1
Q
What controls the periodic nature of inspiration and expiration?
A
The central pattern generator
It comprises groups of neurons located in the pons and medulla.
2
Q
Where is the medullary respiratory center located?
A
In the reticular formation of the medulla beneath the floor of the fourth ventricle
This area is crucial for respiratory control.
3
Q
What is the Pre-Botzinger complex associated with?
A
Generation of the respiratory rhythm
It is located in the ventrolateral region of the medulla.
4
Q
What is the primary function of the Dorsal Respiratory Group?
A
Associated with inspiration
It is one of the groups of neurons in the medulla.
5
Q
What is the primary function of the Ventral Respiratory Group?
A
Associated with expiration
It is another group of neurons in the medulla.
6
Q
What property do the groups of cells in the medullary respiratory center have?
A
Intrinsic periodic firing
This property is responsible for the basic rhythm of ventilation.
7
Q
What happens to the respiratory rhythm when all known afferent stimuli are abolished?
A
Cells generate repetitive bursts of action potentials
This results in nervous impulses going to the diaphragm and other inspiratory muscles.
8
Q
What is the initial phase of the intrinsic rhythm pattern of the inspiratory area?
A
A latent period of several seconds during which there is no activity
This phase precedes the appearance of action potentials in the inspiratory area.
9
Q
Describe the pattern of action potentials during the inspiratory phase.
A
Action potentials increase in a crescendo over the next few seconds
This pattern correlates with increasing inspiratory muscle activity.
10
Q
How does the inspiratory muscle activity change during the inspiratory phase?
A
It becomes stronger in a ‘ramp’-type pattern
This ramp pattern characterizes the increase in muscle activity during inspiration.
11
Q
What happens to inspiratory action potentials at the end of the inspiratory phase?
A
They cease, and inspiratory muscle tone falls to its preinspiratory level
This marks the end of the inspiratory effort.
12
Q
How can the inspiratory ramp be shortened?
A
By inhibiting impulses from the pneumotaxic center
This leads to an increase in breathing rate.
13
Q
Which cranial nerves modulate the output of the inspiratory cells?
A
Impulses from the vagus and glossopharyngeal nerves
These impulses terminate in the tractus solitarius, influencing the inspiratory area.
14
Q
What is the role of the expiratory area during normal quiet breathing?
A
It is quiescent; exhalation is passive at rest
The diaphragm is the primary muscle involved in this process.
15
Q
What occurs to the ventral respiration group during more forceful breathing?
A
Expiration becomes active due to the activity of the expiratory cells
This contrasts with normal quiet breathing where expiration is passive.
16
Q
Is there universal agreement on how the intrinsic rhythmicity of respiration is regulated?
A
No
The mechanisms underlying respiratory rhythmicity remain a topic of research.
17
Q
What is the apneustic center?
A
An area in the lower pons that causes prolonged inspiratory gasps interrupted by transient expiratory efforts
Named because sectioning the brain above this site leads to apneuses in experimental animals
18
Q
What happens when the apneustic center is stimulated?
A
It has an excitatory effect on the inspiratory area of the medulla, prolonging ramp action potentials
Its role in normal human respiration is not known
19
Q
What is the pneumotaxic center?
A
An area in the upper pons that inhibits inspiration and regulates inspiration volume and respiratory rate
Demonstrated through direct electrical stimulation in experimental animals
20
Q
What is the primary function of the pneumotaxic center?
A
To fine-tune respiratory rhythm
21
Q
Where are the respiratory centers located?
A
In the medulla and pons of the brainstem
22
Q
What inputs do the respiratory centers receive?
A
From chemoreceptors, lung and other receptors, and the cortex
23
Q
What is the major output of the respiratory centers?
A
To the phrenic nerves and other respiratory muscles
24
Q
You’re doing a case study of a patient who damaged their pneumotaxic center. Your friend, Zendaya, says, “The patient can’t generate a normal breathing rhythm anymore!”
Is Zendaya correct?
A
No. The pneumotaxic center only fine tunes the existing rhythm
25
What is the extent of voluntary control over breathing?
Breathing is under voluntary control to a considerable extent
26
Which part of the brain can be overridden by the cortex during breathing?
The brainstem
27
What can happen when arterial Pco2 is halved by hyperventilation?
