Respiratory physiology and disease

sophietevans
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sophietevans
Created by sophietevans over 7 years ago
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From the 29/10/13 Human Physiology lecture.

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Question Answer
What is the function of the respiratory system? To supply the body with oxygen and remove carbon dioxide.
Which four processes does the respiratory system use to perform its function? Pulmonary ventilation, external respiration, transport, and internal respiration.
What maximises air flow? What maximises gaseous exchange? What kind of compromise therefore exists in the lungs? Minimal airway resistance maximises air flow, and a large surface area maximises gaseous diffusion, so the lungs are a compromise of wide airways and many alveoli which allows for both criteria to be met without each detrimentally affecting the other.
Complete the equation: alveolar ventilation = ... frequency x depth of breaths
What is the lung capacity? ~6L/min
What is a typical rate and depth of breathing over a minute? 12 breaths of 500 mL.
The structure of the lungs is a compromise between minimal airway resistance and maximal exchange surface area. But how is the work of lungs also a compromise? Breathing could either be low frequency but deep, which would have low resistance but require work to expand the thorax quite far, or it could be high frequency and shallow, which would only expand the chest minimally, but more work would be require to overcome the resistance of these breaths. General function is a compromise of both (12 breaths of 500 mL per min) to reduce overall work as much as possible.
With regard to resistance, how is the pulmonary system the same as the vascular system? Resistance is dictated primarily by radius of bronchi (and vessels) because the length of the airways (and vessels) is constant. Further, it is the medium-sized bronchi (like the medium-sized arterial vessels, arterioles) that offer the most resistance to air flow as they are large in number and can constrict and relax.
What is compliance? The ease with which lungs can be expanded, or the change in lung volume that occurs with a given change in transpulmonary pressure (which establishes a pressure gradient) i.e. stiffer lungs would require a larger pressure to push air through.
What is lung compliance determined by? The distensibility of the lung tissue and thoracic cage, and the surface tension of the surfactant coating the inside of the alveoli.
Which are firmer: smaller or larger surfactant bubbles in alveoli? Why? Smaller bubbles of surfactant in alveoli are ‘firmer’ than larger ones, as the radius is smaller so the pressure is bigger.
What is the Law of LaPlace? P = 2T/r, i.e. recoil pressure = 2 x surface tension / radius of the bubble of surfactant in the alveoli.
Without surfactant, what is the tendency of air movement between a large and a small alveolus that are connected? Given that the pressure is higher in the smaller alveolus due to its smaller radius, there is a tendency for air to be forced from the smaller alveolus to the larger alveolus in an interconnection (which alveoli are) in order to prevent itself from collapsing.
Which cells produce surfactant? Type II alveolar cells.
What size alveoli contains more surfactant? Smaller alveoli contain more surfactant than larger alveoli as their radius is smaller and so pressure is higher, meaning more support is required to prevent them from collapsing.
What are the effects of surfactant presence? It reduces surface tension to prevent alveoli from collapsing, which keeps them in equilibrium so there is no air exchange between different sized alveoli. This also reduces the amount of work done to expand lungs and force alveoli to expand.
What is the 'dead space' in the lungs? The area of non-exchange tissue in the upper respiratory tract (the trachea and primary bronchi).
What volume of air does the 'dead space' of the lungs store? ~150 mL.
Why is only 350 mL of air exchanged, despite the fact that the average inspiration is ~500mL? The presence of the dead space in the lungs accounts for only 350 mL of air being exchanged. This means that at the end of inspiration, the dead space is storing 150mL of fresh air – which is the first to be exhaled. So during exhalation, one exhales only 350mL ‘stale’ air. This means in the next inspiration, the first 150 mL to be inhaled is the stale air from the dead space! So only 350mL is exchanged.
Why might alveoli be said not to be ventilated? Alveoli aren’t exactly ventilated, as, though the velocity of air is relatively high in the trachea, the division of the airways results in a larger cross-sectional area so the velocity of the air gets smaller to the point that the bulk flow is near zero at the alveoli.
Why might minimal velocity at the alveoli be necessary/beneficial? This helps keep the alveolar composition relatively constant and exchange with blood fairly constant in the face of intermittent breathing, as rapidly oscillating O2 levels would mean that blood concentration would change with each breath, rather than remain stable (homeostasis).
