Week 1/2 - B - Phsyiology 2-6 - Volumes, spirometry, compliance, dead space, O2/Hb curve, myoglobin, Resp centres/chemoreceptors Flashcards
What are the major respiratory muscles of inspiration? What are the accessory muscles of inspiration and when do they contract? What are muscles of expiration an when do they contract?
Inspiration - active process * Major muscles - diaphragm and external intercostals * Accessory muscles (during forceful inspiration) - sternocaleidomastoid, scalenus and pectoral muscles Expiration - passive process * Contract only during active (forceful) expiration - abdominal muscles and internal intercostal muscles
We will now discuss lung volumes and capacities Define the different lung volumes (try include volumes) * Tidal volume * Inspiratory reserve volume * Expiratory reserve volume * Residual volume
* Tidal volume (TV) - volume of air entering or leaving the lungs during a single breath (0.5L) * Inspiratory reserve volume (IRV) - extra volume of air that can be maximally inspired over and above the typical resting tidal volume (3L) * Expiratory reserve volume (ERV) - extra volume of air that can actively expired by maximum contraction beyond the normal volume of air after a resting tidal volume (1L) * Resdiual volume (RV) - minimal volume of air remaining in the lungs even after a maximal expiration (1.2L)
Define the different lung capacities (try include volumes) * Inspiratory capacity * Functional residual capacity * Vital capacity * Total lung capacity
* Inspiratory capacity (IC) - maximal volume of air that can be inspired at the end of a normal quiet expiration (IC=TV+IRV = 3.5L) * Functional residual capacity (FRC) - volume of air left in lungs at the end of a normal passive expiration (FRC=RV+ERV=2.2L) * Vital capacity (VC) - maximal volume of air that can be moved out in a single breath following a maximal inspiration (VC=IC(TV+IRV)+ERV=4.5L) * Total lung capacity (TLC) - total volume of air the lungs can hold (TLC = RV+ERV (FRC) + TV+IRV (IC) = VC + TV = 5.7L
Describe how the total lung capacity can hold 5.7L in words? Total lung capacity (TLC) - total volume of air the lungs can hold (TLC = RV+ERV (FRC) + TV+IRV (IC) = VC + TV = 5.7L
* The minimal air left in the lungs after maximal expiration is 1.2L. (RV). The extra volume of air that can be expired over and after a normal passive expiration is 1L. (ERV) * The normal volume left in the lungs after a normal passive expiration is therefore 2.2L (FRC). * The normal volume of air that is inspired after normal expiration is 0.5L (TV). The extra volume of air that can be inspired over and above typical resting tidal volume is 3L (IRV) * Maximal volume that can be expired at the end of a normal quiet expiration is therefore 3.5L (IC). Adding the IC & FRC = total lung capacity (5.7L).
Spirometry is a common test used to assess how well your lungs work by measuring how much you exhale and how quickly you exhale How is spirometry helpful?
Spirometry is helpful in diagnosing and differentiating between obstructive and restrictive lung disorders It is also useful for monitoring the progression of COPD
Spirometry is often displayed as a volume time curve Dynamic Lung Volumes useful in the diagnosis of Obstructive and Restrictive Lung Disease Which dynamic lung volumes are measured? How are they displayed as a ratio?
Forced vital capacity (FVC) - maximum volume that can be forcibly expelled from the lungs after a maximal expiration (remember should be ~4.5L) Forced Expiratory volume in one second (FEV1) - Volume of air that can be expired during the first second of expiration in an FVC FEV1/FVC - the proportion of the FVC that can be expired in one second
What is the normal FEV1? What is the normal FVC? What is the normal FEV1/FVC?
Normal FEV1 >80% predicted Normal FVC >80% predicted Normal FEV1/FVC > 70%
Explain the results of spirometry in obstructive lung disease and explain why?
Obstructive lung disease causes shortness of breath due to difficulty exhaling all the air from the lungs. Because of damage to the lungs or narrowing of the airways inside the lungs, exhaled air comes out more slowly than normal * FEV1 FEV1/FVC is <70% ((inability to exhale 70% of their air in one second)
Explain the results of spirometry in restrictive lung disease and explain why?