It may cause alkalosis, leading to tetany and carpopedal spasm
28
By how much does arterial pH increase when Pco2 is halved?
About 0.2 units
29
What is more difficult to achieve than hyperventilation?
Voluntary hypoventilation
30
What limits the duration of breath-holding?
Arterial Pco2 and Po2
## Footnote
other unknown factors too
31
What effect does hyperventilation have on breath-holding time?
It increases breath-holding time, especially if oxygen is breathed
## Footnote
Does this through changing PCO2 and PO2
32
What can allow for a further period of breath-holding at the breaking point? What are the implications?
Inhaling a gas mixture that raises arterial Pco2 and lowers Po2. Partial pressure alone does not limit voluntary hypoventilation
33
What are the primary muscles of respiration?
Diaphragm
intercostal muscles
abdominal muscles
34
What are the accessory muscles of respiration?
sternocleidomastoids
scalenes
35
When do the accessory muscles of respiration become active?
forced breathing
respiratory distress
36
What is the role of the nasopharyngeal muscles?
Maintain patency of the upper airways
## Footnote
This is particularly important during sleep.
37
What is essential for the control of ventilation?
Coordinated activity of various muscle groups
## Footnote
This coordination is managed by the central controller.
38
What issue can occur in some newborn children regarding respiratory muscles?
Uncoordinated respiratory muscle activity
## Footnote
This is especially common in premature newborns.
39
Fill in the blank: The _______ is responsible for coordinating the activities of respiratory muscles.
central controller
40
True or False: Thoracic muscles may inspire while abdominal muscles expire in some premature newborns.
True
41
What happens to respiratory muscle coordination during sleep in some newborns?
It may become uncoordinated
## Footnote
This can lead to ineffective breathing patterns.
42
What is a chemoreceptor?
A receptor that responds to a change in the chemical composition of the blood or other fluid around it.
## Footnote
Chemoreceptors play a crucial role in monitoring and regulating physiological processes.
43
Where are the most important chemoreceptors for ventilation control located?
Near the ventral surface of the medulla in the vicinity of the exit of the 9th and 10th nerves.
## Footnote
These receptors are critical for minute-by-minute control of ventilation.
44
What stimulates breathing within a few seconds when applied locally to the central chemoreceptors?
H+ or dissolved CO2.
## Footnote
This rapid response is vital for maintaining appropriate levels of gases in the blood.
45
What was once thought about the medullary respiratory center's role in CO2 action?
It was thought to be the site of action of CO2.
## Footnote
Current understanding indicates that the chemoreceptors are anatomically separate from the respiratory center.
46
How far below the ventral surface of the medulla do some chemoreceptors lie?
About 200 to 400 μm.
## Footnote
This anatomical detail helps in understanding the precise location of chemoreceptors in the respiratory control system.
47
What do central chemoreceptors respond to?
Changes in H+ concentration in the brain extracellular fluid
## Footnote
Central chemoreceptors are sensitive to the acidity of the extracellular fluid, which is influenced by H+ ions.
48
What effect does an increase in brain ECF H+ concentration have on ventilation?
Stimulates ventilation
## Footnote
Increased acidity (higher H+ concentration) leads to increased breathing rates.
49
What effect does a decrease in brain ECF H+ concentration have on ventilation?
Inhibits ventilation
## Footnote
Lower acidity (lower H+ concentration) results in decreased breathing rates.
50
What factors govern the composition of extracellular fluid around central chemoreceptors?
Cerebrospinal fluid (CSF)
local blood flow
local metabolism
## Footnote
These factors influence the chemical environment surrounding the chemoreceptors.
51
Which factor is considered the most important in governing brain extracellular fluid composition?
Cerebrospinal fluid (CSF)
## Footnote
CSF plays a crucial role in maintaining the chemical balance necessary for chemoreceptor function.
52
What separates the cerebrospinal fluid from the blood?
Blood-brain barrier
## Footnote
This barrier restricts the passage of certain ions and molecules, including H+.
53
How does CO2 affect the cerebrospinal fluid (CSF)?
CO2 diffuses into the CSF, liberating H+ ions
## Footnote
This process occurs when blood Pco2 rises, leading to increased acidity.
54
What is the primary way CO2 regulates ventilation through the central receptors?
