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Medicine Respiratory > Physiology > Flashcards

Physiology Flashcards

1
Q

Internal respiration

A

Intracellular mechanisms which consumes O2 and produces CO2

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2
Q

External respiration

A

The sequence of events that lead to the exchange of O2 and CO2 between the external environment and the cells of the body

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3
Q

4 steps of external respiration

A

Ventilation - mechanical process of moving gas in and out of the lungs
Gas exchange between alveoli and blood - exchange of O2 and CO2 between air in the alveoli and blood in pulmonary capillaries
Gas transport in the blood - binding and transport of O2 and CO2 in circulating blood
Gas exchange at tissue level - exchange of O2 and CO2 between blood in systemic capillaries and the body cells

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4
Q

4 body systems involved in external respiration

A

Respiratory system, cardiovascular system, haematology system, nervous system

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5
Q

Ventilation

A

The mechanical process of moving air between the atmosphere and the alveolar sacs

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6
Q

Boyle’s Law

A

At any constant temperature, the pressure exerted by a gas varies inversely with the volume of gas (as the volume of gas increases the pressure of the gas decreases)

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7
Q

Relating to Boyle’s law, how is air taken into the lungs during inspiration?

A
  • Air flows down a pressure gradient (high to low)
  • Intra-alveolar pressure must be < atmospheric pressure for air to flow into lungs.
  • Before inspiration intra-alveolar pressure = atmospheric pressure but during inspiration the thorax and lungs expand as a result of contraction of inspiratory muscles
  • Increase in size of lungs means intra-alveolar pressure ↓
  • Air enters until intra-alveolar pressure = atmospheric pressure
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8
Q

2 forces holding the thoracic wall and lungs in close opposition

A
  • Intrapleural fluid cohesiveness - water molecules in intrapleural fluid are attracted to each other and resist being pulled apart hence pleural membranes stick together
  • Negative intrapleural pressure - sub-atmospheric intrapleural pressure creates a transmural pressure gradient across the lung wall and chest wall so lungs are forced to expand outward while chest is forced to squeeze inwards
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9
Q

Atmospheric pressure

A

Pressure caused by the weight of the gas in the atmosphere on the Earth’s surface. Normally 760mmHg at sea level

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10
Q

Intra-alveolar pressure

A

Pressure within the lung alveoli. 760mmHg when equilibrated with atmospheric pressure

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11
Q

Intrapleural pressure

A

Pressure exerted outside the lungs within the pleural cavity. Usually less than atmospheric pressure

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12
Q

What does inspiration depend on?

A

It is an active process dependent on muscle contraction

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13
Q

Muscular movement during inspiration

A

Volume of thorax increased vertically by contraction of the diaphragm, flattening out its dome shape, controlled by the phrenic nerve from cervical 3, 4, 5
The external intercostal muscle lifts the ribs and moves out the sternum aka the ‘bucket handle mechanism’

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14
Q

What is normal expiration brought about by?

A

It is a passive process brought about by relaxation of inspiratory muscles

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15
Q

Relating to Boyle’s law, how is air expelled from the lungs during expiration?

A
  • Chest wall and lungs return to their preinspiratory size
  • Recoil of lungs means ↑intra-alveolar pressure
  • Air leaves lungs down a pressure gradient until intra-alveolar pressure = atmospheric pressure
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16
Q

Changes in intra-alveolar and intra-pleural pressures during the respiratory cycle

A

They both decrease during inspiration and increase during expiration

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17
Q

Pneumothorax

A

Air in the pleural space that can be spontaneous, traumatic or iatrogenic

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18
Q

Symptoms and signs of pneumothorax

A

Symptoms - shortness of breath, chest pain, hypoxia

Signs - Hyperresonant percussion note, decreased/absent breath sounds, tachycardia, reduced chest expansion

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19
Q

How can pneumothorax lead to a lung collapse?

A

Air enters the pleural space from outside or from the lungs and this can abolish the transmural pressure gradient

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20
Q

What causes the lungs to recoil during expiration?

