Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Physiology > Control of Breathing (B2: W7) > Flashcards

Control of Breathing (B2: W7) Flashcards

1
Q

Where is the “central controller” for respiration?

A
  • Brainstem
  • Cortex - voluntary control
  • Limbic system, hypothalamus
    • Lesser degree
    • E.g. fear and rage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Where are the respiratory centers in the breainstem?

A

In the pons and medulla

  • Poorly defined collection of neurons rather than discrete nuclei
  • 3 main groups of neurons
    • Medullary respiration center (main headquarters)
    • Apneustic center
    • Pneumotaxic center
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What two regions of the medullary response center are overlapping, and what is each responsible for?

A

Dorsal respiratory group = inspiration

Ventral respiratory group = expiration

DIVE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the organization of the medullary respiratory center?

A

Reticular formation below the 4th ventricle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Where is the pre-Botzinger complex, and what is it responsible for?

A

Medullary respiratory center

  • Intrinsic respiratory rhythm generator (liken to SA node)
    • Mechanism unknown
  • Caudal to Botzinger complex
  • Rostral to the ventral respiratory group
    • Located in the reostral ventrolateral medulla (RVLM)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How do pre-Botzinger complex nuclei affect inspiration?

A
  • Starts with a latent period
  • Crecendo of action potentials
    • Causes stronger inspiratory muscle activity (ramp-type pattern)
  • Action potentials then cease
    • Inspiratory muscle tone falls to pre-inspiratory level
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the motor nucleus of CN IX and CN X, and what are the implications if it is destroyed?

A

Nucleus ambiguus

  • If destroyed, there is complete respiratory failure
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does the pneumotaxic center (dorsal) affect inspiration?

A

Input from the pneumotaxic center shortens breathing

  • Breathing rate increases
  • Breathing rate is also modulated by glossopharyngeal and vagal nerves
    • Terminate in the tractus solitarus, close to the inspiratory center
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where do afferent signals from airways, lungs, heart, and peripheral chemoreceptors terminate?

A

CN IX and CN X

  • Glossopharyngeal and vagal
  • These nerves go into tractus solitarus
    • Part of the medulla
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe the expiratory area during normal breathing

A
  • Quiescent during normal quiet breathing
    • Ventilation in this state is achieved by active contraction of inspiratory muscles (mainly diaphragm)
    • Followed by passive relaxation of the chest wall
  • More forceful breathing: increased activity of expiratory cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What happens in animals if there is a transection above the apneustic center (lower pons)?

A

Affects breathing patterns

  • Expiramental sectioning leads to prolonged inspiratory gasps (apneuses)
    • Interrupted by transient expiratory efforts
  • Apneuses are seen in severe breain injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What effect do impulses from the apneustic center have on inspiration?

A

Excitatory effect on the inspiratory center of the medulla

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the role of the pneumotaxic center (upper pons) on inspiration?

A
  • Inhibits inspiration and controls inspiratory volume
  • Involved in fine tuning of respiratory rhythm
    • If ablated, normal respiratory rhythm intact
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What effect does a transection of the pneumotaxic center have on breathing?

A

Irregular rate or depth of breathing

  • Gasping, ataxic, or both
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What areas are damaged, causing transient vs. permanent apnea?

A
  • Transient apnea: lesion in the temporal lobe
  • Permament apnea: lower pons and medulla (around nucleus ambiguus)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What causes central neurogenic hyperventilation?

A

Medial reticular formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is Ondine’s curse and what causes it?

A

Loss of automaticity

  • When you fall asleep, you lose the ability to breathe on your own
  • Medial reticular formation or anterolateral C2 (reticulospinal pathway from cordotomy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe Cheyne-Stokes respirations

A
  • 10-20 second periods of apnea followed by equal periods of hyperpnea
    • Seen with high altitude, severe heart disease, or sever neurological injury
  • Unstable feedback in respiratory control system
    • Overblow the PCO2 so that it is too low, then breathing has to stop (apnea) to bring it back up
    • Then PCO2 will be too high, and rapid breathing returns
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How does the cortex influence breathing?

A

Cortex can override the function of the breainstem within limits

  • Voluntary hyperventilation can halve the PCO2 to the point of muscular tetany
    • Will increase pH by 0.2
  • Voluntary hypoventilation is more difficult
    • Influenced by PCO2 and PO2
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What sensors in the body affect drive of breathing?

A
  • Central chemorecptors
  • Peripheral chemoreceptors
  • Lung receptors
  • Other receptors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Where are the central chemoreceptors located?

A
  • Rostral zone
    • Lateral to pyramids
    • Medial to CN VII to X rootlets
  • Caudal zone
    • Lateral to pyramids
    • Medial to CN XII rootlet
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What changes are central chemoreceptors responsive to?

