Lecture 5 Flashcards

1
Q

Where are the 2 classes of chemoreceptors found and what stimuli activates them?

A

Central and Peripheral.

Central is in medulla, responds directly to H+ (directly reflecting PCO2), primary ventilatory drive.

Peripheral is in carotid and aortic bodies, responding primarily to PO2 (less than PCO2) and plasma[H+]. Secondary ventilatory drive.

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2
Q

What factors are involved in changing “resp. drive” (rate and depth of breathing)

A

Main factor is Chemical composition of plasma, (esp PaCO2)

PaO2 and plasma pH are secondary roles,

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3
Q

How do central chemoreceptors serve to regulate arterial PCO2 by monitoring the pH of CSF

A
Increasse in arterial PCO2. 
CO2 crosses into CSF 
CO2 +H20 - H2CO3 - H+ + HC3-
Central Chemoreceptors respond to H+
Feedback via resp centers in the medulla to increase ventilation
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4
Q

How do peripheral chemoreceptors become important during hypoxia?

A

Detect changes in arterial PO2 (PaO2) and [H+]. Located in Carotid and aortic bodies.
Reflex stimulation of ventilation following significant fall in arterial PO2 (<60mmHg) (not O2 content)

Does this by low PO in blood vessel means no O2 combining with O2 sensor (KO2 channel) on cells. Therefore decrease in K+ permeability depolarising cell, causing exocytosis of dopamine cont. vesicles - attatch to dopamine receptor in sensory neuron which signals to medullary center to increase ventilation.

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5
Q

How are respiratory motor movements affected by CNS?

Which nerves are innervated to which muscles?

A

think CNS rep think interview nerve breaths - CV ME. Chemical comp of blood(Chemoreceptor input - most important), Vountary override, Mechano-sensorary, Emotion.

Resp centers (Pons and Medulla) have rhythm moulated by:
Emotion (via brains limbic system)
Voluntary over-ride (hgher centers in the brain)
Mechano-sensory input from the thorax (stretch reflex)
Chemical composition of the blood (PCO2, PO2 and pH), detected by chemoreceptors.

Inspiration : Phrenic nerve (diaphragm), intercostal nerves (external intercostal muscles).

From Pons and Medulla (resp. centers)

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6
Q

What are the 2 groups of neuros coming from the pons and medulla?

A

DRG - Dorsal Resp Group (goes to inspiratory muscles)

VRG - Ventral Respiratory Group pf Neurons (goes to Tounge, pharynx, larynx and expiratory muscles.

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7
Q

What are the 2 groups of neuros coming from the pons and medulla?

A

DRG - Dorsal Resp Group (goes to inspiratory muscles)

VRG - Ventral Respiratory Group pf Neurons (goes to Tounge, pharynx, larynx and expiratory muscles.

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8
Q

What is Hypercapnea?

A

raised CO2

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9
Q

What is Hypercapnea?

A

raised CO2

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10
Q

What do people with Chronic lung disease become reliant on to stimulate ventilation?

A

Changes in PaO2 (and therefore peripheral chemoreceptors) as PaCO2 can become chronically elevated and therefore desensitised to PCO2 changes.

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11
Q

What affect do most anasthetic agenst have on RR, TV and AV?

A

Increase RR, decrease TV and therefore decrease AV

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12
Q

What affect do most anasthetic agenst have on RR, TV and AV?

A

Increase RR, decrease TV and therefore decrease AV

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13
Q

How do Barbiturates and OPiods affect respiratory centers?

A

They depress respiratory centers, decreasing sensitivity to pH and therefore responce to PCO2. Also decreases peripheral chemoreceptor response to low PO2.

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14
Q

How do Barbiturates and OPiods affect respiratory centers?

A

They depress respiratory centers, decreasing sensitivity to pH and therefore responce to PCO2. Also decreases peripheral chemoreceptor response to low PO2.

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15
Q

What is Nitrous oxide used for? How does it work? When would it be problematic?

A

Common sedative/light anasthetic agent. Blunts peripheral chemoreceptors response to falling PaO2..

Ploblematic in Chronic Lung Disease as they are often reliant on “hypoxic drive” (peripheral chemoreceptors to kick in due to chronic high levels of PCO2). Administering O2 aggrevates situation.

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16
Q

Additionally to a change in PO2 what else do the peripheral Chemoreceptors detect?

