Question 1

In the face of hyperoxia, what is the response of the peripheral chemoreceptors to hypercapnia?

Accepted Answer

High arterial PO₂ (hyperoxia) decreases the peripheral chemoreceptors' PCO₂ sensitivity to almost zero.

Question 2

In the face of chronically elevated levels of CO₂, what happens to the response mediated by the central chemoreceptors?

Accepted Answer

The stimulatory effect of chronically high CO₂ on the central chemoreceptors gradually declines over 1 or 2 days, because the kidneys retain bicarbonate ions in response to respiratory acidosis, bringing the blood pH level back toward normal.

Question 3

Why does it take approximately 24 hr for a full ventilatory response to develop to acute hypoxemia?

Accepted Answer

High altitude causes a healthy person's ventilation to increase because low barometric pressure decreases the inspired PO₂, and thus the arterial PO_2,which in turn raises the sensitivity of peripheral chemoreceptors to hydrogen ions. The resulting increase in ventilation is less than expected though, because hyperventilation lowers the PaCO₂ and raises arterial pH. The increased pH depresses the medullary respiratory center, counteracting the excitatory effect of a low PaO₂ on peripheral chemoreceptors.

Question 4

Which of the following causes hypoxic stimulation of the carotid bodies? 1) Large decrease in arterial PO₂ 2) Large decrease in O₂ content 3) CO poisoning

Accepted Answer

The carotid bodies are primarily sensitive to changes in arterial PO2, not O2 content. CO poisoning does not decrease PO2, so it does not stimulate the carotid bodies.

Question 5

How should O₂ therapy be administered to chronically hypercapnic patients?

Accepted Answer

Oxygen should never be withheld from acutely hypoxemic COPD patients for fear of inducing hypoventilation and hypercapnia. Tissue oxygenation is an overriding priority; O₂ must never be withheld from exacerbated, hypoxemic COPD patients for any reason. This means the clinician must be prepared to mechanically support ventilation if O₂ administration induces severe hypoventilation.

Question 6

When given high concentrations of O₂, a patient with chronic hypercapnia may develop a more serious respiratory acidosis. Which of the following might be contributing to the patient's increased PCO₂? 1) Worsening ventilation-perfusion (VV/QQ) balance 2) Desensitization of the carotid bodies 3) Removal of the hypoxic stimulus

Accepted Answer

High concentrations of O2 can worsen ventilation-perfusion balance and remove the hypoxic drive, leading to increased PCO2.

Question 7

Stimulation to increase ventilation does not occur until the PaO₂ falls below what level?

Accepted Answer

When pH and PaCO₂ are normal (pH = 7.40 and PaCO₂ = 40 mm Hg), the carotid bodies' nerve-impulse transmission rate does not increase significantly until the PaO₂ decreases to approximately 60 mm Hg.

Question 8

Which of the following is indirectly responsible for minute-to-minute control of breathing?

Accepted Answer

As the H⁺ ions in the CSF are generated in direct relation to the level of arterial PCO₂, it is really the arterial PCO₂ that (indirectly) controls primary minute-to-minute ventilation.

Question 9

What is the response of a patient with chronic hypercapnia to a sudden acute rise in carbon dioxide?

Accepted Answer

Chronic hypercapnia does not mean that the medullary chemoreceptors cannot respond to further acute rises in PaCO₂. A sudden elevation in PaCO₂ immediately crosses the blood-brain barrier into the cerebrospinal fluid, generating H⁺ ions that subsequently stimulate the medullary chemoreceptors. This will increase the drive to breathe.

Question 10

Which of the following will occur during even strenuous exercise in a normal healthy individual?

Accepted Answer

Strenuous exercise increases carbon dioxide production and O₂ consumption by as much as 20-fold. Ventilation normally keeps pace with CO₂ production, keeping PaCO₂, PaO₂, and arterial pH constant. Because arterial blood gases do not change, elevated carbon dioxide or hypoxia does not stimulate ventilation in healthy individuals during exertion.

Question 11

In what manner would O₂ therapy induce worsening mismatch and thus a further elevation in CO₂ in a chronically hypercapnic patient?

Accepted Answer

Oxygen breathing causes more blood flow to be directed to poorly ventilated alveoli, which takes blood flow away from well-ventilated alveoli. The key point is that when already under-ventilated alveoli receive additional blood flow, blood PCO₂ rises further. These events can occur without a fall in overall minute ventilation.