CO2 in the CSF releases H+ through its reaction with water
## Footnote
Changes in CO2 levels influence H+ concentration and thus ventilation rates.
55
True or False: The central chemoreceptors respond to changes in Po2.
False
## Footnote
Central chemoreceptors are primarily responsive to H+ levels, not Po2.
56
What is the consequence of hyperventilation on blood Pco2?
Reduces Pco2 in the blood
## Footnote
Hyperventilation decreases the concentration of CO2 in the bloodstream.
57
What physiological change in the brain accompanies increased arterial Pco2?
Cerebral vasodilation
## Footnote
This allows for enhanced diffusion of CO2 into the CSF and brain extracellular fluid.
58
Fill in the blank: The central chemoreceptors do not respond to changes in _______.
Po2
## Footnote
Their main focus is on H+ concentration rather than oxygen levels.
59
What is the normal pH of the CSF?
7.32
## Footnote
CSF stands for cerebrospinal fluid.
60
How does the protein content of CSF compare to that of blood?
CSF contains much less protein than blood.
61
What is the buffering capacity of CSF compared to blood?
CSF has a much lower buffering capacity than blood.
62
What happens to CSF pH with a change in Pco2?
The change in CSF pH for a given change in Pco2 is greater than in blood.
63
Does CSF pH usually return all the way to 7.32 after displacement?
No, CSF pH does not usually return all the way to 7.32.
64
How does the speed of CSF pH change compare to arterial blood pH change?
CSF pH changes more promptly than arterial blood pH.
65
How long does renal compensation take to affect blood pH?
2 to 3 days.
66
What effect does rapid CSF pH change have on ventilation and arterial Pco2?
CSF pH has a more important effect on changes in the level of ventilation and the arterial Pco2.
67
What is one example of a patient condition affecting CSF pH and ventilation?
A patient with chronic lung disease and CO2 retention.
68
What might a patient with chronic lung disease have regarding CSF pH and ventilation?
Nearly normal CSF pH and abnormally low ventilation for arterial Pco2.
69
What can cause hypoventilation in very obese patients?
Abnormal respiratory mechanics and alterations in ventilatory control.
70
What happens to normal subjects exposed to an atmosphere containing 3% CO2 for some days?
They may experience a similar pattern of changes as those with chronic lung disease.
71
Fill in the blank: The CSF has a _______ buffering capacity compared to blood.
much lower
72
True or False: CSF pH returns to its normal value more slowly than blood pH.
False
73
Where are peripheral chemoreceptors located?
In the carotid bodies at the bifurcation of the common carotid arteries and in the aortic bodies above and below the aortic arch.
74
Which peripheral chemoreceptors are most important in humans?
Carotid bodies.
75
What types of glomus cells are found in the carotid bodies?
* Type I cells
* Type II cells
76
What is a notable characteristic of Type I cells in the carotid bodies?
They show an intense fluorescent staining due to large content of dopamine.
77
What is the relationship between Type I cells and the carotid sinus nerve?
Type I cells are in close apposition to endings of the afferent carotid sinus nerve.
78
What additional feature is present in the carotid body besides glomus cells?
A rich supply of capillaries.
79
What is the current understanding of the mechanism of the carotid bodies?
The precise mechanism is still uncertain.
80
What do many physiologists believe about glomus cells?
They are the sites of chemoreception.
81
How does the discharge rate of the carotid body afferent fibers get affected?
By modulation of neurotransmitter release from glomus cells by physiological and chemical stimuli.
82
What do peripheral chemoreceptors respond to?
Decreases in arterial Po2 and pH, increases in arterial Pco2
## Footnote
Peripheral chemoreceptors are sensitive to changes in blood gas levels.
83
At what arterial Po2 level does sensitivity in peripheral chemoreceptors begin?
Around 500 mm Hg
## Footnote
This threshold indicates the beginning of their sensitivity to changes in arterial Po2.
84
Describe the relationship between firing rate and arterial Po2.
Very nonlinear; little response until Po2 is below 100 mm Hg, then rate rapidly increases
## Footnote
This nonlinear relationship highlights the chemoreceptors' sensitivity to severe hypoxemia.
85
What is notable about the blood flow in carotid bodies?
Very high blood flow for their size
## Footnote
This high blood flow is essential despite their high metabolic rate.
