W1 - Respiratory Physiology (4-5) Flashcards

1
Q

Define ventilation and perfusion. In what unit are they measured?

A

Ventilation - amount of air getting to alveoli

Perfusion - local blood flow

Both are in l/min

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2
Q

What term describes the following:

Ideally the amount of air getting into the lungs should be equal to the amount of blood flowing past the lungs, but this isn’t the case across the lung, since both decrease with height across the lung.

A

Ventilation-perfusion mismatch

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3
Q

Describe ventilation and blood flow at the base of the lung and apex of the lung. Provide a reason for each.

A

Base - blood flow exceeds ventilation, due to arterial pressure exceeding alveolar pressure

Apex - ventilation exceeds blood flow, as blood flow is low as arterial pressure is less than alveolar pressure

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4
Q

At the level of which rib does ventilation perfectly match with perfusion?

A

At rib 3, ventilation=perfusion

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5
Q

On a graph showing ventilation and perfusion, does blood flow or ventilation decline faster?

A

Blood flow declines faster than ventilation

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6
Q

Where does majority of ventilation-perfusion mismatch take place in the lung?

What % of the height of the health lung performs well in matching blood and air?

A

Over 75%

Majority of mismatch takes place in the apex

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7
Q

In an upright position, why does the ratio of ventilation to perfusion in the lung increase from base to apex?

A

Gravity

The low pressure circuit is more susceptible to the effects of gravity, giving rise to a great degree of variability in blood flow in lungs. Base is highly perfused compared to apex

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8
Q

Provide systolic and diastolic values for pulmonary arterial pressure

A

Systolic P ~25mm Hg
Diastolic P ~8mm Hg

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9
Q

Why do we need a big partial pressure gradient for gas exchange of O2?

A

It’s not very soluble in plasma, unlike CO2

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10
Q

Describe gas exchange in poorly ventilated regions of the lung

A

Blood takes O2 faster than its being replenished, leading to a fall in partial pressure, which means we can’t get rid of CO2 in pulmonary arterial blood

Alveolus gets CO2 from the blood faster than it can blow off, so CO2 builds up.

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11
Q

Define shunt

A

When blood returns to circulation still with CO2 and little O2 - so it’s shunted from the right side of the heart to the left without undergoing gas exchange. It dilutes oxygenated blood from better ventilated lung areas.

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12
Q

Describe the local control mechanism to try to keep ventilation and perfusion matched following shunt

A

Decreased tissue PO2 around under ventilated alveoli constrict their arterioles, which diverts blood to better-ventilated alveoli

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13
Q

Provide 2 reasons why constriction of arterioles following shunt is beneficial

A
  • Blood is redirected to better ventilated regions of the lung, allowing for better gas exchange
  • The constriction increases partial pressure, which dilates bronchial smooth muscle, further improving ventilation
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14
Q

Define alveolar dead space in terms of partial pressure, and provide 2 reasons for when it might occur

A

Alveolar dead space - when ventilation exceeds blood flow.
- Increase in partial pressure of O2
- Decrease in partial pressure of CO2

Occurs:
- To a small extent at the apex of normal lung
- Pulmonary embolism

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15
Q

Describe the following factors in terms of shunt and alveolar dead space:
Ventilation
Perfusion
Alveolar PO2
PCO2
Pulmonary
Bronchial

A

Ventilation - low in shunt, high in ADS
Perfusion - high in shunt, low in ADS
Alveolar PO2 - falls in shunt, rises in ADS
PCO2 - rises in shunt, falls in ADS
Pulmonary - vasoconstriction in shunt, vasodilation in ADS
Bronchial - dilation in shunt, constriction in ADS

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16
Q

Define alveolar dead space, anatomical dead space and physiological dead space

A

Alveolar dead space - alveoli that are ventilated but not perfused

Anatomical dead space - air in the conducting zone of the respiratory tract unable to participate in gas exchange as walls of airways in this region (nasal cavities, trachea, bronchi, upper bronchioles) are too thick

