RS Lecture 17 - Control of Breathing Asleep

Question 1

What are the 5 stages of sleep?

Answer 1

Stage 1-4, then REM sleep

Question 2

How long are our cycles of sleep?

Answer 2

90 minute cycles

Question 3

What are the 3 controls of breathing?

Answer 3

Brainstem (reflex/automatic); motor cortex (voluntary/behavioural); limbic system (emotional)

Question 4

What is the control of breathing when asleep?

Answer 4

Brainstem -> automatic/reflex

Question 5

Where is the motor cortex for voluntary/behavioural control of breathing on the motor homonculus?

Answer 5

Between the shoulder and the trunk is the diaphragm, and other respiratory muscles

Question 6

Where is the automatic control of breathing located?

Answer 6

Pre-Botzinger complex -> present in rostral ventral respiratory group -> situated on edge of medulla, close to CSF, so appropriate breathing due to PaCO2 -> not pacemaker cells, and perpetuate respiratory rhythm

Question 7

How do we define emotional control of breathing?

Answer 7

Lack of input from other breathing controls -> like in locked-in syndrome

Question 8

What happens to your minute ventilation when you go to sleep?

Answer 8

It reduces by 10% -> don’t breathe more; due to reduced tidal volume

Question 9

What is an issue about reduced minute ventilation in patients with COPD?

Answer 9

Losing 10% of their minute ventilation would reduce their O2 saturation to 80%, which could be a problem, and taking blood gases in the morning is bad as they will have accumulated CO2 overnight

Question 10

How does CO2 change during sleep?

Answer 10

PaCO2 goes up by 0.5kPa -> otherwise you won’t breathe during sleep, as you need to stimulate the chemoreceptors

Question 11

What happens if PaCO2 doesn’t rise above apnoeic threshold during sleep?

Answer 11

Breathing will stop -> Central sleep apnoea

Question 12

Why does CO2 need to increase?

Answer 12

The central chemoreceptors reduce sensitivity to PaCO2 during sleep -> everyone has different sensitivities which can be plotted on a CO2 sensitivity graph

Question 13

What is obstructive sleep apnoea?

Answer 13

Reduced upper airway muscle activity during sleep, plus extra luminal pressure and negative intraluminal pressure can result in occlusion of the phalangeal airway during sleep -> mechanical problem

Question 14

Which upper airway muscles reduce their activity during sleep?

Answer 14

Genioglossus and Levator palatini

Question 15

Why do we snore?

Answer 15

Turbulent airflow over the vocal cords, result of airflow getting less during sleep

Question 16

What is the cycle of obstructive sleep apnoea?

Answer 16

Question 17

What is the difference between central and obstructive sleep apnoea?

Answer 17

Central has no thoracic/abdominal effort involved (equal and opposite in obstruction) -> central is chemosensitivity, obstructive is mechanical

Question 18

How does heart failure cause central sleep apnoea?

Answer 18

HF can be exacerbated by sleep-related changes in breathing because 50% of patients hyperventilate (pulmonary oedema, stimulating J-receptors which causes over-breathing), so have a low PaCO2 (below apnoeic threshold)

Question 19

What is the purpose of gas exchange systems?

Answer 19

Transport of O2 to tissues, removal of waste products (CO2)

Question 20

What is the role of O2?

Answer 20

Required for production of energy -> combustion of glucose, lipids and proteins

Question 21

What is the respiratory quotient and what is it for fat, protein and glucose?

Answer 21

It is the CO2:O2 ratio -> lowest for fat (0.696), next protein (0.818) and highest for glucose (1 - theoretical maximum) -> routine fuels almost entirely glucose and fat

Question 22

What is the at rest O2 requirement of the average human?

Answer 22

3.5ml/min/kg of O2 = 1MET (metabolic equivalent)

Question 23

How much MET is used in standing, walking slowly, cycling and running?

Answer 23

Standing=1-2, walking=2.3, cycling>4, running>7

Question 24

What is the muscle’s response to exercise?

Answer 24

Onset of exercise - stored energy (ATP/creatine phosphate) causes muscular contraction -> inorganic phosphates, ADP, creatine drive oxidative phosphorylation -> Kreb’s cycle and glycolysis increase, O2 consumption at the muscle increases -> initially CO2 only slightly increases (buffered as HCO3-) but then rises, matching O2

Question 25

What does exercise look like when plotted on a VO2/time graph?

Answer 25

Question 26

What is the circulation’s response to exercise?

Answer 26

Heart rate increases over time, CO increases over time and SV increases but then decreases after a 600 seconds

Question 27

What occurs to oxygen consumption and cardiac output when exercising?

Answer 27

CO rises 4-7 fold; O2 consumption rises 10-15 fold, with mixed venous stats 75-80% and up to 85% of O2 can be extracted

Question 28

What is the lungs response to exercise?

Answer 28

Tidal volume increases as V.E (respiratory minute volume); increased VQ matching improves PaO2

Question 29

What happens to aerobic metabolism during exercise?

Answer 29

O2 flow matches demand, so RQ rises towards 1 as glucose becomes predominant fuel source -> ventilation increases to match CO2 production and attempts to maintain steady state BUT anaerobic metabolism occurs during first minutes of exercise until steady state is reached

Question 30

How does the body deal with metabolic acidosis from exercise?

Answer 30

Lactate forms excess H+, which are buffered by HCO3-, forming CO2 and H2O, which leads to increased ventilation, pH remains stable (low); H+ exceeds HCO3- and hyperventilation occurs

Question 31

What occurs in the aerobic and anaerobic phase of exercise to VE, VCO2 and VO2?

Answer 31