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50 Cards in this Set
- Front
- Back
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muscles for ventilation?
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accessory: - sternocleidomastoid
-scalenes group -pectoralis minor principal: - external intercostalis -internal intercostalis -diaphragma abdominalis |
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overview gas exchange, 4 steps
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Gas (O2, CO2) exchange between atmosphere and lungs (ventilation, inspiration, expiration)
-gas exchange between lungs and blood -transport of gases in blood -gas exchange between blood and cells in peripheral tissues |
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lower respiratory tract
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-trachea
-2 primary bronchii -bronchial branches -lungs |
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trachea
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grote en kleine bronchien-->bronchioli (zonder krakbeen)-->bronchioli terminalis-->bronchioli respiratori (met alveolen)-->sacculi alveolaris met alveoli pulmonis
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respiratory mebrane:
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-nucleus of type 1 (squameous epithelial cel
-alveolar epithelium -fused basement mebranes of the alveolar epithelium and the capillary endothelium -capillary endothelium |
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cellen in alveoli
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-type I epithelium for gas exchange
-type II epithelium secretes surfactant -capillary endothelium -macrophages |
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gas laws
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-gas moves down pressure gradients
-total pressure of mixed gases equals sum of individual gases (daltons law) -changes in gas volume relate inversely to changes in pressure (P1 x V1=P2 x V2; boyles law) -pressure and volume of gas dtetermined by number of molecules n, gas constant R, and temperature T (iseal gas law PV=nRT |
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lung compliance
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-compliance is the ability of the lungs to strecht
-highly compliant lungs stretch easily -poorly compliant lungs stretch poorly (more work for inspiration needed) |
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lung elastance
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elastance is the ability of the lung to return to its resting volume
-highly compliant lung does not mean highly elastic! -good elasticity is rquired for proper expiration |
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ventilatory work determined by?
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compliance, sufactant, resistance
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surfactant?
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-alveolar cells are covered with a thin fluid layer
-if cells are stretched (inspiration), tension increases -in bubbles, like alveoli, tension directs towards the center resulting in pressure towards the bubble -LaPlaces law: P=2T/r -higher pressure in smaller bubbles -rufactant reduces T, thus, comliance increases and work drops |
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resistance
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-length of the system (constant)
-viscosity of the air (fairly constant) -diameter of the airways r R= L n/r^4 l is constant, n is constant so major effects of changes in diameter |
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changes in diameter:
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upper airways: physical obstruciton
lower airways: bronchoconstriction( parasymp, histamine) -bronchodilatation (CO2, adrenalin, beta 2 receptores) |
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ventilation rate and depth?
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total pulmonary ventilation: 6L/min
total alveolar ventilation 4,2l/min maximal voluntary ventilation 125-180 l/min respiratory rate 12-20 brath/min |
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ventilation and perfusionß
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-pulmonary blood flow (perfusion) depends on properties of capillaries and pO2 and pCO2
-hydrostatic pressure results in open capillary bed in the base of the lungs -with increasing blood pressure more capillaries open -locally (at alveolar and arteriole level) body attemps to match air flow and blood flow -brnonchiolar diameter mediatet by CO2 in exhaled air (more CO2 dilatation) -pulmonary arteries constrict upon low pO2 to shift flow to better ventilated areas (in contrast to systemic circulation) |
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ventilatio and perfusion are matched serves to
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-have optimal gas exchange in the ventilated and perfused alveoli
-rapidly adopt to changes in availibility and demand |
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ficks law-->rate of diffusion across an exchange surface depends on (quicker when)?
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-surface area across within diffusion occurs (larger)
-thickness of mebranes (thinner) -difference in conentration grade (larger) -(diffusion distance) -(surface area*difference in conc.)/thickness of surface -distance, thickness and surface area fairly constant in physiology -so concentration gradient (in resp. physiology defined as part. pressure of gas) most important factor |
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if gas is in contact with fluid and pressure gradients exist-->
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-gas molecules move from one phasse into the other
-if pressure fluid>gas, molecules leave fluid into gas - and the other way araound |
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solubility is directly proportional to the:
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-pressure gradient of gas
-solubility of gas in the fluid -temperature |
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hypoxia
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-hypoxic hypoxia: low arterial pO2 (altitude, alveolar hypoventilation, decreased capacit for lung diffusion, abnormal ventilation/diffsuion)
-enmic hypoxia: decrease O2 binding to Hb (blood loss, anemia, CO poisoning) ischemic hypoxia: reduced blood flow (cardiac failure, peripheral hypoxia, thrombosis) |
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emphysema
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-loss of alveolar surface area
-cig smoke induced induction of elastase -->high compliance, low elastic recoil lung --> fewer, larger, lower surface alveoli |
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fibrosis
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-alveolar mebrane thicken due to scar tissue
-poor gas exchange across scar tissue ->30% of exchange epithelium must be damaged before PaO2 drops significantly |
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edema
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-excess fluid between alveolis and capillaries
-increased diffusion distance -due to increased pulmonary blood pressure(increase hydrostatic pressure in lung capillaries) -commonly via LV dysfunction or mitral valve disf -O2 solubilty in body fluid is low in contrast to CO2 |
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asthma
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-increased airway resistance
-decreases airway ventilation -bronchioles constricted - |
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O2 transport in blood
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1. dissolved in blood plasma
2. bound to Hb (<98%) according to law of mass action -Hb + O2 -->HbO2 -in pulonary capillaries high pO2 equilibrium shifts to the reiqght o2 binds -in periphere capillaries pO2 low equilibrium shifts to the left and O2 is released |
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amaount of HB bound depends on
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-the pO2 in plasma sourrounding the blood cells
-on the number of binding sites available in the red blood cells -depends on number of HB molecules -hb comprises 4 iron containing heme groups (70% of the body's iron in in heme) -every heme group can reversely bind to one O2 |
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o2 binding
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-o2 dissolved in plasma fiffuses into erys where it is bound to hb
-thus o2 dissolved in plasma decreases, facilitating more =2 from the alveolis into plasma (occurs fast) -usually the limitation is in the number of erys -in peripheral tissues the reverse occurs -increased rates of metabolism maintain difference in pO2 -muslce contains myoglobin as a O2 binding buffer |
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% of saturation
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= percent potential binding sites actually binding O2
-if all Hb molecules contain 4 (3) O2 molecules-->100% (75%) -if saturation approaches 100% the only way to enhance O2 transport capacity is to increase the number of Hb molecules |
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oxyhemoglobin dissociatiekurve
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-at normal alveolar pO2 (100mmHg) all O2 binds to hb (98% saturation)
-if pO2>100mmHg saturation barely increases -as long as pO2 > 60mmHg 90-98% saturation -at resting tissue level pO2 40mmhG saturation is still 70 - |
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verschuving van curve naar rechts?