86
What drives the response of peripheral chemoreceptors?
Po2, not oxygen concentration
## Footnote
This distinction emphasizes the receptors' specific sensitivity to partial pressure of oxygen.
87
How quickly can the discharge rate of peripheral chemoreceptors alter?
Very fast; can change during the respiratory cycle
## Footnote
Small cyclic changes in blood gases affect their discharge rate.
88
What is the primary role of peripheral chemoreceptors in humans?
Responsible for all increase of ventilation in response to arterial hypoxemia
## Footnote
This highlights their critical function in respiratory regulation.
89
What can happen in the absence of peripheral chemoreceptors during severe hypoxemia?
Ventilation may be depressed
## Footnote
This occurs presumably through a direct effect on the respiratory centers.
90
What has been shown in patients with bilateral carotid body resection?
Complete loss of hypoxic ventilatory drive
## Footnote
This indicates the importance of carotid bodies in regulating ventilation during hypoxia.
91
Is there variability in hypoxic ventilatory response among individuals?
Yes, considerable variability exists
## Footnote
This suggests that genetic or environmental factors may influence sensitivity.
92
What physiological change occurs in persons exposed to chronic hypoxia?
Hypertrophy of their carotid bodies
## Footnote
This adaptation may enhance their ability to respond to low oxygen levels.
93
What is the relative importance of peripheral chemoreceptors compared to central chemoreceptors in response to arterial Pco2?
Less important than central chemoreceptors
94
What percentage of the ventilatory response can be attributed to peripheral chemoreceptors when a normal subject breathes a CO2 mixture?
Less than 20%
95
What is a key advantage of peripheral chemoreceptors in ventilation response?
More rapid response to abrupt changes in Pco2
96
Which bodies respond to a fall in arterial pH in humans?
Carotid bodies
97
Do aortic bodies respond to a fall in arterial pH?
No
98
What types of causes can lead to a fall in arterial pH that carotid bodies respond to?
Respiratory or metabolic causes
99
How does the activity of chemoreceptors respond to decreases in arterial Po2?
Potentiated by increases in Pco2 and decreases in pH
100
Fill in the blank: In humans, the carotid bodies respond to a fall in arterial _______.
pH
101
True or False: Peripheral chemoreceptors are the primary responders to changes in arterial Pco2.
False
102
What are pulmonary stretch receptors also known as?
Slowly adapting pulmonary stretch receptors
## Footnote
They are believed to lie within airway smooth muscle.
103
What triggers the discharge of pulmonary stretch receptors?
Distension of the lung
## Footnote
Their activity is sustained with lung inflation and shows little adaptation.
104
Through which nerve do impulses from pulmonary stretch receptors travel?
Vagus nerve
## Footnote
They use large myelinated fibers.
105
What is the main reflex effect of stimulating pulmonary stretch receptors?
Slowing of respiratory frequency
## Footnote
This is due to an increase in expiratory time.
106
What is the Hering-Breuer inflation reflex?
A reflex that slows respiratory frequency due to lung inflation
## Footnote
Demonstrated in rabbit preparations.
107
What effect does inflation of the lungs have on inspiratory muscle activity?
Inhibits further inspiratory muscle activity
## Footnote
This is part of the Hering-Breuer reflex.
108
What occurs during lung deflation regarding respiratory activity?
Initiates inspiratory activity
## Footnote
This is known as the deflation reflex.
109
What is the role of the Hering-Breuer reflexes in ventilation?
Determining the rate and depth of breathing
## Footnote
They modulate the “switching-off” mechanism in the medulla.
110
What happens when bilateral vagotomy is performed?
Causes slow, deep breathing in most animals
## Footnote
This removes the input of pulmonary stretch receptors.
111
In which population are Hering-Breuer reflexes more important?
Newborn babies
## Footnote
Recent studies suggest they are largely inactive in adult humans unless tidal volume exceeds 1 liter.
112
What happens when transient bilateral blockade of the vagus nerves occurs in awake humans?
Does not change either breathing rate or volume
## Footnote
Suggests low activity of Hering-Breuer reflexes in adults.
113
What are irritant receptors thought to lie between?
Airway epithelial cells
114
What stimulates irritant receptors?
Noxious gases, cigarette smoke, inhaled dusts, and cold air
115
How do impulses from irritant receptors travel?
