exam 1 Flashcards

Question

1-trachea 2-bronchi 3-bronchioles 4-cough reflex

Answer 1

1-membranous tube from larynx to level of sternal angle - patecy of tracheal airway is maintained by c shaped tracheal cartilage= deficient posteriorly to permit passage of food through adjacent esophagus - termiantes by bifrucating into r. & l. primary bronchi - carina= keel shaped projection of last tracheal cartialge, marks tracheal bifurcation internally 2-primary (r &l)= term branches of trachea---supply r & l lung---walls of primary bronchi have c shaped cartilage rings - r. primary= shorter, braoder & more vertically orietned - at hilus, primary bronchi divide into secondary lobar bronchi, supplies a single lobe - w/in lobe...2ndary bronchi divide into tertiary segmental bronchi 3-tertiary bronchi give rise to mult. generations of bronchioles, terminate in resp region of lung 4-tracheal & carina mucosae have sensory receptors for reflex in response to irritation or foreign objects. aspirated object that reach bronchi can be silent---differences in shape of bronchi direct aspirated objects towards r. lung

Answer 2

1-region of lung tissues supplied by single tertiary bronchus---8-10 named segments - bronchipulmonary segment is the smallest functionally self contained unit of lung tissueA - separted from adjacent segments by CT septa - supplied by tertiary branches of pulm arteries - each lobe has several adjacent segments---& functionally autonomous -segmental structure of lung= surgical resection of 1 or more segments (segmentectomy) or entire lobe (lobectomy) w/ little impage on pulm tissue

Answer 3

1-pulm vesses carry deoxy blood to lung & return oxygenated blood to heart - pulm arteries (r. & l.) term branches of pulm trunk---located anterior & superior to primary bronchus at hilus - branches of pulm arteries off tree= secondary (lobar)& tertiary (segmental) pulm arteries - tertiary pulm arteries= intersegmental---tertiary branch supplies singl ebronchopulm segment and no arterial anastomosis between adjacent segments 2-interruption of perfusion of supplied region of lung tissue & acute respiratory distress...bc of blood clots, fat flobules or gas bubbles

Answer 4

1-2 per side...superior and inferior - located anterior & inferior to prim bronchus at hilus - w/in lungs, tributaries of pulm veins go independently of arteries - individual bronchopulm segments are drained by pulm vein tributes= intersegmental---venous communication 2-supply CT of lungs & conducting portions of bronchial tree 3-arise as direct branches of descending aorta, follow branching of bronchial tree 4-drain to azygos vein system -much of blood distributed by bronchial arteries returns via pulm vein system...bronchial veins= smaller than bronchial arteries

Answer 5

1-lymph drainage of lungs follows bronchial tree, pulm lumph nodes drain to bronchopulm nodes at hilus of lung -bronchopulm nodes drain to tracheobronchial nodes, that are superior & inferior to bifurcation of trachea 2-sentinel nodes= enlargement of nodes bc of infection, lymphoma or tumor metastasis= deviation of carina seen via bronchoscopy... enlarged tracheobronchial nodes interfere w/ swallowing or impinge on l. recurrent laryngeal nerve= hoarsness 3-via anterior & posterior pulm plexuses...surround bifurcation of trachea & extend laterally between layers of pulm ligaments

Answer 6

1-presynaptic symp arise in upper thoracic spinal and synapse on postsynaptic cell bodies in symp trunk - inhibits SM and glands of bronchial tree= bronchodilation & reduced secretion - stimulates SM in pulm vesses= vasoconstriction 2-presynaptic parasymp fibers are carried by vagus (10) post synp cell bodies in pulm plexuses and on bronchial tree - stimualtes SM & glands of bronchial tree= bronchoconstriction & inc secretion - inhibits SM in pulm vessels= vasodilation 3-from bronchial mucosa (cough reflex), bronchial tree (monitor bronchioconstriction) & pulm vessels (chemo & baro) are carried by vagus nerve CN X -visceral afferent nerve fibers conveying other sensations from bornchial tree & visceral pleurae follow symp pathways

