Respiratory rate

List physiological factors which increase respiratory rate. Include a brief explanation of the mechanism by which each achieves this increase (02B10) (1995)

Controller of respiration

1. Respiratory centre
2. Cortex
   - can override respiratory centre to limited extent
3. Others
   - limbic system and hypothalamus can alter patterns of respiration

Respiratory centre:

• controlled respiratory rate
• located in medulla and pons (in the brain stem)
• output via phrenic nerve

Sensors for respiratory centre

1. Central chemoreceptors
2. Peripherial chemoreceptors
3. Lung receptors
4. Other receptors

1. Central chemoreceptors

• Detects changes in PaCO2
• NOT: PaO2

2. Peripheral chemoreceptors

Stimulated by:

• Decreased PaO2, ie. hypoxemia (main role)
• Increased PaCO2, ie. hypercapnia
• Decreased pH, i.e. acidosis
• Hypoperfusion (e.g. by severe hypotension)
• Hyperthermia
• Chemical stimulation

3. Lung receptors

• Pulmonary stretch receptor
  (slow adapting)
  1.  Hering-Breuer reflex
  => distension of lung -> stimulation -> increase in expiration time and decrease in RR
  => Acts primarily to limit or prevent hyperinflation, and are less important for controlling respiratory rate.
  2. Deflation reflex
  => deflation of lung
  => tends to initiate inspiratory effort
• Irritant receptors
  => irritation (noxious gas, cigarette, dusts, cold air) -> bronchocontriction, hypercapnoea
• J receptors
• Bronchial receptors

4. Other receptors

• Arterial baroreceptors
  => decreased BP -> hyperventilation
• Pain and temperature
  => Pain -> apnoea, then hyperventilation
  => Heating of skin -> hyperventilation
• Joint/muscle receptor
  => Stimulates ventilation at early stages of exercise

Work of breathing and respiratory rate

Work against elastic recoil

(For a given minute volume)

• the greater the rate, the less the work due to elastic recoil resistance

Work against air flow resistance

(For a given minute volume)

• the greater the rate, the more the work due to air flow resistance

Optimal respiratory rate

Human tend to breath at a respiratory rate close to the one that minimises work of breathing.

• Increased elastic recoil => higher optimal rate
• Decreased air flow resistance => higher optimal rate

[See diagram 20050306(1) - "Work of breathing vs respiratory rate"]

Factors which INCREASE respiratory rate

1. low pH (acidosis)
   - via: peripheral
2. high PaCO2 (hypercapnoea)
   - via: (mainly) central, peripheral
3. low PaO2 (hypoxemia)
   - via: peripheral
4. raised temperature (hyperthermia)
   - via: peripheral, skin
5. pain
6. severe hypotension
   - via: peripheral, arterial baroreceptor
7. some chemicals and irritants
8. exercise
   - via: joint/muscle receptor
9. voluntarycontrol (to limited extent)
10. Increased elastic recoil AND/OR
    lower airway resistance

Additional Notes

Respiratory centre include:

1. Medullary respiratory centre (excitatory, both inspiratory and expiratory)
2. Apneustic centre (excitatory, inspiratory only) 
3. Pneumotaxic centre (inhibitory on inspiration)

Output via phrenic nerve

1. Medullary respiratory centre

Located in reticular formation of medulla, beneath floor of 4th ventricle

Has 2 parts:

1. Dorsal respiratory group (excitatory, inspiratory)
2. Ventral respiratory group (excitatory, expiratory)

Dorsal respiratory group

• Mainly associated with inspiratory
• "May" have intrinsic periodic firing
  => responsible for basic rhythm
• Inhibited by pneumotaxic centre
• Stimulated by apneustic centre
• Also modulated by vagal (CN10) and glossopharyngeal (CN9)

Ventral respiratory group

• Mainly for expiration
• Not active during quiet breathing
• During exercise, causes active expiration

2. Apneustic centre

Located in lower pons

Causes excitatory effect on dorsal respiratory group
=> longer inspiration
=> thus slower rate

3. Pneumotaxic centree

Located in upper pons

Inhibits dorsal respiratory group
=> shorten inspiration
=> thus faster (not slower) rate

Central chemoreceptors

• Located in ventral surface of medulla, near exit of CN9 and CN10.
• Surrounded by CSF and local blood flow
• Detects only changes in PaCO2.
  => Thus responsible for hypercapnic drive
  NB: Peripheral chemoreceptor also contribute somewhat to hypercapnic drive

Changes in PaCO2 leads to changes in PCO2 in CSF.

Since there are less protein and haemoglobin in CSF (i.e. less buffer),

=> changes in PCO2 in CSF leads to great changes in pH.

When PaCO2 increase, cerebral vessels dilate,

=> faster diffusion of CO2

=> faster changes in pH in CSF

(Normal pH in CSF = 7.32)

When changes are prolonged,

=> HCO3 - moves across the blood-brain barrier to buffer the pH change in CSF (unknown if transport is active or passive)

=> CSF pH change is buffered BEFORE renal compensation of blood pH changes

=> Respiratory change is reduced

Peripheral chemoreceptors

Located as:

1. Carotid bodies (important) - common carotid bifurcation
2. Aoric bodies - above and below aortic arch

Rapid response.

Stimulation of the carotid bodies has predominantly respiratory effect.

Stimulation of the aortic bodies have a greater cardiovascular effect.

Carotid bodies

Contains glomus cells (type I and type II)

• type I - rich in dopamine, in close apposition to afferent carotid sinus nerve endings
• Very rich capillary supply - respond to arterial changes (not venous)

Peripheral chemoreceptors

Responds to:

• Decreased PaO2 (hypoxemia)
  => Main function
• Increased PaCO2 (hypercapnoea)
  => not as significant as central chemoreceptor
• Decreased arterial pH (acidosis)
  => carotid bodies only
• Hypoperfusion (e.g. by severe hypotension)
• Hyperthermia
• Chemical stimulation
  1. Nicotine, acetylcholine => stimulates sympathetic ganglia
  2. Cyanide, carbon monoxide => blocks cytochrome oxidase (histotoxic hypoxia)
  3. Other drugs doxapram, almitrine

Peripheral chemoreceptor stimulation also causes (in addition to increased ventilation):

• bradycardia
• hypertension
• bronchiolar tone
• adrenal secretion

Others

• Hyperthermia in itself also enhances ventilatory response to hypoxia and CO2.  

Additional notes

Examiner's comment

• At least mention hypoxia, hypercapnia, acidosis
• Also menion exercise, voluntary control, pulmonary stretch reflex, ?depression of respiratory centers
• Need to mention: hypoxia and hypercapnia are synergistic in increasing RR.
• Respiratory control mechanism is NOT required.
• Pulmonary stretch reflex acts primarily to limit or prevent hyperinflation, and are less important for controlling respiratory rate.

To be added later

Can add more notes on responses to O2, CO2, pH, exercise, diving