Mashour: Control of Breathing Flashcards

1
Q

Reticular formation below the fourth ventricle

A

Medullary respiratory center

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2
Q

Intrinsic respiratory rhythm generator, likened to the SA node

A

Pre-Botzinger complex

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3
Q

2 regions of the medullary respiratory center

A
  1. dorsal respiratory group = inspiration

2. ventral respiratory group = expiration

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4
Q

Where is the pre-Botzinger complex located?

A

Caudal to the Botzinger complex
Rostral to the ventral respiratory group
Located in the Rostral ventrolateral medulla

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5
Q

Discuss how the Pre-Botzinger Complex works?

A

starts with a latent period
crescendo of action potentials
stronger inspiratory muscle activity (ramp-type pattern)
action potentials then cease
inspiratory muscle tone falls to pre-inspiratory level

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6
Q

Motor nucleus of CN IX and CN X

A

Nucleus ambiguus

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7
Q

If this is destroyed, may cause respiratory failure

A

Nucleus ambiguus (seen in polio)

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8
Q

Fasciculus solitarious

A

Smaller collection of neurons similar to nucleus ambiguus

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9
Q

Inspiratory ramp can be turned off by this center. It can cause shortened inspiration and an increased breathing rate.

A

Pneumotaxic center

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10
Q

Inspiration can also be modulated by these two nerves

A

Glossopharyngeal and vagal nerves

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11
Q

The medulla is the (blank) area

A

Expiratory

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12
Q

During quiescent breathing, ventilation is achieved by (blank) contraction of inspiratory muscles, followed by (blank) relaxation of chest wall

A

Active; passive

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13
Q

This is found in the lower pons

A

Apneustic center

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14
Q

Impulses from this center have an excitatory effect on the inspiratory center of the medulla

A

Apneustic center (sectioning in experiments above this area leads to prolonged inspiratory gasps interrupted by transient expiratory efforts

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15
Q

This is found in the upper pons

A

Pneumotaxic center

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16
Q

This inhibits inspiration and controls inspiratory volume. Involved in fine tuning of respiratory rhythm

A

Pneumotaxic center

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17
Q

10-20 second periods of apnea followed by equal periods of hyperpnea. Seen with high altitude, severe heart disease, or neurological injury

A

Cheyne-Stokes respirations

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18
Q

Describe apneustic breathing

A

Deep breath in, hold it, then exhale

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19
Q

This structure can override the function of the brainstem within limits

A

Cortex

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20
Q

Which is easier, voluntary hyperventilation or voluntary hypoventilation?

A

Voluntary hyperventilation, because when you hold your breath, it becomes very uncomfortable, and your midbrain will override your cortex and cause you to start breathing

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21
Q

Involved in affective states such as fear and rage

A

Limbic system and hypothalamus

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22
Q

Sensors for drive of breathing

A

Central chemoreceptors
Peripheral chemoreceptors
Lung receptors

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23
Q

These receptors respond to changes in H+ concentration. Increase in [H+] stimulates ventilation

A

Central chemoreceptors

24
Q

How does CO2 levels in the blood regulate ventilation?

A

By its effect on pH in the CSF

25
As arterial PCO2 rises, what occurs to ensure that the brain does not become too acidified?
Cerebral vasodilatation → increases CO2 washout in brain → results in reduced brain acidification → reduces increased ventilatory drive from central chemoreceptors
26
The point at which rhythmic ventilation ceases at a given pCO2
Apneic threshold
27
What is the normal pH of CSF?
7.32
28
For a given increase in PCO2, is there a greater change in pH in the CSF or blood?
CSF
29
If CSF pH is displaced for a prolonged period of time, there will be a compensatory change in (blank)
[HCO3-]
30
With the high levels of CO2, does the CSF pH return all the way to 7.32?
No, but the response occurs more rapidly than in blood.
31
Renal compensation for high pCO2 takes 2-3 days, while CSF pH is mitigated much more rapidly. What does the more rapid compensation for rising CO2 in the CSF mean?
The CSF is more important in its effect on changes in arterial pCO2 and level of ventilation
32
Located in the bifurcation of the common carotid arteries (carotid bodies) and above and below the arch of the aorta (aortic bodies)
Peripheral chemoreceptors
33
2 cell types in the carotid bodies that work hand in hand to modulate our response to pO2
``` Type I (large amount of dopamine) Type II (rich capillary supply) ```
34
Three things peripheral chemoreceptors respond to
1. arterial pO2 (chief stimulant) 2. pH 3. arterial pCO2 increases
35
When does sensitivity to changes in arterial pO2 begin? What level in mmHg?
Less than 50mmHg
36
Responsible for all of the increase in ventilation in response to arterial hypoxemia
peripheral chemoreceptors
37
Hypotension provides a clinical example of how the peripheral chemoreceptors work. Discuss.
With hypotension, there is decreased blood flow or O2 delivery to the carotid bodies, and this leads to an increase in ventilation.
38
3 types of lung receptors
1. pulmonary stretch receptors 2. irritant receptors 3. J receptors
39
lie within the airway smooth muscle discharge in response to distention of the lung activity is sustained with lung inflation
Pulmonary stretch receptors
40
Stimulating these receptors will increase expiratory time and therefore reduce the respiratory rate
Pulmonary stretch receptors
41
Important reflex in newborns, in which inflation of the lungs further prohibits inspiratory activity, while deflation initiates inspiratory activity.
Hering-Breuer inflation reflex
42
lie between airway epithelial cells | stimulated by noxious gases, smoke, dust, and cold air
Irritant receptors
43
When you have a stimulus like smoke, it may cause broncoconstriction, which can be especially problematic for what type of patients?
Patients with COPD
44
Pulmonary edema is a classic example of activation of these receptors.
J receptors
45
These are located in the alveolar walls near the capillaries
J receptors
46
What’s the net effect of activation of the J-receptors?
Rapid, shallow breathing. When a patient comes in with pneumonia, this can be relevant.
47
engorgement of the pulmonary capillaries and increases in the interstitial fluid volume of alveolar wall activates what type of receptors?
J receptors
48
This system is located in the intercostal muscles and the diaphragm. Senses elongation and dyspnea (inability to breathe). Think of COPD, flattened diaphragm, so more work involved.
Gamma system
49
Concerning the arterial baroreceptors, a decrease in BP causes
hyperventilation
50
The most important factor in the control of ventilation under normal conditions is
Arterial pCO2
51
You only need a slight change in (blank) to cause a response in ventilation rate, but a larger change in (blank) to cause a response in minute ventilation rate.
CO2, O2
52
(blank) has little effect in day-to-day management of minute ventilation.
O2
53
Does hypoxemia have an effect on central chemoreceptors?
No
54
If no peripheral chemoreceptors, what would occur in the case of hypoxemia?
Respiratory depression
55
If you reduce pH without an increase in pCO2, this can produce an increase in (blank)
Ve (minute volume)
56
Minute volume (Ve)
Minute volume= tidal volume * respiratory rate