Restrictive lung diseases restrict the lungs from fully expanding and therefore the vital capacity of the lungs is reduced. Both FEV1 and FVC are reduced ( * FEV1/FVC is >70%
* Obstructive lung disease - affects the ability to exhale as quickly due to narrowing of the airways (bronchioles) - decreased FEV1, normal or low FVC. FEV1/FVC * Restrictive lung disease - prevents full expansion of the lungs, therefore decreased FVC and less decreased FEV1. FEV1/FVC >70% Name obstructive and restrictive lung diseases? What would a combination of the two cause?
Obstructive lung disease - COPD, asthma, cystic fibrosis Restictive lung diseases - anything inflaming the lungs - fibrosis, pleural effusion, CTD, pneumoconisosi, sarcoidosis A combination of the two diseases would cause a decreased FEV1 and decreased FVC however the FEV1/FVC would also be low
Flow = Pressure/Resistance Resistance to flow in the airway normally is very low and therefore air moves with a small pressure gradient What is the primary determinant of airway resistance? What autonomics control broncodilation and constriction?
The primary determinant of airway resistance is the radius of the conducting airway - narrowing or obstruction therefore will cause an increase in resistance decrease the flow of air rate * Parasympathetic control –> bronchoconstriction * Sympathetic control –> bronchodilation (ie SABA (short acting beta2-adrenoreceptor agonsit) given to dilate the airways in asthma)
Describe pulmonary compliance?
Pulmonary compliance is the ease at which the lungs expand The less compliant the lungs are, the more work required to produce inflation
What could cause a decreased pulmonary compliance? What type of pattern may decreased compliance show in spirometry?
Decreased pulmonary compliance - where it requires a greater pressure to produce a given change in the lung volume may produce a restrictive pattern of lung disease on spirometry Diseases causing include - fibrosis, pneumonia, lung collapse, absence of surfactant
What may caused an increased pulmomnary compliance? How does emphysema cause this?
Increased pulmonary compliance (too easy to inflate the lungs) could be caused when the elastic recoil of the lungs is lost In people with emphysema, alveoli are damaged. Over time, the inner walls of the alveoli weaken and rupture therefore losing the elastic tissue. - this makes it harder to get air out of your lungs leading to hyperinflation
Work of breathing is increased in the following situations * When pulmonary compliance is decreased * When airway resistance is increased * When elastic recoil is decreased * When there is a need for increased ventilation What normal process increases pulmonary compliance?
Normal pulmonary compliance increases with age
Pulmonary Ventilation: Is the volume of air breathed in and out per minute (approx 6 litres/min) Alveolar Ventilation: Is the volume of air exchanged between the atmosphere and alveoli per minute (approx 4.2litres/min) Why is there a difference in the volumes between pulmonary and alveolar ventilation?
Pulmonary ventilation = tidal volume x breaths per minute (usually approx 6L/min) Alveolar ventilation = (tidal volume - dead space) x breathing rate is less due to their being anatomical dead space - area in the airways that do not particpate in gas exchange (air left in bronchi and trachea)
Alveolar ventilation is more important than pulmonary ventilation as it represents the new air available for gas exchange with blood To increase pulmonary ventilation (e.g. during exercise) both the depth (tidal volume) and rate of breathing (RR) increase. Increasing which factor is more important?
It is more advantageous to increase the depths of the inhalation (tidal volume now using some of that inspiratory reserve volume) because of the alveolar dead space
* The match between air in the alveoli and the blood in the pulmonary capillaries is not always perfect * Local controls act on the smooth muscles of airways and arterioles to match airflow to blood flow What does accumulation of CO2 in the alveoli as a result of increased perfusion cause? What does accumulation of O2 in the alveoli as a result of increased ventilation cause?
Accumulation of CO2 in the alveoli as a result of increased perfusion causes a decreases in airway resistance (dilation of airways) (sympathetic stimulation causes bronchodilatation) leading to increased airflow Accumulation of O2 in the alveoli as a result of increased ventilation causes pulmonary vasodilation which increases blood flow to match the larger airflow
What effect does sympathetic and parasympathetic innervation have on the blood vessels and bronchioles?
