Respiratory System Theme 2
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- Created by: Splodge97
- Created on: 21-05-17 16:59
What is anatomic dead space?
The volume of air held by the conducting airways (around 150ml)
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What is alveolar dead space?
Volume of air entering the alveoli which doesn't undergo perfusion (increases with age)
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What is physiologic dead space?
Sum of anatomic and alveolar dead space, so indicates the diffusion capacity of the lung
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How is physiologic dead space measured via the Fowler's method?
A pure gas (not N2) inhaled and then N2 conc measured; volume exhaled when first N2 detected indicates dead space
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What are the pores of Kohn?
Present between alveoli to allow an equilibrium between the amount of air in each alveolus (so more are well perfused)
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What is the diffusion capacity of the lung?
Amount of transferance between the alveolar air and blood, measured in mmol/min/KPa; depends upon the solubility and concentration of the gas being measured.
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How may gases be perfusion/diffusion limited?
Perfusion limited = when equilibrium met before the end of the capillary. Diffusion limited = sufficient diffusion not achieved by the end of the capillary to meet equilibrium.
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What is Dalton's law?
States the total pressure of a gas mixture is the sum of the partial pressure of all the individual gases
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Why is venous pressure lower than arterial pessure? Why does it vary more?
Lower as increase in PCO2 less than decrease in PO2 as for every molecule of O2 we use we produce
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What is Henry's Law?
States amount of a gas dissolved in a liquid is determined by the partial pressure of the gas and its solubilty in the liquid
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Why is there a larger pressure difference between the blood/alveoli and alveoli/tissues for O2 than CO2?
As solubility of O2 in water musch lower so greater concentration gradient needed so CO2 and O2 reach equilibrium at same point along capillary (meaning same volume inhaled and exhaled)
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What are the festures of chronic obstructive pulmonary diseases?
Obstruct airways so difficulty in inhalation. Occurs due to bronchoconstriction in asthma/excess mucous in bronchitis. Observed as low PO2 (less supplied) and high PCO2 (less removed).
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What are the features of restrictive pulmonary diseases?
Restrict lung expansion (as in fibrosis), causing increased workload and iinadequate ventilation. Causes difficulty exhaling, often due to smoking.
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Why is PO2 affected more than PCO2 in pulmonary oedema?
As O2 less soluble in water, so cant diffuse across excess fluid (meaning severely reduced, whereas PCO2 normal)
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What ooccurs if patients with pulmonary oedema are placed in a semi-supine position?
Fluid redistributed to accumulate at the base of the lung so difficulty breathing
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Why are alveoli at the base of the lung bettter perfused?
Due to the effect of gravity - as intrapleural pressure higher towards the base alveoli less distended than at apex. This, along with flattening of diaphragm in inspiration, means they undergo a larger increase in diameter (are better ventilated).
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Why are the alveoli at the base better perfused (to match their greater ventilation)?
As they are less distended so capillaries surrounding them noot compressed (as in apex), allowing greater flow. Also because pulmonary circulation has pressure too low to pass sufficient blood to the vessels at the apex.
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What is the V/Q ratio?
Amount of air reaching the alveoli per minute : amount of blood reaching the alveoli per minute; best matched at 3rd rib
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What is a pulmonary embolus?
Blockage of a pulmonary artery (appearing as a transparent area when xenon 133 injected into the blood)
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How is V/Q matched at the apex of the lung?
Low V/Q occurs (as ventilation
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How is V/Q matched at the base of the lung?
High V/Q occurs (as ventilation>perfusion); to match vasodilation (to increase perfusion) and bronchoconstriction (to decrease ventilation)
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How is perfusion increased to the apex of the lung during exercise?
Right ventricle works harder to incerase pressure in the pulmonary circulation (though may cause pulmonary oedema)
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Why is there a lower pH at the base of the lung?
Because PCO2 is higher (and PO2 lower) as better ventilation leads to a greater transference
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When does hypoxic pulmonary vasoconstriction occur?
In infants post natal when O2 first reaches the lungs and when lungs are poorly ventilated in COPD (however this increases pulmonary blood pressure, causing heart failure/hypertrophy or pulmonary oedema)
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How is hypoxic pulmonary vasoconstriction brought about?
Independant of ANS (occurs after transplant). Mitochondria of vessels sense hypoxia through increased ADP + NADH. Initiates ADP-->AMP-->AMPK. Inactivates K+ channels so less K+ removed, activating Ca2+VGC's to open (Ca2+ influx causes contraction).
