Respiratory - Control of Ventilation

Question 1

How does the respiratory centre control ventilation - list the name and function of the four areas

Answer 1

Dorsal Respiratory Group (of neurons)

• Inspiratory neurons
• Controls diaphragm
• Normal tidal ventilation

Ventral Respiratory Group (of neurons)

• Inspiratory and expiratory neurons
• Intercostal muscles
• Increases force of inspiration and expiration

Apneustic

• Lower pons
• Inhibits overexpansion by DRG neurons
• Ablation results in pathologically long and deep breaths

Pneumotaxic

• Upper pons
• Modulates DRG to modify respiratory pattern

Question 2

Summarise the inputs to the respiratory center

Answer 2

Peripheral chemoreceptors
- Aortic and Carotid bodies
Central chemoreceptors
Mechanoreceptors 
Other factors

Question 3

Describe the location and function of the peripheral chemoreceptors

Answer 3

PERIPHERAL CHEMORECEPTORS
Location:
- Carotid bodies (glossopharyngeal afferent)
- Aortic bodies (vagus afferent)

Stimulated by

• Low PaO2 (not O2 content!)
• High PaCO2 (contributes 20% of response)
• pH < 7.35 (carotid bodies only)
• Low BP

Faster response time than central chemoreceptors: 1 - 3 seconds

Question 4

Describe the location and function of the central chemoreceptors

Answer 4

Ventral Surface of the medulla (Close to but separate from VRG)

Stimulated by
- Change CSF pH ONLY

But H+ and HCO3- cannot cross BBB, only CO2 can. CO2 crosses BBB into CSF to form H ions.

• Minimal protein in CSF (vs. plasma) –> minimal buffer
• CSF is hence more sensitive to small changes in PCO2 than plasma.

Question 5

Which affects central chemoreceptors more: respiratory acidosis or metabolic acidosis

Answer 5

Respiratory acidosis.
Metabolic acidosis –> H ions cannot cross into CSF –> carotid body (peripheral chemoreceptor) responsible for Kussmaul respiration characteristic of metabolic acidosis.

Question 6

How does cerebral vasodilatation associated with hypercapnoea influence central chemoreceptor function

Answer 6

It enhances it. VD –> increase blood supply to medulla and increased delivery of CO2 to central cehmoreceptors

Question 7

How does the body adjust to chronic hypercapnoea

Answer 7

1. BBB actively secretes HCO3 - into CSH to normalize CSF pH and reduce hyperventilatory drive
2. Kidneys actively reabsorb and regenerate HCO3- which increases plasma pH reducing hyperventilatory drive from the peripheral chemoreceptors.

Myth –> COPD patients rely on hypoxic ventilatory drive

Excessive O2 administration can lead to respiratory failure in some patients with COPD.
Mechanism
1. Disrupted compensatory hypoxic pulmonary vasoconstriction –> blood now flows to poorly ventilated alveoli
2. Disruption of the recruited Haldane effect –> Excess O2 leads to right shift of CO2 Hb saturation curve. Oxy Hb has reduced ability to form carbamino compounds vs deoxyHb. Therefore with excessive O2 the Ability to transport excess CO@ to lungs from tissue for excretion is thwarted by approximately up to 25%. Leading to worsening CO2 retention

Never withhold O2 from critically ill hypoxic COPD patient. BUT titrate sats 88 - 92 !

Question 8

How do mechanoreceptors in the chest affect ventilation

Answer 8

Lung stretch receptors
- Overinflation sensed –> apneustic centre –> reduce depth inspiration

Muscle spindles
- Responsible for the respiratory response to exercise

Question 9

List the inputs from the CNS and the PNS that influence the respiratory centre and ventilation

Answer 9

JUXTACAPILLARY RECEPTORS (J-RECEPTORS)
- Pulm emboli and oedema

IRRITANT RECEPTORS
- Noxious chemicals

PAIN RECEPTORS
- Pain

THALAMUS
- Increase body temperature

LIMBIC
- Extreme emotion

CEREBRAL CORTEX
- Voluntary control

Question 10

What is the location and function of J receptors

Answer 10

JUXTACAPILLARY RECEPTORS (J-RECEPTORS)
- Non-myelinated C fibres alveolar walls
- Stimulated by pulmonary oedema and embolism 
Activation:
--> Increase ventilation
--> dyspnoea sensation
--> Bradycardia
--> Hypotension

Question 11

Where are irritant receptors located in the lungs and what does activation cause

Answer 11

In the airway epithelium.

Activation causes bronchoconstriction and hyperventilation

Question 12

What is the ‘break-point’ with regard to voluntary control of ventilation

Answer 12

One cannot hold breath indefinitely –> after a short period of apnoea, chemoreceptor stimulation by hypoxaemia and hypercapnoea overrides voluntary control. This is called the breakpoint.

Question 13

In the absence of peripheral chemoreceptors, what is the ventilatory response to hypoxaemia

Answer 13

Hypoxia in the CNS leads to depression of the ventilatory response –> apnoea

Question 14

Differentiate the effects of opioids versus anaesthetic agents on the control of ventilation

Answer 14

Anaesthetic agents

• Respiratory centre depression
• Peripheral chemoreceptor depression
• Central chemoreceptor depression
• –> Reduced ventilatory response to hypercapnoea and hypoxaemia (shift the CO2 response curve to the right)

Opioids
- Respiratory centre depression only

—> Reduced ventilatory response to hypercapnoea and hypoxaemia (shift the CO2 response curve to the right)

Question 15

What is the pre-Botzinger complex

Answer 15

Contained within the DRG of neurons in the brainstem, the pre-Botzinger complex, is a cluster of neurons thought to be the respiratory pacemaker.

Ablation of this area abolishes respiratory drive

Question 16

What is the Hering-Breuer reflex

Answer 16

Overinflation of the lungs is detected by lung stretch receptors located within bronchial smooth muscle. This impulses are conveyed to the apneustic centre in the brainstem by the vagus nerve which leads to a reduction in the depth of inspiration