Sympathetic Activates when perfusion is greater than ventilation (pic on front of card) * Bronchodilation * Vasoconstriction Parasympathetic Activates when ventilation is greater than perfusion (pic on left) * Bronchoconstriction * Vasodilation
As well has sympathetic and parasympathetics having different effects on resistance between blood vessels and bronchioles * Sympathetic - vasoconstriction and bronchodilation * Parasympathetic - vasodilation and bronchoconstriction The effects of low O2 also differ between pulmonary and systemic arterioles - how?
Pulmonary arterioles * Decreased O2 - vasoconstriction (trying to match perfusion to ventilation) * Increased O2 - vasodilation (trying to match perfusion to ventilation) Systemic arterioles * Decreased O2 - vasodilation * Increased O2 - vasoconstriction
How may haem groups are there in a haemoglobin molecule? What are the units in which the haem group is contained known as?
4 haem groups in a molecule - 2 alpha and 2 beta in adult haemoglobin
What type of curve is the oxygen haemoglobin dissociation curve and why?
More molecules bind as the oxygen partial pressure increases until the maximum amount that can be bound is reached. As this limit is approached, very little additional binding occurs and the curve levels out as the hemoglobin becomes saturated with oxygen. Hence the curve has a sigmoidal or S-shape.
Discussing the significance of the sigmoid oxygen haemoglobin dissociation curve - remember this shape because as the Hb becomes bound to more oxygen, less sites are available - eventually there will be saturation leading to a flattened curve What does the flat upper portion of the curve mean for oxygen loading should the alveolar PO2 fall? What does the steep lower portion of the curve mean for peripheral tissues should the capillary PO2 fall?
Upper portion of sigmoidal curve A moderate drop in alveolar PO2 will not have much affect on oxygen loading on Hb Lower portion of sigmoidal curve A small drop in capillary CO2 mean peripheral tissues still receive oxygen
What is the structure of foetal haemoglobin? (HbF) How does it react with 2,3- Biphosphoglycerate? (2,3 BPG is important in maintaining the balance of haemoglobin oxygenation)
HbF has 2alpha subunits and 2gamma subunits HbF reacts less with 2,3BPG as 2,3BPG tends to binds to the beta chains in haemoglobin and HbF contains none
Is the affinity of HbF higher or lower than the affinity of adult Hb for oyxgen What does this allow for?
HbF has a higher affinity for oxygen than HbA This means if the PO2 was low, O2 would still be able to transfer from mother to foetus
Haemoglobin is the iron- and oxygen-binding protein in blood, specifically in the red blood cells. What is the iron and oxygen binding protein in muscle known as? Raised in eg rhabdomyolysis or heart attacks Does it have a greater or less than affniity for O2 than HbF/HbA?
This would be myoglobin Myoglobin has the highest affinity for oxygen > HbF > HbA In humans, myoglobin is only found in the bloodstream after muscle injury.
Binding of one O2 to Hb increases the affinity of Hb for O2 What is this known as? Is this present in myoglobiin? What type of curve is the oxyegn myoglobin curve?
Binding of O2 to Hb increases the affinity of Hb for O2 - this is co-operative binding - not present in myoglobin as it is 1oxyegn : 1myoglobin molecule binding It is a hyperbolic curve
What is the ratio of oxygen molecules to myoglobin molecules? What is the ratio of oxygen molecules to haemoglobin molcules?
Not present in myoglobin as there is 1:1 binding per molecule (one haem group per myoglobin molecule) There are 4 haem groups per haemoglobin molecules therefore (4oxygen to 1 Hb molecule)
What causes the oxygen haemoglobin curve to shift to the right? What is this effect known as?
Oxygen haemoglobin curve shifts to the right when oxygen is offloaded from the haemoglobin - this is due to a decreasing pH in the bloodstream Increase in CO2 Increase in H+ ions Increase in 2,3, BPG Increased temperature Hypoxia - offload oxygen in blood to tissues THE BOHR EFFECT
Describe the Haldane effect?
* Te Haldane effect describes how oxygen concentrations determine hemoglobin affinity for CO2 * Removal of O2 from Hb increases the ability of haemoglobin to pick up CO2 and CO2 generated H+
Where is the respiratory rhythm control centre in the brain and what is thought to be the pacemaker part of this area that generates the breathing rhythm?