Question 12

What happens in chronic hypercapnia? 1) The central chemoreceptive response to CO₂ is decreased. 2) The cerebrospinal fluid pH is restored to normal. 3) Responsiveness to increased CO₂ is decreased.

Accepted Answer

In chronic hypercapnia, the body adapts to the elevated levels of CO2. The central chemoreceptors' response to CO2 is decreased, allowing the body to tolerate higher levels of CO2. Additionally, mechanisms such as renal compensation help restore cerebrospinal fluid pH to normal, despite the elevated CO2 levels. This adaptation also leads to a decreased responsiveness to further increases in CO2, as the body's baseline has shifted to accommodate the chronic condition.

Question 13

What group of nerve cells senses and responds to changes in the chemical composition of its fluid environment?

Accepted Answer

Hypercapnia, acidemia, and hypoxemia stimulate specialized nerve structures called chemoreceptors.

Question 14

What has the primary responsibility for sensing and responding to changes in blood levels of CO₂?

Accepted Answer

Hydrogen ions stimulate highly responsive chemosensitive nerve cells, located bilaterally in the medulla. Nevertheless, these central chemoreceptors are extremely sensitive to CO₂ in an indirect fashion. Through the hydrolysis reaction, as CO₂ increases there is a greater release of hydrogen ions to which the chemoreceptors respond.

Question 15

Which respond more rapidly to high levels of CO₂?

Accepted Answer

The carotid chemoreceptors respond to increased arterial hydrogen ion concentration more rapidly than do the central chemoreceptors.

Question 16

Both anemia and carbon monoxide (CO) poisoning can cause severe hypoxia, yet neither condition results in a major stimulation of breathing. Why is this so?

Accepted Answer

Because of their extremely high blood-flow rates, the carotid bodies respond to decreased arterial partial pressure of O₂ rather than to an actual decrease in arterial O₂ content.

Question 17

Coexisting arterial hypoxemia, acidemia, and high PaCO₂ (i.e., asphyxia) will have what effect on the peripheral chemoreceptors?

Accepted Answer

Coexisting arterial hypoxemia, acidemia, and high PaCO₂ (i.e., asphyxia) maximally stimulate the peripheral chemoreceptors.

Question 18

Adjustment of respiratory muscle contractions to accommodate varying loads is regulated by which of the following?

Accepted Answer

Muscle spindles in the diaphragm and intercostal muscles are part of a reflex arc that helps the muscles adjust to an increased load.

Question 19

Which of the following centers responds more strongly to high levels of CO₂?

Accepted Answer

For a given increase in PaCO₂ or hydrogen ion concentration, the carotid bodies are less responsive than the central chemoreceptors. The peripheral chemoreceptors account for only 20% to 30% of the ventilatory response to hypercapnia.

Question 20

Where are the peripheral chemoreceptors located?
1) In the arch of the aorta
2) In the bifurcations of carotid arteries
3) On the ventrolateral surfaces of the medulla

Accepted Answer

Peripheral chemoreceptors are located in the carotid bodies at the bifurcations of the carotid arteries and in the aortic bodies in the arch of the aorta.

Quiz 15: Regulation of Breathing

In the face of hyperoxia, what is the response of the peripheral chemoreceptors to hypercapnia?

In the face of chronically elevated levels of CO2, what happens to the response mediated by the central chemoreceptors?

Why does it take approximately 24 hr for a full ventilatory response to develop to acute hypoxemia?

Which of the following causes hypoxic stimulation of the carotid bodies? 1) Large decrease in arterial PO2 2) Large decrease in O2 content 3) CO poisoning

How should O2 therapy be administered to chronically hypercapnic patients?

Stimulation to increase ventilation does not occur until the PaO2 falls below what level?

Which of the following is indirectly responsible for minute-to-minute control of breathing?

What is the response of a patient with chronic hypercapnia to a sudden acute rise in carbon dioxide?

Which of the following will occur during even strenuous exercise in a normal healthy individual?

In what manner would O2 therapy induce worsening mismatch and thus a further elevation in CO2 in a chronically hypercapnic patient?

What happens in chronic hypercapnia? 1) The central chemoreceptive response to CO2 is decreased. 2) The cerebrospinal fluid pH is restored to normal. 3) Responsiveness to increased CO2 is decreased.