Up the vagus in myelinated fibers
116
What are the reflex effects of irritant receptors?
Bronchoconstriction and hyperpnea
117
What alternative name do some physiologists use for irritant receptors?
Rapidly adapting pulmonary stretch receptors
118
Why are irritant receptors called rapidly adapting pulmonary stretch receptors?
They show rapid adaptation and are involved in additional mechanoreceptor functions
119
In addition to noxious stimuli, what else do irritant receptors respond to?
Stimuli on the airway walls
120
What role might irritant receptors play in asthma attacks?
Bronchoconstriction due to response to released histamine
121
What are J Receptors?
Endings of nonmyelinated C fibers, believed to be in the alveolar walls near capillaries
## Footnote
The term 'juxtacapillary' refers to their location close to capillaries.
122
Where are J Receptors believed to be located?
In the alveolar walls, close to the capillaries
## Footnote
This location is supported by their response to chemicals injected into the pulmonary circulation.
123
What type of fibers do J Receptors use to transmit impulses?
Slowly conducting nonmyelinated fibers
## Footnote
These fibers pass impulses up the vagus nerve.
124
What physiological responses can J Receptors trigger?
Rapid, shallow breathing or apnea with intense stimulation
## Footnote
Apnea is a temporary cessation of breathing.
125
What activates J Receptors?
Engorgement of pulmonary capillaries and increases in interstitial fluid volume
## Footnote
These changes occur in the alveolar wall.
126
What conditions may J Receptors be associated with?
Left heart failure and interstitial lung disease
## Footnote
They may contribute to rapid, shallow breathing and dyspnea.
127
True or False: J Receptors are involved in the sensation of difficulty in breathing.
True
## Footnote
This sensation is referred to as dyspnea.
128
What supplies bronchial C fibers?
Bronchial circulation
## Footnote
Unlike J receptors, which are supplied by pulmonary circulation
129
What do bronchial C fibers respond quickly to?
Chemicals injected into the bronchial circulation
130
What are the reflex responses to stimulation of bronchial C fibers?
* Rapid shallow breathing
* Bronchoconstriction
* Mucous secretion
131
What do the nose, nasopharynx, larynx, and trachea contain?
Receptors that respond to mechanical and chemical stimulation
132
What are the reflex responses described in relation to upper airway receptors?
Sneezing, coughing, bronchoconstriction
133
What may occur if the larynx is irritated mechanically?
Laryngeal spasm
134
What is a common cause of laryngeal spasm?
Insertion of an endotracheal tube with insufficient local anesthesia
135
Fill in the blank: The receptors in the upper airway are an extension of the _______ receptors.
Irritant
136
What is the role of joint and muscle receptors during exercise?
They are believed to be part of the stimulus to ventilation during exercise, especially in the early stages.
137
What do muscle spindles in muscles like the intercostal muscles and diaphragm sense?
They sense elongation of the muscle.
138
How do muscle spindles contribute to respiratory control?
The information from muscle spindles is used to reflexly control the strength of contraction.
139
What sensation may be involved due to the activity of muscle spindles during respiratory efforts?
The sensation of dyspnea.
140
What can cause reflex hypoventilation or apnea?
An increase in arterial blood pressure through stimulation of the aortic and carotid sinus baroreceptors.
141
What is the effect of a decrease in blood pressure on ventilation?
It may result in hyperventilation.
142
Fill in the blank: Muscle spindles are involved in the sensation of _______ when respiratory efforts are unusually large.
dyspnea
143
True or False: Arterial baroreceptors only respond to decreases in blood pressure.
False
144
True or False: the response to central receptors is faster than peripheral since they are closer to the brain
False. However, central receptors provide a stronger stimulus
145
What is the typical respiratory pattern following pain stimulation?
Apnea followed by hyperventilation
## Footnote
Pain often leads to a temporary cessation of breathing (apnea) followed by increased breathing rate (hyperventilation).
146
What effect does heating of the skin have on ventilation?
Hyperventilation
## Footnote
Heating the skin can trigger an increase in the rate and depth of breathing.
147
What is the most important factor in the control of ventilation under normal conditions?
The Pco2 of the arterial blood
## Footnote
The sensitivity of this control is remarkable.
148
How much does the arterial Pco2 vary during daily activities?