A

Elastic tissue in the lungs and alveolar surface tension

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21
Q

Alveolar surface tension

A

Attraction between water molecules at liquid air interface and in the alveoli this produces a force which resists the stretching of the lungs
but if the alveoli were lined with water alone the surface tension would be too strong and the alveoli would collapse

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22
Q

The law of LaPlace

A

P=2T/r where P = inward directed collapsing pressure, T = surface tension and r=radius. This means that the smaller the alveoli the more likely they are to collapse

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23
Q

Pulmonary surfactant:

  • What is it?
  • What does it do?
A
  • It is a complex mixture of lipids and proteins secreted by type II alveoli
  • It reduces the alveolar surface tension and prevents smaller alveoli from collapsing and emptying their air contents into the larger alveoli
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24
Q

How does pulmonary surfactant lower the alveolar surface tension?

A

It insperses between the water molecules lining the alveoli

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25
Q

Does alveoli lower the surface tension more in smaller or larger alveoli

A

Smaller

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26
Q

Respiratory distress of the newborn

A

Foetal lungs do not synthesise surfactant until late into pregnancy so premature babies may not have enough pulmonary surfactant. This causes the baby to make very strenuous inspiratory efforts in an attempt to overcome the high surface tension and inflate the lungs

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27
Q

Alveolar interdependence

A

If an alveolus starts to collapse, the surrounding alveoli are stretched and recoil exerting expanding forces in the collapsing alveolus to open it

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28
Q

Forces keeping the lung open

A

Transmural pressure gradient, pulmonary surfactant, alveolar interdependence

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29
Q

Forces promoting alveolar collapse

A

Elasticity of stretched lung connective tissue, alveolar surface tension

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30
Q

Major inspiratory muscles

A

Diaphragm and external intercostal muscles

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31
Q

Accessory muscles of inspiration (contract during forceful inspiration)

A

Sternocleidomastoid, scalenus, pectoral

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32
Q

Muscles of active expiration (contracts only during active expiration)

A

Abdominal muscles and internal intercostal muscles

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33
Q

Tidal volume (TV)

A

Volume of air entering or leaving the lungs in a single breath. Average value = 0.5L

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34
Q

Inspiratory reserve volume (IRV)

A

Extra volume that can be maximally inspired over and above the typical resting tidal volume. Average value = 3.0L

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35
Q

Expiratory reserve volume (ERV)

A

Extra volume of air that can be maximally expired by maximal contraction beyond the normal volume of air after a resting tidal volume. Average value = 1.0L

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36
Q

Residual volume (RV)

A

Minimum volume of air remaining in the lungs even after a maximal expiration. Average value = 1.2L

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37
Q

Inspiratory capacity (IC)

A

Maximum volume of air that can be inspired at the end of a normal quiet expiration (IC = IRV + TV). Average value = 3.5L

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38
Q

Functional residual capacity (FRC)

A

Volume of air in the lungs at the end of normal passive expiration (FRC = ERV + RV). Average value = 2.2L

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39
Q

Vital capacity (VC)

A

Maximum volume of air that can be moved out during a single breath following a maximal inspiration (VC = IRV + TD + ERV). Average value = 4.5L

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40
Q

Total lung capacity (TLC)

A

Maximum volume of air that the lungs can hold. (TLC = VC + RV). Average value = 5.7L

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41
Q

Can residual volume be measured by spirometry?

A

No therefore it is impossible to measure the total lung capacity by spirometry

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42
Q

When does residual volume increase?

A

When the elastic recoil of the lung is lost (e.g. in emphysema)

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43
Q

What does a volume time curve allow you to determine?

A

Forced vital capacity (FVC), forced expiratory volume in one second (FEV1) and the FEV1/FVC ratio

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44
Q

Forced vital capacity

A

The volume of air that can be forcibly expelled by the lungs following a maximum inspiration

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45
Q

Forced expiratory volume in one second

A

Volume of air that can be expelled during the first second of expiration in an FVC determination

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46
Q

FEV1/FVC ratio

A

The proportion of the forced vital capacity that can be expired in the first second. Normally >70%

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47
Q

Dynamic lung volumes in obstructive lung disease

A

FVC will be normal or low but FEV1 will be low. FEV1/FVC ratio will be <70% (low)

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48
Q

Dynamic lung volumes in restrictive lung disease

A

Both FVC and FEV1 will be low but the FEV1/FVC ratio will be normal

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49
Q

Dynamic lung volumes in combination of obstructive and restrictive lung disease

A

FVC, FEV1 and FEV1/FVC ratio will all be low

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50
Q

What is the primary determinant of airway resistance

A

The radius of the conducting (F=∆P/R)

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51
Q

Sympathetic and parasympathetic stimulation on the radius of airways

A 
Sympathetic = bronchodilatation
Parasympathetic = bronchoconstriction
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52
Q

Intrapleural pressure in inspiration and expiration

A

Intrapleural pressure falls during inspiration (due to airways being pulled open by the expanding thorax) and rises during expiration (due to the lungs recoiling)

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53
Q

Why does dynamic airway compression make active expiration more difficult in patients with airway obstruction?

A

The driving pressure between the alveolus and the airway is lost over the obstructed segment, causing a fall in airway pressure along the airway downstream resulting in airway compression by the rising compression by the rising pleural pressure during active respiration

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54
Q

Dynamic airway compression

A

The rising pleural pressure during active respiration causes the pressure to be applied to the alveoli which helps push air air out of the lungs and pressure is also applied to the airway, which is not desirable as it tends to compress it

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55
Q

Why does dynamic airway compression cause no problems in people with normal airways?

A

The increased airway resistance causes an increase in airway pressure upstream, helping open the airways by increasing the driving pressure between the alveolus and the airway

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56
Q

Peak flow meter:

  • What does it measure and assess?
  • This is useful for assessing patients with what category of lung disease?
  • How is it measured?
A
  • It measures peak flow rate which assesses the airway function
  • It is useful in assessing patients with obstructive lung disease (e.g. asthma, COPD)
  • The patient gives a short, sharp breath into the peak flow meter and the best of three attempts is usually taken
57
Q

Pulmonary compliance

A

A measure of effort that has to go into stretching or distending the lungs.
Volume change per unit of pressure change across the lungs

58
Q

Decreased pulmonary compliance:

  • Which factors can decrease pulmonary compliance?
  • Why does this cause shortness of breath on exertion?
  • What may it show in spirometry?
A
  • Pulmonary fibrosis, pulmonary oedema, lung collapse, pneumonia and absence of surfactant
  • It means that a greater change in pressure is needed to produce a given change in volume
  • A restrictive pattern
59
Q

Increased pulmonary compliance:

  • What causes this?
  • Which condition does this occur in?
  • Which physiological mechanism can cause this?
A
  • When the elastic recoil of the lungs is lost
  • Emphysema - causes hyperinflation of lungs
  • It increases with age
60
Q

How much energy expenditure does quiet work of breathing normally require?

A

3% of total energy expenditure

61
Q

When is work of breathing increased?

A

When pulmonary compliance is decreased
When airway resistance is decreased
When elastic recoil is decreased
When there is a need for increased ventilation

62
Q

Anatomical dead space

A

Air that remains in the lungs that is not available for gas exchange

63
Q

What is the formula for calculating pulmonary ventilation? What is the average value under resting conditions?

A

Pulmonary ventilation = tidal volume x respiratory rate

Average value - 0.5 x 12 = 6L/min under resting conditions

64
Q

What is the formula for calculating alveolar ventilation?

What is the average value under resting conditions?

A

Alveolar ventilation = (tidal volume - alveolar dead space) x respiratory rate
Average value - (0.5 - 0.15) x 12 = 4.2L/min under resting conditions

65
Q

Why is alveolar ventilation less than pulmonary ventilation?

A

Due to the presence of anatomical dead space

66
Q

Pulmonary ventilation

A

The volume of air breathed in and out per minute

67
Q

Alveolar ventilation

A

The volume of air exchanged between the atmosphere and the alveoli per minute (more important as it represents new air available for gas exchange)

68
Q

What must increase to increase pulmonary ventilation

A

Rate of breathing and depth of breathing. Depth of breathing is more advantageous due to alveolar dead space)

69
Q

Ventilation and perfusion definitions

A 
Ventilation = the rate at which gas is passing through the lungs
Perfusion = the rate at which blood is passing through the lungs
70
Q

What is the result of blood flow and ventilation varying from the bottom to the top of the lung?

A

The average arterial and alveolar partial pressures of oxygen are not exactly the same. This is normally insignificant but can be in disease

71
Q

Alveolar dead space

A

Ventilated alveoli that are not adequately perfused by blood

72
Q

Result of accumulation of CO2 in the alveoli as a result of increased perfusion

A

Decreased airway resistance causing increased airflow

73
Q

Result of increase in alveolar O2 as a result of ventilation

A

Pulmonary vasodilation which increases blood flow to match the larger airflow

74
Q

What happens in an area in which perfusion>ventilation?

A

CO2 increases, O2 decreases, dilatation of local airways, constriction of local blood vessels, airflow increases and blood flow decreases

75
Q

What happens in an area in which ventilation>perfusion?

A

CO2 decreases, O2 increases, constriction of local airways, dilatation of local blood vessels, airflow decreases and blood flow increases

76
Q

4 factors influencing the rate of gas exchange across the alveolar membrane

A
  • Partial pressure gradient of O2 and CO2
  • Diffusion coefficient for O2 and CO2
  • Surface area of alveolar membrane
  • Thickness of alveolar membrane
77
Q

Dalton’s law of partial pressures

A

The total pressure exerted by a gaseous mixture = the sum of the partial pressures in each individual component in the gas mixture. Ptotal = P1 + P2 + …. + Pn

78
Q

What is partial pressure of a gas?

A

The pressure that one gas in a mixture of gases would exert if it were the only gas present in the whole volume occupied in the mixture at a given temperature

79
Q

Alveolar gas equation

A

PAO2 = PiO2 - (PaCO2/0.8) where PAO2 = partial pressure of O2 in alveolar air, PiO2 = partial pressure of of O2 in inspired air, PaCO2 = partial pressure of CO2 in arterial blood and 0.8 is the respiratory exchange ratio

80
Q

Values of O2 partial pressure gradient and CO2 partial pressure gradient in pulmonary and systemic capillaries

A

Pulmonary - O2 = 60mmHg, CO2 = 6mmHg

Systemic - O2 = >60mmHg, CO2 = >6mmHg

81
Q

The diffusion coefficient

A

The solubility of gas in membranes

82
Q

What does a big gradient in PAO2 and PaO2 indicate?

A

Problems with gas exchange in the lungs or a left to right shunt in the heart

83
Q

Fick’s law of diffusion

A

The amount of gas that moves across a sheet of tissue in a unit of time is proportional to the area of the sheet but inversely proportional to its thickness

84
Q

What do alveolar walls consist of?

A

Flattened type I alveolar cells

85
Q

Non-respiratory functions of the respiratory system

A

Route for water loss and heat elimination, enhances venous return, helps maintain a normal acid/base balance, enables vocalisations, defends against inhaled foreign matter, nose serves as the organ of smell

86
Q

Henry’s law

A

The amount of a given gas dissolved in a given type and volume of liquid at a constant temperature is proportional to the partial pressure of the gas in equilibrium with the liquid

87
Q

2 forms in which oxygen is present in the blood

A

Bound to haemoglobin (most oxygen is transported this way) and physically dissolved (very little is dissolved)

88
Q

How many harm groups does one haemoglobin molecule contain?

A

4

89
Q

How many oxygen molecules can each haem group bind to?

A

Each haem group reversibly binds to 1 oxygen molecule

90
Q

When is haemoglobin fully saturated?

A

When all the haemoglobin present is carrying its maximum oxygen load

91
Q

What is the primary factor which determines the percentage saturation of haemoglobin with oxygen?

A

Partial pressure of oxygen

92
Q

What is haemoglobin made up of?

A

Alpha chains, beta chains and haem groups (iron)

93
Q

Cardiac index

A

Cardiac output to the body surface area

94
Q

Oxygen delivery index equation

A

DO2I = CaO2 x CI where DO2I is oxygen delivery index, CaO2 is the oxygen content of arterial blood and CI is the cardiac index

95
Q

What is the oxygen content of arterial blood determined by?

A

The haemoglobin concentration and the saturation of haemoglobin with oxygen

96
Q

What volume of oxygen does one gram of haemoglobin carry when fully saturated?

A

1.34ml

97
Q

Oxygen content of arterial blood equation

A

CaO2 = 1.34 x [Hb] x SaO2

98
Q

Which things can impair oxygen delivery to the tissues?

A

Decreased partial pressure of inspired oxygen
Respiratory disease (decrease PAO2, hence Hb saturation with O2 decreases, O2 content of blood decreases)
Anaemia (Hb concentration decreases, O2 content decreases)
Heart failure (decreases cardiac output)

99
Q

What does partial pressure of inspired oxygen depend on?

A

Total pressure and proportion of oxygen in a gas mixture

100
Q

Partial pressure of oxygen in the alveolar air equation

A

PAO2 = PiO2/[PaCO2/0.8] where PiO2 is the partial pressure of oxygen in inspired air, PaCO2 is the partial pressure of carbon dioxide in arterial blood and 0.8 is the respiratory exchange ratio

101
Q

Co-operativity

A

Binding of one oxygen to haemoglobin increases the affinity of haemoglobin to oxygen, producing a sigmoid curve on a diagram

102
Q

Significance of flat upper portions and steep lower part in the sigmoid curve

A

Flat upper portions - moderate fall in PaO2 will not affect oxygen loading much
Steep lower part - peripheral tissues get a lot of O2 for a small drop in papillary PO2

103
Q

What affect does the Bohr effect have on the oxygen dissociation curve and what causes this?

A

A shift of the curve to the right. Caused by increased release of O2 by conditions at the tissues (e.g. increased PCO2, increased haemoglobin, increased temperature, 2,3-Biphosphoglycerate)

104
Q

Structure of foetal haemoglobin

A

It is made up of 2 alpha and 2gamma subunits

105
Q

Why does foetal haemoglobin have a higher affinity for oxygen compared to adult haemoglobin?

A

Foetal haemoglobin reacts less with 2,3-Biphosphoglycerate in red blood cells (meaning the oxygen haemoglobin curve for foetal haemoglobin is shifted to the left)

106
Q

Where is myoglobin present?

A

Skeletal and cardiac muscles

107
Q

How many haem groups are there per myoglobin molecule?

A

1 haem group her myoglobin molecule

108
Q

What does myoglobin do?

A

Releases oxygen at very low PO2 and provides short-term storage of oxygen for anaerobic conditions

109
Q

What shape is the dissociation curve for myoglobin?

A

Hyperbolic

110
Q

What does presence of myoglobin in the blood indicate?

A

Muscle damage

111
Q

How can carbon dioxide be transported in the blood?

A

In solution (10%), as bicarbonate (60%), as carbamino compounds (30%)

112
Q

Which is more soluble - CO2 or O2?

A

Carbon dioxide

113
Q

How is bicarbonate formed in the blood?

A

Carbonic anhydrase in red blood cells

114
Q

Carbamino compounds:

  • How are they formed?
  • Example
A
  • By combination of CO2 with terminal amine groups in blood proteins
  • Binds to globin of haemoglobin to give carbamino-haemoglobin
115
Q

The Haldane effect

A

Removing O2 from Hb increases the ability of Hb to pick up CO2 and CO2 generated H+

116
Q

What do the Bohr effect and the Haldane effect work in synchrony to facilitate?

A

O2 liberation and uptake of CO2 and CO2 generate H+ at tissues

117
Q

Affect of the Bohr effect on the oxygen haemoglobin curve

A

Shift to the right

118
Q

Affect of the Haldane effect on the carbon dioxide dissociation curve

A

Shift to the right

119
Q

Which part of the brain is the major rhythm detector?

A

Medulla

120
Q

Pre-Botzinger complex:

  • Function
  • Location
A
  • Network of neutrons that display pacemaker activity and are believed to be where the breathing rhythm is generated
  • Located near the upper end of the medulla respiratory centre
121
Q

What gives rise to inspiration?

A
  • Rhythm generated by Pre-Botzinger complex
  • Excited dorsal respiratory group neurones
  • Fire in bursts
  • Firing leads to contraction of inspiratory muscles - inspiration
  • When firing stops, passive expiration occurs
122
Q

Muscle contraction in inspiration

A

Volume of thorax is increased vertically by contraction of diaphragm, flattening out its dome shape, via phrenic nerve from CN III, CN IV, CN V. The external intercostal muscle contraction lifts the ribs and moves out the sternum via the ‘bucket handle’ mechanism

123
Q

“Active” expiration during hyperventilation

A

Increased firing of dorsal neurones excites ventral respiratory group neurones, which excite internal intercostals, abdominals etc and cause forceful expiration

124
Q

The rhythm generated in the medulla can be modified by what?

A

Neurones in the pons

125
Q

Pneumotaxic centre:

  • What does it do?
  • When is it stimulated?
  • What happens without pneumotaxic centre stimulation?
A
  • Stimulation terminates inspiration
  • When dorsal respiratory neurones fire
  • Breathing is prolonged inspiratory gasps with a brief expiration (apneusis)
126
Q

Apneustic centre:

  • What do impulses from these neurones excite?
  • What does it do?
A
  • Inspiratory area of medulla

- Prolongs inspiration

127
Q

Involuntary modifications of breathing

A

Pulmonary stretch receptors hering-breuer reflex, joint receptors reflex in exercise, stimulation of respiratory centre by temperature, adrenaline or impulses from cerebral cortex, cough reflex

128
Q

Pulmonary stretch receptors:

  • Which reflex are they related to?
  • When are they activated?
  • When are they thought to be important?
A
  • Hering-breuer reflex
  • During inspiration at large >1L tidal volumes
  • Maybe important in newborn babies and may prevent overinflation of the lungs in hard exercise
129
Q

Factors that may increase ventilation during exercise

A

Reflexes originating from body movement, adrenaline release, impulses from the cerebral cortex, increase in body temperature

130
Q

Cough reflex - how does it occur?

A

Afferent charge stimulates: short intake of breath, then closure of the larynx, then contraction of abdominal muscles, opening of the larynx and expulsion of air at a high speed

131
Q

What do peripheral chemoreceptors do?

A

Sense tension of oxygen, carbon dioxide and H+ in the blood

132
Q

Central chemoreceptors:

  • Where are they situated?
  • What do they respond to?
A
  • Near the surface of the medulla of the brainstem

- Respond to the H+ of the cerebrospinal fluid

133
Q

Hypoxic drive of respiration:

  • What is the effect via?
  • When is it stimulated?
  • When is it important?
A
  • The peripheral chemoreceptors
  • Stimulated when arterial PO2 falls to low levels (<8.0kPa)
  • Important at high altitudes and may become important in patients with chronic CO2 retention
134
Q

What is hypoxia at high altitudes caused by?

A

Decreased partial pressure of inspired oxygen

135
Q

Acute response of hypoxia at high altitudes

A

Hyperventilation and increased cardiac output

136
Q

Symptoms of acute mountain sickness

A

Headache, fatigue, nausea, tachycardia, dizziness, sleep disturbance, exhaustion, shortness of breath, unconsciousness

137
Q

Chronic adaptions to high altitudes hypoxia

A
  • ↑ RBC production (↑ O2 carrying capacity of blood)
  • ↑ BPG produced within RBC (O2 offloaded to tissues easier)
  • ↑ number of capillaries (blood diffused more easily)
  • ↑ number of mitochondria (O2 used more efficiently)
  • Kidneys conserve acid (arterial pH ↓)
138
Q

H+ drive of respiration:

  • What is the effect via?
  • What is it important in?
A
  • Peripheral chemoreceptors

- Acid-base balance

139
Q

How do the peripheral chemoreceptors play a major role in adjusting for acidosis caused by addition of non-carbonic acid H+ to the blood?

A

Their stimulation by H+ causes hyperventilation and increases elimination of CO2 from the body

Medicine Respiratory (12 decks)

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