Control of breathing

Question 1

How is the breathing system controlled?

Answer 1

• Volume of air Inspired and Expired are tightly controlled by the frequency of breath and tidal volume painting PCO2, PO2, &pH

1) Sensors:

• Chemoreceptors
• Mechanoreceptor in the Lung receptors

2) Central controller

• Pons
• Medulla
• Cerebral cortex for voluntary commands “which can override the brain stem”
• ETC

3) Effector Organ

• Resp muscles

Question 2

Which neurons in the brain stem (pons, & medulla) control respiration?

Answer 2

1) Medullary Respiratory Centre

• located in the reticular formation

1a) The inspiratory center (dorsal-respiratory-group-of-neurons), associated with inspiration regulating the basic rhythm of breathing by setting the frequency of inspiration, these neurons are located in the NUCLEUS TRACTUS SOLITARIUS (NTS)

1b) Expiratory center (ventral-respiratory-group-of-neurons), responsible for expiration (DOESN’T WORK AT REST)

2) Apneustic center

• Abnormal pattern of breathing that occurs in pathological conditions
• Prolongs the inspiratory gaps, followed by brief expiration by exciting the inspiratory center of the medulla & by prolonging the AP and contraction of the phrenic nerve and diaphragm relatively
• They are located in the lower pons

3) Pneumotaxic center

• It fine-tunes the respiratory Rhythm
• It is located in the upper pons
• It inhibits the inspiratory center, limiting the tidal volume

Question 3

Where is the inspiratory center “dorsal respiratory group of neurons” located?

Answer 3

In the NUCLEUS TRACTUS SOLITARIUS

Question 4

Where is the apneustic center located?

Answer 4

In the LOWER PONS

Question 5

Where is the pneumotaxic center located?

Answer 5

In the Upper Pons

Question 6

What is the sensory and motor input of the medullary Inspiratory center?

Answer 6

1) Sensory input

• Peripheral chemoreceptors (via nerves 9 and 10)
• Mechanoreceptors of the lungs

2) Motor input

• The diaphragm via the phrenic nerve

Question 7

What controls voluntary breathing?

Answer 7

• The cerebral cortex

1) Voluntary hyperventilation
2) Decreased arterial PCO2 and increased pH
3) Unconsciousness
4) Return to normal breathing

1) Voluntary hypoventilation
2) Decreased oxygen levels
3) Increased arterial PCO2
4) String drive for ventilation

Question 8

What controls the inspiratory center?

Answer 8

1) Peripheral chemoreceptors (more sensitive to O2)

2) Central chemoreceptors (most imp “sensitive to PC02 in arterial blood”)

3) Lung stretch receptors (if the lungs are excessively stretched this will inhibit inspiration)

4) Muscle & Joint receptors (Important during exercise)

5) Apneustic center, which accelerates it

6) Pneumotoxic center inhibits respiration

• This will all ultimately lead to the increase or decreased AP to the phrenic nerve which controls the diaphragm

Question 9

Where are the central chemoreceptors located?

Answer 9

In the brain stem, the ventral surface of the medulla, near the point of exit of the 9th nerve and 10th nerve, and only a short distance from the DRG thus communicating directly with the inspiratory center, on the ventral surface of the medulla close to the inspiratory center

Question 10

What is the function and mechanism of the central chemoreceptors?

Answer 10

• They drive alveolar ventilation, control the breathing rate & maintain arterial PCO2 in normal range
• They are directly activated by the pH of the CSF and indirectly by the arterial PCO2 (dec in pH = more breathing, Inc in breathing = less breathing)

Question 11

What is the effect of the pH on the central chemoreceptors?

Answer 11

1) CO2 crosses the blood-brain barriers well from the capillaries to the CSF, as CO2 is lipid-soluble

2) In the CSF CO2 will combine with H2O producing hydrogen ions and HCO3, the hydrogen ion will act directly on the central chemoreceptors

3) An increase in PCO2 and H+ stimulates breathing while a decrease inhibits it, which returns them back to normal

• A pt with meningitis is expected to hyperventilate due to the excessive H+ from the infections which stimulate central receptors

Question 12

What is the main drive for alveolar ventilation in normal sea-level individuals?

Answer 12

The effect of the arterial PCO2 and CSF on the central chemoreceptors

• CSF H+ directly influences the central chemoreceptors while the arterial PCO2 indirectly affects the central chemoreceptors because it increases the CSF H+.

Question 13

What is the location of the peripheral chemoreceptors?

Answer 13

• In the carotid bodies (the bifurcation of common carotid arteries), & aortic bodies (aortic arch)

Question 14

What is the function and mechanism of the peripheral chemoreceptors?

