L9 Control of Ventilation Flashcards

1
Q

What is minute ventilation?

A

This is the amount of breaths taken in by the lungs in a minute and so the volume of air inhaled.

In a healthy human:
5L/min = 10 breaths * 500ml (tidal volume)

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2
Q

How does dead space affect minute ventilation?

A

Dead space decreases the amount of air that takes place in gases exchange. The volume of air that actually participates in gas exchange is 350ml rather than 500ml. The last 150ml is lost in the conducting bronchioles.

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3
Q

What factors can affect oxygen consumption?

A
  • Exercise - Exercise increases the rate of ventilation to keep up with the increasing oxygen demand. A build up of carbon dioxide can lead to acidosis, hence why we hyperventilate to reduce blood pH. In this case ventilation rate can increase by 10 fold.
  • Physiological conditions - Being at altitude means that the partial pressures of oxygen is significantly lower despite the oxygen concentration remaining constant. Ventilation therefore increases to maintain blood gas pressures.
  • Disease - In some diseases the lung volume participating in gas exchange decreases.
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4
Q

How is ventilation controlled by the medulla oblongata?

A

The medulla oblongata houses the respiratory centre of the brain. It includes a dorsal respiratory group (DRG) and a ventral respiratory group (VRG). The DRG is required for inhalation. The VRG is slightly higher than the DRG. It is responsible for a bit of inspiration but mainly for expiration. It is stimulated in active expiration.

The DRG inhibits the VRG and vice versa. This helps to create cyclical breathing pattern

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5
Q

How is ventilation controlled by the pons?

A

The pons houses the apneustic and the pneumotaxic areas.

The apnesustic area: Responsible for prolonging inspiration by delaying the inspiration off switch.

The pneumotaxic area: Responsible for encouraging the inspiration off switch and so reducing the time spent in inspiration.

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6
Q

What is feature of the brain is necessary for life?

A

The DRG. Inspiration is active and so requires innervation. Expiration however is passive and relies only on the elasticity on the lungs and its tendency to recoil. At the end of normal inspiration, there is a function residual capacity left in the lung. This is the point the chest we all movement out and the lung tissue collapse is in balance.

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7
Q

What factors can affect inspiratory activity?

A

Inspiratory activity can be depresses by hypoxia, a wide variety of therapeutic drugs (opiates, barbiturates - stimulate GABA A receptors causing hyperpolarisation of the nerves and so depression of respiratory neurones - and anaesthetic agents) and inhibition of blood supply.

A hypoxemic circulation will cause breathing rate to increase however past a point, this causes the brain to 'shut down'.
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8
Q

What receptors are involved in the control fo ventilation?

A
  • Chemoreceptors
  • J receptors - These are receptors found near the capillaries (C-afferent) that are sensitive to diseases that cause hypoxia. They are activated by ‘traumas’ such as pulmonary oedema, inflammatory agents and pneumonia. There activation triggers ventilation.
  • Cough and irritant receptors
  • Muscle spindles
  • Joint proprioceptors - involved in exercise and movement. This feeds into the brain to increase ventilation.
  • Arterial baroreceptor - These receptors detect changes in pressure in the arterial wall.
  • Nasal and upper airway receptors
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9
Q

What are higher brain influences on ventilation?

A

Cortical and hypothalamic influences. Cortical control can override the effects of stimuli. For example, individuals can voluntary hyperventilate causing alkalosis - this however is under conscious control and cannot be overridden. Voluntary breath holding causes hypoxia which is unsustainable (this will lead to the individual passing out and starting to breath again).

Hyper thalamic centres have an effect on breathing rate through emotions and sensory reflexes. Both anger and anxiety (in fight or flight mode), and pain and cold tough cause hyperventilation. Hyperventilation can lead to pins and needle, or tetany. The symptoms cause them to hyperventilate more. A brown paper bag is used to recycle the carbon dioxide.

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10
Q

How is a low pH sensed by the brain?

A

The acidosis of the blood cannot transfer across to the blood brain barrier. Carbon dioxide can however dissolve and pass through the CSF. This can lead to an acidotic CSF as well as a high H+ concentration in the blood. A high carbon dioxide concentration CSF can then be detected.

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11
Q

Where are peripheral chemoreceptors located?

A

In aortic bodies and carotid bodies. The peripheral chemoreceptors based in the aortic bodies and the carotid bodies are sensitive to hypoxia, hypercapnia and acidosis. The peripheral chemoreceptors are more sensitive to metabolic acidosis than the central chemoreceptors.

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12
Q

What is a gloms cell?

A

In the carotid body (and aortic bodies), the glomus cell is the translator, the sensor that causes signal transduction to the afferent nerve which then sends information to the brain. This is the main organ that helps respiratory function in patients with hypoxic drive following chronic hypercapnia. Glomus type I cells are peripheral chemoreceptors which sense the oxygen, carbon dioxide and pH levels of the blood.

Hypoxia triggers calcium ion influx into the gloms cell via depolarisation. The calcium influx triggers the release of transmitters which imitate action potentials in the afferent nerve. Dopamine is one transmitter released, but the excitation is from ATP and acetylcholine.

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13
Q

What are pulmonary stretch receptors?

A

Afferent fibres from the smooth muscle of the bronchi and the trachea. They run to the vagus nerve to the respiratory centre in the medulla. As inspiration progresses, the bronchi and trachea stimulate the pulmonary stretch receptors sending the information to the brain to reduce inspiration so you do not over-inflate the lungs.

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14
Q

What are cough receptors?

A

There are receptors throughout the airways which when stimulated initiate an explosive expiration – a cough.
Afferent fibres from these receptors run in the vagus to the respiratory centre.
Others, also found in the upper airways and nose are irritant receptors. Stimulation leads to hyperpnoea (deep inhalation), and airway constriction which can lead on to coughing and also contribute to sneezing

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