A
  • Respond to change in H+ concentration
    • Increase in [H+] stimulates ventilation, and vice versa
  • Composition of the extracellular fluid is managed by CSF, local blood flow, and local metabolism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

How do CO2 levels in the blood regulate ventilation?

A

CSF = most important region

  • CO2 levels in blood regulate ventilation by its effect on pH in the CSF
  • CSF is impermeable to H+ and HCO3- ions
  • Permeable to CO2 from cerebral blood vessels
    • Will liberate H+ from the CSF
    • Stimulates chemoreceptors
    • Hyperventilation
24
Q

WHat happens in the brain as arterial PCO2 rises?

A

Cerebral vasodilatation

  • Results in increase CO2 washout in brain PCO2 levels
    • Leads to reduced brain acidification
    • Causes a reduction in the increased ventilatory drive from central chemoreceptors
  • This is the reason for morning headaches in people who have sleep apnea
    • Apnea → increased PCO2
    • Vasodilation in the brain
25
Q

How does hyperventilation affect pH in CSF?

A

Decrease in PCO2 → increase in pH in CSF

  • Less acidic
26
Q

What is the apneic threshold?

A

The point at which rhythmic ventilation ceases at a given PCO2

  • PCO2 is so low that breathing stops
27
Q

What is the normal pH of the CSF?

A

7.32

  • Due to reduced protein in fluid and less buffering capacity
  • Change in CSF pH for a given PCO2 is much greater than with blood
28
Q

What happens if CSF pH is displaced for a prolonged period of time?

A
  • A compensatory change in [HCO3-] occurs as a result of transport across the blood-brain barrier
  • CSF pH does not return all the way to 7.32, but occurs more rapidly than blood
    • Renal compensation takes 2-3 days
  • More rapid compensation means CSF is more important in effect on changes in arterial PCO2 and level of ventilation
29
Q

What happens to the CSF of patients with chronic lung disease and chronic CO2 retention (i.e. advanced COPD or idiopathic pulmonary fibrosis)?

A

These patients have normal CSF pH

  • Have abnormally low ventilation for their given PCO2
  • They breathe normally, but the PCO2 is elevated
    • Compensation
    • Do not hyperventilate to blow off CO2
30
Q

Where are peripheral chemoreceptors located?

A

Carotid bodies: In the bifurcation of the common carotid arteries

Aortic bodies: Above and below the arch of the aorta

31
Q

What are the two cell types in the carotid body peripheral chemoreceptors?

A
  1. Type I: glomus cells
    1. Large amounts of dopamine
  2. Type II: sustentacular cells
    1. Rich capillary supply
    2. Modulation of neurotransmitter release by physiologic and chemical stimuli affects discharge rate of carotid afferent fibers
32
Q

What changes do peripheral chemoreceptors respond to?

A
  • Arterial PO2 (chief stimulant)
    • Sensitivity to changes areound 75 mm Hg
    • Increases markedly PO2 < 50 mm Hg
  • pH
  • Arterial PCO2 increases
33
Q

What happens in the absence of peripheral chemoreceptors?

A

Severe hypoxemia depresses ventilation

  • Presumed through a direct effect on respiratory centers
  • These receptors are responsible for all of the increase in ventilation in response to arterial hypoxemia
34
Q

How does hypotension affect the peripheral chemoreceptors and subsequently ventilation?

A
  • With hypotension, there is decreased blood flow to the carotid bodies
    • Decreased O2 delivery
  • Increase in ventilation
35
Q

What are the different lung receptors that have an effect on breathing?

A
  • Pulmonary stretch receptors
  • Irritant receptors
  • J receptors
36
Q

Where are pulmonary stretch receptors and when are tehy activated?

A
  • Lie within the airway smooth muscle
  • Discharge in response to distention of the lung
  • Activity is sustained with lung inflation
37
Q

What happens upon stimulation of pulmonary stretch receptors?

A

Increase expiratory time

  • Reduced respiratory rate (Hering-Breuer inflation reflex)
  • Inflation of the lungs further inhibits inspiratory muscle activity
  • Deflation will initiate inspiratory activity (deflation reflex)
    • Negative feedback loop
38
Q

Why are plumonary stretch receptors more important in infants?

A
  • In infants: as the lung is stretched, there is a reflexive decrease in respiration
    • Can reduce minute volume
  • These reflexes are inactive in adults unless large tidal volumes are encouraged
    • E.g. exercise with > 1L tidal volumes
39
Q

How does a transient bilateral blockade of the vagus nerve affect respiration?

A

Bilateral blockade of vagus does not affect respiratory rate or volume

40
Q

Where are the irritant receptors of the lung and how are they activated?

