Control of Ventilation

Question 1

what nerves control skeletal inspiration muscles

Answer 1

the phrenic (to diaphrgam) and intercostal nerves (to external intercostal muscles

Question 2

where do phrenic and intercostal nerves come from

Answer 2

within ill defined centres located in the pons and medulla (Respiratory Centres)

Question 3

where is severed if breathing stops

Answer 3

spinal cord above origin of phrenic nerve (C3-5) breathing ceases

Question 4

how do respiratory centres set an automatic rhythm of breathing

Answer 4

through co-ordinating the firing of smooth and repetitive bursts of action potentials in DRG – travel to inspiratory muscles, which is adjusted in response to stimuli

Question 5

what is the respiratory rhythm modulated by

Answer 5

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

Question 6

what do ventral respiratory group send nerves to

Answer 6

Tongue, pharnyx, larynx, expiratory muscles

Question 7

what do dorsal respiratory group send nerves to

Answer 7

inspiratory muscles Via phrenic and intercostal nerves

Question 8

central chemoreceptors

Answer 8

medulla
respond directly to H+ (directly reflects PCO2)
- primary ventilatory drive

Detect changes in [H+] in CSF around brain
Cause reflex stimulation of ventilation following rise in [H+] (driven by raised PCO2 = Hypercapnea)

Question 9

Peripheral Chemoreceptors

Answer 9

carotid and aortic bodies
respond primarily to plasma [H+] and PO2 (less so to PCO2)
Cause reflex stimulation of ventilation following significant fall in arterial PO2 (consider haemoglobin dissociation) or a rise in [H+]
Respond to arterial PO2 not oxygen content
Increased [H+] usually accompanies a rise in arterial PCO2

• secondary ventilatory drive

Question 10

what is ventilation reflexly inhibited by

Answer 10

a decrease in arterial PCO2 (reduces CSF [H+])
(hyperventilation)
Do not respond to direct changes in plasma [H+]

Question 11

hypoxic drive

Answer 11

Most people rely on CO2 levels for stimulation of ventilation
In chronic lung disease PCO2 is chronically elevated
Individuals become desensitised to PCO2 and instead rely on changes in PO2 to stimulate ventilation

Question 12

if plasma pH falls ([H+] increases)

Answer 12

ventilation will be stimulated (acidosis) by peripheral chemoreceptor pathways
Increased ventilation drives the equation to the left (by blowing off CO2) and lowers [H+]

Question 13

if plasma pH increases ([H+] falls)

Answer 13

e.g.vomiting (alkalosis), ventilation will be inhibited by peripheral chemoreceptor pathways
Decreased ventilation drives the equation to the right (by retaining CO2) and increases [H+]

Question 14

Voluntary aspects of control of breathing

Answer 14

Descending neural pathways from cerebral cortex to respiratory motor neurons allow a large degree of voluntary control over breathing
Cannot over ride involuntary stimuli such as arterial PCO2 or [H+]
Breath-holding

Question 15

hyperventilation

Answer 15

Ventilation is reflexly inhibited by an increase in arterial PO2 or a decrease in arterial PCO2/[H+]

Question 16

why is high CO2 distressing

Answer 16

Our bodies are wholly programmed to get rid of CO2. If unable to, extreme distress is experienced. In the above example breathing in CO2 increases PACO2 and thus impairs the partial pressure gradient that normally allows CO2 removal from the pulmonary artery. CO2 remains in the blood and therefore the partial pressure gradient at the periphery that pulls CO2 out of cells is also lost causing CO2 to build up in cells.

Question 17

swallowing

Answer 17

Respiration is inhibited during swallowing to avoid aspiration of food or fluids into the airways. Swallowing is followed by an expiration in order that any particles are dislodged outwards from the region of the glottis.

Question 18

Common drugs affecting respiratory centres

Answer 18

Barbiturates and opioids depress respiratory centre – overdose often results in death as a result of respiratory failure.

Most gaseous anaesthetic agents increase RR but decrease TV so decrease AV.

Nitrous oxide, a common sedative/light anaethetic agent, blunts peripheral chemoreceptor response to falling PaO2. Very safe in most individuals, problematic in chronic lung disease cases where individual often on “hypoxic drive”. Administering O2 to these patients aggravates situation.