Answer 14

• Controls breathing rate & drive alveolar ventilation when arterial oxygen is below 60 mmHg
• It does that by detecting arterial PO2, PCO2, & pH, then it sends the information to the inspiratory center via cranial nerves 9 and 10, regulating the breathing
• Peripheral chemoreceptors in the carotid body can sense pH changes while the one in the aortic arch cannot

Question 15

During which conditions will the breathing rate increase?

Answer 15

1) Decreased arterial oxygen partial pressure “especially when <60”

2) Increased in arterial carbon dioxide partial pressure

3) Decrease in the arterial pH

Question 16

Why should we not give COPD patients 100% oxygen?

Answer 16

Because the main drive for alveolar ventilation is the low oxygen if 100% oxygen is given = stop breathing

• You should give them a mix of CO2 and oxygen

Question 17

What is the effect of decreased PO2 in the arterial blood, on the peripheral chemoreceptors?

Answer 17

Stimulates hyperventilation when PO2 decreases below 60 mmHg “emergency mechanism”

Question 18

What is the effect of decreased PCO2 in the arterial blood, on the peripheral chemoreceptors?

Answer 18

Weak stimulant of hyperventilation

Question 19

What is the effect of decreased H+ in the arterial blood, on the peripheral chemoreceptors?

Answer 19

It stimulates it, and it is important in the acid-base balance

Question 20

What is the effect of decreased PO2 in the arterial blood, on the central chemoreceptors?

Answer 20

It directly depresses it and the respiratory center itself when <60 mmHg

Question 21

What is the effect of decreased PCO2 in the arterial blood, on the central chemoreceptors?

Answer 21

Strongly stimulates, the dominant control of ventilation

Question 22

What is the effect of increased H+ in the arterial blood, on the central chemoreceptors?

Answer 22

It doesn’t affect anything as it can’t penetrate the blood-brain barrier

Question 23

What is the mechanism of action of the lung stretch receptors?

Answer 23

• They prevent the hyperventilation of the lungs
• They are mechanoreceptors located in the smooth muscles of the airway, that are stimulated by the distention of the lungs and airway
• They decrease inspiration and ventilation “Hering-Breuer reflex” prolonging the expiratory period

Question 24

Describe the function of the joint and muscle receptor

Answer 24

• They are mechanoreceptors that are located in the joints and muscles
• They detect the movement of the limbs, instructing the inspiratory center to increase the breathing rate
• Important during exercise

Question 25

What is the function and location of the irritant receptors?

Answer 25

• They are located between the epithelial lining of the airway
• They respond to noxious chemicals (dust, pollen, etc) and particles through the cranial nerve 10, causing a reflex that increases the breathing rate & constricts the bronchial smooth muscle

Question 26

What is the function and location of the (Juxtacapillary) J-receptors?

Answer 26

• They are located in the alveolar wall (near to the pulmonary capillaries)
• They detect engorgement of blood and increase in interstitial fluid, increasing breathing rate (like in left-side HF, this will cause rapid sallow breathing & dyspnea)

Question 27

What is the abnormal pattern of breathing, Cheyne-strokes “periodic breathing”?, and what is the mechanism behind it?

Answer 27

• Periods of hyperventilation (40-60 sec) altering with the same periods of apnea
• During apnea, increased brain PCO2, stimulates ventilation maximally, decreases alveolar PCO2 below the set point, inhibits respiration
• In this way, the chemoreceptors will receive information too late to regulate ventilation properly

When a person overbreathes, thus blowing off too much CO2 from the pulmonary blood while at the same time increasing blood O2, it takes several seconds before the changed pulmonary blood can be transported to the brain and inhibit the excess ventilation.

By this time, the person has already overventilated for an extra few seconds.

Therefore, when the overventilated blood finally reaches the brain respiratory center, the center becomes depressed to an excessive amount, at which point the opposite cycle begins—that is, CO2 increases and O2 decreases in the alveoli.

Again, it takes a few seconds before the brain can respond to these new changes. When the brain does respond, the person breathes hard once again and the cycle repeats.

Question 28

What are the causes of abnormal breathing?

