Module 3 Section 7

Question 1

what is central control of breathing

Answer 1

• unlike the heart which can generate its own rhythmic heartbeat, the lungs themselves do not contain the means to generate the rhythmic, cyclic pattern of breathing
• the lungs rely completely on external control to changes that alter the matched intake of oxygen and release of carbon dioxide
• this higher level of control occurs in the respiratory control center of the medulla and in the brain stem

Question 2

explain the generation of the alternating inspiration/expiration rhythm

Answer 2

this occurs in the medullary respiratory center that sends its output to the respiratory muscles. two clusters of neurons:
1. dorsal respiratory group (DRG) neurons are the inspiratory neurons whose firing causes inspiration, and cessation of firing causes expiration
2. ventral respiratory group (VRG) neurons are both inspiratory and expiratory. there are interneurons between the DRG and VRG to allow for recruitment when there is increased output form the DRG during increased ventilator demand

Question 3

explain the regulation of the level of respiration to match metabolism

Answer 3

(rate and depth)
this is controlled by the brain stem under the influence of receptors involved in respiration

Question 4

explain modulation of respiratory activity for other purposes

Answer 4

these may be either voluntary, as in speech, or involuntary, as in cough or sneeze

Question 5

what are the 2 classes of receptors

Answer 5

1. mechanical
2. chemical

Question 6

what are the 3 mechanical receptors

Answer 6

1. pulmonary receptors
2. rib cage receptors
3. diaphragm receptors

Question 7

what are the 3 classes of pulmonary receptors

Answer 7

1. slowly adapting receptors
2. rapidly adapting receptors
3. C-fibres

Question 8

explain slowly adapting receptors

Answer 8

• these have endings in the airway smooth muscle and respond to changes in lung volume
• their rate of discharge increases as the lungs inflate

Question 9

explain rapidly adapting receptors

Answer 9

• these have endings in the epithelia of larger airways and respond to both mechanical and chemical stimuli
• their activation can cause the airways to narrow and cough, this is a protective reflex to prevent inhalation of irritants
• their activation can also cause mucus production to further trap inhaled particles

Question 10

explain C-fibres

Answer 10

• these endings close the pulmonary capillaries and detect increases in pulmonary arterial pressure and pulmonary oedema
• they also respond to chemical stimuli such as capsaicin, that signal inflammation
• activation causes bronchoconstriction and rapid shallow breathing

Question 11

explain rib cage receptors

Answer 11

• the muscles of the chest wall are highly innervated with muscles spindles with a few golgi tendon organs
• their role in respiration is unclear
• these spindles detect discrepancies in actual chest wall distention from the distention that was expected
• if there was a smaller distention than expected then the spindles receptors would discharge to “unload” the spindle and permit greater distention
• the intercostal muscles, also play a role in posture, so it is possible that their physiological function is more related to posture regulation and respiratory control

Question 12

explain diaphragm receptors

Answer 12

• the diaphragm contains very few mechanical receptors
• it is likely that the diaphragm’s key roles in respiration has limited these types of receptors within it
• there are many other kinds of receptors tough
• the diaphragm has many small myelinated and unmyelinated afferents that respond to local metabolic conditions

Question 13

explain chemical control in breathing

Answer 13

• no matter how much oxygen the tissues consume nor how much carbon dioxide the tissues release, the PO2 and PCO2 of the arterial blood remain remarkably constant
• this maintenance of the arterial blood gases is achieved by carrying the rate and depth of breathing to match metabolic demand
• if metabolism increases, then ventilation also increases
• this is achieved by information about the chemical composition of the blood being sent to the medullary control center

Question 14

explain decreased arterial PO2

Answer 14

• arterial PO2 is monitored by peripheral chemoreceptors located int he carotid bodies and the aortic bodies
• they are different from the baroreceptors of the cartoid sinus and aortic arch
• the carotid chemoreceptors respond to changes in arterial PO2 whereas the aortic chemoreceptors respond to changes in oxygen content
• the cartoid chemoreceptors are relatively insensitive to small change sin arterial PO2 until the PO2 drops below 60mmHg, the level at which oxygen desaturation could impair peripheral tissue functioning

Question 15

what does PO2 activation cause

Answer 15

• causes an increase in ventilation to increase arterial PO2
• the reason for not being activated above a PO2 of 60mmHg is that above this level, increasing alveolar PO2 has little effect on oxygen content as the blood is near saturated already
• activation of the aortic chemoreceptors when oxygen content decreases does not affect ventilation, but rather increases cardiac output to increase systemic oxygen delivery

Question 16

explain the role of CO2 in minute-to-minute control in ventilation

Answer 16

CO2 is the most important factor regulating minute-to-minute ventilation when at rest
- this makes sense since changes in ventilation have immediate effects on arterial PCO2
- even slight increases in PCO2 stimulate the respiratory centres to increase ventilation to remove this excess CO2
- a fall in PCO2 decreases ventilation to allow metabolically-derived CO2 accumulate until PCO2 is normalized

Question 17

explain central chemoreceptors and CO2-mediated ventilatory control

Answer 17

• despite the important role CO2 plays in controlling ventilation, there are no peripheral chemoreceptors that play any significant role
• the central chemoreceptors are lcoated in the medulla near the respiratory centres
• these chemoreceptors do not monitor CO2 itself, but monitor CO2-induced changes in H+ concentration in the brain extracellular fluid

Question 18

how does CO2 cause changes in ventilation (part 1)

Answer 18

• CO2 readily crosses the blood-brain barrier so any increase in arterial PCO2 will cause an increase in brain extracellular fluid PCO2
• the law of mass action says that if you increase CO2, you will get a rise in H+
• this increase in H+ stimulates the central chemoreceptors to increase ventilation

Question 19

how does CO2 cause changes in ventilation (part 2)

Answer 19

• as the excess PCO2 is exhaled, the reaction reverses to decrease H+ again
• H+ does not readily cross the blood-brain barrier so plasma H+ concentrations do not influence respiration
• the effects of increasing H+ are so powerful that they can override voluntary inhibition of breathing
• this is a major but not the sole determinant of breath-hold duration as the blowing of air in the mouth and out the nostrils can prolong breath-hold duration with no effect on arterial PCO2

Question 20

explain the effects of exercise on ventilation

Answer 20

• during exercise, alveolar ventilation can increase up to 20-fold
• during exercise, arterial PO2 generally remains normal or may even be flghtly elevated, PCO2 also remains normal or may even decrease due to the increased ventilation, and brain extracellular fluid H+ also remains constant since arterial PCO2 does not change
• the exercise-induced increase in ventilation occurs very fast

Question 21

what are the factors that can play a role in exercise-induced increases in ventilation

Answer 21

1. relfexes originating from body movements
2. increased body temperature
3. epinephrine release
4. impulses from the cerebral cortex

Question 22

explain relfexes originating from body movements

Answer 22

• muscle mechanoreceptors excited during muscle contraction reflexly stimulate the respiratory centre to increase ventilation
• even minor movements can have a large effect on ventilation rates

Question 23

explain increased body temperature

Answer 23

• sweating alone cannot counter the heat generated during exercise so body temp rises slightly
• since we know that increasing body temp increases ventilation, this is likely a contirbutor to the control of ventilation

Question 24

explain epinephrine release

Answer 24

the release of epinephrine from the adrnela medulla stimulates ventilation

Question 25

explain impulses from the cerebral cortex

Answer 25

- at the onset of exercise, it is believed that the motor areas of the cerebral cortex simultaneously stimulate the medullary respiratory neurons and activate the motor neurons of the exercising muscles - this is a feedforward mechanism that can occur before any homeostatic factors could occur