Respiratory Physiology Flashcards
V
Volume of gas
L
V̇
Rate of change of volume of a gas
L/min
P
Pressure
mmHg
F
Fractional concentration of a gas
C
Content of a gas in blood
mL/L
f
Frequency of respiration
I
Inspired gas
E
Expired gas
A
Alveolar
T
Tidal
D
Dead space
B
Barometric
a
Arterial
v
Venous
c
Capillary
FAO2
Fraction of O2 in alveolar air
V̇O2
Volume of O2 consumed per minute
PcO2
Partial pressure of O2 in capillary blood
Total lung capacity
Achieved by maximal inspiration
The largest amount of air that can possibly be held in the lungs
Maximal inspiration
The maximum amount of air you can inhale
Maximal expiration
Maximum amount of air you can exhale - not all air can be expelled from the lungs
Tidal volume
VT
The volume of a single breath
Functional residual capacity
Amount of air in the lungs at the end of a normal relaxed expiration
Residual volume
VR
Minimal volume of air that can be left in the lung
Ventilation at rest
0.5 L x 12 min = 6 L/min
Ventilation while exercising
3 L x 40 min = 120 L/min
Describe the equation V̇ ∝ (PB - PA)
Rate of flow is directly proportional to the barometric/alveolar pressure gradient
In order for air to move a pressure gradient must exist so air can only enter the lungs if alveolar pressure is less than barometric pressure. The wider the difference the faster air can flow
The pressure gradient is caused when the ribcage expands, increasing thoracic volume and decreasing alveolar pressure
Alveolar pressure increases with the inhalation of air into the lungs. When the alveolar pressure excess the barometric pressure exhalation occurs
Describe the equation V̇ = (PB - PA) / R
Rate of flow equal to the barometric/alveolar pressure gradient divided by the resistance to air flow
The rate at which the lungs expand or deflate is reduced by any factor that increases resistance to air flow allowing the direct proportionality to be converted into a calculable equation
Sub-atmospheric pressure
When alveolar pressure is less than barometric pressure it is considered sub-atmospheric
Occurs whens thoracic volume increases by descent of diaphragm and rib cage elevation
Pip
Intrapleural pressure
Pressure within the pleural cavity, normally slightly less than barometric pressure and therefore considered negative
Describe the balance of forces during breathing
The lungs experience a force that causes a tendency for them to collapse because of elastic recoil from stretched elastic fibres and surface tension from surfactant
The chest wall experiences a force that causes a tendency for it to spring outward because of stretched tissues in the sterno-costal and costo-vertebral joints
The collapsing tendency exactly counteracts the expanding tendency causing equilibrium at functional residual capacity
Where opposing forces are equal
At functional residual capacity
Describe why the intrapleural space is filled with fluid
Serous fluid in the IP space connects the lungs and the ribcage via the parietal and visceral pleura. The moist membranes are impossible to pull apart and so move together to achieve equilibrium of the opposing forces
Describe the equation Fcw = -FL
The force of the chest wall is equal to the opposite force of the lung
Occurs when the lung relaxes and brings the chest wall with it and vice versa
Pneumothorax
A penetrating injury of the chest wall resulting in a connection between the external environment and the intrapleural space
Pressure gradients between the intrapleural space and lung can’t be set up because the intrapleural pressure is equal to the barometric pressure - 0
The intrapleural space can’t increase the volume and decrease the pressure meaning the lungs can’t move with it and expand when the diaphragm and external intercostal muscles contract
Introduction of air into the intrapleural space disrupts the adhesive forces set up by the serous fluid, allowing the visceral and parietal pleura to move apart and resulting in a collapsed lung
Describe how intrapleural pressure changes during a quiet breath
In a human lung the intrapleural pressure is always slightly subatmospheric so at rest the pressure is around -3 mmHg
Diaphragm and external intercostal muscles contract causing active inspiration as the intrapleural pressure decreases to about -5 mmHg
Passive expiration occurs by relaxation of the diaphragm and external intercostal muscles, decreasing the volume of the intrapleural space and thus increasing the intrapleural pressure back to -3 mmHg
Describe how alveolar pressure changes during a quiet breath
Immediately before inspiration alveolar pressure is equal to barometric pressure, therefore 0 mmHg
Contraction of the diaphragm and external intercostal muscles enlarges the thoracic cavity, increasing the volume and decreasing the alveolar pressure to subatmospheric levels around -1 mmHg
The area of the curve during active inspiration is equal to the peak of tidal volume
Alveolar pressure returns to barometric pressure causing the diaphragm and external intercostal muscles to relax
Intrapleural pressure rises and the lungs recoil causing the gases still in the alveoli to become compressed and increasing the alveolar pressure causing a pressure gradient pushing the air back from the lungs to the atmosphere
Factors affecting air exchange
Muscular effort Compliance Resistance Dead space Diffusion
Pulmonary compliance
A measure of the distensibility of the lungs and chest wall
