Control of Breathing Flashcards

1
Q

Describe the composition of atmospheric, dry air.

A
  • N2 = 79.04%
  • O2 = 20.93%
  • CO2 = 0.03%
  • Others = <1%
  • Atmospheric pressure = 760mmHg at sea level.
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2
Q

What is partial pressure (Pgas)?

A
  • Partial pressure of a gas in a mixture is the pressure which that gas contributes to the total pressure.
    • So total pressure is the sum of all the partial pressures in a mixture of gases.
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3
Q

How do you calculate the partial pressure of a gas in atmospheric air?

Use N2 as an example.

A
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4
Q

What happens to barometric pressure at varying altitudes?

What are the implications for oxygen availability?

A
  • Barometric pressure decreases as altitude increases.
    • There are implications for oxygen availability.
  • PO2 sea level = 160mmHg.
  • PO2 Mt Blanc 16,000ft = 90mmHg.
  • PO2 Mt Everest 30,000ft = 43mmHg.
  • PO2 commercial aircraft 33-36, 000ft = 35mmHg.
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5
Q

What happens to liquid which is exposed to a gas mixture?

A
  • If a liquid is exposed to a gas mixture, some gas will become dissolved in it.
  • Dissolved gas has Pgas (or gas tension).
  • The amount of gas dissolved in liquid (e.g. blood) depends upon:
    • Solubility of gas in blood (e.g. around alveolus) = constant.
    • Pgas in alveolar air = variable.
  • So, amount of dissolved gas is the alveolar PCO2 and PO2.
  • Alveolar Pgas “holds” gas in solution.
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6
Q

What happens to gas in a partial pressure gradient?

Describe this in relation to the alveoli and pulmonary capillaries.

A

Gas will always diffuse DOWN a partial pressure gradient.

  • If PO2 alveoli > PO2 blood in pulmonary capillaries:
    • O2 diffuses into blood until [PO2 Alveolar = PO2 Blood].
  • If PCO2 alveoli > PCO2 blood in pulmonary capillaries:
    • CO2 diffuses out of blood until [PCO2 Blood = PCO2 Alveoli].
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7
Q

How does alveolar PO2 differ from atmospheric PO2?

A
  • It becomes saturated with H2O vapour.
  • PH2O at body temp = 47mmHg.
    • Pgas for other gas is diluted by 47mmHg (~6%)
  • So, to calculate initial PO2 in alveolar air:
    • PO2 = (760 - 47) x 21/100
    • = 150mmHg.
  • For alveolar PCO2:
    • PCO2 = (760 - 47) x 0.03/100
    • = 0.21mmHg.
  • For alveolar N2:
    • PN2 = (760-47) x 79/100
    • = 563mmHg.
  • These factor in that air is diluted by water vapour in the alveoli.
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8
Q

Describe the effect of dead space in the lungs.

A
  • Because of dead space not all air is fresh after every breath.
  • PO2 is already lowered 150mmHg because of H2O vapour.
  • Only 350/500mL is ‘new’ air.
  • So, alveolar PO2 = ~100mmHg (cf 160mmHg in atmospheric air).
  • PO2 remains fairly constant during respiratory cycle because:
    • Only quite small change in alveolar air / breath.
    • O2 being removed by passive diffusion into blood.
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9
Q

Why does PCO2 remain fairly constant?

A
  • Tissues produce CO2, but PCO2 remains quite constant because:
    • CO2 is removed from blood into the alveoli by passive diffusion.
      • I.e. 46mmHg → 40mmHg
    • CO2 leaves alveoli in expiration.
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10
Q

How do partial pressure gradients drive gas exchange across capillaries?

A
  • Across pulmonary capillaries:
    • O2 partial pressure gradient rom alveoli to blood = 60mmHg (100 ⇒ 40).
    • CO2 partial pressure gradient from blood to alveoli = 6mmHg (46 ⇒ 40mmHg).
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11
Q

Describe the effects of varying pulmonary ventilation.

A
  • PCO2 and [H+] must be controlled within narrow limits.
  • Alveolar Pgas change ⇒ Pgas change in pulmonary capillaries ⇒ Pgas change in systemic arterial blood.
  • Achieved by varying pulmonary ventilation.
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12
Q

Explain this equation.

A
  • VE = minute ventilation.
    • The volume of air inspired and expired in 1 minute.
  • TV = tidal volume.
    • The volume of air inspired and expired per breath - ~500ml during breath at rest.
  • RF = frequency.
    • The number of breaths per minute - approximately 12-15 at rest.
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13
Q

How can the rate and depth of breathing be altered?

A

By changing the discharge of the motor neurons supplying the respiratory muscles.

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14
Q

What does increased VE achieve?

A
  • CO2 gets flushed out of body so alveolar PCO2 decreases.
    • Alveolar PO2 increases and approaches atmospheric PO2
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15
Q

What does decreased VE achieve?

