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BMS 242 - CVS respiratory > Respiration IV > Flashcards

Respiration IV Flashcards

1
Q

What is the BASIC respiratory rhythm pattern generated by?

How do we know this?

A

Centres in the MEDULLA

Know this because:
- Lesion between the medulla and the pons - maintain basic breathing pattern

  • Lesion BELOW the level of the medulla - basic breathing rhythm is LOST
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2
Q

What MODIFIES the basic respiratory pattern?

A

Inputs from various regions of the brain

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3
Q

How can breathing be CONSCIOUSLY altered?

A
  • Hyperventilating

- Breath holding

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4
Q

What are the 2 respiratory groups in the medulla?

A

1) DORSAL respiratory group

2) VENTRAL respiratory group

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5
Q

What does the dorsal respiratory group in the medulla control?

A

Inspiration

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6
Q

What does the ventral respiratory group in the medulla control?

A

FORCED inspiration and FORCED expiration

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7
Q

How does quiet EXPIRATION occur?

A

Passive process - elastic recoil

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8
Q

Where do the INSPIRATION outputs from the medulla go to?

A

1) Down the PHERNIC NERVE to control the diaphragm

2) Down the SPINAL NERVES to control the external intercostal muscles

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9
Q

Where do the EXPIRATION outputs from the medulla go from/to?

A

From: the VENTRAL RESPIRATORY GROUP

To:

  • INTERNAL intercostal muscles
  • ABDOMINAL muscles
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10
Q

What complex in the medulla controls the basic breathing pattern?

How do we know this?

A

PRE-BOTZINGER COMPLEX

Know this because:
The activity in the HYPOGLOSSAL nerve matches the Pre-Botzinger complex output

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11
Q

Where is the pre-botzinger complex present?

A

At the top of the ventral respiratory group

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12
Q

What 3 basic types of pattern output does the Pre-Botzinger complex generate?

A

1) Eupneic
2) Sigh
3) Gasp

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13
Q

What is a eupneic breathing pattern?

A

Basic, standard breathing

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14
Q

What happens to the activity of the Pre-Botzinger complex when there is a sigh?

A

Increase INTENSITY of spike rate

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15
Q

What does a sigh help with?

A

Gas exchange

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16
Q

What happens to the activity of the Pre-Botzinger complex when there is a gasp?

A

Short, rounded activity spike

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17
Q

When does a gasp occur?

A

When there is shortage of oxygen

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18
Q

What are the 2 main classes of neurons in the Pre-Botzinger complex?

A

1) Pacemaker cells

2) Non-pacemaker cells

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19
Q

What is the difference between pacemaker and non-pacemaker cells?

A

Pacemaker - able to generate their OWN rhythmic action potential

Non-pacemaker - NOT able to generate their own rhythmic action potential

20
Q

Describe the activity of the pacemaker cells in the PB complex

A

1) Spiking phase - slow, background depolarisation called the SODIUM LEAK CURRENT
2) Reaches point where the membrane remains depolarised
3) Activation of a PERSISTANT SODIUM CURRENT
- Causes BURSTING phase of action potentials –> inspiration
4) Eventually, deactivation of the persistant sodium current
5) Repolarisaion back to normal membrane potential
6) No further inspirations until the activation of the persistant sodium current again

21
Q

What is NALCN?

A

The sodium leak channel

22
Q

What occurs in a mouse with NALCN KO?

A

No sodium leak - membrane is hyperpolarised:

  • Breathing stops for 5 seconds, 5 times in one minute
  • Very IRREGULAR breathing pattern
  • Don’t survive past 24 hours
23
Q

What does K+ do?

A

Determine the resting membrane potential through the K+ gradient across the membrane

24
Q

What does increase in K+ cause?

What does this allow?

A

Depolarisation

More of a chance for the neuron to enter BURSTING activity

25
Q

What does the transition to bursting activity depend upon?

A

2 different types of inward current:
1) Persistant sodium current (Inap)

2) CAN cation current (Ican)

26
Q

What is the CAN cation current activated by?

When is the CAN cation current activated more?

A

Ca2+ influx

Activated more during the ‘sigh’ breathing pattern

27
Q

What classes are the pacemaker cells split into?

A

2 classes:

1) Cadmium SENSITIVE
- Neurons relying on Ican for bursting

2) Cadmium INSENSITIVE
- Neurons relying on Inap for bursting

28
Q

What alters the background depolarisation of the pacemaker cells?

What does this determine?

A

Altered by inhibitory and excitatory inputs on the neurons of the Pre-Botzinger

Determines when the neurons are in spiking phase or in bursting phase

29
Q

What is hypoxia?

A

LACK of oxygen

30
Q

What impact does hypoxia have on the Pre-Botzinger complex?

A

Normal breathing –> sighing –> gasping:
- Loss of the IPSCs on the Pre-Botzinger complex

  • Loss of autonomous spiking neurons
  • Loss of cadmium sensitive neurons
  • Cadmium insensitive neurons remain
31
Q

What are cadimium insensitive neurons responsible for?

A

The GASPING pattern of breathing

32
Q

How does the dorsal respiratory group control quiet inspiration?

A

Sending signals to the inspiratory muscle

33
Q

When is the dorsal respiratory group active?

A

Spontaneously active:

1) Period of ACTIVITY
- Activity in the PB sends signals to the DRG, activating it

2) Shuts OFF
- No signalling of the PB to the DRG

3) Period of activity again

34
Q

What happens when the dorsal respiratory group is inactive?

A

Passive expiration

35
Q

When is the VRG inactive?

A

During quiet respiration

36
Q

When is the VRG active?

A

During FORCED inspiration/expiration (eg. exercise)

37
Q

How do signals from the pons act on the PB?

What does it regulate?

A

Can have STIMULATORY or INHIBITORY impacts on the PB

To REGULATE the RATE and DEPTH of breathing

38
Q

What are the centres in the pons that send signals to the PB?

A

1) Pneumotaxic centre

2) Apeneustic centre

39
Q

What does the Pneumotaxic centre do?

A

INHIBITORY effect on the INSPIRATORY centre

  • -> Reducing/shortening inspiration phase
  • -> Shallower breathing (increase rate, reduce depth)
40
Q

What does the Apneustic centre do?

A

STIMULATES the INSPIRATORY centre

  • -> PROLONGS inspiration phase
  • -> INCREASES DEPTH and REDUCES RATE
41
Q

How is the breathing pattern determined?

A
  • MANY inputs on the PB complex (inhibitory/excitatory)
  • SUM of all the inputs determine the output of the PB (which controls the basic breathing pattern, gasping, sighing etc)
42
Q

What is the Hering-Breuer reflex?

Describe this reflex

A

Negative feedback loop controlling the stretch of the lung:

  • Stretch receptors in the lung send signals BACK to the medulla when the diaphragm contracts and the lungs INCREASE in volume
  • Signal via the VAGUS NERVE to the INSPIRATORY centre
  • -> SHUTS OFF inspiration, to prevent over-inflation of the lungs
43
Q

What is the ‘inspiratory centre’?

A

The dorsal respiratory group

44
Q

What do CENTRAL chemoreceptors do?

How?

A

Monitor conditions in the CEREBRO-SPINAL fluid such as CO2 and pH

Increase in CO2 –> acidification

45
Q

Where are PERIPHERAL chemoreceptors located?

A

In the carotid body and the aortic arch

46
Q

What do the peripheral chemoreceptors respond to?

A

Increase in Co2
Decrease in pH
Decrease in O2

47
Q

What does the stimulation of the chemoreceptors cause?

A

Increase in ventilation

BMS 242 - CVS respiratory (15 decks)

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