Session 5 - Control of breathing, Hypoxia and Respiratory Failure Flashcards
1
Q
What is hypoxia?
A
• A fall in alveolar, thus arterial pO2
2
Q
What is hypercapnia?
A
• A rise in alveolar, thus arterial CO2
3
Q
What is hypocapnia?
A
• A fall in alveolar, thus arterial CO2
4
Q
What is hyperventilation?
A
- Ventilation increases with no change in metabolism
* (breathing more than you actually have to)
5
Q
What is hypoventilation?
A
- Ventilation decreases with no change in metabolism
* (breathing less than you have to)
6
Q
How does hyperventilation affect plasma pH?
A
- pCO2 down
* pH increases
7
Q
How does hypoventilation affect CO2 and plasma pH?
A
- pCO2 up
* pH down
8
Q
What is the normal metabolic pH?
A
• 7.4
9
Q
What is the body’s normal pH range?
A
• 7.38 - 7.42
10
Q
What happens if plasma pH falls below 7.0?
A
- Plasma k+ rises to dangerous levels and enzymes are lethally denatured
- Function of heart affected
11
Q
What happens if plasma pH rises above 7.6?
A
- Free calcium concentration falls enough to produce fatal tetany
- Calcium salts soluble in acid conditions - In alkalosis, calcium forms complexes. Nerves become excitable, causing tetany
12
Q
Give two events which will occur when hypoventilation occurs?
A
- Hypercapnia
- Respiratory acidosis
- pH falls below 7.0
- Enzymes become lethally denatured
13
Q
Give two events which will occur when hyperventilation occurs?
A
• Hypo capnia and respiratory alkalosis
• pH rises above 7.6
• Free calcium concentration falls enough to produce fatal tetany
○ Ca2+ is only soluble in acid, so pH rises Ca2+ cannot stay in blood. Nerves become hyperexcitable.
14
Q
What is respiratory acidosis?
A
- CO2 produced more rapidly than it is removed by the lungs (hypoventilation).
- pCO2 rises, so (dissolved CO2) rises more than HCO3-, producing a fall in plasma pH
15
Q
What is compensated respiratory acidosis?
A
• Respiratory acidosis persists, and the kidneys responsd to low pH by reducing excretion of HCO3-, thus restoring ratio of (dissolved CO2) to (HCO2-), producing a rise in pH
16
Q
How long does compensation take?
A
• 2-3 days
17
Q
What is respiratory alkalosis?
A
- CO2 is removed from alveoli more rapidly than it is produced (hyperventilation)
- Alveolar pCO2 decreases, changing the ratio of (dissolved CO2) to (HCO3-) producing an increase in plasma pH
18
Q
What is compensated respiratory alkalosis?
A
• Respiratory Alkalosis persists, and the kidneys respond to the high pH by excreting HCO3-, thus restoring the ratio of [Dissolved CO2] to [HCO3-], and therefore the pH.
19
Q
What is metabolic acidosis?
A
- HCO3- displaced by metabolically produced acids
* Blood pH form
20
Q
How can metabolic acidosis be compensated for?
A
• Ratio of (dissolved CO2) to (HCO3-) may be restored to near normal by increasing ventilation rate to decrease pCO2
21
Q
What does acidosis mean?
A
- Reduction in HCO3-
* NOT PH
22
Q
What is metabolic alkalosis?
A
- Plasma HCO3- rises, causing the pH of blood to rise (after vomiting?)
- Stomach produces HCO3- when acid generated
- If acid removed from stomach, gastrin released which produces more acid
- HCO3- produced in excess as a result of this increased production
23
Q
How can metabolic alkalosis be compensated for?
A
- Ratio of dissolved CO2 to HCO3- may be restored to near normal by raising pCO2
- Lungs decrease ventilation to correct pH
- Dangerous
24
Q
What is the control of our breathing moderated by?
A
- pH
* Oxygen requirements are secondary
25
Give three variables which affect breathing?
* pH
* Decrease O2
* Increased CO2
26
What occurs when there is falling inspired pO2?
* Detected by peripheral chemoreceptors located in carotid and aortic bodies
* Increase the tidal volume and rate of respiration
* Changes in circulation direction more blood to the brain and kidney
* Increased pumping of blood by the heart
27
What occurs when there is an increase in inspired pCO2
* Central chemoreceptors in medulla more sensitive than peripheral
* Small rise in pCO2 -> Increase ventilation
* Small decrease in pCO2 -> Decrease ventilation
* Basis of negative feedback control of breathing
28
What is low O2 detected by?
• Peripheral chemoreceptors
29
Where are peripheral chemoreceptors found?
* Carotid bodies
| * Aortic bodies
30
Why do peripheral chemoreceptors only respond to large changes in O2?
* High blood flow in carotid and aorta
| * Lots of O2, usually
31
What are peripheral chemoreceptors stimulated by?
* Low O2
| * High CO2 (minor function)
32
Give three ways in which chemoreceptors response to a decrease in O2
* Increase tidal volume and rate of respiration
* changes in circulation directing blood to the brain and kidney
* Increased pumping of blood by the heart
33
What is a central chemoreceptor and where is it found?
* Found in medulla of the brain
| * Much more sensitive, altering breathing on a second to second basis
34
What do the central chemoreceptors do in response to arterial pCO2?
* Small rise in pCO2 -> Increase ventilation
| * Small fall in pCO2 -> Decrease ventilation
35
hat do central chemoreceptors respond to?