Probably held to within 3 mm Hg
## Footnote
During sleep, it may rise a little more.
149
What is are two methods to measure the ventilatory response to CO2?
Having the subject inhale CO2 mixtures or rebreathe from a bag
Measure the inspiratory pressure after brief airway occlusion
## Footnote
This allows the inspired Pco2 to gradually rise.
150
What is the composition of the gas mixture used in the rebreathing technique for measuring ventilatory response?
7% CO2 and 93% O2
## Footnote
As the subject rebreathes, metabolic CO2 is added to the bag.
151
At what rate does the Pco2 of the bag gas increase during the rebreathing technique?
About 4 mm Hg·min−1
## Footnote
The O2 concentration remains relatively high.
152
What happens to ventilation for a given Pco2 when Po2 is lowered?
Ventilation is higher and the slope of the line becomes steeper
## Footnote
There is considerable variation between subjects.
153
How much does ventilation increase for each 1 mm Hg rise in Pco2 with normal Po2?
About 2 to 3 liters·min−1
## Footnote
This is based on experiments adjusting the inspired mixture to yield a constant alveolar Po2.
154
What equipment is used to measure inspiratory pressure during airway occlusion?
A mouthpiece attached to a valve box
## Footnote
The inspiratory port has a shutter that closes during expiration.
155
What is the purpose of the shutter in the valve box during the measurement process?
To occlude the airway during the first part of the next inspiration
## Footnote
The subject is unaware of the shutter's operation.
156
What is P0.1 in the context of measuring respiratory drive?
The pressure generated during the first 0.1 s of attempted inspiration
## Footnote
It serves as a measure of respiratory center output.
157
How does P0.1 relate to the mechanical properties of the respiratory system?
It is largely UNaffected by the mechanical properties of the respiratory system
## Footnote
However, P0.1 is influenced by lung volume.
158
What variables can the method of measuring P0.1 be used to study?
Respiratory sensitivity to CO2, hypoxemia, and other variables
## Footnote
This highlights the method's versatility in respiratory studies.
159
Fill in the blank: The pressure generated during the first 0.1 s of attempted inspiration is known as _______.
P0.1
160
True or False: The shutter during the measurement process remains open during expiration.
False
## Footnote
The shutter closes during expiration.
161
What effect does a reduction in arterial Pco2 have on ventilation?
It reduces the stimulus to ventilation
## Footnote
For example, hyperventilating can temporarily eliminate the urge to breathe.
162
What happens to an anesthetized patient who is overventilated?
They may stop breathing for a minute or so.
163
Why do some swimmers hyperventilate on the starting block?
To reduce the urge to breathe during the race.
164
What factors reduce the ventilatory response to CO2?
Sleep
Increasing age
Genetic factors
Drugs
Training
165
How do trained athletes and divers typically respond to CO2?
They tend to have a low CO2 sensitivity.
166
Which drugs are known to depress the respiratory center?
* Opiates
* Barbiturates
167
What is a common result of overdosing on opiates or barbiturates?
Marked hypoventilation.
168
What happens to the ventilatory response to CO2 when the work of breathing is increased?
It is reduced.
## Footnote
The drive is still strong but the external resistance reduces the resulting ventilation
169
What mechanism can partly explain the small ventilatory response to CO2 in patients with chronic lung disease?
Increased airway resistance.
170
What effect do bronchodilators have on patients with chronic lung disease?
They often increase the ventilatory response.
171
What evidence exists regarding the respiratory center in patients with chronic lung disease?
The sensitivity of the respiratory center is reduced.
172
Why does increasing work of breathing or chronic lung disease cause a decrease in respiratory drive in response to CO2?
trick question! Respiratory drive is not reduced, but it is not translated into more ventilation. Similar to how the same effort will move a light weight quickly but a heavy weight slowly
173
What is the main stimulus to increase ventilation in response to PCO2?
The main stimulus comes from the central chemoreceptors.
174
How do central chemoreceptors respond to increased arterial PCO2?
They respond to the increased H+ concentration of the brain extracellular fluid near the receptors.
175
What additional stimulus affects ventilation besides central chemoreceptors?
Peripheral chemoreceptors are an additional stimulus.
176
What conditions do peripheral chemoreceptors respond to?
They respond to both the rise in arterial PCO2 and the fall in pH.
