?

Answer 33

The total volume changes of the FVCs are not greatly different, indicating only a moderate differenec in basic lung volumes.

Question 34

What is FEV1?

Answer 34

The Forced Expiratory Volume in 1 second is the volume of air that a person can forcefully exhale in the first second of a forced breath.
[It is usually expressed as a percentage of the total Forced Vital Capacity.]

Question 35

What is the FEV1/FVC% in a normal person?

Answer 35

In a normal person, 80% of the FVC is expired in the first second (FEV1/FVC%).

Question 36

What is pulmonary emphysema?

Answer 36

This is a condition characterized by permanent enlargement of air spaces in the lungs as a result of damage to the alveoli.

Question 37

Discuss the major pathophysiological changes in the lungs due to pulmonary emphysema.

Answer 37

💨 Chronic infection caused by inhaling smoke or other irritants leads to deranged protective mechanisms of the airways, partial paralysis of the cilia, excess mucus secretion and inhibition of alveolar macrophages.
💨 This then results in chronic obstruction of many smaller airways due to excess mucus and inflammatory edema of the bronchiolar epithelium.
💨 One will therefore experience difficulty in expiring air, causing entrapment of air in the alveoli, overstretching them, and marked destruction of alveolar walls [50 - 80%].
💨 [Diagram]
💨 Gallery: [Image 1] [Image 2] [Image 3]

Question 38

What are the physiological effects of chronic emphysema?

Answer 38

💨 Increased airway resistance due to bronchiolar obstruction, resulting in increased work of breathing, especially during expiration.

💨 Decreased diffusing capacity of the lung due to the marked loss of alveolar walls, reducing the ability to oxygenate blood and remove CO2.

💨 Abnormal ventilation-perfusion ratios, with some parts of the lungs being well ventilated and others poorly ventilated, causing physiological shunt and dead space.

💨 Decreased number of pulmonary capillaries due to the loss of alveolar walls, leading to increased pulmonary vascular resistance, pulmonary hypertension, and right-sided heart failure.

Question 39

What are the long term effects of chronic emphysema?

Answer 39

Both hypoxia and hypercapnia develop due to hypoventilation of many alveoli and loss of alveolar walls. The net result is severe, prolonged, and devastating air hunger [aka. dyspnea] that can last for years until hypoxia and hypercapnia cause death.

Question 40

Define “pneumonia”.

Answer 40

The term “pneumonia” includes any inflammatory condiiton of the lung in which some or all of the alveoli are filled with fluid and blood cells.

Question 41

How does bacterial pneumonia affect the alveoli and spread in the lungs?

Answer 41

Bacterial pneumonia begins with infection in the alveoli, causing the pulmonary membrane to become inflamed and highly porous, leading to fluid and blood cells leaking into the alveoli. The infected alveoli become filled with fluid and cells, and the infection spreads from alveolus to alveolus, eventually consolidating large areas of the lungs.

Question 42

What are the two major pulmonary abnormalities caused by pneumonia, and what are their effects?

Answer 42

(1) reduction in the total available surface area of the respiratory membrane, and
(2) a decreased ventilation-perfusion ratio. These effects cause hypoxemia (low blood O2) and hypercapnia (high blood CO2).

Question 43

What does FEV1/FVC measure and why will the ratio increase with lung fibrosis?

(a) the forced expiratory volume in one second in relation to the total forced vital capacity; lung fibrosis causes the lungs to become less pliable

(b) the functional expiratory volume in one second in relation to the total functional vital capacity; lung fibrosis causes the lungs to become less pliable

(c) the functional expiratory volume in one second in relation to the total functional vital capacity; lung fibrosis causes the lungs to decrease in size

(d) the forced expiratory volume in one second in relation to the total forced vital capacity; lung fibrosis causes the lungs to decrease in size

(e) none of the above

Answer 43

(a) the forced expiratory volume in one second in relation to the total forced vital capacity; lung fibrosis causes the lungs to become less pliable

Question 44

An anesthetized male is breathing with no assistance. He is then artificially ventilated for 10 min at his normal tidal volume but at twice his normal frequency. He is ventilated with a gas mixture of 60% O₂ and 40% N₂. The artificial ventilation is stopped and he fails to breathe for several minutes. This apneic episode is due to which of the following?
(a) Low arterial PCO₂ suppressing the activity of the peripheral chemoreceptors
(b) Low arterial PCO₂ suppressing the activity of the medullary chemoreceptors
(c) High arterial PCO₂ suppressing the activity of the peripheral chemoreceptors
(d) Decrease in arterial pH suppressing the activity of the peripheral chemoreceptors
(e) High arterial PCO₂ suppressing the activity of the medullary chemoreceptors

Answer 44

(b) Low arterial PCO₂ suppressing the activity of the medullary chemoreceptors

Question 45

The peripheral chemoreceptors are most active when
(a) PaO₂ levels are greater than 90 mmHg
(b) pH of arterial blood rises
(c) pH of arterial blood falls
(d) PaO₂ levels are below 60 mmHg
(e) PaCO₂ levels are below 40 mmHg

Answer 45

(d) PaO₂ levels are below 60 mmHg

Question 46

The effect of a fall in arterial pH on the central chemoreceptors:
(a) occurs indirectly through CO2 entry across the blood brain barrier
(b) results in hypoventilation
(c) occurs directly as H+ passes through the blood brain barrier
(d) results in respiratory alkalosis
(e) has a negligible effect on ventilation

Answer 46

(a) occurs indirectly through CO2 entry across the blood brain barrier

Question 47

What conditions of the lungs would cause a an increase in FEV1/FVC? What about a decrease FEV1/FVC?
(a) This ratio increases as the lungs become stiff and less pliable, decreasing when there is increased resistance in the lung.
(b) This ratio decreases as the lungs become stiff and less pliable, decreasing further when there is increased resistance in the lung.
(c) This ratio increases as the lungs become stiff and less pliable, increasing further when there is increased resistance in the lung.
(d) This ratio decreases as the lungs become stiff and less pliable, increasing when there is increased resistance in the lung.
(e) All of the above

Answer 47

(a) This ratio increases as the lungs become stiff and less pliable, decreasing when there is increased resistance in the lung.