Control of Ventilation

Question 1

What must be stimulated for inspiration?

Answer 1

Skeletal muscles of inspiration.
Phrenic nerve - the diaphragm.
Intercostal nerves - external intercostal muscles.

Question 2

What must be stimulated for expiration?

Answer 2

Nothing - it is passive.
No neural input is required.

Question 3

Where is the site of ventilatory control?

Answer 3

Ill-defined centres in the pons and medulla.
The respiratory centres.

Question 4

How are the respiratory centres controlled?

Answer 4

Normally subconscious.
Can be voluntarily modulated.
Dependent on brain signalling.

Question 5

What can cause breathing to cease?

Answer 5

Severing the spinal cord above the origin of the phrenic nerve (C3-C5).

Question 6

How do the respiratory centres work?

Answer 6

Sets an automatic rhythm of breathing.
Co-ordinates firing of smooth and repetitive bursts of action potentials in the DRG.
Adjusts rhythm in response to stimuli.

Question 7

What modulates the rhythm of the respiratory centres?

Answer 7

Emotion (via the limbic system in the brain).
Voluntary override (via higher centres in the brain).
Mechanosensory input from the thorax (such as the stretch reflex).

The most significant input is the chemical composition of the blood (PCO2, PO2, pH - via chemoreceptors).

Question 8

What do the DRG and VRG influence?

Answer 8

DRG - inspiratory muscles.
VRG - tongue, pharynx, larynx, expiratory muscles.

Question 9

Where are central chemoreceptors found, and what is their function?

Answer 9

In the medulla.
Detects changes in [H+] in the CSF around the brain (directly reflects PCO2).
The primary ventilatory drive.

Question 10

Where are peripheral chemoreceptors found, and what is their function?

Answer 10

In the carotid and aortic bodies.
Detects changes in (primarily) arterial PO2 and plasma [H+] (not oxygen content).
The secondary ventilatory drive.

Question 11

When do central chemoreceptors cause a reflex stimulation of ventilation?

Answer 11

Following a rise of H+.
Driven by a raised PCO2 (hypercapnia).

Question 12

What equation links CO2, H2CO3 and HCO3-?

Answer 12

CO2 + H2O <–> H2CO3 <–> H+ + HCO3-.

Question 13

When are central chemoreceptors reflexively inhibited?

Answer 13

A decrease in arterial PCO2.
Reduced CSF [H+] via hyperventilation.
They do not respond to direct changes in plasma [H+].

Question 14

What happens when arterial PCO2 increases?

Answer 14

CO2 crosses the blood-brain barrier (not [H+]).
Central chemoreceptors monitor the PCO2 indirectly in the CSF.
CO2 forms H+ and HCO3-, and receptors respond to the H+.
Feedback via the respiratory centres increases ventilation in response to an increased arterial PCO2.

Question 15

What is chronic lung disease?

Answer 15

PCO2 is chronically elevated.
Individuals become desensitised to PCO2 and rely on changes in PO2 to stimulate ventilation - a ‘hypoxic drive’.

Question 16

When do peripheral chemoreceptors cause a reflex stimulation of ventilation?

Answer 16

Following a significant fall in arterial PO2 (Hb dissociation) or a rise in [H+].
Increased [H+] is usually accompanied by a rise in arterial PCO2.

Question 17

What alters ventilation via peripheral chemoreceptor pathways?

Answer 17

Changes in plasma pH.

Decrease in pH = increase in [H+].
Ventilation is stimulated (acidosis).

Increase in pH = decrease in [H+].
Ventilation is inhibited (alkalosis).
Vomiting can cause this.

Question 18

What happens to RR in an anaemic patient with normal lung function, who has a blood O2 content half the normal value?

Answer 18

Normal lungs = PaO2 is normal.
RBCs are 98% saturated.
No change in RR.

Question 19

How do gaseous anaesthetic agents affect the respiratory centres?

Answer 19

Increases RR.
Decreases TV and AV.

Question 20

How do barbiturates and opioids affect the respiratory centres?

Answer 20

Depresses them. Overdose often results in death via respiratory failure.

Question 21

How does NO affect the respiratory centres?

Answer 21

A common sedative.
Blunts the peripheral chemoreceptors response to falling arterial PO2.

Question 22

Why is NO problematic in those with chronic lung disease?

Answer 22

Subjects have no means of controlling ventilation as ‘hypoxic drive’ is affected.
Administering O2 aggravates the situation.

Question 23

How does ventilation affect [H+] and CO2?

Answer 23

Increased ventilation produces CO2 and lowers [H+].
Decreased ventilation produces [H+] and retains CO2.

Question 24

What occurs in hypoventilation and hyperventilation?

Answer 24

Hypoventilation - CO2 increases, H+ increases, and respiratory acidosis occurs.
Hyperventilation - CO2 decreases, H+ decreases, and respiratory alkalosis occurs.

Question 25

What is pH proportional to?

Answer 25

HCO3 / CO2.
HCO3 - controlled by the kidneys.
CO2 - controlled by the lungs.

Question 26

What allows a large degree of voluntary control over breathing?

Answer 26

Descending neural pathways from the cerebral cortex to respiratory motor neurons.

Question 27

What involuntary stimuli for ventilation cannot be overridden?

Answer 27

Arterial PCO2.
[H+].

Question 28

How does swallowing control breathing?

Answer 28

Respiration is inhibited, to avoid aspiration of food or fluids into the airways.
Swallowing is followed by expiration, so any particles are dislodged outwards from the region of the glottis.

Question 29

How does a high PCO2 cause distress?

Answer 29

Impairs the partial pressure gradient that removes CO2 from the pulmonary artery.
CO2 remains in the blood. The partial pressure gradient that pulls CO2 out of cells is also lost.
CO2 builds up in cells.

Question 30

How does ventilation change during exercise?

Answer 30

Moderate exercise - increases in proportion to metabolism. PO2 and PCO2, and therefore ventilation, remain unchanged.

Strenuous exercise - increases more than metabolism. Arterial [H+] increases because of increased lactate production.