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What does venous adimixture refer to?
Blood passing through the lung without being properly oxygenated
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How does a V/Q mismatch (physiologic shunt) cause venous adimixture?
In 4-5% of cases. More blood in a capillary than can be oxygenated by alveolar air due to a failure of hypoxic pulmonary vasoconstriction (through mucous plugs/tumours/oedema).
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How does an anatomical shunt cause venous adimixture?
In 1-2%. Blood bypasses the lungs through a channel (e.g. a leaking hert septum, cardiac vein or bronchial vein), usually into left ventricle. Example where bronchial veins accept all deoxygenated blood from bronchioles so some enters pulmonary vein.
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How is ventilation maintained during an asthma attack?
Purse the lips to increase resistance to the outflow of air (helps regulate breathing and extend expiration)
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Why should O2 not be given to those with respiratory conditions?
Ineffective as will only increase O2 slighly (at higher partial pressures). Dangerous as may prevent ventialtion, cause CO2 retention (acidosis) or prevent CO2 entering the alveoli (so they deflate, causing lung collapse/atelectasis).
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Why are men more likely to suffer heart failure?
Have a higher Hb mass in their erythrocytes (required as their androgens are vasoconctrictors, whereas oestrogens are vasodilatory). Means viscosity of blood increased so heart must work harder to pump.
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What causes the oxygen dissociation curve to move to the right (oxygen release to tissues)?
Bohr effect (low pH), Haldane effect (CO2 increase in exercise) and 2,3-DPG (produced by erythrocytes in greater concentrations during hypoxia)
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How is CO2 present in the body?
23% bound to Hb at amino terminus (though unnecessary due to high solubility), 7% as solute and 70% in bicarbonate buffer system
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How does the bicarbonate buffer system operate?
RBC's take up CO2 in tissues, converted to HCO3- and H+ by carbonic anhydrase, products released to prevent reverse reaction. In lungs HCO3- and H+ enter RBC's and are converted to CO2 + H20 by carbonic anhydrase; released in expiration.
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How does HCO3- transport occur at the erythrocyte membrane in the bicarbonate buffer system?
Via a chloride shift - always transferred with Cl- to prevent changes to Vm
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Where does the medullary respiratory control centre recieve signals from?
Cerebral cortex (hypothalamus, limbic system, hemispheres), chemoreceptors and mechanoreceptors.
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What is the role of the dorsal and ventral respiratory groups?
Dorsal = mainly gererates inspiratory drive by activating inspiratory muscles via the phrenic nerve. Ventral = Pre-Botzinger complex present, gives output via exppiratory (mainly) and inspiratory neurones.
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Where are peripheral chemoreceptors present?
Aortic bodies of the arotic arch (send impulses to the RCC via the vagus nerve) and carotid bodies (glomus cells) at the bifurcation of the common carotid (send impulses to RCC via glossopharyngeal nerve, greater influence than arotic bodies)
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What is the role of peripheral chemoreceptors?
Coordinate O2 response and 15% of the CO2 response (quicker than central chemoreceptors). Their sensitivity is increased by low pH/high CO2; response still sluggish (only triggered at
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Describe type I glomus cells and their action
Very small (so increased SA) and well perfused. Supported by type II glomus cells. Low PO2 causes low ICF O2 so K+ channels close; no efflux causes depolarisation so Ca+VGC's open (influx initiates dopamine vesicles, activating IX to signal RCC).
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Why do anaesthetics/drugs often reduce the respiratory drive?
As glomus cells are very sensitive to them (so won't sense O2 as effectively)
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Where are central chemoreceptors present?
At the ventrolateral surface of the medulla, bathed in CSF
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How do central cemoreceptors coordinate the reamining 85% of the response to CO2?
Increase in PCO2 leads to increase in CO2 entering CSF where it combines with H20 to form HCO3- and H+ via carbonic anhydrase; as H+ can't enter blood/brain barrier all H+ due to CO2. More H+ atoms bind to receptors more AP's to RCC.
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Why is the response by central chemoreceptors slow?
Requires two step process to convert CO2 to H+ and diffusion of CO2 into CSF occurs slowly
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Why is CO2 the main factor influencing the respiratory drive?
Because CO2 isn't buffered by Hb (whereas O2 is) so produces a rapid laminar increase in ventilation (not as sluggish as with O2). Below 30mmHg has no effect. Effect increased in acidosis and decreased in sleep/narcotic overdose.
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What is synergy?