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T hoog, PCO2 hoog, 2,3 DPG hoog, pH laag
affiniteit van Hb voor O2 verlaaging |
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verschuiving van curve naar links door?
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T laag, PCO2 laag, pH hoog
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effect verschuiving curve?
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- steep part is profoundly effected
- O2 binding in 90-100mmHg range is maintained, but release in 20-40mmHg is significantly effected |
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bohr effect?
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shift in curve due to pH chnage
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2,3 DPG effect on curve?
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-derived from glycolysis intermediates
-chronic hypoxia triggers 2,3 DPG synthesis - hypoxia and anemia result in RIGHT shits on the curve - 2,3 DPG binds to deoxyHb, diminishing O2 affinity, thus releasing O2 more readily |
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CO2 transport in blood
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-CO2 solubility in body fluids >O2 soulbility
-CO2 production may exceed solubiltity - only 7% of total venous blood is dissolved in plasma - remaining 93% diffuses into erys - in erys 70& is converted to HCO3- and 23% binds to Hb -CO2 must be removed from the blood to prevent hypercapnia-induced acidosis |
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conversion of CO2 into HCO3- serves to:
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-additional means to transport CO2 and extract CO2 from the tissue
-HCO3- serves as a buffer for metabolic acids |
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conversion of CO2 into HCO3-:
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CO2 + H2O-->H2Co3--> H+ + HCO3-
-H2CO3 is instable thus: CO2 + H20--> H+ + HCO3- -H2O is not limiting thus to keep the reaction going H+ and HCO3- must be removed from the plasma -if H+ and HCO3- is kept low, CO2 is continously removed from the plasma--> more CO2 can be extrected from the tissue--> HCO3- is remved from the erys in exchange of Cl- (chloride shift, neutral chemic gradient) -Hb can buffer the H+: H+ + Hb --> HbH -if the Hb buffer can not keep up, excess H+ ends up in the plasma--> respiratory acidosis |
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Hb and CO2?
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-about 23% CO2 entering the erys is bound to Hb
-upon removal of O2 from Hb at the cellular level, CO2 binds to Hb CO2 --> HbCo2 -Hb.CO2 known as carbaminohemoglobin |
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CO2 removal at the lungs?
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-reversal preocesses at cellular level
-PCO2 in alveoli lower than in venous pulonary blood--> CO2 from blood in alveoli - CO2 + H2O --> H+ + HCO3- -more CO2 is removed from the ery --> H+ leaves Hb -newly released H+ generates H2CO3 and H20 and CO2 -CO2 leaves the erythrocyte and via plasma to alveoli |
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sensors for insp exp?
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-cycles of insp and exp under control of neurons activated by sensory input from:
-chemoreceptors for CO2 -chemoreceptors for O2 -chemoreceptors for Ph |
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Where does regulation take place?
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-respiratory neurons in medulla control in and expiratory muscles
-neurons in the pons integrate sensory information and interact with medulla to regulate ventilation -rythm originates from spontaniously discharging neurons in a network -vetilation continously modified by reflexive input from chemo- and mechanoreceptors and higher brain centers |
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primary stimulus for ventilation?
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-CO2
-O2 and pH are less of importance - peripheral chemorecteptors for O2 and Co2 are in carotic and aortic arteries - central chemoreceptors in the medulla (brain) sense CO2 |
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borstademhaling?
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-pump-handle
-bovenste ribben worden opgetild, voorachterwaartse diameter worst groter -grootste toename ter hoogde van het onderste gedeelte van het sternum |
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flankademhaling
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-onderste ribben bewegen naar lateraal
-transversale diameter van de long neemt toe -bucket handel beweging |
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beweging van . intercost ex/int?
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externeus: van craniaal/lateraal naar caudaal mediaal
internus: van mediaal craniaal naar lateraal caudaal |
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waar hecht de de diafragama aan?
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ribbeboog, sternum werfels
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welke buizen gaan door diafragma?
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a. aorta, v cava inf, oesphagus--> gaan door hiatus
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vertakking bronchus principalis?
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-bronchus principalis dexter wijst meer naar verticaal en is korter
-bronch princip dexter vertakt in 3 bronchi lobares, die zich op hun beurt weer vertakken in 10 bronchi segmentalis -bronch princ sinsiter vertakt in 2 bronchi lobares en verv in 9 bronchi segmentalis |
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waar bevindtt zich de grootste longmassa?
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posterior, lateraal
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6 structuuren in het mediastinum?
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-hart
-thymus -aorta descendes -v. cava v. et a. pulonalis |