The change in volume that accompanies a small change in pressure
Describe the equation Compliance = ΔV / ΔP
Compliance = change in volume divided by change in pressure
A small change in pressure + large volume change = high compliance
Describe how compliance is affected in emphysema
Destruction of elastic fibres in the alveolar walls causes inability to recoil, therefore increased compliance
Little pressure required to fill lungs during inspiration but because lungs are limp and soft without elastic fibres expiration is much more difficult resulting in shortness of breath
Elastance
Describes the stiffness of the lung tissue
Resistance
ΔP / ΔFlow
Describe why air filled lungs are less compliant than saline filled lungs
Alveoli has moist surface meaning under normal circumstance an air-water surface tension exists that must be overcome during inspiration
When filling a lung with saline no air-water interface exists meaning less pressure needs to be overcome and disrupting the compliance = ΔV / ΔP equation to the point where compliance is massively increased in a saline filled lung
Describe resistance at different stages of the airways
Resistance starts high in the trachea and increases through the bronchi . It is highest at the level of the tertiary bronchi and decreases rapidly as total cross sectional area increases in the smaller respiratory airways
Resistance is highest in the smallest airways when looking at them individually because it varies inversely with airway radius, however the small airways tend to be arranged in parallel meaning the TOTAL resistance is lowest in the smallest airways
Anatomic dead space
The volume of the conducting airways
About 3% of total lung capacity
Air that consists of no oxygen that you can never get rid of - always the first to enter the lung and the last to leave but owing to the fact you can only inhale and exhale so much, this dead air takes up valuable space in the lung and is consistently taken in and out with every breath
Dilution of tidal inspiration with alveolar air remaining from previous expiration
Describe where oxygen and carbon dioxide move between
Between alveoli and pulmonary capillary blood
Between systemic capillary blood to cells
Ficks Law
Volume of gas transported across a membrane per unit of time is directly related to the difference in partial pressure of the gas across the membrane and the area of the membrane
Volume of gas transported across a membrane per unit of time is inversely related to the length of the diffusion pathway and the square root of the molecular weight of the gas
Respiratory Distress Syndrome
Common in premature babies because of underdeveloped surfactant
Air-water interface in the alveoli causes surface tension. Sufficient pressure is needed to overcome both the elastic recoil of the lung tissue and the air-water surface tension
Decreased surfactant means higher intrapleural pressure is required to separate the pleura and inflate the lungs - more muscular effort needed causing fatigue
Emphysema
Characterised by destruction of alveolar and peribronchial tissue which normally holds the smallest bronchioles open during expiration
Destruction causes bronchiole collapse upon expiration causing trapped air in the donwstream alveoli and a condition called barrel chest - you can get air in but not out, impairing passive deflation
Functional Residual Capacity is increased and disadvantages inspiratory muscles
Asthma
Characterised by bronchiolar restriction by smaller radius
Increased resistance in the bronchioles which increases the pressure required to achieve tidal volume and therefore increased muscular effort
Pulmonary edema
Characterised by increased diffusion distance by fluid build up in the tissues and the lungs
Decreased gas exchange causing shortness of breath
Can be treated somewhat by increasing partial pressure of oxygen
The universal gas law
P = nRT / V
The pressure of a gas is inversely related to its volume
Daltons law
P(total) = ΣP
Total pressure of gas is equal to the sum of pressures of each of its parts
Henrys law
C = σP
Concentration of a dissolved gas varies directly with its partial pressure
σ is a solubility constant depending on the gas
Oxygen content of blood
Total amount of oxygen carried in whole blood
Sum of oxygen combined with haemoglobin inside erythrocytes and oxygen dissolved in plasma
Amount of oxygen that can be bound to haemoglobin per litre of blood
200 mL per L of blood
Whole blood of healthy adults contains about 150g of haemoglobin per litre of blood, each gram binding 1.34 mL oxygen
Saturation of haemoglobin
Amount of oxygen actually bound to haemoglobin relative to the maximum amount that could be bound (normally 200 mL per L of blood)
Normal saturation level of haemoglobin
98% (arterial blood)
197 mL oxygen per litre of blood bound to haemoglobin
Other 3 mL dissolved in plasma
Cooperative binding
The first oxygen molecule is difficult to bind haemoglobin but binding becomes progressively easier as more oxygen binds haemoglobin
Effect of pH on affinity of haemoglobin for oxygen
High blood pH (7.6) increases haemoglobin saturation
Low blood pH (7.2) decreases haemoglobin saturation
Effect of carbon dioxide partial pressure on affinity of haemoglobin for oxygen
Low blood CO2 increases haemoglobin saturation
High blood CO2 decreases haemoglobin saturation
Factors affecting the haemoglobin-oxygen equilibrium
pH decrease
CO2 partial pressure increase
temperature increase