When the effect on respiration of CO2 and O2 concentration is greater than the sum of PO2 and PCO2 (hypercapnia/hypoxia) acting individually
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What is sudden infant death syndrome?
Lack of development means chemoreceptors less sensitive so reduction in respiratory drive in sleep can cause ventilation to stop/infant death
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What is the effect of hyperventilation?
Minimal PO2 increase but large PCO2 decrease so respiratory drive significantly reduced (when levels below 30mmHg). If passes out conscious control of ventilation lost so stops.
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How do mechanoreceptors signal the RCC?
Via the vagus nerve
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How do slowly adapting pulmonary stretch receptors act?
In large airways and visceral pleura; terminate inspiration, extend inspiration and limit tidal volume (by inhibiting pre-Botzinger complex upon inspiration). Without them phrenic would continue to fire, prolonging inspiration.
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How do rapidly acting irritant pulmonary receptors operate?
Beneath the epithelium at airway bifurcations. When air flow changes to protect from dust/smoke/noxious fumes cause rapid, shallow breathing and augmented (held) breaths. Unlike slowly adapting inactive after initial stimulus (don't continue AP's).
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What is the role of juxtapulmonary capillary (J) receptors?
Present in alveolar septa, transmit AP's via C fibres to cause apnoea (cessation of breathing) followed by rapid, shallow breathing and bronchoconstriction. Triggered in oedema and presence of histamine (in inflammation). Their function is unknown.
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How do the inspiratory and expiratory neurones match the rate/depth of inspiration and expiration?
They are mutually inhibitive (so have equal and opposite effects); this can be disrupted by neurones from the CNS to allow integration of respiration with other functions (vocalisation).
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What is the role of the pre-Botzinger complex?
This is in the ventral respiratory group and is the main ventilatory rhythm generator in adults; if experienced a bilateral lesion irreversible ataxic (uncoordinated) breathing would result.
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What are the (non essential) effects of the parasympathetic nervous system on the lungs?
Causes bonchoconstriction, mucous secretion and vasodilation (via Ach/muscarinic receptors)
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What are the (non esssential) effects of the sympathetic nervous system on the lungs?
Bronchodilation and vasoconstriction (via nor-adrenalin/B2 receptors)
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What is Cheyne-Stokes respiration (congentital central hypoventilation syndrome)?
Delay in the time it takes for the central chemoreceptors to send impulses to the RCC so periods where breathing absent followed by short rapid breathing; causes over and under correction of arterial PCO2
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What is the respiratory response to exercise?
Proportional increase in rate/depth of breathing; means Hb saturated and no V/Q mismatch. Initial rise via cortex (as PO2/PCO2 normal until CO2 blown off after 70% max); stretch receptors, increased K+, peripheral chemoreceptors and RCC maintain.
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Why is there a slow rreturn to normal ventilation after exercise?
To fulfil the oxygen debt created by replenishing ATP and phosphocreatine stores
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What is the respiratory response to high altitude?
Decrease in PO2 causes increase in ventilation after 3000m (via peripheral chemoreceptors). This hyperventilation reduces PCO2 so respiratory drive reduced with only a small increase in Hb saturation.
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What are the short term adaptations to high altitude (in first three days)?
Hypoxic pulmonary vasoconstriction (so blood to better ventilated areas, though causes oedema/fluid on brain), HCO3- lost in urine so central chemoreceptors reset (improves respiratory drive but must drink to compensate) and capillary recruitment
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What are the long term adaptations to high altitude?
Increased synthesis of 2,3-DPG by RBC's; however means less O2 from lungs so erythropoiesis increased. High PCV increases viscosity so heart failure or gangrene/frostbite (no blood to extremities). Mitochondria and capillaries increased.
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What are the symptoms of altitude sickness?
Occurs >5000m. Causes headaches (fluid accumulates in brain), pulmonary oedema, lack of BF to gut to increase to muscles/brain (causing malaise, loss of apetite, nausea and vomiting), disturbed sleep (as respiratory drive disrupted) and cyanosis.
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What exacerbates altitude sickness?
Climbing faster (less time to adapt), sleeping higher, longer exposure, greater exertion, dehydration (as less HCO3- removal in urine) and high fat/protein diets (as fewer glycogen stores).
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Other cards in this set
Card 2
Front
What is alveolar dead space?
Back
Volume of air entering the alveoli which doesn't undergo perfusion (increases with age)
Card 3
Front
What is physiologic dead space?
Back
Card 4
Front
How is physiologic dead space measured via the Fowler's method?
Back
Card 5
Front
What are the pores of Kohn?
Back
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