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Flashcards in Control of respiration Deck (17):
1

Describe the function of the main respiratory center in the brain

The respiratory rhythm is generated in the medulla. The breathing rhythm drives the respiratory motoneurons and interneurons in the spinal cord, which then drive the respiratory muscles, both inspiratory and expiratory (only during exercise or forced expiration)

2

What modulates the rhythm and frequency of breathing

The medulla generates the breathing rhythm while imput from other areas can modulate the frequency of breathing.

3

Describe the locations of peripheral chemoreceptors.

Carotid group is located in carotid bodies (bifurcation of carotid arteries). The aortic group is located in the aortic bodies in the arch of the aorta.

4

What stimulates the peripheral chemoreceptors

decreases in arterial PO2 or increases in PCO2. The carotid group is also stimulated by decreased arterial pH

5

General function of peripheral chemoreceptors

Cardiovascular and respiratory regulation. Carotid group exerts dominant effect on respiration

6

Function of carotid bodies

Increases ventilation in response to low arterial O2 (main function), high PaCO2 (only 20% of the ventilation response but fast which is necessary during exercise) and low arterial pH (fast, only mediator of response)

7

Describe the location of central chemoreceptors.

Close to the ventral surface of the medulla

8

Function of central chemoreceptors

Stimulates breathing in response to high PaCO2 (CO2 crosses BBB then dissociates into protons which are directly bound by central chemoreceptors). There are no central chemoreceptors for oxygen

9

Describe CSF buffering capacity and how this relates to central chemorecptors

Since the CSF contains much less protein than blood, it has a much lower buffering capacity. As a result, the change in CSF pH for a given change in PCO2 is greater than in blood. This is why central chemoreceptors have such a strong response to changes in PaCO2

10

Speed of central chemoreceptors

Slow- it takes minutes for CSF to equilibrate with blood PCO2

11

Speed of pH recovery in CSF in response to elevated PCO2

slow- It takes time for bicarb ions to pass across the BBB to lower the pH

12

Describe the role of the blood-brain barrier in determining the function of central chemoreceptors.

Limits (slows) diffusion of CO2 from blood, prevents diffusion of protons from blood.

13

Describe other inputs into the respiratory center

Cortex, pons (fine control of respiratory rhythm), pulmonary stretch receptors (in airway smooth muscle and activate in response to lung distension to inhibit inspiration), pulmonary irritant receptors (cause hyperpnea-increased ventilation w/out decreased PACO2), Juxtapulmonary capillary receptors (activated by increased pulm interstitial fluid), nose/ upper airway receptors, joint and muscle receptors, gamma system, arterial baroreceptors, pain and temp

14

Describe the integrated response to changes in altitude in terms of the control of respiration.

Low inspired PO2 > increased ventilation > decreased blood PCO2 and increased blood/CSF pH oppose increased ventilation by suppressing peripheral chemoreceptors > ventilation decreases > eventually CSF bicarb decreases which lowers CSF pH and excretion of bicarb by kidneys lowers blood pH. This eliminates the suppression of peripheral chemoreceptor activity and allows ventilation to increase again, raising blood PO2

15

How long does compensation for altitude take

2-3 days for normal PaO2 to be obtained

16

Long term adaptations to altitude

Polycythemia (increased RBCs), increased vascularity of heart and striated muscles

17

Describe the integrated response to exercise in terms of the control of respiration.

Increased PaCO2 and decreased pH during exercise lead to activation of central and peripheral chemoreceptors which increase ventilation ( increased breathing frequency and tidal volume). This increase in ventilation increases linearly at moderate exercise, then even more (steeper) at intense exercise due to liberation of lactic acid