All 3 of these occur during exercise in order to offload oxygen into tissues faster
Effect of anaemia on oxygen transport
Haemoglobin is reduced which in turn substantially reduces the total oxygen bound even though haemoglobin saturation level is still 98%
Fall in oxygen levels causes no shift but the sigmoidal curve becomes depressed
Effect of carbon monoxide of oxygen transport
Carbon monoxide has a much higher affinity for haemoglobin than oxygen so oxygen binding in blocked
Less oxyhaemoglobin saturation causing no sigmoidal relationship
Describe why a sigmoidal curve is desirable for haemoglobin saturation
Partial pressure drives diffusion so it is ideal to keep this value relatively stable
A sigmoidal curve allows a large drop in haemoglobin saturation with only a small drop in partial pressure
Summarise gas exchange and transport in lungs and tissues using haemoglobin onload and offload
Haemoglobin binds oxygen in the lungs
Oxyhaemoglobin moves to tissues where oxygen is offloaded
Oxygen is converted into carbon dioxide and water
All oxygen is used up in the tissues. Haemoglobin is forced to pick up carbon dioxide because of lack of oxygen
Carboxyhaemoglobin moves back to the lungs where carbon dioxide is offloaded
Haemoglobin is now free to pick up oxygen again
Describe the equation V̇A = fR x (VT - VD)
The alveolar volume is the difference between the tidal volume and the dead space volume
The rate at which the alveolar volume is ventilated is proportional to the alveolar volume and the frequency of breathing
Hyperventilation
Rapid breathing
Eliminating CO2 at a faster rate than metabolism can produce it
Raises alveolar O2 partial pressure towards inspiration rate
Consequences of hyperventilation
Accumulation of oxygen in alveoli leads to increased alveolar and arterial oxygen partial pressures
Decrease of carbon dioxide in the alveoli leads to decreased alveolar and arterial carbon dioxide partial pressures, increase of arterial pH and respiratory alkalosis
Eventually alkalotic coma
Hypoventilation
Slow or absent breathing
Carbon dioxide builds up by metabolism in the body but is not expired quickly enough
Decreases alveolar oxygen partial pressure
Consequences of hypoventilation
Decreases oxygen in the alveoli leads to decrease oxygen alveolar and arterial partial pressures
Accumulation of carbon dioxide in the alveoli increases alveolar and arterial carbon dioxide partial pressure, decreases pH and causes respiratory acidosis
Eventually acidotic coma
Describe the response to altered inspiratory partial pressures of oxygen and carbon dioxide
Respiratory system is unaware of oxygen content of any tissue and is unaware of venous oxygen partial pressure
Not very responsive to arterial oxygen partial pressures
Appears to be more sensitive to carbon dioxide partial pressures - sensed centrally and peripherally by chemoreceptors
Respiratory centres in the CNS
Breathing relies on neural input to ventilation muscles from the medulla oblongata
Basic rhythm determined by two groups of neurons in medulla called DRG and VRG
The brainstem communicates with cranial motor neurons and spinal cord which cause contraction of ventilation muscles
DRG
Dorsal Respiratory Group
Medullary centre containing neurons primarily active during inspiration
VRG
Ventral Respiratory Group
Medullary centre containing neurons with activity split between inspiration, expiration and the transition between the two
Airway feedback
Slowly adapting stretch receptors in the bronchi and bronchiole walls send signals via the vagus nerve to respiratory centres
Irritant sensors in airways respond to noxious mechanical and chemical stimuli, histamine and prostaglandins, lung hyperinflation
Chemoreceptor feedback
Peripheral sensors in the carotid bodies and aortic bodies detect arterial oxygen and carbon dioxide partial pressures, informing the central respiratory control centre if more ventilation is required to maintain appropriate gas levels
Central sensors on the ventral surface of the medulla are sensitive to cerebrospinal fluid pH
Carotid bodies
Located at the bifurcation of the common carotid arteries
Highly vascularised
Well suited to sense oxygen and carbon dioxide levels in the blood
Respond to decrease of oxygen arterial partial pressure or increase of carbon dioxide arterial partial pressure
Afferents from carotid bodies travel along carotid sinus nerve which joins the IXth cranial glossopharyngeal nerve as it enters the medulla
Aortic bodies
Found in the aortic arch and subclavian arteries
Afferents travel in the vagus nerve
Intrinsic sensitivity to oxygen and carbon dioxide arterial partial pressures
Ventilation is most sensitive to peripheral arterial carbon dioxide partial pressure and central medullary pH
The body is very sensitive to both carbon dioxide and oxygen but oxygen sensitivity is masked to keep carbon dioxide to a non-poisonous level
Residual volume calculation
FRC - ERV
1200 mL
Tidal volume calculation
Inspiratory capacity - IRV
500 mL
Functional residual capacity calculation
ERV + residual volume
2400 mL
Total lung capacity calculation
Vital capacity + residual volume
6000 mL
Vital capacity calculation
IRV + ERV + tidal volume
4800 mL
Expiratory reserve volume
1200 mL
Amount that can be actively expired past normal tidal breathing, not including residual volume
Inspiratory reserve volume
3100 mL
Amount that can be actively inspired past normal tidal breathing