What is the respiratory zone defined/characterised by? The presence of alveoli.
What does the respiratory zone consist of? The terminal bronchioles, respiratory bronchioles, alveolar ducts, and clusters of alveoli.
What process occurs in the respiratory zone? External respiration.
Roughly how many alveoli are there in the lungs? ~300 million
What size are alveoli? ~0.3mm in diameter
What structure composes the majority of the lung tissue? Alveoli.
What type of cells do alveoli consist of a single layer of? Squamous epithelial cells.
What is the diffusion distance across the respiratory membrane? ~1μm
What components does the respiratory membrane consist of? The alveolar epithelial cells, the capillary endothelial cells, and the fused basal lamina of both.
Gaseous exchange across a respiratory membrane can be calculated thus: D = (s / √MW) * ΔP * (A/d). What does this mean? Diffusion rate = (solubility / √molecular weight of the gas) * partial pressure difference * (diffusion area/diffusion distance).
What is the diffusion distance in the gaseous exchange equation D = (s / √MW) * ΔP * (A/d) ? The distance between the erythrocyte and the air, which can be as little as 0.5 microns.
What is the diffusion area of the lungs? What volume of blood is distributed over this area? A = 70m2 over which a monolayer of 100ml of blood is distributed.
What is Dalton's law of pressure? Dalton’s law of partial pressures states that the total pressure exerted by a mixture of gases is the sum of that exerted independently by each gas in the mixture (its partial pressure). The partial pressure of the gas is proportional to its percentage in the mixture.
How do gases diffuse with regard to pressure gradients? Gases diffuse independently down their partial pressure gradients, regardless of other gases present, but these are not reflective of concentration gradients so it is not correct to think of them in this way.
What is Henry's law? Henry’s Law states that when a liquid is exposed to a mixture of gases, each gas dissolves in proportion to its partial pressure. The amount of gas dissolved depends on its solubility. So the partial pressures of the gases will be equal in and out of the liquid at an interface, but the concentrations may or may not be equal.
What is the pressure gradient of CO2 between the venous blood and the alveoli? PCO2 = 5mmHg: 45mmHg in venous blood vs 40 mmHg in alveoli – CO2 is very soluble in plasma but the gradient is sufficient to exchange the CO2.
What is the pressure gradient of O2 between the alveoli and the blood? PO2 = 64mmHg: 40mmHg in venous blood vs 104mmHg in alveoli – O2 is much less soluble in plasma than CO2.
How does the respiratory membrane have ~230ml/min O2 diffuse across it at rest? Its diffusing capacity is ~21ml O2/min/mmHg, so given that its average partial pressure gradient is 11 mmHg, the diffusing capacity of the respiratory membrane for O2 is ~230ml/min at rest.
How can the diffusing capacity of the lungs be increased? By increasing perfusion of under-perfused parts of the lungs, and increasing the cardiac output. The latter may seem counterintuitive, but only 1/3 of the time an erythrocyte spends travelling through a capillary is spent oxygenating, so pushing through 3x faster is not detrimental.
How are ventilation and perfusion of the lungs coupled? If there is low [CO2] in the alveoli, constriction of bronchioles results so ventilation is reduced and excess work not put in to ventilate lung tissue with little CO2. If there is low [O2] in alveoli, there is constriction of arterioles so lung tissue with little O2 to pick up is not perfused.
What are the four mechanisms by which CO2 is removed from plasma? That dissolved in plasma diffuses across the respiratory membrane into the alveoli. That contained in HCO3- ions in plasma, is converted: HCO3- + H+ → H2CO3 → H2O + CO2 (slow) which diffuses. That combined with haemoglobin (carbaminohaemoglobin) dissociates then diffuses through plasma. The majority dissociates from H2CO3 catalysed by carbonic anhydrase to speed it up: HCO3- + H+ → H2CO3 (CA) → H2O + CO2.
What is the chloride shift? The chloride shift in erythrocytes exchanges HCO3- in for Cl- out.
What are the two mechanisms by which oxygen is delivered to the plasma and erythrocytes? Diffusion into the plasma, which it then dissolves in. Binding to haemoglobin: O2 + HHb → HbO2 + H+.
