Control of respiration

Question 1

Control of Respiration involves

Answer 1

• Factors responsible for generating the alternating inspiration/expiration rhythm
• Factors that regulate the magnitude of ventilation to match body needs
• Factors that modify respiratory activity to serve other purposes such as speech, coughing, holding one’s breath

Question 2

Three lines of defense against changes in non-CO2 induced [H+] to maintain the [H+] of body fluids at a nearly constant level:

Answer 2

Chemical buffer system – immediate response Respiratory compensation – few-minute delay (breathing heavier)
Renal compensation – hours to days delay (kidneys hang on to carbonate)

Question 3

The causes of increased ventilation during exercise are NOT

Answer 3

Arterial PO2
Arterial PCO2
Arterial [H+}

Question 4

*** The causes of increased ventilation during exercise IS A COMBINATION OF

Answer 4

Joint and muscle receptors?
Body temperature?
Adrenaline?
Cerebral cortex?

Question 5

Non-respiratory factors influencing ventilation

Answer 5

Involuntary control
 protective reflexes such as coughing and sneezing
  pain
  emotions (laughing, crying, sighing,
groaning)
Voluntary control
  speaking, singing, whistling

Question 6

Apnea

Answer 6

During apnea, a person subconsciously “forgets to breathe”.
Victims of sleep apnea stop breathing for seconds, even minutes, for up to 500 times a night.
Apnea can lead to respiratory arrest. SIDS may be a form of apnea.

Question 7

Dyspnea

Answer 7

During dyspnea, a person consciously feels that ventilation is inadequate.

Question 8

Respiratory compensation in acidosis

Answer 8

increase in arterial non-CO2-H+ > increase peripheral chemoreceptors > increases activity in medullary respiratory centre > increase ventilation > decrease arterial Pco2 > decrease arterial CO2-H+ > relieves acidosis

• No central chemoreceptor influence as can’t penetrate blood brain barrier

Question 9

Oxygen therapy for such patients has to be carefully monitored. Why?

Answer 9

Because such patients may rely on the life saving mechanism of the peripheral chemoreceptors (PO2 under 60 mm HG) for ventilation. This is called ‘hypoxic drive to breathe’. O2 therapy will increase arterial PO2 above 60 mm Hg and thus decrease the patients drive to breathe. They may stop breathing all together and need to be mechanically ventilated.

Question 10

WHEN ARTERIAL PO2 > 70-80 mm Hg

hyperoxia

Answer 10

become unconscious

high arterial Pco2 > increase central chemoreceptors (increase in brain ECF Pco2 and ecf H+) as well as weak input to peripheral chemorecptors > increases activity in medullary respiratory centre > increses ventilation > decreaes arterial Pco2

Question 11

central chemoreceptors

Answer 11

MONITOR EXTRA CELLULAR
FLUID NOT OXYGEN
- compensatory adjustments in ventilation

• CO2 TRAVELS EASILY INTO EXTRA CELLULAR
  FLUID OF BRAIN

Question 12

peripheral chemoreceptors

Answer 12

MONITOR O2 AND
BLOOD PH

chemoreceptors input to the brain stem modifies the rate and depth of breathing so that, under normal conditions, arterial PCo2, pH, and Po2 remain relatively constant.

Question 13

hypoxia

WHEN ARTERIAL PO2 < 60mm Hg

Answer 13

emergency life-saving mechanism which increase peripheral chemoreceptors > increases activity in medullary respiratory centre > increases ventilaton > increases Arterial Po2

• central chemoreceptors have no effect on medullary respiratory centre