Answer 7

1-lung volume is maintained by physical forces that resist tendency of elastic lung tissue to recoil (collapse) - --serous fluid tension & neg pressure w/in pleural cavity (due to lymph drainage of serous fluid) causes lungs to expand and contract in response to changes in intrathoracic volume - --loss of neg pressure in pleural cavity= due to accum of air (pneumothorax), fluid (hydrothorax), or blood (hemothorax) causes lung collapse

Answer 8

1-when inc, the lungs expand and intrapulm pressure dec---air passes in to equalize intrapulm & atmospheric pressure - descent of diaphragm= inc superoinferior diameter - elevation of ribs (bucket handle action) inc transverse diameter - elevation of sternum (pumphandle) inc AP diamter 2-normal breathing= diphragm intercostal muscles stiffen thoracic wall & external intercostals actively elevate ribs 3-accessory muscles of respiration---sternocleidomastoid, serratus anterior, scalenes, pec minor...elevate sternum & ribs 4-via passive recoil of lungs as diaphragm relaxes & ascends 5-contraction of ab muscles= inc intraab pressure and forcefully depresses lower ribs 6-injuries w/ air into pleural cavity (pneumothorax) equalize pleural & atmospheric pressures=lung collapsed - open pneumothorax (sucking chest wound)= resp movememnts cause air to run in & out of thorac via open wound - tension pneumothorax= tissue flap admits air but prevents its escape - rapid accum of air in thorax displaces & compresses mediastinum & interferes w/ venous return to heart= jugular vein distention & tracheal shift towards uninjured side

Answer 9

1-process of moving O2 from atmosphere to cells & moving CO2 from cells to atmosphere 2-movement of air in/out of lungs 3-alveolocapillary---gas exchange---movement of O2 from alveoli to capillaries & of CO2 from capillaries to alveoli...diffusion is driven by each gases partial pressure gradient 4-blood gas transport---transport of O2 in blood from lungs to tissues & CO2 from tissues to lungs 5-capillary tissue---gas exchange---movement of O2 from capillaries to cells and CO2 in opposite direction...respective to partial pressure gradients 6-metabolic process used to convert biochemical energy into ATP

Answer 10

1-obtain O2 from environment, remove CO2 from body, in conjunction w/ kidney...regulates body acid/base balance 2-lungs & vocal cords produce sounds for comm. 3-resp system has surface area 30 x's larger than surface area of skin...so defends against air born microbes---hair & mucous trap particles are larger than 10 um w/in nasal...smaller parties entering are trapped and elimated by mucociliary elevator. lymphoid tissues & adenoids= more defense 4-blood through pulm capillaries, small clots are trapped & dissovled before they reach the brain or other vital organs 5-pulm circulation= compliant...lungs= blood reservoir, especially when supine 6-endothelial cells line pulm capillaries can activate/inactivate blood borne chem messengers w/in lung...angiotensin I is converted to angiotensinIII by ACE bradykinin and serotonin are either removed or inactivated as they pass through pulm circulation

Answer 11

1-warm, moisten, & filter inspired air and dehumidify expired air(lose 350 mL of water bc of it) - moistening of inspired= alveolar viability - nasal hair---vibrissae, filter large particles - small particles are trapped in moist mucous membranes that line nasal conchae & rest of cavity 2-frontal, sphenoidal, ethmoidal, & maxillary -warm & moisten inspired air & reduce weight of skull -sinusitis= inflammation of mucous membranes that line sinuses bc of colds, allergies, deviated septum (take decongestant to reduce flow to sinuses) steroids for reduction in inflam, antibiotics for bacterials, and antihistamines for allergies 3-conducting pathway for resp & digestive systems -respiratory only and gives connection w/ middle ear & eustachian tube...oropharynx= passage for inhaled air & foods. air can bypass nose when clogged

Answer 12

1-maintains open airway to lungs & involved in production of sounds - mucosal surface of larynx= pseudostrat ciliated columnar epithelium - epiglottis= prevents swallowed food/water from entering airways 2-connects larynx to lungs---16-20 hyaling cartilage C rings for suppor...mucosal surface of trachea is lined w/ pseudostra cili columnar epitheloum 3-conducting airways w/in lung that lead to alveoli 4-primary bronchi divides into 2ndary bronchi and divide into tertiary bronchi...contain SM and irregular cartilage plates. SM in walls of bronchi can constrict/relax and will change the airway diameter of bronchi 5-airways that dont have cartilage anymore 6-end of conducting zone after first 16 divisions...no gas exchange occuring w/in first 16 divisions 7-contain alveoli & mark beginning of resp zone