A
  • Lie between airway epithelial cells
    • Travel via the vagus nerve
  • Stimulated by nocious gases, smoke, dust, and cold air
    • All of these are important stimulators of COPD and asthma exacerbations
41
Q

How do the irritant receptors of the lung respond to stimulation?

A

Reflex effects include bronchoconstriction and hyperpnea

  • May play a role in bronchoconstriction of asthma attacks in response to released histamine
42
Q

Where are the J (juxta-capillary) receptors of the lung and how are they activated?

A
  • Located in the alveolar walls near the capillaries
    • Travel up vagus nerve slowly in non-myelinated fibters
  • Respond quickly to chemicals injected into the pulmonary circuit
  • Net effect: rapid, shallow breathing
    • Intense stimulation = apnea
43
Q

What is the significance of the nasal and upper airway receptors?

A
  • Respond to mechanical and chemical stimulation
    • An extension of teh irritant receptors
  • Reflex responses include sneeze, cough, bronchoconstriction, and laryngeal spasm
44
Q

What is the significance of the joint and muscle receptors?

A
  • Impulses from moving limbs in early stage exercise will stimulate ventilation
    • Increase in minute volume
45
Q

What is the significance of the gamma system?

A
  • Located in intercostal muscles and diaphragm
  • Sense elongation
  • Involved in the sensation of dyspnea
    • Dyspnea = shortness of breath
    • Large respiratory efforts that are required to move lung and chest wall
46
Q

How are arterial baroreceptors involved with ventilation?

A
  • Increase in blood pressure - hypoventilation or apnea
    • Not very common
  • Decrease in blood pressure - hyperventilation
    • Common
    • E.g. sepsis with shock
47
Q

How do pain and temperature play a role in ventilation?

A
  • Pain - apnea followed by hyperventilation
  • Heating of skin - hyperventilation
48
Q

What is the most important factor in the control of ventilation under normal conditions?

A

Arterial PCO2

  • Variation of PCO2 curing the day is about 3 mm Hg
    • Tight control
49
Q

How does PCO2 affect minute ventilation?

A

For every 1 mm Hg rise in PCO2, there is a 2-3 L/min increase in minute ventilation (Ve)

  • Large effect
  • Higher Ve for given PCO2 - the synergistic response
  • Lowering PO2
50
Q

What are the various factors that decrease PCO2?

A
  • Sleep
  • Increased age
  • Genetics
  • Race
  • Personality factors
  • Trained athletes
  • Divers
  • Narcotics
  • Increased work of breathing
51
Q

A small change in PCO2 has a large effect on minute ventilation; how much of a change in PO2 is necessary to affect Ve?

A

Arterial PO2 has to be reduced to <50 mm Hg in order to produce an increase in Ve

  • Versus slight increase in PCO2 that produces the same effect
  • Increased PCO2 will increase Ve at PO2 < 100 mm Hg
    • Hypoxia and hypercarbia synergistic
  • PO2 has little effect on day-to-day management of minute ventilation
    • Except at high altitudes
    • Leads to a large increase in Ve
52
Q

Why is hypoxic ventilatory drive extremely important in patients with chronic lung disease?

A
  • These patients have chronic retention of CO2
    • High PCO2 is normal for them
    • The body doesn’t try to change it
    • Brain ECF pH near normal - little pH stimulation in peripheral chemoreceptors
  • Their breathing is driven by hypoxia
    • Hypoxia increases breathing rate
    • These patients need to be kept on reduced oxygen percentages
      • If O2 saturation is too high, they hypoventilate
53
Q

What effect does hypoxemia have on central chemoreceptors?

A

None

54
Q

What happens when there is hypoxemia in the absence of peripheral chemoreceptors?

A

Hypoxemia produces respiratory despression

  • When hypoexemia is prolonged, it can cause mild cerebral acidosis
    • Leads to increase in minute ventilation (Ve)
55
Q

Does reduced pH without increased PCO2 have an effect on minute ventilation?

A

Yes

  • E.g. diabetic ketoacidosis
    • PCO2/bicarbonate is very low
    • Minute volume/ventilation (Ve) is very high
    • Blowing off a lot of CO2
      • Bicarbonate in blood is down less than a 5
    • pH can get to 6.6
  • Peripheral chemoreceptors - chief site of action
    • Need ventilation to get the minute volume back up
56
Q

Can central chemoreceptors be involved in minute ventilation in response to pH?

A

Can be involved if the change in serum pH is large enough

  • The blood-brain barrier will become partially permeable to H+ ions
57
Q

How does minute ventilation increase during exercise?

A
  • Mechanism unknown
  • Can increase Ve 15-fold
  • PCO2 falls slightly
  • PO2 remains nearly constant
  • Arterial pH falls with heavy exercise due to lactic acidosis

Physiology (29 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions