Respiratory Anatomy and Physiology Flashcards
1
Q
Describe the anterior and middle scalene
A
Attached to the first rib from the cervical vertebra
2
Q
Describe the posterior scalene
A
Attached to the second rib from the cervical vertebrae.
3
Q
Describe the sternocleidomastoid muscle
A
Attached to the first rib from the mastoid process
4
Q
What is compliance work?
A
The energy required to expand the lungs against the lung and chest elastic forces
5
Q
What is tissue resistance work?
A
The energy required to overcome the viscosity of the lung and chest wall structures
6
Q
What is airway resistance work?
A
The energy required to overcome airway resistance to movement of air into the lungs.
7
Q
What is work of breathing?
A
The energy expended during respiration
8
Q
Is there a positive or negative pressure within the pleural space?
A
Negative
9
Q
Define compliance
A
A measure of the disposition of the lungs to expand under traction or pressure
10
Q
Define elastance
A
A measure of the disposition of the lungs to return to resting position due to intrinsic elasticity
11
Q
Define Hooke’s law
A
The force needed to extend or compress a string is proportional to that distance.
Not quite relevant to the lung - the lung is stiffer at high and low volumes
12
Q
Does emphysema increase or decrease compliance?
A
Increase
13
Q
Does fibrosis increase or decrease compliance?
A
Decrease
14
Q
What cells secrete surfactant?
A
Type II epithelial cells (pneumocytes)
15
Q
What is the major ingredient in surfactant?
A
Phospholipids (dipalmitoyl phosphatidylcholine)
16
Q
As well as phospholipids, what other important substances are in surfactant?
A
Surfactant proteins A B C D
17
Q
Which surfactant proteins activate macrophages and bind to pathogens?
A
A and D
18
Q
Which nerve stimulates contraction of bronchial smooth muscle?
A
Vagus nerve CN X
19
Q
Which type of drugs are used in the treatment of asthma? Which receptors do they act on?
A
Beta - agonists
B2 receptors.
20
Q
What three things determine airway resistance?
A
Autonomic nervous system
Lung volume
Turbulent/laminar flow
21
Q
What is vital capacity?
A
The difference in volume between maximum inhalation and maximum exhalation
22
Q
What drug type is usually in a reliever inhaler?
A
Beta agonist
23
Q
What drug type is usually in a preventer inhaler?
A
Steroid
24
Q
What is residual volume?
A
The amount of air that remains in the lungs after full exhalation.
25
What is tidal volume?
The normal volume of air displaced between normal inhalation and exhalation, usually around 500mL
26
What is functional residual capacity?
The volume of air remaining in the lungs after expiration of a normal breath
27
What is the best indication of lung restriction on spirometry?
A reduction in vital capacity
28
What is the best indication of airways obstruction on spirometry?
An increase in residual volume
29
What would you expect to see on a restrictive spirometry?
Decreased inspiratory reserve volume
Decreased expiratory reserve volume
Decreased reserve volume
Decreased total lung capacity
Decreased forced vital capacity.
30
What would you expect to see on an obstructive spirometry?
```
Increased total lung capacity
Decreased inspiratory reserve volume
Increased expiratory reserve volume
Increased reserve volume
Same or decreased forced vital capacity
```
31
Define metabolic acidosis
pH <7.35
Low HCO3-
32
Define respiratory acidosis
pH <7.35
High PaCO2
33
Define metabolic alkalosis
pH >7.45
High HCO3-
34
Define respiratory alkalosis
pH >7.45
Low PaCO2
35
What is the area of the thorax called where the heart and great vessels sit?
Mediastinum
36
What vertebral level is the suprasternal notch?
T2
37
What vertebral level is the sternal angle?
T4/5
38
What vertebral level is the xiphoid process?
T9/10
39
Name the three portions of the sternum
Manubrium
Body
Xiphoid process
40
Which rib sits at the sternal angle?
Rib 2
41
Why is the posterior angle of the rib an important anatomical landmark?
Used to perform intercostal nerve blocks.
42
Where is the neurovascular bundle?
In the costal groove
43
What is in the neurovascular bundle?
Posterior/anterior intercostal artery
Vein
Nerve
44
What joints sit between the ribs and vertebrae?
Synovial joints
45
Which ribs are vertebrosternal?
Ribs 1-7
46
Which ribs are vertebrocostal?
Ribs 8-10
47
Which ribs are floating ribs?
11 & 12
48
From outside in, name the 3 layers of intercostal muscle
External intercostal muscle
Internal intercostal muscle
Innermost intercostal muscle
49
Between what muscle layers does the neurovascular bundle run?
Internal and innermost intercostal muscles
50
Where does the internal thoracic artery arise from?
Subclavian artery
51
What comes off the internal thoracic artery?
Anterior intercostal artery
52
Name the right sided vein of the thoracic wall
Azygous vein
53
Name the left sided veins of the thoracic wall
Where do they drain into?
Accessory azygous vein
Hemiazygous vein
Both drain into the azygous vein on the right hand side which drains straight into the SVC
54
Where does the majority of the body's lymph fluid drain into?
Where does the thoracic duct start?
Most of the lymph drains into the left subclavian vein (produces Virchow's node in GI cancers)
Cisterna chyli
55
At what level does the IVC pierce the diaphragm?
T8
56
At what level does the oesophagus pierce the diaphragm?
T10
57
At what level does the aorta pierce the diaphragm?
T12
58
In what 3 ways is CO2 transported?
Dissolved CO2 (10%)
Cabamino compounds (21%)
HCO3- (69%)
59
What determines the concentration of H+ ions in the plasma?
Concentration of CO2
Concentration of HCO3-
60
Does arterial or venous blood carry more H+?
Venous blood
| Deoxygenation results in uptake of H+
61
What is the Bohr effect?
Uptake of CO2 reduces the affinity of haemoglobin for O2
62
What is the Haldane effect?
Giving up O2 increase the carriage of CO2
63
What decreases haemoglobin's affinity for O2?
Increased H+ ions
Increased CO2
Increased temperature
Increased 2,3-biphosphoglyceric acid.
64
How are carbamino compounds formed?
When CO2 reacts with protein amino groups
65
How is H+ linked to Ca2+?
Low H+ is linked with increase binding of Ca2+ to albumin
66
What 3 mechanisms minimise the changes in pH?
Buffer systems
Lungs - adjusting CO2
Kidneys - adjust the excretion of H+ into the urine
67
What is a buffer?
Any substance that can reversibly bind H+
68
What are the factors affecting diffusion in the respiratory system?
Surface area
Permeability of membrane
Pressure gradient (osmotic gradient)
69
What is the pO2 in the alveoli and circulatory system?
Alveoli - 13.3 kPA
| Circulation - 6.0 kPa
70
What is the pCO2 in the alveoli and circulatory system?
Alveoli - 5.3 kPa
| Circulation - 6.5 kPa
71
What limits O2 transfer?
O2 transfer is perfusion limited- limited by how much blood we can push through the lungs
72
When is O2 diffusion limited?
If the diffusion barrier is thickened e.g. fibrosis
73
What are the four lung volumes of spirometry?
Tidal volume
Inspiratory reserve volume
Expiratory reserve volume
Residual volume
74
How do you calculate total lung capacity?
IRV+TV+ERV+RV
75
How do you calculate Inspiratory capacity?
IRV+TV
76
How do you calculate vital capacity?
IRV+TV+ERV
77
How do you calculate functional residual capacity?
ERV+RV
78
What is minute ventilation (MV)?
The amount of air moved into and out of the lungs per minute
79
How do you calculate minute ventilation?
```
Volume moved per breath (tidal volume, Vt)
Respiratory rate (RR)
```
MV = Vt x RR
80
What is alveolar ventilation rate (AVR)?
The amount of air that actually reaches the alveoli per minute
81
What are the two types of dead space?
Serial and distributive
82
Define serial dead space
The volume of the conducting airways (a.k.a. ‘anatomical dead space’)
83
Define distributive dead space
Some parts of the lung are not airways, but do not support gas exchange
e.g. damaged alveoli or alveoli with poor perfusion
84
How do you calculate alveolar ventilation rate?
(Vt - Vds) x RR
```
Vt = tidal volume
Vds = dead space volume
RR = resp rate
```
85
What alters the partial pressure gradient in the alveoli?
Alveolar ventilation rate
86
What is the ventilation perfusion ratio?
Ideally a ratio of 1, when the ventilation and perfusion are in equilibrium.
Mismatches cause a change in the V/Q ratio.
87
Does the V/Q ratio increase or decrease as you move towards the base of the lungs?
V/Q ratio decreases to less than 1 at the base of the lungs.
Perfusion increases, ventilation decreases
88
Why is ventilation greater at the bases of the lungs?
Because the basal lung is relatively compressed compared to the apex - more potential for expansion
89
Why does TB tend to consolidate at the apex of the lung?
Because the bacteria likes a well perfused area to grow in
90
What pathophysiology results in a reduction of ventilation?
Pneumonia
Therefore blood is less oxygenated
Decreases V/Q ratio
91
What pathophysiology results in reduced perfusion?
PE
Increases V/Q ratio
92
Where is the respiratory centre located?
Pons and medulla
93
What are the two respiratory centres called?
Dorsal and ventral respiratory centres
94
What are the two respiratory centres responsible for?
Rhythm of breathing
95
Which respiratory centre is found in the pons?
Pneumotaxic centre
96
What does the pneumotaxic centre do?
Regulates respiratory rate
| Decreases tidal volume
97
How do central chemoreceptors monitor pH?
They are found in the brainstem and monitor arterial pCO2 through the pH of CSF.
98
Which chemoreceptors monitor pO2?
Peripheral chemoreceptors
99
Where are peripheral chemoreceptors found?
Aortic and carotid bodies
100
Which 2 nerves does the respiratory centre control?
Phrenic motor nerves (C3, 4, 5)
Vagus nerve (CNX)
101
What is the hypoxic drive?
The need to provide tissues with oxygen
102
Define hypercapnia
Rise in PaCO2
103
Define hypocapnia
Fall in PaCO2
104
Define hypoxia
Fall in PaO2
105
What are normal pAO2 and pACO2 values?
A = alveolar
pAO2 = 13.6 kPa
pACO2 = 5.3 kPa
106
What causes a rise in pAO2?
Increased ventilation
Decreased perfusion
107
What causes a rise in pACO2?
Decreased ventilation
Increased perfusion
108
At what pO2 does ventilation begin to increase and Hb start to desaturate?
8 kPa
109
Between which arteries does the carotid body sit?
Internal and external carotid artery
110
Via which nerve are impulses sent to the medulla from the carotid bodies?
CN IX
111
What is the principle function of the carotid bodies?
What other functions can it perform?
Stimulating the response to hypoxia
Detecting changes in pCO2, hypotension, temperature, some chemicals, pH
112
Which chemoreceptors detect hypoxia?
Which nerve detects this?
Where does it send messages to?
The carotid bodies between the internal and external carotid.
CN IX
Respiratory centres in the medulla
113
What actions are taken as a result of hypoxia detected?
Increased rate and depth of respiration
| Increased BP, adrenal secretion
114
Where are the principle sensors of pCO2?
The ventral surface of the medulla.
Detect the composition of CSF
Information is then sent to the medullary centre which controls ventilation rate
115
Where is CSF secreted from?
The chyroid plexus
CSF is protein free
116
What is the blood brain barrier permeable to?
What is it impermeable to?
Why does this allow central chemoreceptors to respond to CO2?
Permeable to CO2
Impermeable to HCO3- and
H+
pCO2 is the same in arterial blood and CSF
117
What is base excess?
The amount of strong acid that must be added (or removed) for each litre of fully oxygenated blood to return the pH to 7.40 at a temperature of 37°C and a pCO2 of 5.3 kPa
118
What does a positive base excess mean?
```
Metabolic alkalosis
(more acid needs to be added to maintain pH)
```
119
What does a negative base excess mean?
```
Metabolic acidosis
(less acid needs to be added to maintain pH)
```
120
What are the 5 causes of metabolic acidosis?
Lactic acidosis
Ketoacidosis
Acute renal failure
Excessive loss of HCO3- (raised plasma chloride)
All other causes e.g. poisons (aspirin, methanol)
121
What is a cute respiratory failure?
When the pulmonary system is no longer able to meet the metabolic demands of the body
122
Describe type 1 respiratory failure
Hypoxaemic respiratory failure
| PaO2 <8 kPa when breathing room air
123
Describe type 2 respiratory failure
Hypercapnic respiratory failure
PaCO2 >6.7 kPa
(May also be hypoxaemic depending on FiO2)
124
What causes type 1 (hypoxic) respiratory failure?
Reduced diffusion or diffusion capacity
- low pO2 (altitude)
- reduced surface area
125
What causes type 2 (hypercapnic) respiratory failure?
Reduced alveolar ventilation
126
What determines arteriole pO2?
Alveolar pO2
Diffusion capacity of alveolar membrane
Ventilation
Perfusion
V/Q
127
What would cause the V/Q ratio to be 0?
If ventilation stops.
| shunting
128
What can cause shunting?
Pneumonia
Pulmonary oedema
Atelectasis
Lung collapse
Pulmonary haemorrhage or contusion
Congenital heart disease (patent foramen ovale - right to left shunt - hypoxix vasoconstriction).
129
What are the clinical features of respiratory failure?
Respiratory compensation
Sympathetic stimulation
Tissue hypoxia
Hb desaturation
Hypercapnia
130
What are the signs of respiratory compensation?
Tachypnoea
Use of accessory muscles
Intercostal recession
Nasal flaring
Splinting of accessory muscles
131
What are some of the signs of tissue hypoxia?
Altered mental state
Lactic acidosis (anaerobic metabolism)
Low HR and BP
132
What are the signs of hypercapnia?
Flapping tremor
Confusion --> coma
Sympathetic stimulation
Respiratory acidosis
133
What are the two types of asthma?
Extrinsic (atopic) eosinophilic
| Intrinsic (non-atopic) neutrophilic
134
What are the triad of features in asthma?
Airway obstruction
Airway hyper-responsiveness
Airway inflammation
135
What are the signs of an asthma attack?
```
Incomplete sentences
Wheeze
Tachypnoea
Tachycardia
Use of accessory muscles
Reduced breath sounds
```
136
What is the principle muscle of respiration?
What is its innervation?
The diaphragm
Phrenic nerve C3, 4, 5
137
What muscles stabilise the position of the 1st rib?
Anterior and middle scalene
Sternocleido-mastoid
138
What is work of breathing?
What are its 3 components?
The energy expended during respiration
1. Energy required to expand lungs against elastic forces (compliance)
2. Energy required to overcome viscosity of lung (tissue resistance work)
3. Energy required to overcome airway resistance to movement of air into lungs (airway resistance work)
139
Inhalation and exhalation in quiet breathing are.....
Inhalation is active - lungs need to be pulled open against elastic tissues promoting recoil and resistance of airways
Exhalation is passive - lungs return to functional residual capacity where opposing forces of lung and chest wall are in balance
140
Which muscles are at work in forced exhalation?
Extracartilaginous portion of internal intercostals - move ribs downwards
Abdominal muscles - push diaphragm upwards
Muscles of abdominal wall
Pectoral girdle muscles
141
What are the accessory muscles of respiration?
Scalene muscles - elevating the first 2 ribs
SCM muscles - raising the sternum
142
Which 5 muscles are used in inhalation?
Scalenes - elevate 1st and 2nd rib
SCM - raising sternum
External intercostals
Intercartilaginous internal intercostals
Diaphragm
143
Define functional residual capacity
The lung volume at which the opposing forces of the expansile skeletal structure of the chest wall (with muscles at rest) and the contractile lung are in balance with each other
144
Why do movements of the diaphragm and chest wall permit expansion of the lung?
Parietal pleura = chest wall
Pleural fluid
Visceral pleura = lung surface
This provides a pleural seal
During inhalation, the chest wall is expanded. Pleural space is stretched which decreases intrapleural pressure
Because of pleural seal, the lung is expanded because of the movement of the chest wall as the force of the lung's elastic recoil is exceeded
145
What lung volume is represented when the forces inflating and deflating the lungs are equal?
At what phase of the respiratory cycle does this occur?
Functional residual capacity
End of exhalation of quiet breathing
146
The lungs are not adherent to the inside of the thoracic cavity. What stops them from collapsing away from the chest wall?
Negative pressure within the pleural space
147
What will a pneumothorax do to the intrapleural pressure?
What effect will this have?
It will raise the intrapleural pressure
The lung will collapse because of the unopposed force of it's elastic recoil (no longer attached to the chest wall)
148
Which way does the trachae deviate in a pneumothorax?
To the contralateral side
149
What signs can be seen on an Xray in a tension pneumothorax?
Lung completely compressed
Tracheal deviation to contralateral side
Heart shifted to contralateral side
Ipsilateral hemidiaphragm compression
150
What is compliance?
A measure of the disposition of the lungs to expand under traction or pressure
A measure of the stiffness of the respiratory system
151
What is elastance?
A measure of the disposition of the lungs to return to resting position due to their intrinsic elasticity
152
Describe the effect of emphysema on compliance
Compliance is increased in emphysema as there is less tissue to stretch due to tissue destruction
153
Describe the effect of fibrosis on compliance
Compliance is reduced in fibrosis
154
What effect does emphysema have on functional residual capacity?
Emphysema increases FRC because there is less elastic recoil to 'close' the lungs
155
What effect does fibrosis have on functional residual capacity?
Fibrosis decreases FRC
156
Describe why surface tension is an important factor in compliance
Which law is relevant to this idea?
Attractive forces between molecules of a liquid are stronger than those between liquid and gas
Surface tension of water is high and lungs would be difficult to expand in the absence of an agent to lower the surface tension
Lungs have surfactant to lower the surface tension and reduce the work of respiration
LAPLACE'S LAW
157
Name the cells that secrete surfactant
Where are they found?
What is the major component of surfactant?
Type II epithelial cells (pneumocytes)
Lining the alveoli
Phospholipid and surfactant proteins
158
List the 5 functions of surfactant
Reduce surface tension, increase compliance at low lung volumes
Reduce the liklihood of tissue fluid transudation
Lipids have antioxidant activity
Surface proteins A and D can bind to pathogens
Surface proteins A and D can activate macrophages and neutrophils
159
Describe the interdependence of the lungs and why this is
The packing of alveoli supports each other
This is an additional factor limiting any tendency of the lungs to collapse
160
Describe Poiseuille's Law
For individual tubes (airways) with laminar flow, the resistance rises with the fourth power of the radius
161
Where does the main part of airways resistance lie?
Smallest airways are many in number and collectively have the lowest resistance
Greatest resistance is in medium sized bronchi
162
In health, what are the limiting factors to max inspiratory and expiratory flow?
Muscle strength
Resistance is negligible in health
163
In disease, what is airway flow limited by?
Resistance
164
What does peak expiratory flow rate measure?
Airways resistance
165
List 3 factors that determine airways resistance
Autonomic NS
- contraction of smooth muscle narrows airways
- relaxation of muscle is generated by adrenaline acting on B2 receptors.
Lung volume
- increased lung volume increases airway radius
Turbulent vs laminar flow
- larger airways are more prone to turbulent flow than smaller airways
166
Discuss Hooke's Law
The force needed to extend/compress a spring by a distance is proportional to that distance
The lung is not an ideal spring
The lung is stiffer at low and high lung volumes
167
What does the dorsal respiratory group contain?
Where is it found?
Inspiratory neurons
Medulla
168
What does the ventral respiratory group contain?
Where is it found?
Inspiratory and expiratory neurons
Medulla
169
What inputs do the respiratory centres receive?
Stretch receptors in lung
Higher centres
Central chemoreceptors
- pH of CSF
Peripheral chemoreceptors
- arterial pO2
170
What will happen if ventilation increases without a change in the use of O2?
PaO2 will rise
PaCO2 will fall
171
What will happen if ventilation decreases without a change in the use of O2?
PaO2 will fall
PaCO2 will rise
172
Suppose that pO2 has fallen and pCO2 has risen (hypoventilation): how can this be corrected?
Increase the ventilation rate
173
What happen if pO2 falls but pCO2 stays the same?
When you try and increase ventilation to increase pO2, this will cause a fall in pCO2 (hypocapnia)
This can happen in ventilation-perfusion mismatch
174
At what level of pO2 does ventilation substantially rise?
If pO2 falls below 8kPa, ventilation will rapidly increase
175
Which nerve carries impulses to the respiratory centre in the medulla?
CN IX (glossopharangeal)
176
Describe the process of metabolic acidosis and the respiratory response to acidosis
When acids dissociate, they produce H+
In metabolic acidosis, production of acids overwhelms the buffering capacity of HCO3-
This limits the removal of H+ leading to metabolic acidosis
Excess CO2 will be excreted more rapidly than it is produced due to the effects of acidosis
Less CO2 is being made because there is less HCO3- relative to H+ to go to the other side of the equation
CO2 levels will drop
To compensate for acidosis, resp increases to excrete CO2 to reduce PaCO2
The ratio of HCO3- and CO2 is restored to a near normal value but both values are low: this is acidosis with compensation
Only way to restore normal ratios and values is to remove excess H+ e.g. sort out DKA
177
Describe the process of metabolic alkalosis and the respiratory response to alkalosis
E.g. prolonged vomitting causes loss of H+
Loss of H+ means there is an increase in HCO3- and a metabolic alkalosis
CO2 will fall and less will be excreted from the lung
Compensation by decreasing respiratory rate
Decreasing respiratory rate and restoring CO2 levels above normal will restore pH.
But this is not normal because HCO3- and CO2 are above normal limits
This is compensated metabolic alkalosis
178
What is normal FiO2 on room air?
0.21
21 kPa
179
Define acute respiratory failure
When the pulmonary system is no longer able to meet the metabolic demands of the body
180
What is hypoxaemic respiratory failure?
What is it?
Reduced diffusion or diffusion capacity
- low pressure of inspired O2 (altitude)
- surface area
- diffusion coefficient (alveolar membrane)
PaO2 <8kPa on room air
181
What is hypercapnic respiratory failure?
What is it?
Reduced alveolar ventilation
PaCO2 >6.7 kPa
182
What is the oxygen cascade?
What is Pb?
kPa of O2 in different parts of the body
Pb is the barometric pressure = 101kPa at sea level
183
What is RQ?
The respiratory quotient
The ratio of CO2 eliminated to O2 consumed
Usually 0.8
(10 litres of O2 inspired, 8 litres of CO2 produced)
184
What 3 things can influence the arterial partial pressure of oxygen?
PaO2
Diffusing capacity
Lung perfusion
Ventilation-perfusion matching
185
How do you calculate alveolar partial pressure of oxygen?
PAO2
Using the alveolar gas equation
186
Describe the A-aO2 gradient
The different between the alveolar and arterial concentration of oxygen
Used to diagnose the extent of hypoxaemia
1. Calculate PAO2
2. Then calculate A-a O2
Normal values
16yo: 1.1kPa
80yo: 3.1 kPa
187
How do you calculate PAO2?
PiO2 - PaCO2
OVER
R
188
How do you calculate A-a O2?
PAO2 - PaO2
189
The alveolar pressure is equal to.....
the sum of the partial pressures of the gases within the alveolus
190
What is a shunt in regards to V/Q ratio?
What would the V/Q ratio be in this situation?
Non-ventilated alveoli remain perfused, but blood is poorly oxygenated. Blood leaving the lungs is not fully saturated.
Lungs are still perfused but not ventilated
V/Q = 0
191
Outline the difference in V/Q ratios between the top and bottom of the lungs
Apex of lung – higher
Base of lung – lower
When someone is standing, the apex of the lung shows higher V/Q ratio, while at the base of the lung the ratio is lower but nearer to the optimal value for reaching adequate blood oxygen concentrations.
While both ventilation and perfusion increase going from the apex to the base, perfusion increases to a greater degree than ventilation, lowering the V/Q ratio at the base of the lungs.
The principal factor involved in the creation of this V/Q gradient between the apex and the base of the lung is gravity (this is why V/Q ratios change in positions).
192
What is dead space ventilation?
What would the V/Q ratio be?
Ventilation is optimal, but there is no perfusion
V/Q can reach infinity
193
For a constant metabolic rate, PaCO2 is largely dependent on alveolar ventilation.
What is the equation for alveolar ventilation?
What affects this equation?
Resp rate X (Vt - Vd)
```
Vt = tidal volume
Vd = dead space
```
Vd is made up of anatomical dead space, and physiological dead space as a result of V/Q mismatching
194
What 3 things can cause hypoxaemia?
Low PiO2
Hypoventilation
V/Q mismatch
- shunting, dead space
- diffusion abnormality
195
Where in the body can disease cause hypoventilation?
Airway
Lung
Pleura
Chest wall
Brainstem
Spinal cord
Nerve root
Nerve
NMJ
Respiratory muscle
196
Describe the effect of hypoxic pulmonary vasoconstriction
Alveolar hypoxia causes local vasoconstriction
Reduction of perfusion to abnormal area means the proportion of shunted blood is reduced in that area
197
What can cause shunting?
Pneumonia
Pulmonary oedema (HF)
Atelectasis
Lung collapse
Pulmonary haemorrhage/contusion
Any cause of right to left cardiac shunt
198
Describe diffusion abnormalities
Abnormalities in the alveolar membrane or a reduction in capillaries can result in a reduction in the alveolar surface
Hallmark of disease is desaturation on exercise
Caused by ARDS and alveolitis
199
List the 5 causes of hypoxaemia
Low PiO2
Hypoventilation
V/Q mismatching or shunting
Diffusion abnormality
Low cardiac output
200
Give some signs of respiratory compensation and sympathetic stimulation in respiratory failure
Tachypnoea
Accessory muscle use
Intercostal recession
Nasal flaring
Splinting of accessory muscles
High HR
High BP
Sweating
201
Give some sources of error in pulse oximetry
Poor perfusion
Poor probe position
False nails/nail varnish
Lipaemia
Excessive motion
SpO2 <85% less accurate
202
What happens to O2 and CO2 if ventilation increases?
PP of O2 increases
PP of CO2 decreases
203
What happens to O2 and CO2 if perfusion increases?
PP of O2 decreases
PP of CO2 increases
204
What layers does oxygen have to travel through to reach a haemoglobin molecule?
Through gas to alveolar wall
Epithelial cell of alveolus
Epithelial basement membrane
Tissue fluid and connective tissue
Capillary basement membrane
Endothelial cell of capillary
Plasma
Red cell membrane and cytoplasm
205
What factors can affect the diffusion rate of a gas?
Think of the equation
Diffusion rate
Area X diffusion constant X partial pressure difference
OVER
Thickness
206
Oxygen has fully saturated haemoglobin by....
What does this mean in regards to oxygen transfer?
Why is this helpful?
....the time it is 25% along the capillary
This implies that oxygen transfer is perfusion limited
Perfusion limitation is seen for O2 and CO2 under normal conditions
This is helpful because it means there is a reserve if perfusion were to increase e.g. exercise
207
What pathophysiology would lead to diffusion limited oxygen saturation?
Explain
Fibrosis would lead to diffusion limited oxygen transfer
Thickening of the alveolar membrane means it takes longer for the Hb to pick up oxygen, sometimes not fully saturated 100% of the way along the capillary
There is no reserve to cope with exercise and other demands in diffusion limitation
208
What is total or minute ventilation?
How is it calculated?
The amount of air moved into and out of the lungs per minute
MV = tidal volume X RR
Tidal volume is the volume moved per breath
209
What is the alveolar ventilation rate?
The amount of air that reaches the alveoli per minute
Calculation must allow for dead space
210
What are the 2 types of dead space?
Describe them
Serial dead space = the volume of the conducting airways, anatomical dead space
Distributive dead space - some parts of the lungs that are not airways but do not support gas exchange, damaged alveoli or poorly perfused areas
The total of both is the physiological dead space
211
Describe the difference in ventilation and perfusion between the apex and bottom of the lungs
What will this do to O2 and CO2 concentrations?
Increased ventilation at bases - because there is more potential for expansion
Increased perfusion at the bases - because of gravity
V/Q ratio decreases moving down the lung
Apical alveolar pO2 is relatively high to to the lower blood flow, and oxygen is perfusion limited
During exercise, apical capillaries can open further to meet oxygen demands
212
What would pneumonia and a PE do to the V/Q ratio?
Pneumonia would reduce ventilation to an area. This would decrease V/Q ratio
PE would reduce perfusion. This would increase V/Q ratio
213
What could atrophy in the 1st dorsal webspace indicate?
A rib that starts at C7 not T1
Compresses the brachial plexus
214
Where would you find the neurovascular bundle?
In the costal groove on the inferior margin of the ribs
215
What do the ribs articulate with?
The bodies of their own vertebrae and the one above it
The transverse process of their own vertebrae
216
What type of joints are found between the ribs and the vertebrae?
Synovial joints
217
Which ribs are vertebrosternal?
Ribs 1-7
218
Which ribs are vertebrocostal?
Ribs 1-8
219
Which ribs are floating ribs?
Ribs 11 & 12
220
Where do the intercostal nerves arise from?
What do they provide?
The ventral rami of the spinal nerves
Provide motor and sensory innervation to intercostal space and surrounding tissue in a DERMATOMAL PATTERN
221
Which artery is used for a CABG?
Internal thoracic artery
222
Where do some of the posterior intercostal veins at the top of the chest drain into?
Some drain straight into R and L brachiocephalic instead of draining into azygous vein
223
Which ribs does the diaphragm attach to?
Where does the diaphragmatic crura attach?
Costal margin of ribs 10-12
The lumbar vertebrae
224
The lungs fill most of the space around the....
Mediastinum
225
Describe the embryological development of the respiratory system
Develops as an outgrowth of the gut tube
The respiratory diverticulum appears at week 4
Diverticulum forms lung/bronchial buds
Buds grow into splanch0-pleuric mesoderm
Mesoderm of the embryo forms blood vessels, lymph, cartilage, smooth muscle and visceral pleura
Endoderm forms lining and glands
Septum between the oesophagus and trachea is formed between weeks 4 + 5
226
Why is it difficult for babies to survivie before 26 weeks?
Simple squamous epithelium has not formed - hard to exchange gases
227
Are the pulmonary arteries superior or inferior to the pulmonary veins?
Pulmonary artery is superior to the pulmonary veins
228
Where do the phrenic and vagus nerve pass in relation to the hilum of the lungs?
Phrenic nerve passes anterior to hilum
Vagus nerve passes posterior to hilum
229
Where are the parietal and visceral pleura?
Visceral pleura - covers lung surface and into the fissures then reflected as:
Parietal pleura - lines the pleural cavity walls
Only a potential space between the parietal layers
230
What 6 things would be seen on an X-ray in a tension pneumothorax?
Mediastinal shift
Tracheal deviation
Diaphragmatic depression
Unilateral hyperinflation
Increased intercostal space size
Hyper-resonant
231
What surface marking tells you where the middle lobe becomes the inferior lobe of the right lung?
6th rib mid-clavicular line
232
What is the surface marking for the horizontal fissure of the right lung?
4th costal cartilage
233
Where is the triangle of safety for safe chest drain insertion?
Apex – base of the axilla (3rd rib)
Anterior – lateral border of pectoralis major
Posterior – mid-clavicular line
Inferior – 5th intercostal space
Needle should go in either the 3rd or 4th intercostal space
234
Which nerve is at risk if you insert a chest drain too far posteriorly?
The long thoracic nerve runs just behind the mid-axillary line
235
Describe the lymphatic drainage from the lungs
All goes to the right lymphatic duct/right subclavian vein
EXCEPT
Left upper lobe to left thoracic duct/subclavian vein
236
List some causes/triggers of asthma
Occupational exposure
Exercise
Atmospheric pollution
Drugs
Genetic factors
Viral infections
Cold air
Emotion
Irritant vapours and fumes
237
Name the 2 types of asthma
Intrinsic
Extrinsic
238
Describe extrinsic asthma
'Atopic'
The result of an inappropriate adaptive immune response to an inhaled antigen
Typical onset in childhood
Associated with atopy e.g. eczema
Sensitisation and effector phases
239
Describe intrinsic asthma
'Non-atopic'
No personal/family history
Typical onset in middle age
Often onset following URTI
240
Describe some of the macroscopic changes seen in asthma
Increased mucus
Increased goblet cells
Thickening of basement membrane and smooth muscle
Increased glands
Increased macrophages, eosinophils, lymphocytes and neutrophils
241
Describe the pathophysiology of extrinsic asthma (type I hypersensitivity reaction)
First contact:
Allergen is picked up by dendritic cell (antigen presenting cell) that presents it via MHCII to T helper 2 cells
Th2 stimulates B cells via IL-4 and IL - 13 to differentiate into plasma cell and bind IgE to mast cells
Mast cells release histamine, leukotrines, prostaglandins, and cytokines - these promote vascular permeability, smooth muscle contraction and mucus production
Mast cells release chemokines - direct the recruitment of eosinophils via IL-5
Eosinophils release pro-inflammatory mediators
Contact again:
Allergen directly stimulates mast cell to release histamine, cytokines and leukotrines
242
What are the 3 phases of asthma pathogenesis?
Early
Late
Remodelling (chronic)
243
What changes are seen in chronic asthma (re-modelling)?
Smooth muscle hypertrophy
Smooth muscle and epithelial cell hyperplasia
Epithelial damage
Basement membrane thickening
244
What primary pathogensis is seen in early asthma?
Constriction of smooth muscle cells
IgE release promoting release of histamine and PGs from mast cells
245
What primary pathogensis is seen in late asthma?
Vascular leak
Eosinophil and neutrophil recruitment
Mucus secretion
246
Asthma - history and symptoms
Chronic condition with acute exacerbations
Cough, wheeze, chest tightness, SOB, worse at night
Closely associated with atopy/allergy
247
Signs of asthma exacerbation
Difficulty completing sentences
Wheeze
Tachypnoea
Tachycardia
Use of accessory muscles
Reduced breath sounds
248
Asthma - diagnosis
Trial of treatment and assess response
Reversibility on spirometry before/after salbutamol
Diurnal variation on peak flow
Fractional exhaled nitric oxide - measures eosinophilic inflammation in airways
249
Acute asthma management
O2 - sats 94-98%
B2-agonist bronchodilators
- salbutamol nebs repeated 15-30 minute intervals
Corticosteroids
- prednisolone 40-50mg
- hydrocortisone 100mgs QDS IV
- continue for minimum 5 days
Ipratropium nebuliser
Magnesium sulphate - bronchodilator. Only severe asthma
Antibiotics - if signs of infection
250
What do B2 agonists, anticholinergics and leukotrine antagonists do in asthma?
Reverse smooth muscle dysfunction
| - reverse bronchoconstriction and airway hyper-reactivity
251
What do glucocorticoids do in asthma?
Reverse airway inflammation
252
Describe chronic bronchitis (COPD)
Seen in larger airways
Mucus gland hypertrophy and hyperplasia
Hypersecretion of mucus
253
Describe emphysema
Lobules/acini
Air space enlargement - destruction of alveolar walls, decreases surface area for gas diffusion to take place
Alveolar wall destruction
Less alveoli means 'old air' is not forced out and sits in the lungs
254
What 3 things can lead to alveolar wall destruction in emphysema?
Oxidative stress, increased apoptosis and senescence
Inflammatory cells and inflammatory mediators
Protease anti-protease imbalace
255
Why can emphysema cause a pneumothorax?
Air escapes into the interpleural cavity via broken/damaged alveoli that cause 'plebs' and build cause secondary spontaneous pneumothorax
256
List 3 reversible causes of airflow obstruction in COPD
Accumulation of inflammatory cells, mucus and plasma in bronchi
Smooth muscle contraction
Dynamic hyperinflamtion during exercise
257
List 3 irreversible causes of airflow obstruction in COPD
Fibrosis and airway narrowing
Loss of elastic recoil due to alveolar destruction
Destruction of alveolar support that mains patency of small airways
258
List some clinical features seen in COPD
Productive cough
Wheeze
Dyspnoea
Frequent infective exacerbations with purulent sputum
Signs of respiratory failure
259
How is COPD diagnosed?
Spirometry
- reduced FEV1 : FVC ratio
CXR - may show hyperinflation
Haemoglobin - may be raised in chronic hypoxia
260
COPD - management
Smoking cessation
Bronchodilators
- salbutamol (B2 agonist)
- ipratropium (anticholinergic)
Combination therapy
- long-acting B2 agonist and inhaled steroid
- long-acting anticholinergic
Home O2
Pulmonary rehab and MDT management
Vaccinations
- pneumococcal
- flu
261
Acute exacerbation of COPD - management
Inhalers
Nebs
Corticosteroids
- PO prednisolone 7/7
Abx?
- ECOPD is bronchitis
NIV
262
What are the 'main' cells in asthma and COPD?
Asthma - mast cells
COPD - macrophage
263
BAM Lu-Glu
BAM (bronchodilation)
- B2-agonist
- Anticholinergics
- Mthylxanthines
Lu-Glu (anti-inflammatory)
- Leukotrine receptor antagonists
- Glucocorticoids
264
Sever acute asthma treatment
Oxygen
Salbutamol (beta2 agonist)
Hydrocortisone (glucocorticoid)
Ipratropium (anticholingergic)
Theophylline (methylxanthine)
265
What type of nervous system response drives bronchodilation?
Sympathetic responses drive bronchodilation
266
What type of nervous system response drives bronchoconstriction?
Parasympathetic response drives bronchoconstriction
267
Give the MoA of B2-adrenoreceptor agonists
Stimulates B2 adrenergic receptors on bronchiolar smooth muscle cells
Increases action of adenylate cyclase which increases cAMP
cAMP activates protein kinase A which moves Ca2+ into storage vesicles
Protein kinase A inactivates MLCK and drives dephosphorylation of myosin light chain
Reduced cytoplasmic Ca2+ reduces smooth muscle constriction
Inactivation of MLCK and dephosphorylation of myosin light chain reduces smooth muscle contraction
268
Give some examples of B2-adrenoreceptor agonists
Salbutamol & Terbutaline (short-acting)
Salmeterol & Formoterol (long-acting)
269
Give some side effects of B2 adrenoreceptor agonists
Tremor
Tachycardia
Cardiac arrhythmia
270
Which enzyme inactivates cAMP?
Phosphodiesterase enzyme
271
What 3 actions does PKA have on bronchiole smooth muscle cells?
Reduces intracellular calcium
Reduces activity of MLCK
Dephosphorylation of myosin light chain
272
Give the MoA of anticholinergics
Blocks M3 muscarinic acetylcholine receptors on bronchiolar smooth muscle cells
Reduces the action of phospholipase C enzyme, reducing Ca2+ release into the cytoplasm
Reducing cytoplasmic Ca2+ reduces smooth muscle contraction, resulting in bronchodilation
273
Give some examples of anti-cholinergics
Ipratropium (short-acting)
Tiotropium (long-acting)
274
What are the side effects of anti-cholinergics?
Dry mouth
Constipation
Urinary retention
275
Give the MoA of methylxanthines
Blockade of phosphodiasterase enzymes in bronchiolar smooth muscle cells
Sustains cAMP levels by inhibiting its breakdown
Promotes activity of cAMP --> PKA
Reduces intracellular Ca2+ which reduces smooth muscle contraction
276
Give some examples of methylxanthines
Theophylline
Aminophylline
277
What are the side effects of methylxanthines?
Very toxic cardiac and neurological side effects
Cardiac arrhythmias
Seizures
278
Give the MoA of leukotrine receptor antagonists
Mast cells secrete leukotrines which act on leukotrine receptors on bronchiole smooth muscle cells causing contraction
Leukotrine receptors of eosinophils guide eosinophil chemotaxis to site of inflammation
Leukotrine receptor antagonists target CysLT1 receptors on eosinophils in the lungs and bronchiole smooth muscle cells
This reduces inflammation (eosinophils) and bronchospasm (smooth muscle)
279
Give some examples of leukotrine receptor antagonists
Montelukast
Zafirlukast
280
Give some side effects of leukotrine receptor antagonists
Abdominal pain
Headaches
281
Give the MoA of glucocorticoids
Targets the intracellular glucocorticoid receptor in immune cells of the lung (macrophages, T-cells, eosinophils)
Activated GR interacts with nuclear DNA and influences gene expression:
- suppresses pro-inflammatory mediators
- expresses anti-inflammatory products
Up-regulates B2-adrenoreceptors
282
What genetic deficiency is though to have an effect in COPD?
a1 antitrypsin deficiency
Decrease in a1 antitrypsin causes a protease/antiprotease imbalance which leads to alveolar wall destruction
283
Give the names of some glucocorticoids
Beclomethasone (inhaled)
Fluticasone (inhaled)
Prednisolone (PO)
Hydrocortisone (IV)
284
Give some side effects of glucocorticoids
Moon face
Weight gain
Osteoporosis
Hyperglycaemia
285
Why do test lung function?
Useful in symptomatic patients and those at risk of pulmonary disease
The evaluation of lung function patterns provides an aid to diagnosis
Drs can follow changes in lung function over time and in response to treatment
Can assess changes in response to specific stimuli in lab or environment
286
What is vital capacity?
The volume of air moved from max inhalation to max exhalation
287
What is residual volume?
The amount of air left in the lungs after full expiration
288
What is expiratory peak flow?
Why is it useful?
What variability is diagnostic of asthma?
Easy to perform
Cheap equipment
Maximum achievable flow is determined by diameter of bronchiole tree and muscle power available
Blow down peak flow meter at maximum inhalation
>20% variability in maximum peak flow is diagnostic of asthma
289
Give some pros and cons to spirometry
Most readily available and useful test
10-15 minutes, cheap instrument, little risk
Achieving expertise takes training
Internationally accepted criteria ensures optimal and repeatable results
Normal values have been defined to differ between populations
290
What is FEV1?
Forced expiratory b=volume in 1 second
291
Describe some characteristics of a restrictive spirometry
A reduction in vital capacity
Decreased total lung volume
FEV1:FVC ration increased to over 70% because the FVC is the reduced factor
292
Describe some characteristics of an obstructive spirometry
Reduced FEV1
Reduced FEV1 :FVC ratio below 70% because FEV1 is the most reduced factor
293
List some contraindications to performing lung function tests
Haemoptysis
Closed/recent pneumothorax
Pre-eclampsia
HTN
Aneurysms
Acute illness that may alter results
Recent thoracic, ear, ocular, abdo surgery
294
How many ATPs are made from one glucose molecule?
38 in presence of O2
2 in anaerobic conditions
295
What does blood oxygen reversibly combine with?
Haem
Porphyrin compound coordinated to a single iron atom in its ferrous form Fe2+
296
Describe haemoglobin
2 alpha and 2 beta globulin chains
Variable quaternary structure
Has 'relaxed' and 'tense' forms
Relaxed has higher O2 affinity - allows O2 access to haem groups
Tense quaternary structure inhibits O2 binding, 500x less available to O2
297
Describe the concept of the minimum threshold for O2 and haem binding
When environmental O2 is low, no O2 is bound to haem and quarterny structure is tense
Hard to bind first O2 in this state
Initial binding requires threshold minimum O2
As O2 binds to one chain, others become more easily available
298
At total saturation, the amount of O2 binding is dependent on.....
The amount of Hb available (anaemia)
Saturation is independent of Hb concentration
299
At what kPa is Hb half saturated with O2?
3.5kPa
300
Where on the dissociation curve is Hb on a plateau?
Above 8kPa
Hb is 90% saturated at this point
301
Alveolar pO2 is 13.3kPa. What does this mean in relation to Hb saturation of O2?
Hb will be almost fully saturated at 95%
For typical Hb levels, O2 content in fully saturated blood is 200ml/L plus dissolved O2
302
How much of its O2 does Hb give up at the tissues?
What is the saturation of Hb at the tissues?
Hb is 65% saturated at the tissues
Hb gives up 30% of its O2 at the tissues
60ml of O2 delivered per litre
303
Why is it useful that Hb only gives off half of its O2 at the tissues?
Leaves room for reserve if demand increases e.g. exercise
Hb can give off more O2 if needed
304
How does O2 diffuse from Hb to the tissues?
Down a concentration gradient
If the tissue pO2 is low, more O2 will be given up
Hb has less affinity for O2 as number of molecules bound decreases
There is a limit to how low tissue O2 concentration can drop before diffusion to cells is compromised
305
Why can heart muscle tolerate a greater fall in tissue pO2 than other tissue?
Because it has high capillary density
With high capillary density, diffusion occurs across shorter distance and higher surface area
This allows maintenance of gradient between capillaries and cells
306
What environmental factors can shift the Hb dissociation curve?
Acidic environments make Hb more tense - less affinity for O2
Increasing temperature makes Hb more tense - less affinity for O2
307
What 4 factors will cause a 'shift to the right' in the O2 dissociation curve?
Acidity
Pyrexia
Increased CO2
Increased 2,3-DPG
Major shift favouring O2 offloading occurs at tissues where it is needed
308
When is 2,3-DPG released?
What does it do?
Levels of 2,3-DPG in RBCs increases in response to hypoxia
This stabilises a tense state - less affinity for O2
309
Describe the Bohr effect/shift
Acidic conditions O2 dissociation curve shifts right
Due to H+ ion and CO2 binding which stabilise Hb in the tense state
Result is at any give pO2 Hb binds less O2
O2 is released more easily in tissues with low pH and high CO2
310
Describe the Haldane effect
Increasing O2 binding to Hb in lungs reduces the affinity for CO2 and H+ by modifying the quaternary
Effective in pulmonary capillaries as more CO2 is offloaded in the lungs
311
How does an increase in metabolism affect O2 dissociation?
pH decreases with metabolism
Low pH through lactic acid and increased CO2 means tissues are metabolically active and need O2
Hb has increasingly less O2 affinity and releases 70% of its O2
312
Outline the long-term physiological adaptations to chronic hypoxia
Chronic hypoxia triggers responses to try and increase O2 delivery to cells
Increased erythropoietin
Increased tissue capillary density
Increase 2,3-DPG levels
Increased ventilation
313
What does dissolved CO2 react with?
Water in plasma
Water in RBCs
314
Define acid
Any chemical that can donate H+ proton
| HCl
315
Define base
Any chemical that can accept H+
| NaOH
316
What is a strong acid?
One that completely dissociates in water releasing large amounts of H+
HCl --> H+ + Cl-
317
What is a weak acid?
Incompletely dissociate in water. Reaches equilibrium with its conjugate base forming a buffer pair that can reversibly bind H+
H2CO3 H+ + HCO3-
318
How is acidity measured?
pH scale
Measures the concentration of H+ ions in a solution
pH = negative logarithm to base10 [H+]
319
What is the average pH of blood?
What is the range?
pH 7.4
7.36 - 7. 44
320
A 1 unit change in pH is equivalent to...
A 10-fold change in H+
321
What are the 2 sources of H+ in the body?
Volatile acids (easily vapourised)
Non-volatile acids (fixed/non-respiratory)
322
Discuss volatile acids as a source of H+ in the body
Large amounts generated ach day from aerobic metabolism and CO2 production (H2CO3)
Can leave solution & enter atmosphere
Excreted by lungs
323
Discuss non-volatile acids as a source of H+ in the body
Small amount generated each day from other metabolic process e.g. sulphuric acid, lactic acid, keto acid
Excreted by kidneys
324
When does a buffer system work best?
Why is the HH equation different?
Buffer systems usually work best at a pH close to their pK
HH is a physiological buffer where physiological mechanisms control HCO3- and pCO2. Not just affected by the equation itself
This means pH can vary from pK and still be alright because there are other buffers
325
Outline the respiratory portion of physiological buffering
If acid is produced, H+ reacts with HCO3- to give CO2.
C)2 is breathed out, restores pH
326
Outline the renal portion of physiological buffering
If pCO2 is too high, kidneys excrete less HCO3-
Plasma HCO3- is raised, restoring pH
327
Where in the blood is carbonic anhydrase found?
What does this mean?
RBCs, NOT in plasma
Reaction occurs more rapidly in RBCs
H+ is buffered Hb and HCO3- is transferred to plasma
328
List some common places where carbonic anhydrase is found
In tissues whree HCO3- or proton production is coupled to transport
```
Salivary gland
Stomach
Pancreas
Renal tubular epithelium
Choroid plexus
Ciliary body
```
329
What can H+ be buffered by?
Outline this process
Can be buffered by Hb to give HHb
Buffering ability of Hb is enhanced by deoxygenation
Venous blood can carry more H+
330
What makes HCO3- leave a cell?
How does it leave the cell?
An increase in intracellular HCO3-
Cl-/HCO3- exchanger
331
What happens if Hb gives off O2 without taking up CO2?
Cellular pH will rise (alkalosis)
Because Hb is deoxygenated, it will pick up excess H+, removing it from the environment
332
Which effect allows O2 to be moved to tissues?
Bohr effect:
Taking up of CO2 reduces O2 affinity of Hb
333
Which effect allows CO2 to be removed from tissues?
Haldane effect:
Releasing O2 increase CO2 carriage by blood
334
How is CO2 transported as carbamino compounds?
Formed when CO2 reaction with protein amino groups (especially in Hb)
CO2 + protein-NH2
Protein-NHCOOH
Reaction with Hb results in carbaminohaemoglobin
Conformation change in Hb reduces affinity for O2 contributing to Bohr effect
