Lecture # 11 Regulation of Respiration Flashcards

1
Q

______ and _____ are specific areas of the brain stem that make up the respiratory center of the brain.

A

Medulla Oblongata and Pons

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2
Q

The 3 major groups of neurons located in the brain stem (medulla obglongata and Pons) that control respiration are:

A
  1. Dorsal Respiratory Group (DRG)
  2. Ventral Respiratory Group (VRG)
  3. Pneumotaxic center
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3
Q

Which of the 3 major groups of neurons in the brain stem plays the most fundamental role in control of breathing?

A

DRG (Dorsal Respiratory Group)

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4
Q

Dorsal Respiratory Group:

Does the DRG controls inspiration, expiration or both?

A

Inspiration. (remember, expiration is passive at rest)

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5
Q

Dorsal Respiratory Group:

Does the DRG control respiratory rate, rhythm, or depth? or all?

A

Rhythm.

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6
Q

Dorsal Respiratory Group:

Which 2 cranial nerves deliver sensory information to the DRG?

A

Glossopharyngeal (IX) and Vagus (X) nerves.

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7
Q

Dorsal Respiratory Group:

The Dorsal Respiratory Group (DRG) recieves peripheral sensory information through the Glossolpharyngeal and vagus nerves. There 3 peripheral sensory sources for this information, what are they?

A
  1. Peripheral Chemoreceptors
  2. Baroreceptors
  3. Lung receptors.
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8
Q

Dorsal Respiratory Group:

What is the Inspiratory “Ramp” Signal?

A
  • The DRG neurons emit repetitive bursts of inspiratory action potentials in a rhythmic fashion to the diaphragm.
  • The motor signals are NOT transmitted in an instantaneous action potential burst, but begins weakly and increases steadily in a “ramp-like” manner for 2 seconds to cause contraction of the diaphragm (inspiration).
  • the excitatory signal abruptly stops for the next 3 seconds to allow relaxation of diaphragm (passive expiration)
  • The advantage of the ramp signal is that it causes a steady increase in inspiratory volume, rather than a quick twitch of the diaphragm, which would not allow full inflation of lungs.
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9
Q

Dorsal Respiratory Group:

The DRG is responsible for control of respiration during rest or exercise?

A

Rest.

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10
Q

Ventral Respiratory Group:

The VRG controls Inspiration, Expiration or both?

A
  • The VRG is active only with stress or exercise and inactive during normal quiet breathing.
  • It controls BOTH inspiration and expiration during high levels of pulmonary ventilation. (exercise of stress).
  • the VRG stimulates the abdominal muscles to assist in forced exhalation.
  • VRG contributes to respiratory drive to increase pulmonary ventilation and does not appear to participate in basic rhythmic oscillation which controls respiration.
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11
Q

Pneumotaxic Center:

What are the major functions of the Pneumotaxic Center.

A
  • Functions to limit inspiration phase of breathing cycle and secondarily to increase rate of breathing.
  • Controls the “switch-off” point of the inspiratory point and shortens entire respiratory cycle.
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12
Q

Pneumotaxic Center:

Strength of inhibitory signal determines the filling phase and rate of breathing cycle. Therefore, a strong pneumotaxic signal will _____ the inspiration phase and _____ the respiratory rate.

A
  • A strong pneumotaxic signal will SHORTEN the inspiration phase and INCREASE the respiratory rate.
  • A weak pneumotaxic signal will LENGTHEN the inspiration phase and REDUCE respiratory rate.
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13
Q

The Apneustic Center works with which respiratory group of neurons?

It works with the ______ (answered above) to control the _______ of inspiration.

A

Pneumotaxic Center.

Pneumotaxic Center; INTENSITY

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14
Q

T/F: The Hering-Breuer Reflex is responsible for the involuntary gasp one makes when surprised.

A

False: I just made that up.

  • The Hering-Breuer Reflex is a protective feed-back reflex which limits the over-inflation of the lungs.
  • Stretch receptors in the muscular portions of the bronchi an bronchioles transmit signals via the VAGUS nerve to the DRG when lung is overstretched (Tidal volume >1.5L)
  • Feedback response switches off the inspiratory ramp and stops further inflation.
  • This reflex also increases the rate of respiration.
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15
Q

T/F: Much like preload and cardiac output in the CV system, respiratory system control is increased or decreased to match the ventilatory needs of the body.

A

TRUE

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16
Q

Chemical Control of the Respiration:

T/F: Both O2 and CO2 have direct effects on the respiratory centers on the brain.

A

FALSE

Excess CO2 or H ions in the blood act DIRECTLY on the respiratory center to increase strength of both inspiratory & expiratory motor signals.

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17
Q

Chemical Control of the Respiration:

Oxygen does NOT have a direct effect on respiratory centers but acts on peripheral chemoreceptors in the _____ and ______.

A

Carotid and Aortic Bodies.

18
Q

_______ is the area of the brain stem that is highly responsive and sensitive to changes in blood pCO2 or H ion concentrations.

A

The ventral medulla surface.

19
Q

Place in order by which has the most direct stimulus on the respiratory center.

pO2, pH (or H ions), pCO2

A
PCO2 = most direct stimulus
pH= less direct stimulus
pO2= least and is stimulated peripherally
20
Q

T/F: CO2 is highly permeable to the blood-brain barrier so blood and brain concentrations of CO2 are equal.

A

Girl you know it’s TRUE!

21
Q

T/F: [H] ions cross the blood brain barrier easily.

A

Nope! they do not!

22
Q

Excitation of respiratory center is great in the first few house of carbon dioxide increase. After 1-2 days of carbon dioxide exposure the stimulatory response declines. Why?