Physiological Dead Space - alveolar DS plus anatomical DS

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17
Q

Define respiratory sinus arrhythmia, why it’s useful and what physiological mechanism is behind it

A

In health, HR increases during inspiration and decreases during expiration

It minimises ventilation-perfusion mismatch

It occurs due to increased parasympathetic vagal activity during expiratory phase, i.e. as HR increases, we have decreased vagal activity; as HR decreases, we have increased vagal activity

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18
Q

What is the O2 demand of resting tissue in ml/min?

What percent of arterial O2 is extracted by peripheral tissues at rest?

A

250 ml/min

25% of arterial O2 is extracted at rest

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19
Q

How much O2 is there per litre of whole blood, and in what 2 ways does O2 travel around the body?

A

200ml O2 per litre whole blood

Solution in plasma - only 3ml O2 dissolved per litre plasma

Bound to haemoglobin protein in RBCs -197ml of which is bound to haemoglobin

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20
Q

What type of haemoglobin do adults primarily have, and how many polypeptide chains do they have? What type of reaction do they undergo? What’s the major determinant of the degree to which haemoglobin binds to oxygen?

A

Haemoglobin A
4 polypeptide chains: 2 alpha, 2 beta
Oxygenation reaction (not oxidation)

Partial pressure of O2 in blood is the major determinant of the degree to which haemoglobin binds oxygen

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21
Q

How does O2 bind and unbind to haemoglobin? What’s the name for this process?

A

When O2 binds to haemoglobin, polypeptide chains shuffle to allow more O2 to bind.

When O2 leaves haemoglobin, we get another confirmational change to make it less attractive to O2

It’s a cooperative binding relationship of oxygen with haemoglobin

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22
Q

How long does it take for haemoglobin to be saturated by alveoli?

A

0.25s contact for saturation to complete

Total contact: 0.75s

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23
Q

In an oxygen-haemoglobin dissociation curve, once partial pressure of O2 falls below what level, haeme groups have a lower affinity for O2

A

Partial pressure of O2 below 60

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24
Q

Define anaemia and explain what PO2, total blood O2 and RBCs might look like for someone with anaemia

A

Anaemia - any condition where O2-carrying capacity of blood is compromised (e.g. iron deficiency, haemorrhage, vit B12 deficiency)

PO2 is normal
Total blood O2 is low

So RBCs can still be fully saturated with O2 in anaemia, as PO2 is normal

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25
Q

What 4 factors affect the oxyhaemoglobin dissociation curve?

A

pH
Partial pressure of CO2
Temperature
DPG (2,3-diphosphoglycerate)

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26
Q

What effect does vigorous exercise have on pH, CO2 and temperature? How would these affect an oxyhaemoglobin dissociation curve?

A

pH - decreases (more acidic)
CO2 - increases
Temp - increases

The curve moves right

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27
Q

Define Bohr effect

A

Bohr effect - decreased affinity of O2 for heme, it aids oxygen unloading at peripheral tissues as haeme is less saturated with O2

28
Q

What makes DPG, what does it do and what 3 things generate more DPG?

A

2,3 diphosphoglycerate is a by-product of RBC metabolism

It reduces affinity of haeme for O2 so helps maintain O2 release in tissues

More DPG is generated in hypoxia, heart or lung disease, living at high altitude

29
Q

In what 3 ways is CO2 carried in blood? Include percentages

A

7% remains dissolved in plasma and RBCs

23% combines in RBCs with deoxyhemoglobin to form carbamino compounds

70% combines in RBCs with water to form carbonic acid

30
Q

What happens to carbonic acid formed from RBCs+water? Where is the process reversed?

A

They dissociates to yield bicarb and H+ ions. Most bicarb moves out of RBCs into plasma in exchange for Cl- ions. Excess H+ bind to deoxyhaemoglobin.