A
  • CO2 is retained in the lungs so alveolar PCo2 increases.
    • Alveolar PO2 falls
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16
Q

What are the key elements in the respiratory control system?

A
  • Sensors:
    • Receptors (e.g. chemoreceptors)
    • Gather information and feed it to…
  • Central controller:
    • Pons
    • Medulla
      • Coordinate information and send impulses to:
  • Effectors:
    • Respiratory muscles
      • Cause ventilation
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17
Q

Where is our basic respiratory rhythm generated?

A

Medulla oblongata

18
Q

Where is involuntary respiration controlled from?

A

Respiratory centres of the upper brainstem.

19
Q

What is the pre-Botzinger complex?

A
  • The pre-Botzinger complex drives the dorsal respiratory group of neurons which fire in bursts leading to inspiration.
    • Firing = contraction of inspiratory muscles. When firing stops there is passive expiration.
20
Q

Describe the primary respiratory control centre in the medulla.

A
  • Main function - send signals to the muscles that control respiration.
  • There are 2 respiratory centres in the medulla:
    • Ventral respiratory group stimulates expiratory movements.
    • Dorsal respiratory group stimulates inspiratory movements.
21
Q

When do neurons in the ventral respiratory group become activated?

A
  • In normal quiet breathing, the ventral neurons do not activate expiratory muscles.
  • In forced expiration, the ventral respiratory group neurons excite the intercostal and abdominal muscles.
22
Q

What is the role of the pons in control of breathing?

A
  • Main function is to control the rate or speed of involuntary respiration.
  • 2 main functional regions:
    • Apneustic centre - sends inspiration signals for long, deep breaths.
    • Pneumotaxic centre - sends signals to inhibit inspiration which allows it to finely control respiratory rate.
    • These work against each other to control RR.
23
Q

Desribe the apneustic centre in the pons.

A
  • Controls the intensity of breathing and is inhibited by the stretch receptors of the pulmonary muscles at maximum depth of inspiration, or by signals from the pneumotaxic centre.
  • It increases tidal volume.
24
Q

Describe the pneumotaxic centre in the pons.

A
  • Pneumotaxic centre sends signals to inhibit inspiration.
  • Its signals limit the activity of the phrenic nerve and inhibits the signals of the apneustic centre.
  • It decreases tidal volume.
25
Q

What is the role of the cortex in the control of breathing?

A
  • The primary motor cortex is the neural centre for voluntary respiratory control.
  • Voluntary control is achieved by bypassing the respiratory centres in the brainstem.
  • The cerebral cortex sends signals directly to motor neurons in the spinal cord that supply the respiratory muscles.
  • Voluntary control is needed for speaking and singing.
  • If we hyper- or hypo- ventilate to extremes, this will trigger the respiratory centres in the brainstem and voluntary input will be overridden.
26
Q

What is the role of chemoreceptors in regulation of breathing?

A
  • Central chemoreceptors
    • Ventrolateral surface of the medulla.
    • Detect changes in the pH of the CSF.
    • Can be desensitised over time by chronic hypoxia or hypercapnia.
  • Peripheral chemoreceptors
    • Aortic body - detects changes in O2 and CO2
    • Carotid body - detects changes in O2, CO2 and pH
    • They cannot be desensitised
  • Chemoreceptor regulation of breathing is negative feedback.
  • The goal of this system is to keep the pH of the bloodstream within normal neutral ranges, ~7.35.
27
Q

Describe how respiratory checmoreceptors work.

A
  • The respiratory chemoreceptors work by sensing the pH of their environment through the concentration of hydrogen ions.
  • Because most CO2 is converted to carbonic acid (and bicarbonate) in the bloodstream, chemoreceptors are able to use blood pH as a way to measure the CO2 levels of the bloodstream.
  • Peripheral chemoreceptors have less of an impact on the RR compared to the central chemoreceptors.
28
Q

Describe the proprioceptor regulation of breathing.

A
  • The Hering-Bauer Reflex
    • Triggered to prevent over-inflation of the lungs.
    • Only activated at very large tidal volumes (>1L).
    • When the lungs are inflated to their maximum volume during inspiration, the pulmonary stretch receptors send an action potential signal to the medulla and pons via the vagus nerve.
  • There are many stretch receptors in the lungs, particularly within the pleura and the smooth muscles of the bronchi and bronchioles.
    • They activate when the lungs have inflated to their ideal maximum point.
    • They are mechanoreceptors, which are a type of sensory receptor that specifically detects mechanical pressure, distortion and stretch.
29
Q

What is the inflation reflex?

A
  • The pneumotaxic centre of the pons sends signals to inhibit the apneustic centre of the pons, to prevent it from activating the dorsal medulla and the inspiratory signals that are sent to the diaphragm and accessory muscles stop.
    • This is called the inflation reflex.
30
Q

What is the deflation reflex?