Answer 13

1-site of gaseous exchange---300 mil alveoli ine ach lung= spongy consitency of lung - alveoli supproted by parenchyma= mesh CT that has elastin & collagen - total surface area for gas exchange w/in lung= 60-80 - large surface area of alveoli matched by dense vascular beds w/ 100 capillaries per alveolus 2-portion of lung supplied by resp bronchiole - each acinus has 100 alveolar ducts - duct terminates into 20 alveoli - alveoli w/in last 7 branches are are referred to as resp zone - resp zone= place w/n lungs where gas exchange w/ blood occurs 3-1 cell layer thick w/ simple squamous epithelium type 1 alveolar= major part of alveolar walls & permit diffusion scattered amongst type 1= type 2 alveolar cells that secrete lipoprotein (surfactant) 4-helps prevent alveolar collapse by decreasing surface tension of alveoli -----wandering alveolar macrophages are w/in alveolar lumen

Answer 14

1-r. lung has 3 lobes l. lung is smaller w/ 2 lobes...has a cardiac impression where the heart is situated... mediastinal surface is the mediasl aspect of lung where the pulm vessels pass -costal surface of lung faces the ribs -base of lung sits on top of diaphragm -apec of lung above the clavicle 2-serous membranes that surround the lungs & line thoracic cavity---visceral pleura adheres to outer surface of lungs & parietal pleura lines thoracic walls & surface of diaphragm -pleural cavity is located between the 2 and has fluid that allows movememnt of lung during inspiration/expiration= potential space bc there is no physical separation

Answer 15

1-resp tract to level of bronchioles= larynx & trachea lined w/ pseudostrat ciliated colum epithlium - goblet cells w/in epi = sticky mucopolysacc mucous that traps small inhaled particles that contact walls - cilia move the mucous & any attached inspired particles upward & out of resp system...can be swallowed or coughed out of body - mucociliary elevator is imp defense against bacteria bc bacteria enter body attached to dust - airway branching continues w/in lung, the epi things to a simple cuboidal epithelium...losing cartilage & SM - w/in alveoli the simple squamous epi is flat & enlogated= optimal for gas exchange

Answer 16

1-jutting external portion on face + nasal cavity -warms moistens & filters inhaled air towards pharynx 2-air spaces= ethmoid, sphenoid, maxillary, & frontal -warms & moistens inhaled air, produces mucous, resonance, lightens skull 3-connecting oral & nasal cavities to larynx -passageway for air into larynx & for food into esophagus 4-flap of elastic cartilage attached to entrance of larynx -prevents food & water from entering airways 5-voice box---short passageway that connects pharynx to trachea -serves as passageway for air, produces sounds, prevents foreign from entering traching

Answer 17

1-flexible tubular connection between larynx &bronchial tree -passageway for air, pseudostrat ciliated colum, epithelium cleanses air 2-bronchi & branching bronchioles in lung, tubular connection between trachea & alveoli -passageway for air, continued cleansing of air 3-microscopic membranous air sacs w/in lungs -units of respiration, site of gaseous exchange between resp & circulatory systems 4-organs of respiration, in thoracic cavity -bronchial trees, alveoli, & pulm vessels 5-serous membranes covering lungs & lining thoracic cavity -compartmentalize, protext & lubricate lungs

Answer 18

1-can be measured w/ spirometers that measures volume of aire breathed in & out - has air filled drum floating in water-filled chamber - person breathes in/out...resultant rise & fall of drum are recored as a spirogram changes (V change) - RV residual volume, FRC functional residual capacity, & TLC total lung capacity & anatomic dead space cant be measured w/ simple spirometry. 2-V_T= volume of gas inspired/expired in single resp cycle...~500mL 3-IRV= max vol of gas that can be inspired starting at end of normal inspiration...~3000mL 4-ERV= max vol of gas that can be expired starting from end of normal expiration...~1100 mL 5-RV= vol of gas that remains in lungs after max expiration...~1200 mL

