Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key

image

Play button

image

Play button

image

Progress

1/50

Click to flip

50 Cards in this Set

  • Front
  • Back
muscles for ventilation?
accessory: - sternocleidomastoid
-scalenes group
-pectoralis minor
principal: - external intercostalis
-internal intercostalis
-diaphragma

abdominalis
overview gas exchange, 4 steps
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
lower respiratory tract
-trachea
-2 primary bronchii
-bronchial branches
-lungs
trachea
grote en kleine bronchien-->bronchioli (zonder krakbeen)-->bronchioli terminalis-->bronchioli respiratori (met alveolen)-->sacculi alveolaris met alveoli pulmonis
respiratory mebrane:
-nucleus of type 1 (squameous epithelial cel
-alveolar epithelium
-fused basement mebranes of the alveolar epithelium and the capillary endothelium
-capillary endothelium
cellen in alveoli
-type I epithelium for gas exchange
-type II epithelium secretes surfactant
-capillary endothelium
-macrophages
gas laws
-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
lung compliance
-compliance is the ability of the lungs to strecht
-highly compliant lungs stretch easily
-poorly compliant lungs stretch poorly (more work for inspiration needed)
lung elastance
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
ventilatory work determined by?
compliance, sufactant, resistance
surfactant?
-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
resistance
-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
changes in diameter:
upper airways: physical obstruciton
lower airways:
bronchoconstriction( parasymp, histamine)
-bronchodilatation (CO2, adrenalin, beta 2 receptores)
ventilation rate and depth?
total pulmonary ventilation: 6L/min
total alveolar ventilation 4,2l/min
maximal voluntary ventilation 125-180 l/min
respiratory rate 12-20 brath/min
ventilation and perfusionß
-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)
ventilatio and perfusion are matched serves to
-have optimal gas exchange in the ventilated and perfused alveoli
-rapidly adopt to changes in availibility and demand
ficks law-->rate of diffusion across an exchange surface depends on (quicker when)?
-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
if gas is in contact with fluid and pressure gradients exist-->
-gas molecules move from one phasse into the other
-if pressure fluid>gas, molecules leave fluid into gas - and the other way araound
solubility is directly proportional to the:
-pressure gradient of gas
-solubility of gas in the fluid
-temperature
hypoxia
-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)
emphysema
-loss of alveolar surface area
-cig smoke induced induction of elastase
-->high compliance, low elastic recoil lung
--> fewer, larger, lower surface alveoli
fibrosis
-alveolar mebrane thicken due to scar tissue
-poor gas exchange across scar tissue
->30% of exchange epithelium must be damaged before PaO2 drops significantly
edema
-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
asthma
-increased airway resistance
-decreases airway ventilation
-bronchioles constricted
-
O2 transport in blood
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
amaount of HB bound depends on
-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
o2 binding
-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
% of saturation
= 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
oxyhemoglobin dissociatiekurve
-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
-
verschuving van curve naar rechts?
T hoog, PCO2 hoog, 2,3 DPG hoog, pH laag

affiniteit van Hb voor O2 verlaaging
verschuiving van curve naar links door?
T laag, PCO2 laag, pH hoog
effect verschuiving curve?
- steep part is profoundly effected
- O2 binding in 90-100mmHg range is maintained, but release in 20-40mmHg is significantly effected
bohr effect?
shift in curve due to pH chnage
2,3 DPG effect on curve?
-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
CO2 transport in blood
-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
conversion of CO2 into HCO3- serves to:
-additional means to transport CO2 and extract CO2 from the tissue
-HCO3- serves as a buffer for metabolic acids
conversion of CO2 into HCO3-:
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
Hb and CO2?
-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
CO2 removal at the lungs?
-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
sensors for insp exp?
-cycles of insp and exp under control of neurons activated by sensory input from:
-chemoreceptors for CO2
-chemoreceptors for O2
-chemoreceptors for Ph
Where does regulation take place?
-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
primary stimulus for ventilation?
-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
borstademhaling?
-pump-handle
-bovenste ribben worden opgetild, voorachterwaartse diameter worst groter
-grootste toename ter hoogde van het onderste gedeelte van het sternum
flankademhaling
-onderste ribben bewegen naar lateraal
-transversale diameter van de long neemt toe
-bucket handel beweging
beweging van . intercost ex/int?
externeus: van craniaal/lateraal naar caudaal mediaal
internus: van mediaal craniaal naar lateraal caudaal
waar hecht de de diafragama aan?
ribbeboog, sternum werfels
welke buizen gaan door diafragma?
a. aorta, v cava inf, oesphagus--> gaan door hiatus
vertakking bronchus principalis?
-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
waar bevindtt zich de grootste longmassa?
posterior, lateraal
6 structuuren in het mediastinum?
-hart
-thymus
-aorta descendes
-v. cava
v. et a. pulonalis