Respiratory control centre is in the medulla The pre Botzinger complex is a network of neurones in the medulla thought to display pacemaker activity to generate the breathing rythym
How does the rhythm generated in the pre-Botzinger complex give rise to inspiration?
The pre-Botzinger complex excites dorsal neurones to fire leading to contraction of inspiration muscles - when contraction stops passive expiration occurs
Inspiration is an active procss - pre Botzinger, dorsal neurones, contraction of inspiratory muscles In normal resting conditions, expiration is passive - recoil of connective tissue in lungs and alveolar surface tensions How is active expiration achieved?
Increased firing of dorsal neurones in the medulla excites a second group: The ventral respiratory neurones of the medulla. These excite the intercostal and abdominal muscles to contract –> forceful expiration DIVE Dorsal neurones inspiratory Ventral neurones expiratory
The rhythm generated in the medulla can be modified by neurones in the pons: How does this work?
The pneumotaxic centre of the pons when stimulated will terminate inspiration - it is stimulated by dorsal respiratory neurones firing Impulses from the apneustic centre of the pons excite inspiratory area of medulla prolonging inspiration
Without the pneumotaxic centre terminating inspiration, there would be an abnormal pattern of breathing known as apneustic respiration or apneusis. Describe this breathing?
Apneusis is where there is deep, gasping inspiration with brief insufficient expiration and usually occurs due to damage to the pons or medulla - ie damage to the vagus nerve or pneumotaxic centre
Respiratory centres are influenced by stimuli received eg.- * Higher brain centres * Stretch receptors * Juxtapulmonary receptors * Joint receptors * Baroreceptors Chemical control of respiratory related to central and peripheral chemoreceptors * Describe the pulmonary stretch receptor reflex? How does it prevent hyperinflation? (reflex name)
Pulmonary stretch receptors activated during excessive stretching of the lungs during large inspirations Stretch receptors in the bronchi and bronchioles send signals via vagus nerve to medulla and apneustic cnetre in pona - inhibits dorsal neurons and apnustic centre This is known as the Hering-Bruer reflex
Respiratory centres are influenced by stimuli received eg.- * Higher brain centres * Stretch receptors * Juxtapulmonary receptors * Joint receptors * Baroreceptors Chemical control of respiratory related to central and peripheral chemoreceptors * Where are the peripheral and central chemoreceptors? WHat do they sense?
Peripheral chemoreceptors - in carotid bodies and sinus bodies - sense tension of O2 and CO2 and H+ in the blood Central chemoreceptors - near surface of the medulla - respond to CO2 generated H+ of the CSF due to CO2 readily diffusing through blood brain barrier (H+ and HCO3- are not)
Which blood gas has the dominat control of ventilation due to its levels being detected at central chemoreceptors via the ions it generates?
This would be arterial CO2 Crosses the blood brain barrier and generates H+ ions which is sensed by central chemoreceptors and therefore ventilation changes in response
When hypoxia is so severe, the respiratory centres are actually depressed. Peripheral chemoreceptors sense when O2 levels in the blood fall - below what level? In response to the low O2, the hypoxic drive is stimulated, how does this work?
When O2 levels fall below 8kPa or 60mmHg, the peripheral chemoreceptors send signals to the respiratory centre in the brain to increase breathing
When may the hypoxaemic drive to breathe not work? (example condition)
People who chronically retain carbon dioxide lose their hypercarbic drive to breathe. Thus, according to the theory, since the brain no longer responds to hypercarbia, the only remaining autonomic drive is hypoxemia. It then follows that, should patients in this condition be given enough supplemental oxygen to drive their Pao2 levels much higher than 60 mm Hg, they will also lose their hypoxemic drive to breathe.
As stated the peripheral chemoreceptors sense tension of O2, CO2 and H+ in the blood What is the H+ drive of respiration? (important in acid base balance)
The peripheral chemoreceptors play a major role in adjusting for acidosis (eg DKA or lactic acidosis during exercise)- their stimulation by H+ causes hyperventilation and increases elimination of CO2 from the body
State the effect of each blood gas on peripheral and central chemoreceptors * Arterial PCO2 * Arterial PO2 * Arterial H+
Peripheral PCO2 - weak O2 - only when O2 Central PCO2 - strong - dominant control of ventilation O2 - severe hypoxia depresses resp centres H+ - can’t cross BBB