The reverse occurs in pulmonary capillaries and CO2 moves down its concentration gradient from blood to alveoli

31
Q

What 3 factors increase affinity of haemoglobin for O2? How do they affect an oxyhaemoglobin curve?

A

Increase in pH (more alkali)
Decrease in partial pressure of CO2
Decrease temperature

They move curve left

32
Q

Provide the reaction catalysed by carbonic anhydrase. Where does it occur, and what happens to the product?

A

Carbonic anhydrase catalyses the reaction:
CO2 + H2O ⇌ HCO3- + H+
Occurs in RBCs. HCO3- can then diffuse into plasma to be eliminated

33
Q

Identify the factors which favour CO2 unloading to the alveoli at the lungs

A

Oxyhaemoglobin curve shifting right, so:
* Decrease in pH (more acid)
* Increase partial pressure of CO2
* Increase temp
* Increase DPG

34
Q

Define partial pressure and gas content

A

Partial pressure - the pressure exerted by an individual gas in a mixture

Gas content - the total amount of a specific gas in a given volume

35
Q

Provide a value for oxygen tension

A

When PaO2 is 100mmHg

36
Q

Name the 4 types of haemoglobin

A

92% adult haemoglobin
8% other:
- HbA2 where δ chains replace β
- HbF (foetal haemoglobin) where y chains replace β
- Glycolysated Hb (HbA1a, HbA1b and HbA1c)

37
Q

Glycosylated haemoglobin is important to monitor which disease? Why?

A

Important in diabetes as haemoglobin becomes glycosylated when exposed to high levels of glucose. Since RBCs last 120 days, it tells clinicians whether diabetes has been controlled for last 3 months

38
Q

What is myoglobin?

A

Carries O2 in cardiac and skeletal muscle. It has 1 polypeptide chain and 1 heme group

39
Q

Which 2 types of -globin have higher affinity for O2, and why?

A

Foetal haemoglobin (HbF) and myoglobin have a higher affinity for O2 than HbA

Foetal haemoglobin - to extract O2 from maternal/arterial blood.

Myoglobin - allows cardiac/skeletal muscles to extract more oxygen from blood

40
Q

Define hypoxia and name the 5 types of hypoxia

A

Hypoxia - inadequate supply of oxygen to tissue

Hypoxaemic hypoxia
Anaemic hypoxia
Stagnant hypoxia
Histotoxic hypoxia
Metabolic hypoxia

41
Q

Define hypoaxemic hypoxia

A

Most common

Reduction in O2 diffusion at lungs due to decreased PO2 atmos or tissue pathology, e.g. living at altitude

42
Q

Define anaemic hypoxia

A

Reduction in O2 carrying capacity of blood due to anaemia, e.g. RBC loss, iron deficiency, vit B12 deficiency, haemorrhage

43
Q

Define stagnant hypoxia

A

Heart disease resulting in inefficient pumping of blood to lungs/around body

44
Q

Define histotoxic hypoxia

A

Poisoning, preventing cells from utilising oxygen delivered to them, e.g. CO or cyanide

45
Q

Define metabolic hypoxia

A

Oxygen delivered to tissues does not meet increased oxygen demand by cells, e.g. during exercise

46
Q

Which 2 nerves aid inspiration and which 2 skeletal muscles do they affect?

A

Phrenic nerve - to diaphragm
Intercostal nerve - to external intercostal muscle

47
Q

What are the 2 neural respiratory centres? What neurone is breathing dependent on?

A

Pons and medulla
Dependent on somatic motor neurone input from brain

48
Q

Severing the spinal cord above the origin of what nerve causes breathing to cease? What level of the spine is this?

A

Phrenic nerve (C3-5)

49
Q

Which 3 things do the ventral respiratory group of neurones stimulate? Why?

A

Stimulate tongue, pharynx and larynx during inspiration

Maintain patency

50
Q

What 4 factors change respiratory drive?

