Module 3 Section 7 (Control of Ventilation) Flashcards
Describe the neural control of respiration.
1) Generation of the alternating inspiration/expiration rhythm:
- This occurs in the medullary respiratory centre that sends its output -> respiratory muscles.
- There are two clusters of neurons:
• Dorsal respiratory group (DRG) neurons: inspiratory neurons whose firing = inspiration, and cessation of firing = expiration.
• Ventral respiratory group (VRG) neurons: both inspiratory and expiratory. There are interneurons b/w the DRG and VRG to allow for recruitment when there is incr output from the DRG during incr ventilator demand.
2) Regulation of the level of respiration (rate and depth) to match metabolism:
- This is controlled by the brain stem under the influence of receptors involved in respiration.
3) Modulation of respiratory activity for other purposes:
- These may be either voluntary (ex: speech) or involuntary (ex: cough or sneeze).
Describe the different mechanical receptors involved in respiration.
There are mechanical receptors in the lungs, the diaphragm, and the chest wall (rib cage), which all contribute to the resp pattern.
1) Pulmonary receotors:
- Slow adapting receptors: have endings in the airway smooth muscle; respond to changes in lung V; the rate of discharge incr as the lungs inflate
- Rapid adapting receptors: endings in the epithelia of larger airways (respond to both chemical and mechanical stimuli); activation = airways narrow and cough (protective reflex to prevent inhalation of irritants); activation also = mucus production (traps inhaled particles)
- C-fibres: endings close the pulmonary capillaries; detect increased pulmonary arterial pressure and pulmonary oedema; can also respond to chemical stimuli (ex: capsaicin signals inflammation); activation = bronchoconstriction and rapid shallow breathing
2) Rib Cage Receptors:
- The muscles here are highly innervated w/ muscle spindles with a few Golgi tendon organs. However, their role in resp = unclear
- Spindles detect discrepancies in chest wall distention from what was expected:
• Smaller distention = spindles receptors “unload” the spindle and permit greater distention
- The intercostal muscles play a role in posture
3) Diaphragm receptors:
- Contains few mechanical receptors, likely due to the diaphragm’s key roles in resp.
- It has many small myelinated and unmyelinated afferents that respond to local metabolic conditions.
Describe the chemical control of breathing.
1) Arterial PˇO2:
- Monitored by peripheral chemoreceptors in the carotid and aortic bodies
- The carotid chemoreceptors respond to changes in arterial PˇO2
• Relatively insensitive to small changes in arterial PˇO2 until it drops <60 mmHg (the level where O2 desaturation could impair peripheral tissue functioning
• Their activation incr ventilation to incr arterial PˇO2
• It’s not activated > 60 mmHg b/c above that lebel, increasing alveolar PˇO2 has little effect on O2 content since the blood is near saturated already
- The aortic chemoreceptors respond to changes in O2 content
• Activation when O2 content decr doesnt affect ventilation, it actually just incr CO to incr systemic O2 delivery
2) Arterial PˇCO2:
- CO2 is the most important factor regulating min-to-min ventilation when at rest. This is apparent since changes in ventilation have immediate effects on arterial PˇCO2
- A slight decr in PˇCO2 stimulates the resp centres to incr ventilation to remove this excess CO2
- A fall in PˇCO2 decr ventilation to allow metabolically-derived CO2 to accumulation until PˇCO2 is normal
- There is no peripheral chemoreceptors that play any significant role
- The central chemoreceptors are in the medulla near the resp centres.
• The chemoreceptors ONLY monitor CO2-induced changes in H+ conc in the brain ECF.
Explain how ventilation changes during exercise.
During exercise, arterial PˇO2 remains normal or may be slightly elevated, while PˇCO2 also remains normal or may be slightly decr b/c of incr ventilation. Brain ECF fluid H+ also remains constant since arterial PˇCO2 doesn’t change.
There are several factors that could play a role in exercise-induced increases in ventilation.
1) Reflexes originating from body movements:
- Muscle mechanoreceptors excited during muscle contraction reflexively stimulate the resp centre to incr ventilation.
- Even minor movements can have a large effect on ventilation
2) Epinephrine release:
- The release of Epi from the adrenal medulla stimulates ventilation.
3) Increased body temp:
- Sweating alone can’t counter the heat generated during exercise so body temp rises slightly.
- Since we know that increasing body temp increases ventilation (this occurs during fever), this is a likely contributor to the control of ventilation.
4) Impulses from the cerebral cortex:
- At the onset of exercise, it’s believed that the motor areas of the cerebral cortex simultaneously stimulate the medullary resp neurons and activate the motor neurons of the exercising muscles.
- This is a feedforward mechanism that can occur before any homeostatic factors could occur.
True or false: the lungs rely completely on external control to changes that alter the matched intake of oxygen and release of carbon dioxide.
True
This occurs in the higher control centre of the medulla and in the brain stem.
No matter how much O2 the tissues consume nor how much CO2 the tissues release, the PˇO2 and PˇCO2 of the arterial blood remain remarkably constant. How is this possible?
This maintenance of the arterial blood gases is achieved by varying the rate and depth of breathing to match metabolic demand.
Thus, if metabolism incr, then ventilation incr. This is achieved by info about the chemical composition of the blood being sent to the medullary control centre.
How does CO2 cause changes in ventilation when the central chemoreceptors in the brain (near the medulla and resp centre) detect changes in H+ concentration in the brain ECF?
1) CO2 can easily cross the blood-brain barrier (BBB), thus any incr in arterial PˇCO2 will incr in brain ECF PˇCO2.
- Ex: in the equation where CO2 in converted to bicarbonate, the law of mass said that if you incr CO2, you’ll get a rise in H+. Thus, this incr in H+ stimulates central chemoreceptors which incr ventilation.
2) As the excess PˇCO2 is exhaled, the reaction reverses which then decr H+ again.
- H+ doesn’t readily cross the BBB, so plasma H+ conc don’t influence resp
- The effects of increasing H+ are SUPER powerful and can override the voluntary inhibition of breathing
• This is a major determinant of breath-hold duration since the blowing of air in the mouth and out of the nostrils can prolong the duration of breath-holding with no effect on arterial PˇCO2
** Slide 8**
Using what you have learned about the mechanical and chemical control of breathing, match each term under the correct heading:
- Aortic bodies
- Cardiac receptors
- Carotid bodies
- Decrease in H+
- Diaphragm receptors
- Increase in Arterial PˇCO2
- Increase in brain Na2+
- Increase in brain ECF H+
- Increase in Arterial Pˇ02
- Pulmonary receptors
- Rib cage receptors
1) Mechanical Control
2) Chemical Control
3) Neither
1) Mechanical Control
- Diaphragm receptors
- Pulmonary receptors
- Rib cage receptors
2) Chemical Control
- Aortic bodies
- Carotid bodies
- Increase in Arterial PˇCO2
- Increase in brain ECF H+
3) Neither
- Cardiac receptors
- Increase in Arterial Pˇ02
- Decrease in H+
- Increase in brain Na2+
True or false: during exercise, alveolar ventilation can incr up to 20-fold.
True
True or false: the exercise-induced increase in ventilation occurs very fast.
True
It’s far faster than can be accounted for by metabolic changes.