The movements of O2 and CO2 are driven by partial pressures between what? Between the tissues and the blood, the blood and the alveoli, and the alveoli and the atmosphere.
What is O2's solubility in a litre of blood? 3mL/L of blood - low!
How does haemoglobin's affinity for O2 allow for a greater volume of O2 to be carried in the blood? O2’s solubility is 3mL/L of blood, but haemoglobin increases the amount carried to 200mL/L of blood. Further, haemoglobin’s O2 affinity acts as a buffer, as even if there is a 4x reduction in O2 available, haemoglobin will be ½ saturated. As PO2 increases, Hb saturates further with O2, plateauing at 98% saturated at 100mmHg O2 in alveoli. The plateau prevents desaturation even if PO2 falls. Low PO2 allows for both loading and unloading of O2 to Hb, depending on the pressure gradient.
How many binding sites for O2 does a molecular of haemoglobin have? Four - because it consists of four subunits.
How does the binding/dissociation of O2 change haemoglobin's affinity for O2? The binding of O2 causes a conformational change which increases the affinity of other subunits for O2, whereas the dissociation of O2 from Hb reduces the affinity of other subunits for O2 (unloading).
What percentages of diffused O2 from the alveoli are carried in the plasma and by haemoglobin? 2% is carried dissolved in the plasma, while 98% is bound to haemoglobin and carried in the erythrocytes.
What percentages of CO2 derived from respiring tissues are carried in the plasma, by haemoglobin, and in the form of HCO3- ? 7% is carried dissolved in the plasma, 23% is carried as carboxyhaemoglobin, and 70% is carried as HCO3- in the plasma.
What does the HCO3- form of CO2 transport also aid in the body? It helps to keep the pH of the blood around 7.4, as more acidic blood changes the conformation of haemoglobin so that it has a lower capacity for O2, as well as causing other damage.
What happen's to the blood's capacity to carry oxygen in alkaline and acidic conditions? If the pH is more alkaline (i.e. less CO2: PCO2 20mmHg, pH 7.6) the blood has an increased capacity to carry O2 even at the same PO2, whereas if pH is more acidic (i.e. more CO2: PCO2 80mmHg, pH 7.2) the blood has a decreased capacity to carry O2 even at the same PO2. Normal is: PCO2 40mmHg, pH 7.4, HbO2 98%.
How does the binding of oxygen to haemoglobin help to get rid of CO2? During HHb + O2 → HbO2 + H+, an H+ ion is produced, which is then recycled to get rid of CO2: H+ + HCO3- → H2CO3 → H2O + CO2.
Which factors involved in oxygen transport could be affected in pulmonary pathology, that would affect the PO2 of the plasma? Composition of transpired air; alveolar ventilation (rate and depth of breathing; airway resistance; lung compliance); O2 diffusion between alveoli and blood (surface area; diffusion distance – membrane thickness; amount of interstitial fluid); adequate perfusion of alveoli.
Which factors involved in oxygen transport can be affected by pulmonary pathology, that affect the amount of O2 bound to Hb? % saturation of Hb (pH; temperature; 2,3-diphosphoglycerate – glycolytic intermediate that decreases affinity of Hb for O2); and total number of binding sites (Hb content per RBC; number of RBCs).
What is emphysema? What effect does it have on the lungs and the partial pressures of O2 and CO2? Destruction of alveoli by inflammation and tissue breakdown as a result of (often) tobacco smoking. Reduces total surface area for gas exchange. Results in constant shortness of breath. PO2 in alveoli normal or low. PO2 in blood low.
What is fibrotic lung disease? How does it affect the lungs and the partial pressures of O2 and CO2? A thickened alveolar membrane (as a result of autoimmune disease or exposure to harmful agents such as asbestos) slows gas exchange and loss of lung compliance may decrease alveolar ventilation. PO2 in alveoli normal or low. PO2 in blood low.
What is pulmonary oedema? How does it affect the lungs and the partial pressures of O2 and CO2? Accumulation of fluid in interstitial space (e.g. in heart failure) increases diffusion distance. PO2 in alveoli normal. PO2 in blood low. PCO2 in blood may be normal due to higher CO2 solubility.
What is asthma? How does it affect the lungs and the partial pressures of O2 and CO2? Increased airway resistance as a result of inflammation decreases airway ventilation. Bronchioles are constricted so alveolar PO2 is low, resulting in low arterial PO2.