177
Fill in the blank: The increase in ventilation when arterial PCO2 rises is primarily due to _______.
central chemoreceptors
178
True or False: The only stimulus for increased ventilation is from central chemoreceptors.
False
179
How can the effects of decreases PO2 be studied?
Breathing hypoxic gas mixtures
## Footnote
The study measures end-tidal Po2 and Pco2 as surrogates for arterial values.
180
To what level can the alveolar Po2 be reduced before a significant increase in ventilation occurs?
To the vicinity of 50 mm Hg
## Footnote
This is observed when the alveolar Pco2 is kept at about 36 mm Hg.
181
How does raising Pco2 affect ventilation at any Po2 level?
It increases ventilation
## Footnote
This is supported by comparisons in the study (see Figure 8.4).
182
When Pco2 is increased, at what is the threshold at which Po2 starts to stimulate ventilation?
100mmHg
## Footnote
This is different from the situation when Pco2 is normal.
183
True or False: when you combine the effects of PCO2 and PO2 on ventilation, it equals the sum of both effects
FALSE! The combined effects of both stimuli exceed the sum of each stimulus given separately
## Footnote
This highlights the synergistic effect of CO2 and O2 levels on ventilation.
184
Are there differences in the magnitude of the response to reduced Po2 among individuals?
Yes, there are large differences
## Footnote
Individual variability can influence the respiratory response.
185
What is the role of Po2 in the control of ventilation under normal conditions?
The role of Po2 in the day-to-day control of ventilation is small.
186
What occurs in response to hypoxemia due to pneumonia or ascent to high altitude?
A large increase in ventilation occurs.
187
Why does the hypoxic drive to ventilation become important in patients with severe chronic lung disease?
They have chronic CO2 retention and lost most of their increase in the stimulus to ventilation from CO2.
188
What happens to the pH of the brain extracellular fluid in patients with chronic lung disease?
The pH has returned to near normal despite a raised Pco2.
189
What is the primary stimulus to additional ventilation in patients with chronic lung disease?
Arterial hypoxemia.
190
What may happen if a patient with chronic lung disease is given a high O2 mixture?
Ventilation may decrease significantly.
191
What factors are involved in the response to high O2 mixtures in patients with chronic lung disease?
Release of hypoxic vasoconstriction and changes in ventilation-perfusion matching.
192
How is the ventilatory state best monitored?
By measuring arterial Pco2.
193
How does hypoxemia stimulate ventilation?
By its action on the carotid and aortic body chemoreceptors.
194
Does hypoxemia have any effect on central chemoreceptors?
No, hypoxemia depresses respiration in the absence of peripheral chemoreceptors.
195
What can prolonged hypoxemia cause in terms of cerebral chemistry?
Mild cerebral acidosis.
196
Fill in the blank: Prolonged hypoxemia can stimulate ventilation through _______.
mild cerebral acidosis.
197
What type of change in arterial blood pH increases ventilation
A reduction in arterial blood pH stimulates ventilation
## Footnote
This response can be difficult to separate from the effects of a rise in Pco2.
198
What condition is mentioned that demonstrates increased ventilation due to low pH and low Pco2?
Partly compensated metabolic acidosis, such as in diabetic ketoacidosis
## Footnote
This condition results in increased ventilation, which contributes to the reduced Pco2.
199
Which chemoreceptors are primarily affected by a reduction in arterial pH?
Peripheral chemoreceptors
## Footnote
Central chemoreceptors may also be affected if the change in pH is significant.
200
What happens to the blood-brain barrier when there is a significant change in blood pH?
It becomes partly permeable to H+ ions
## Footnote
This can potentially affect the central chemoreceptors or the respiratory center.
201
True or False: A fall in arterial blood pH can be studied in experimental animals at constant Pco2.
True
## Footnote
This allows for a clear demonstration of the stimulus to ventilation from pH changes.
202
Fill in the blank: Patients with _______ show increased ventilation due to low pH and low Pco2.
partly compensated metabolic acidosis
203
What happens to ventilation during exercise?
Ventilation increases promptly and may reach very high levels during strenuous exertion.
204
How much more is the total ventilation during exercise compared to resting level?
More than 15 times
205
How does ventilation change at low to moderate levels of exercise?
