RS Lecture 17 - Control of Breathing Asleep Flashcards Preview

LSS 1 - Thorax anatomy, Respiratory and Circulatory system > RS Lecture 17 - Control of Breathing Asleep > Flashcards

Flashcards in RS Lecture 17 - Control of Breathing Asleep Deck (31)
Loading flashcards...
1
Q

What are the 5 stages of sleep?

A

Stage 1-4, then REM sleep

2
Q

How long are our cycles of sleep?

A

90 minute cycles

3
Q

What are the 3 controls of breathing?

A

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

4
Q

What is the control of breathing when asleep?

A

Brainstem -> automatic/reflex

5
Q

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

A

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

6
Q

Where is the automatic control of breathing located?

A

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

7
Q

How do we define emotional control of breathing?

A

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

8
Q

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

A

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

9
Q

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

A

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

10
Q

How does CO2 change during sleep?

A

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

11
Q

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

A

Breathing will stop -> Central sleep apnoea

12
Q

Why does CO2 need to increase?

A

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

13
Q

What is obstructive sleep apnoea?

A

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

14
Q

Which upper airway muscles reduce their activity during sleep?

A

Genioglossus and Levator palatini

15
Q

Why do we snore?

A

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

16
Q

What is the cycle of obstructive sleep apnoea?

A
17
Q

What is the difference between central and obstructive sleep apnoea?

A

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

18
Q

How does heart failure cause central sleep apnoea?

A

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)

19
Q

What is the purpose of gas exchange systems?

A

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

20
Q

What is the role of O2?

A

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

21
Q

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

A

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

22
Q

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

A

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

23
Q

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

A

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

24
Q

What is the muscle’s response to exercise?

A

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

25
Q

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

A
26
Q

What is the circulation’s response to exercise?

A

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

27
Q

What occurs to oxygen consumption and cardiac output when exercising?

A

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

28
Q

What is the lungs response to exercise?

A

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

29
Q

What happens to aerobic metabolism during exercise?

A

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

30
Q

How does the body deal with metabolic acidosis from exercise?

A

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

31
Q

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

A

Decks in LSS 1 - Thorax anatomy, Respiratory and Circulatory system Class (27):