Regulation of ventilation drives the rhythmic patterns of skeletal muscles driving ventilation. But where does the central pattern generator receive input from? The cortex, limbic system, and chemoreceptors.
How does neural activity change during inspiration? During inspiration, the activity of inspiratory neurons increases steadily, apparently through a positive feedback mechanism. At the end of inspiration, the activity shuts off abruptly and expiration takes place through recoil of elastic lung tissue.
Where are the pneumotaxic and apneustic centres found in the brain? In the pons.
Where are the dorsal and ventral respiratory groups found in the brain? In the medulla.
Where do continuous inhibitory signals travel to from the pneumotaxic centre in the pons? To the apneustic centre in the pons, and to the dorsal respiratory group in the medulla.
Where do continuous stimulatory signals from the apneustic centre in the pons travel? To the dorsal respiratory centre in the medulla, and from there to the ventral respiratory centre in the medulla.
Which muscles does the ventral respiratory group send stimulatory impulses to once stimulated itself? To the internal intercostals, causing expiration.
Which muscles does the dorsal respiratory group send stimulatory impulses to, when stimulated itself? To the external intercostal muscles and diaphragm, causing inspiration.
Which type of cells do peripheral chemoreceptors consist of? Glomus cells!
Where are peripheral chemoreceptors found? In the aortic arch and carotid bodies.
Chemoreceptors contain receptors for which gases/ions? O2, CO2 and H+.
Where are central chemoreceptors found? There are medullary CO2 receptors.
Which relative concentrations of O2, CO2 and H+ lead to increased ventilation? Low [O2], high [CO2], and high [H+] lead to increased ventilation.
How does low PO2 diffusing from the blood to the glomus cells in the carotid body cause an increase in ventilation? Low PO2 diffuses from the blood to the glomus cell, causing K+ channels to close. This depolarises the cell, causing voltage-gated Ca2+ channels to open. Ca2+ entry to the glomus cell causes exocytosis of dopamine-containing vesicles, and the dopamine activates a receptor in a sensory neuron which signals to the medullary centres (DRG and VRG) to increase ventilation.
What is the negative feedback mechanism for the glomus cell peripheral chemoreceptors responding to changes in blood gas composition? The increase in PO2 and the decrease in PCO2 result in less sensory stimulation of the respiratory centres, and a reduction in the rate of ventilation via a negative feedback mechanism.
How do CO2 chemoreceptors in the medulla increase the rate of ventilation? Why are H+ ions significant? Increased PCO2 in cerebral capillaries increases the PCO2 in the cerebrospinal fluid (the other side of the blood brain barrier, which H+ molecules can’t cross). This CO2: CO2 + H2O → H2CO3 → H+ + HCO3-. Since H+ ions can’t cross the BBB, those from increased PCO2 are the only ones that activate the central chemoreceptor, resulting in sensory input to the respiratory control centres in the medulla, which increases ventilation.
What is the negative feedback mechanism for the central chemoreceptors responding to changes in the blood gas composition? The increase in PO2 and the decrease in PCO2 result in less sensory stimulation of the respiratory centres, and a reduction in the rate of ventilation via a negative feedback mechanism.
Other than the peripheral and central chemoreceptors, which receptors can influence the rate of ventilation? Other receptors exist in: pain/emotional stimuli acting through the hypothalamus; stretch and irritant receptors in the lungs; voluntary control over breathing in cerebral cortex; and receptors in muscles and joints.
How many times can the rate of ventilation increase by in exercise? Up to 20x.
As well as increasing in rate, what happens to the breath in exercise? It becomes deeper and more vigorous.
Is increased ventilation in exercise a response to an increase in CO2 in the blood/a decrease in O2 in the blood/a decrease in pH of the blood? Levels of PCO2, PO2 and pH remain surprisingly constant during exercise so it is not these which prompts the ventilation adjustment, but neural factors including psychological aspects, cortical motor activation, and excitatory impulses from proprioceptors in muscles.
How does the rate of ventilation change between the beginning and the end of exercise? As exercise begins, ventilation increases abruptly, rises slowly, and reaches a steady state. Correspondingly, when exercise stops, ventilation declines suddenly, then gradually decreases to normal.
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