A
  • As inspiration stops, expiration begins and the lungs begin to deflate.
  • As the lungs deflate the stretch receptors are deactivated (and compression receptors called proprioceptors may be activated) so the inhibitory signals stop and inhalation can begin agan.
    • This is called the deflation reflex.
31
Q

Aside from the Hering-Bauer reflex, what are the other forms of reflex control of breathing?

A
  • Input from irritant receptors
    • Free nerve endings between respiratory epithelial cells.
  • Input from J receptors
    • Believed to be in alveolar walls close to the capillaries.
  • Input from upper airway receptors
    • In the nose, pharynx and larynx.
32
Q

Describe the role of irritant receptors in the control of breathing.

A
  • Stimulated by dust, smoke, noxious gases etc.
  • Initiate reflex bronchial and laryngeal constriction, mucous production.
  • Implicated in asthmatic and allergic bronchoconstriction.
  • Play NO role in the normal control of breathing.
33
Q

Describe the role of J-receptors (juxta-capillary receptors) in the control of breathing.

A
  • Impulses pass up the vaus nerve in slowly conducting myelinated fibres and can result in rapid, shallow breathing, although intense stimulation will cause apnoea.
  • They may play a role in the rapid, shallow breathing and dyspnoea associated with left heart failure and interstitial lung disease.
34
Q

Describe the role of upper airway receptors in the control of breathing.

A
  • Stimulated by mechanical and chemical stimuli.
  • Initiate deep inspiration and closure of the glottis.
  • Pressure builds up to give a high pressure blast of expired air to expel the irritant, for example in sneezing or coughing.
  • No role in the control of normal breathing.
35
Q

Describe the cough reflex.

A
  • The respiratory apparatus comes into contact with something it is sensitive to.
  • Receptors trigger afferent impulses via the vagus nerves to the medulla causing this response:
    • Up to 2.5L of air is rapidly inspired.
    • The epiglottis and vocal cords close, trapping air in the lungs.
    • Abdominal muscles contract, pushing up against the diaphragm. Accessory muscles of expiration contract.
    • Pressure in the lungs increases.
    • Epiglottis and vocal cords open suddenly, releasing air at 75-100mph.
    • The force is enough to collapse the bronchi and trachea, air is ejected through narrow slits.
    • Irritant is ejected.
36
Q

Describe the input from joint and muscle receptors in the control of breathing.

A
  • Inpulses from moving limbs reflexly increase breathing believed to contribute to the increased ventilation during exercise.
    • There is no increased demand but the receptors cause an increase in ventilation.
37
Q

Describe the input from the gamma system in the control of breathing.

A
  • Many muscles, including the intercostal muscles and diaphragm contain muscle spindles that sense elongation of the muscle.
  • This information can control strength of contraction.
  • These receptors may be involved in sensing dyspnoea - which occurs when unusually large respiratory effort are required to move the lung and chest wall.
  • This could be due to airway obstruction.
38
Q

Describe the input from arterial baroreceptors in the control of breathing.

A
  • Increase in arterial BP can cause reflex ypoventilation or apnoea through stimulation of the aortic and carotid sinus baroreceptors.
  • A decrease in BP may result in hyperventilation.
39
Q

Which chemical state results in an increase in the rate of ventilation?

A
  • Arterial PO2 is decreased.
  • Arterial PCO2 is increased.
  • Arterial [H+] is increased.
  • Inspiratory centres are automatically triggeres by these factors.
40
Q

Where is arterial PO2 monitored?

A
  • Decreased PO2 is monitored by carotid bodiea and aortic bodies.
    • These are peripheral chemoreceptors.
  • Located on right and left of carotid arteries and arch of the aorta.
41
Q

What happens when arterial PO2 is decreased?

A
  • Receptors respond to chemical changes in arterial blood.
  • Not usually involved in quiet respiration - used in disease or decreased atmospheric pressure / oxygen availability.
  • Sensitive to decreased PO2 but do not initially cause a response.
    • PO2 must fall below 60mmHg (>40% reduction).
      • Recall Hb still 90% saturated at arterial PO2 of 60mmHg.
    • Receptors then send afferent impulse to medullary inspiration neurons to increase ventilation.
      • This is very important at altitude.
42
Q

What happens when arterial PCO2 increases?

A
  • PCO2 is the mst important magnitude regulator in quiet ventilation.
  • Aortic body peripheral receptors are not responsive to change in PCO2. Carotid may respond to change in pH and PCO2 but not usually at sea level in health.
  • Central chemoreceptors monitor changes in PCO2 induced [H+] in the brainstem ECF.
  • Increased PCO2 in brainstem ECF causes increased [H+].
  • In the brain stem:
    • Increased [H+] stimulated cnentral chemoreceptors.
    • Increased ventilation.
    • Increased CO2 blown off.
    • PCO2 decreases.
    • [H+] decreases.