Answer 28

1) Severe hypoxemia (high altitude at night)

2) Lesions in the CNS

3) CVS disease (Severe HF)

Question 29

Describe the relation between the levels of PCO2 in the pulmonary blood and the delayed changes in the PCO2 of the fluids in the respiratory center

Answer 29

The basic cause of Cheyne­-Stokes breathing occurs in everyone. However, under normal conditions, this mecha­nism is highly “damped.” That is the fluids of the blood and the respiratory center control areas that have large amounts of dissolved and chemically bound CO2 and O2. Therefore, normally, the lungs cannot build up enough extra CO2 or depress the O2 sufficiently in a few seconds to cause the next cycle of periodic breathing. However, under two separate conditions, the damping factors can be overridden and Cheyne­-Stokes breathing does occur:

1) Cardiac failure:

• When a long delay occurs for the transport of blood from the lungs to the brain, changes in CO2 and O2 in the alveoli can continue for many more seconds than usual. Under these conditions, the storage capacities of the alveoli and pulmonary blood for these gases are exceeded; then, after a few more seconds, the periodic respiratory drive becomes extreme and Cheyne-­Stokes breathing begins. This type of Cheyne-­Stokes breathing often occurs in patients with severe cardiac failure because blood flow is slow, thus delaying the transport of blood gases from the lungs to the brain. In fact, in patients with chronic heart failure, Cheyne­-Stokes breathing can sometimes occur on and off for months.

2) Damaged respiratory centers in the brain:

• A second cause of Cheyne-­Stokes breathing is increased negative feedback gain in the respiratory control areas, which means that a change in blood CO2 or O2 causes a far greater change in ventilation than normal. For instance, instead of the normal 2­ to 3­ fold increase in ventilation that occurs when the PCO2 rises 3 mm Hg, the same 3 mm Hg rise might increase ventilation 10­ to 20 ­fold. The brain feedback tendency for periodic breathing is now strong enough to cause Cheyne­-Stokes breathing without extra blood flow delay between the lungs and brain. This type of Cheyne-­Stokes breathing occurs mainly in patients with damage to the respiratory centers of the brain. The brain damage often turns off the respiratory drive entirely for a few seconds, and then an extra intense increase in blood CO2 turns it back on with great force. Cheyne-­Stokes breathing of this type is frequently a “prelude to death from brain malfunction”.
• Typical records of changes in pulmonary and res­piratory center PCO2 during Cheyne-­Stokes breathing are shown in Figure 42-12. Note that the PCO2 of the pulmonary blood changes in advance of the PCO2 of the respiratory neurons. However, the depth of respiration corresponds with the PCO2 in the brain, not with the PCO2 in the pulmonary blood where the ventilation is occurring.

Question 30

What is meant by the sleep apnea syndrome?

Answer 30

• They are a group of disorders where breathing during sleeping stops for > 10 seconds, > 20 times in an hour, causing measurable blood deoxygenation

Question 31

What are the different types of sleep apnea?

Answer 31

1) Central sleep apnea

2) Obstructive sleep apnea

3) Mixed central and obstructive sleep apnea

Question 32

What is the cause of central sleep apnea?

Answer 32

It occurs due to the decreased respiratory center output, with longer intervals between each breath

• Disorders that can cause cessation of the ventilatory drive during sleep include damage to the central respiratory centers or abnormalities of the respiratory neuromuscular apparatus.
• In most patients the cause of central sleep apnea is unknown, although instability of the respiratory drive can result from strokes or other disorders that make the respi­ratory centers of the brain less responsive to the stimula­tory effects of CO2 and hydrogen ions.

Question 33

What is the cause of obstructive sleep apnea?

Answer 33

• Upper airway blockage despite normal airflow drive (most common), usually in obese patients occurring in males more than females with excess fat in the neck, associated with snoring
• In a few individuals, sleep apnea may be associated with nasal obstruction, a very large tongue, enlarged tonsils, or certain shapes of the palate that greatly increase resistance to the flow of air to the lungs during inspiration.

Question 34

Describe the pleural pressure and airflow in obstructive sleep apnea

Answer 34

Airflow would be flattened at certain points, however the pleural pressure goes up and down indicating that airflow resistance is very high due to the blockage of the oropharynx by the soft palate or tounge, thus there is still a drive for breathing

Question 35

Describe the airflow, and pleural pressure during central sleep apnea

Answer 35

Both the airflow and pleural pressure are flattened at certain points thus there is no drive for breathing

Question 36

What is the treatment for obstructive sleep apnea?

Answer 36

1) surgery to remove excess fat tissue at the back of the throat (a procedure called uvulopalatopharyngoplasty), remove enlarged tonsils or adenoids, or create an opening in the trachea (tracheostomy) to bypass the obstructed airway during sleep

2) nasal ventilation with continuous positive airway pressure (CPAP).

Question 37

What is the treatment of central sleep apnea?

Answer 37

Medications that stimulate the respiratory centers can sometimes be helpful, but ventilation with CPAP at night is usually necessary