* Changes in the pH of cerebro-spinal fluid (CSF)
| * CSF separated from blood by the blood-brain barrier
36
What is CSH (HCO3-) controlled by?
• Choroid plexus cells
37
What out of HCO3-, CO2 and H+ can cross the BBB
• CO2 only
38
What is the pH of the CSF governed by?
• The ratio of HCO2- to pCO2
39
How is regulation of brain pH different to that of the rest of the body?
• Occurs within hours
40
Apart from pCO2 and pO2, what do the central chemoreceptors respond to?
• Changes in pH of CSF
41
How is the CSF separated from the blood?
• By the blood brain barrier
42
What is the CO2 of the CSF determined by?
* Arterial pCO2
| * HCO3- and H+ cannot cross
43
What is CSF (HCO3-) controlled by?
• Choroid plexus cells
44
What is the pH of CSF determined by?
* The ratio of HCO3- to pCO2
* In the short term HCO3- is fixed, so falls in pCO2 -> increase in pH
* Rise in pCO2 -> lower pH
* Persisting changes compensated for by choroid plexus cells altering CSF
45
What is the oxygen transport chain?
• Air -> Airways -> Alveolar gas -> alveolar membrane -> Arterial blood -> Regional arteries -> Capillary blood -> Tissues
46
Define hypoxia
• A fall in alveolar, thus arterial pO2
47
Give conditions which cause diffusion impairments
• Fibrotic lung disease
○ Thickened alveolar membrane slows gas exchange
• Pulmonary oedema
○ Fluid in interstitial space increases diffusion distance
• Emphysema
○ Destruction of alveoli reduces surface area for gas exchange
48
What is respiratory failure?
* Not enough oxygen enters the blood
| * Not enough CO2 leaves the blood
49
What is type 1 respiratory failure?
* Arterial hypoxia (pO2 below 8kPa), accompanied by normal or low pCO2
* Breathlessness, Exercise intolerance, central cyanosis
50
What alveoli can t1 respiratory failure effect?
• Some or all alveoli
51
Give three symptoms of T1 Respiratory failure
* Breathlessness
* Exercise intolerance
* Central cyanosis
52
Can ventilation perfusion matching bring lungs to 100% capacity
no
53
Give four possible causes of T1 respiratory failure can be caused by conditions affecting some alveoli
* Pulmonary embolism
* Pneumonia
* Consolidation
* Early stages of acute asthma
54
Give two possible causes of T1 respiratory failure which can be caused by conditions affecting most alveoli
```
• Pulmonary oedema
• Fibrosis
○ Pneumoconiosis
○ Asbestosis
○ Extrinsic allergic alveolitis
```
55
What is type 2 respiratory failure?
* Arterial hypoxia, accompanied by an elevated pCO2
| * (Arterial hypoxia = 8kPa)
56
How is O2 saturation measured?
* Pule oximeter
| * Blood gas analysis
57
Give three causes of T2 respiratory failure
```
• Poor respiratory effort
○ Narcotics
○ Muscle weakness (upper and lower motoneurone)
• Chest wall problems
○ Scoliosis/Kyphosis
○ Trauma
○ Pneumothorax
• Hard to ventilate lungs
○ High airway resistance
○ COPD
○ Asthma
```
58
What is emphysema?
* Destruction of lung tissue ( lack of a1-antitrypsin)
* Changes in compliance
* Ventilation perfusion mismatch
* Affects O2 supply
* Initally T1 failure, then T2
59
What happens in the body to solve chronic hypoxia?
* There is a renal correction of acid base balance
| * Increase in ventilation
60
Outline the acute effects of Type 2 respiratory failure
```
• pCO2 rises
• Central chemoreceptors detects
• Breathlessness
○ Some compensation
○ Poor ventialtion prevents full compensation
```
61
What happens in chronic type 2 respiratory failure
* CSF acidity corrected by choroid plexus
* Central chemoreceptors rest to high CO2 level
* Persisting hypoxia
* Reduction of respiratory drive, which is now driven by hypoxia
62
What happens if you give O2 to someone with COPD (T2 respiratory failure)
• They may stop breathing
63
What effect does T2 respiratory failure have on pulmonary circulation?
```
• Effects of hypoxia on pulmonary arterioles
○ Pulmonary hypertension
○ Right heart failure
○ Cor pulmonale
• Increased O2 transport capacity
• Hb increased
• 2,3 BPG
```
64
Give five factors necessary to maintain arterial pO2, problems with which will cause hypoxia
* Low pO2 in inspired air
* Hypoventilation
* Diffusion impairment
* Ventilation perfusion mismatch
* abnormal right to left cardiac shunts
65
What causes low pO2 in inspired air?
• Everything is normal, air has low pO2
66
What is hypoventilation often associated with?
• Increased pCO2 (type 2 respiratory failure)
67
What are neuromuscular causes of hypoventilation?
* Respiratory depression due to opiate overdose • Head injury
* Muscle weakness (NMJ/Nerve/Muscle diseases)
68
What are some Chest wall problems (Mechanical) of hypoventilation
* Scoliosis/kyphosis
* Morbid obesity
* Trauma
* Pneumothorax
69
Give three things which make it hard to ventilate lungs
* Airway obstruction
* COPD & Asthma when the airway narrowing is severe and widespread
* Severe fibrosis