A
  • The decline results for renal adjustment of of hydrogen back to normal or close to normal levels (COPD).
  • The effect decreases to about 1/5th of the initial response.
23
Q

Why do patient’s with COPD have a blunted response to increased CO2?

A

Changes in blood CO2 concentration has a potent ACUTE effect on controlling respiratory drive but a weak CHRONIC effect after a few days (or years) of adaptation.

24
Q

T/F: Changes in Oxygen have virtually NO effect on respiratory center to alter respiratory drive.

A

True!!!!!!!!!!!!!!!

-changes in O2 concentration acts indirectly by peripheral receptors to alter respiratory drive.

25
Q

Blood oxygen levels below pO2 of ___mmHg are sensed by peripheral chemoreceptors.

A

70mmHg. (normal= 80-100mHg)

Oxygen is the back-up stimulation for respiratory regulation. Proper delivery of oxygen occurs despite significant changes in lung ventilation. Hemoglobin-oxygen buffer system delivers normal amounts of O2 to tissures over a wide range of pulmonary O2 partial pressures (60-100mmHg.)

26
Q

Peripheral Chemoreceptors:

They are located in the ______ and ______bodies.

A

Aortic and Carotid bodies;

these are areas of high flow arterial blood supply exposure.

27
Q

Peripheral Chemoreceptors:

What cranial nerve innervates the Carotid body?
Where at on the carotid arteries does the nerve innervate?
Where does this nerve send information to?

A
  • Glossalpharyngeal nerve (IX).
  • At the bifurcations in the common carotid.
  • The vagus nerve relays information to the DRG (Dorsal Respiratory Group).
28
Q

Peripheral Chemoreceptors:

What cranial nerve innervates the Aortic body?
Where on the aorta does the nerve innervate?
Where does this verve send information to?

A
  • Vagus nerve (X).
  • At the aortic arch
  • information sent to DRG (Dorsal Respiratory Group).
29
Q

Peripheral Chemoreceptors:

Stimulation of carotid or aortic chemoreceptors is caused by decreased arterial oxygen content. The impulse rate is sensitive to drops in PaO2 from a range of _____mmHg to _____mmHg.

A

60-30mmHg.

This range is when hemoglobin-oxygen saturation decreases rapidly.

30
Q

T/F: Direct effect of of CO2 and pH is 7 times more powerful but peripheral stimulation occurs 5 times more quickly.

A

T-R-U-E.

Peripheral receptors are important to increase response to CO2 at onset of exercise.

31
Q

Where are glomus cells found and what is their function?

A
  • Glomus cells are grandular-like cells synapsing with nerve endings in carotid and aortic bodies.
  • Glomus cells may function as chemoreceptors with stimulate nerve endings.
32
Q

Low Arterial Oxygen:

When CO2 & pH are NORMAL, ventilatory drive by low blood oxygen content is not significant until P02 falls below _____mmHg.

A

100mmHg.

Ventilation doubles when PaO2 falls below 60mmHg.

33
Q

Acclimatization:

At high altitudes the respiratory center _______(gains or loses) sensitivity to PCO2 & pH changes over 2-3 days.
What is or becomes the respiratory drive at high altitudes?

A

LOSES!

OXYGEN becomes drive for respiratory center at high altitudes.

-Alveolar ventilation increases greater than 400% after acclimatization in response to low PaO2.

  • at 760mmHg (sea level) x 0.21=159 PO2
  • at 300mmHg (altitude) x 0.21= 63 PO2
34
Q

On a graph with ventilation rate on the Y axis and PaCO2 on the X axis. How does the line of the graph shift with changes in pH?

A
  • The curves are displaced to the RIGHT at a HIGHER pH.

- The cures are displaced to the LEFT at a LOWER pH.

35
Q

What causes increases in ventilation during exercise?

A
  • PCO2 and PO2 changes caused by exercising muscles stimulate respiration.
  • hypoxia in muscles during exercise elicits afferent nerve signals to excite respiratory center.
  • joint & muscle proprioceptors transmit excitatory impulses to respiratory center.
  • Brain transmits collateral impulses to brainstem while simultaneously transmitting motor impulses to muscles, VRG.
36
Q

Is voluntary control of ventilation mediated through the respiratory center of the brain?

A

No, it is mediated from cortex and higher centers downward.

37
Q

What are lung J receptors and how are they stimulated?

A
  • J receptors are sensory verve endings in alveolar walls that juxtapose the pulmonary capillaries.
  • J receptors become stimulated when engorged by blood or when pulmonary edema occurs as in CHF
  • Functional role not well understood; their excitation may give the feeling of dyspnea.
38
Q

Respiratory center activity can be depressed or inactivated by what?

A

Acute brain edema (head trauma/concussion)

Blood flow reductions affects cellular metabolism and function. (pressure on the brain stem).

39
Q

Describe Cheyne-Stokes breathing pattern.

A

Short intervals of deep or rapid breathing followed by periods of shallow breaths or apnea.

40
Q

What is the pathophysiologic process behind Cheyne-Stokes breathing pattern?

A

Over-breathing causes a decrease of CO2 and increases blood oxygen level. Respiratory drive decreases due to blowing off the CO2 rapidly. This causes apnea, long pauses between breaths, or shallow breathing. The cycle repeats due to rising CO2 levels during shallow absent breaths.

41
Q

Two separate conditions allow Cheyne-Stokes breathing to occur, what are they?

A
  1. Long delay in transport of blood from lungs to brain (low cardiac output).
  2. Increased negative feeback gain (brain damage) due to hypoxia or severe metabolic abnormality

The potential for C-S breathing is present in everyone. large amounts of dissolved and bound CO2 & O2 in the blood and tissues. Lungs cannot build up enough CO2 or deplete O2 supply in a normal state.