It closely matches the increase in O2 uptake and CO2 output.
206
What is remarkable about the cause of increased ventilation during exercise?
It remains largely unknown.
207
What happens to arterial Pco2 during exercise?
It does not increase and typically falls during severe exercise.
208
What typically happens to arterial Po2 during exercise?
It usually increases slightly, although it may fall at very high work levels.
209
What happens to arterial pH during moderate and high levels of exercise?
It remains nearly constant during moderate exercise but falls at high levels due to lactic acidosis
210
What has been suggested as a stimulus for increased ventilation during exercise?
Passive movement of the limbs
Partial pressure fluctuation
Allostatic control of PCO2 in the brain
Heat
Motor cortex impulses
PCO2 load in the veins
211
Describe the effects that passive limb movements may have on ventilation during exercise
A reflex with receptors presumably located in joints or muscles may help increase ventilation during the first few seconds of exercise
212
What do oscillations in arterial Po2 and Pco2 do during exercise?
They may stimulate the peripheral chemoreceptors.
213
What is one hypothesis regarding central chemoreceptors during exercise?
They increase ventilation to hold arterial Pco2 constant.
The Pco2 setpoint may be reset lower temporarily
214
How is ventilation linked to the additional CO2 load during exercise?
An increase in CO2 load correlates well with ventilation.
215
What is a problem with the hypothesis regarding CO2 load and ventilation during exercise?
No suitable receptor has been found.
216
True or False: All theories proposed for increased ventilation during exercise are completely satisfactory.
False
217
What happens to voluntary control of breathing during sleep?
Voluntary control and other factors that override automatic control of breathing during wakefulness are lost
## Footnote
This loss is due to the absence of excitatory inputs to the medullary centers from the reticular formation and hypothalamus.
218
How do ventilatory responses to Pco2 and Po2 change during sleep?
Ventilatory responses to Pco2 and Po2 are decreased
## Footnote
This decrease affects the body's ability to respond to changes in carbon dioxide and oxygen levels.
219
What happens to the tone of the upper airway dilating muscles during sleep?
The tone of the upper airway dilating muscles decreases
## Footnote
The muscles affected include the genioglossus and palatal muscles.
220
What can the decrease in tone of upper airway muscles during sleep predispose individuals to?
Upper airway obstruction and impaired ventilation
## Footnote
This condition is significant as it can lead to sleep-related breathing disorders.
221
Fill in the blank: During sleep, the wakefulness drive to breathe is mediated by _______.
[excitatory inputs to the medullary centers from the reticular formation and hypothalamus]
222
What is Cheyne-Stokes respiration?
A pattern of periodic breathing characterized by periods of apnea of 10 to 20 seconds, separated by hyperventilation.
## Footnote
This pattern is often seen in subjects with severe hypoxemia during sleep, particularly at high altitudes or in patients with severe heart failure or neurologic injury.
223
What are the typical characteristics of Cheyne-Stokes respiration?
Periods of apnea and hyperventilation with gradually waxing and waning tidal volume.
## Footnote
Apnea lasts 10 to 20 seconds and is followed by equal periods of hyperventilation.
224
In which conditions is Cheyne-Stokes respiration commonly observed?
* High altitude
* Severe heart failure
* Neurologic injury
## Footnote
It is particularly noted at night during sleep.
225
What physiological issue contributes to Cheyne-Stokes respiration?
Problems with feedback control and increased ventilatory responsiveness to changes in Pco2.
## Footnote
This leads to delays in sensing changes in Pco2, causing overshooting of the respiratory center.
226
How can Cheyne-Stokes respiration be experimentally reproduced?
By lengthening the distance blood travels from the lung to the brain.
## Footnote
This results in a long delay before central chemoreceptors sense changes in Pco2.
227
What is another abnormal pattern of breathing that can occur during sleep?
Ataxic pattern of breathing.
## Footnote
This pattern is marked by irregular ventilation and variable periods of apnea, often seen in chronic opiate users.
228
True or False: Cheyne-Stokes respiration is only found in patients with heart failure.
False
## Footnote
It can also occur at high altitudes and in patients with neurologic injuries.
229
Fill in the blank: Cheyne-Stokes respiration is characterized by _______ of 10 to 20 seconds.
apnea
## Footnote
This is a key feature of the breathing pattern.
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