A

Emotion (via limbic system of brain)
Voluntary override (via higher centres in brain)
Mechano-sensory input from thorax
Chemical composition of blood

51
Q

Describe the location of the two classes of chemoreceptors

A

Central chemoreceptors
Peripheral chemoreceptors

52
Q

Where are central chemoreceptors
and peripheral chemoreceptors found? What do they respond to?

A

Central - medulla, respond to changes in H+ in CSF around brain (which directly reflects PCO2)

Peripheral - carotid and aortic bodies, respond to PO2

53
Q

What’s the strongest factor influencing ventilation?

A

Partial pressure of CO2 in plasma (PaCO2)

54
Q

At what arterial PO2 mmHg do peripheral chemoreceptors cause reflex stimulation of ventilation?

A

<60mmHg

55
Q

How are peripheral chemoreceptors important in hypoxia?

A

We’re sensitive to changes in CO2. When arterial PCO2 decreases, it tells the brain there’s not much CO2 to get rid of, so ventilation is switched off

56
Q

Explain the role of peripheral chemoreceptors in chronic lung diseases of diffusion or ventilation. What is this called?

A

Those with chronic lung disease have high PaCO2. They are desensitised to PCO2 so rely on changes in PaO2 and peripheral chemoreceptors to stimulate ventilation

This is hypoxic drive

57
Q

Explain how central chemoreceptors regulate arterial PCO2 by monitoring the pH of CSF

A

When arterial PCO2 increases, CO2 crosses BBB but not H+

Central chemoreceptors monitor PCO2 indirectly in CSF

Bicarb and H_ are formed and receptors respond to H+

Feedback via Resp Centres increase ventilation in response to increased arterial PCO2

Decreased arterial PCO2 slows ventilation rate

58
Q

What effect do gaseous anaesthetic agents have on respiration? What 3 things do barbiturates and opioids do?

A

Most gaseous anaesthetic agents increase RR but decrease TV so decrease AV.

Barbiturates and opioids:
* Depress respiratory centres (overdose causes death from resp failure)
* Less sensitivity to pH and response to PCO2
Less peripheral chemoreceptor response to less PO2

59
Q

Why is nitrous oxide dangerous for those with chronic lung disease? Administering what aggravates the situation?

A

NO blunts peripheral chemoreceptor response to falling PaO2

In chronic lung disease, people on hypoxic drive use peripheral chemoreceptors to breathe.

Administering O2 makes it worse

60
Q

Which way does the following equation go if plasma pH falls or rises?

CO2 (aq) + H2O ⇌ H2CO3 ⇌ HCO3- + H+

Relate it to hyperventilation, hypoventilation, alkalosis and acidosis

A

If plasma pH falls, the reaction goes backwards. This is hyperventilation, leading to alkalosis

If plasma pH rises, the reaction goes forward. This is hypoventilation, leading to acidosis

61
Q

pHa is calculated by what? Which organs control the factors

A

Bicarbonate (controlled by kidneys) divided by Carbon dioxide (controlled by lungs)

62
Q

Outline how the respiratory system can both create, and compensate for, acid-base disturbances

A

Respiratory system can compensate for non-respiratory caused acidosis/alkalosis, known as metabolic acidosis/alkalosis, and vice versa.

63
Q

During moderate exercise, what causes ventilation to increase in exact proportion to metabolism?

A

The signals causing it are not known - we know it’s not blood-gas composition since arterial PO2 and PCO2 remain unchanged

64
Q

What happens to ventilation and metabolism during strenuous exercise? Why does arterial H+ increase?

A

Ventilation increases more than metabolism

Arterial H+ increases due to lactic acid production, causing some hyperventilation

65
Q

What happens while swallowing in terms of respiration?

A

Respiration is inhibited during swallowing to avoid aspiration of food or fluids in airways. Swallowing is followed by an expiration in order that any particles are dislodged outwards from the glottis

66
Q
A