A

Also respond to increasing plasma [H+]

[H+] often comes form CO2 :
CO2 +H20 = H2CO3 = HCO3- + H+

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17
Q

Increasing plasma pH will result in what with regards to ventilation?

A

Ventilation inhibited.

Increasing pH = decreasing [H+]

eg. vommiting (alkalosis), ventilation will be inhibitted

18
Q

What will happen to ventilation is pH falls?

A

Lowe pH = More H+, therefore more CO2, therefore breathing stimulated (increased)

19
Q

What will happen to ventilation is pH falls?

A

Lowe pH = More H+, therefore more CO2, therefore breathing stimulated (increased)

20
Q

What is the normal resting level of minute ventilation?

A

5L/min

21
Q

Will hypOventilation lead to respiratory acidosis or respiratory Alkalosis?

A

Hypoventilation, causing CO2 retention, leads to increased [H+] bringing about respiratory acidosis

22
Q

Will hypERventilation lead to respiratory acidosis or respiratory Alkalosis?

A

Hyperventilation, blowing off more CO2, lead to decreased [H+] bringing about respiratory alkalosis

23
Q

pH α HCO3/CO2 (REMEMBER THIS)

Which factors are controlled by the lungs or the Kidneys?

A

HCO3 controlled by Kidneys

CO2 controlled by lungs

24
Q

What is pH proportional to?

A

pH α HCO3/CO2

25
Q

In strenuous activity, ventilation increases more than metabolism. What accounts for some of this hyperventilation?

A

Lactic acid production increases arterial [H+], detected by the peripheral chemoreceptors only (as H+ can’t cross blood-brain barrier), increased heart rate.

26
Q

In moderate exercise, what happens to arterial PO2 and PCO2

A

They remain the unchanged as ventilation and metabolism increase proportionally (signals causing this unknown).

27
Q

Would it be more distressing being in an environment with low PO2 or high CO2?

A

High CO2 as the body is programmed to mainly just get rid of CO2! High CO2 would impair partial pressure gradient that usually allows for the removal of CO2, therefore CO2 remains in the blood and loses partial pressure pulling CO2 out of cells so CO2 starts to build up in the cells.

28
Q

Do we have large control over our breathing? What stimuli are we unable to override?

A

Yes we do thanks to descending neural pathways from cerebral cortex to respiratory motor neurons.

We are unable to over ride involuntary stimulus eg. arterial PCO2 or [H+]

29
Q

What happens to resp. when swallowing?

A

Inhibited (to avoid choking). Swallowing followed by expiration to ensure anything is dislodged outwards from region of glottis.

30
Q

What type of muscle are the muscles we use for breathing and why is this significant

A

Skeletal, use somatic nerves, have control (to some extent)

31
Q

Where does the phrenic nerve originate

A

C3-5

32
Q

What can modulate the rhythm of the respiratory centers?

A
  1. Emotion (via limbic system in the brain)
  2. Voluntary over-ride (via higher centres in the brain)
  3. Mechano-sensory input from the thorax (e.g. stretch reflex).
  4. Chemical composition of the blood (PCO2, PO2 and pH) – detected by chemoreceptors.
33
Q

Why can CO2 cross the blood brain barrier but H+ can’t?

A

Because gas can cross the blood brain barrier but v tightly regulated so most of the time most ions can’t.

Can get increase in H+ ions through CO2 moving into the cerebrospinal fluid tho:
CO2 + H2O = H2CO3 = H+ + HCO3-

This is then detected by central chemoreceptor and translates message ot resp. control centers.

This means Central Chemoreceptors will only respond to an increase in H+ through CO2 and therefore are directly responding to an increase in H+ in the blood

34
Q

Can high levels of CO2 be lethal?

A

Yes

35
Q

What is the normal pH of extracellular fluid?

A

7.4

36
Q

What is H2CO3 called?

A

Carbonic acid

37
Q

Where do the H+ ions origionate from that are registered at perhipheral and central Chemoreceptors?

A

Perhipheral - can origionate from anywhere as registering it in the plasma

central - CO2 as only this can get through the blood brain barrier as it is a gas

38
Q

As plasma [H+] increases, does Minute Ventilation increase in a linear or nonlinear way?

A

Linear

39
Q

What is metabolic acidosis?

A

An increase in H+ conc. for a reason that’s not a change in resp. function

40
Q

What is the normal value for alveolar ventilation?

A

4.2L/min