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Block 2 Exam 3 > Mashour: Control of Breathing > Flashcards

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
Q

As arterial PCO2 rises, what occurs to ensure that the brain does not become too acidified?

A

Cerebral vasodilatation → increases CO2 washout in brain → results in reduced brain acidification → reduces increased ventilatory drive from central chemoreceptors

26
Q

The point at which rhythmic ventilation ceases at a given pCO2

A

Apneic threshold

27
Q

What is the normal pH of CSF?

A

7.32

28
Q

For a given increase in PCO2, is there a greater change in pH in the CSF or blood?

A

CSF

29
Q

If CSF pH is displaced for a prolonged period of time, there will be a compensatory change in (blank)

A

[HCO3-]

30
Q

With the high levels of CO2, does the CSF pH return all the way to 7.32?

A

No, but the response occurs more rapidly than in blood.

31
Q

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?

A

The CSF is more important in its effect on changes in arterial pCO2 and level of ventilation

32
Q

Located in the bifurcation of the common carotid arteries (carotid bodies) and above and below the arch of the aorta (aortic bodies)

A

Peripheral chemoreceptors

33
Q

2 cell types in the carotid bodies that work hand in hand to modulate our response to pO2

A 
Type I (large amount of dopamine)
Type II (rich capillary supply)
34
Q

Three things peripheral chemoreceptors respond to

A
  1. arterial pO2 (chief stimulant)
  2. pH
  3. arterial pCO2 increases
35
Q

When does sensitivity to changes in arterial pO2 begin? What level in mmHg?

A

Less than 50mmHg

36
Q

Responsible for all of the increase in ventilation in response to arterial hypoxemia

A

peripheral chemoreceptors

37
Q

Hypotension provides a clinical example of how the peripheral chemoreceptors work. Discuss.

A

With hypotension, there is decreased blood flow or O2 delivery to the carotid bodies, and this leads to an increase in ventilation.

38
Q

3 types of lung receptors

A
  1. pulmonary stretch receptors
  2. irritant receptors
  3. J receptors
39
Q

lie within the airway smooth muscle
discharge in response to distention of the lung
activity is sustained with lung inflation

A

Pulmonary stretch receptors

40
Q

Stimulating these receptors will increase expiratory time and therefore reduce the respiratory rate

A

Pulmonary stretch receptors

41
Q

Important reflex in newborns, in which inflation of the lungs further prohibits inspiratory activity, while deflation initiates inspiratory activity.

A

Hering-Breuer inflation reflex

42
Q

lie between airway epithelial cells

stimulated by noxious gases, smoke, dust, and cold air

A

Irritant receptors

43
Q

When you have a stimulus like smoke, it may cause broncoconstriction, which can be especially problematic for what type of patients?

A

Patients with COPD

44
Q

Pulmonary edema is a classic example of activation of these receptors.

A

J receptors

45
Q

These are located in the alveolar walls near the capillaries

A

J receptors

46
Q

What’s the net effect of activation of the J-receptors?

A

Rapid, shallow breathing. When a patient comes in with pneumonia, this can be relevant.

47
Q

engorgement of the pulmonary capillaries and increases in the interstitial fluid volume of alveolar wall activates what type of receptors?

A

J receptors

48
Q

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.

A

Gamma system

49
Q

Concerning the arterial baroreceptors, a decrease in BP causes

A

hyperventilation

50
Q

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

A

Arterial pCO2

51
Q

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.

A

CO2, O2

52
Q

(blank) has little effect in day-to-day management of minute ventilation.

A

O2

53
Q

Does hypoxemia have an effect on central chemoreceptors?

A

No

54
Q

If no peripheral chemoreceptors, what would occur in the case of hypoxemia?

A

Respiratory depression

55
Q

If you reduce pH without an increase in pCO2, this can produce an increase in (blank)

A

Ve (minute volume)

56
Q

Minute volume (Ve)

A

Minute volume= tidal volume * respiratory rate

Block 2 Exam 3 (19 decks)

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