Answer 19

1-sum of 2 or more volumes 2-TLC= total amt of gas in lungs at end of max inspiration (sum of all 4 lung volumes...RV + ERV+ V_T +IRV)...~5800 mL 3-VC= max vol of gas that can be expired after max inspiration (ERV + V_T + IRV)...~4600 mL 4-IC= max amt of gas that can be inspired starting from FRC (VT + IRV)...~3500 mL 5-FRC= amt of gas in lungs at end of normal expiration (ERV + RV)...~2300 mL

Answer 20

1-air is moved in/out of lungs w/ each inspiration ~500mL of air enters body= V_t(tidal volume)...w/in gaseous exchange divison of resp system...O2 diffuses out of alveoli & into blood (VO2) while CO2 diffuses out of blood and into alveoli VCO2 2-V_E amt of air exhaled per minute...equal to product of V_T & resp rate (n)...V_E=V_T \* n -poor measure of fucntional ventilation...bc w/in each V_T there is a vol of gas that doesnt participate (dead space V_D)---dead space= nonfunctional air w/in diffusion -w/in 1st to 16th generations of branching w/in lungs that dont participate in gas exchange= dead space, abt 20-25% tidal volume...parts of resp system that arent gas exchanging= nose, sinuses, pharynx, larynx, conducting and alveoli that arent perfused.

Answer 21

1-vol of air contained w/in nose, sinuses, pharynx, larynx & conducting pathway 2-vol of air contained w/in no perfused alveoli 3-functional measurement bc it is the sum of anatomic & alveolar dead space -in patients w/ lung disease where ventilation doesnt match alveolar perfusion, alveolar dead space = higher so consider that expired CO2 comes from alveoli in which gas exchange occurs 4- V_T=V_{D +}V_A...dead space and alveolar volume volume--- V_E= V_T \* n V_E= (V_D + V_A) \* n ventilation--- V_E= V_D + V_A V_A=V_E-V_D

Answer 22

1-imp functional measurememnt bc it is the vol of air/unit time that participates in gas exchange - minute ventilation can be obtained by measuring exhaled air/time...dead space isnt easily measure and can vary depending on size/posture - rough estimate for dead space is approximated by assuming for every pound of body weight there is 1 mL of dead space - weighs 150 lbs has 150 mL dead space 2-disorganized flow w/ no smooth sheets of flow - greater driving pressure is required vs laminar flow - turblent flow may occur in trachea when flow velocities are high & result in wheezing sound 3-mixture of turbulent flow & laminar flow...transitional flow occurs throughout most of bronchial tree 4-parabolic profile and is smooth flow...rapidly branching system like lung has fully developed laminar flow, only in very small ariways

Answer 23

1-w/o difference in pressure between beginning & end of a tube there isnt flow airflow mL/min in a tube is equal to driving pressure in tube mmHg dividied by resistance to airflow---driving pressure for airflow during respiration is generated by muscles of inspiration working in conjunction w/ recoil forces of lung... V= delta P/ R 2-relationship between pressure & flow V= (P\*pi\*r^4)/ (8\*greek n \* l) greek n=visocisity 3-airflow is: directly proportional to ^4 power of tubes radius directly proportional to driving pressure inversely proportional to viscosity inversely proportional to length 4-substitute poiseuille into ohms---R= P/V= (8 \* greek n \* l)/ (pi \* r^4) 5-resistance to airflow is directly proportional to viscosity directly proportional to length inversely proportional to ^4 power of tubes radius

Answer 24

1-conducting airway branch into lung they become more numerous & narrower bc resistance to ariflow is inverse to radius side...the airway should get inc in resistance in the small airways but actually the pressure drops w/in the airways of the bronchial tree and that the resistance peaks w/in medium sized segmental bronchi small bronchioles= little airway resistance bc total cross sectional area of the airways also increase very rapidly w/ branching so the forward velocity of the gas during inspiration= small in region of resp bronchioles...so when TOTAL airway cross sectional area inc, airway resistance dec

Answer 25

1-supproted by surrounded parenchymal lung tissue -lung vol inc towards TLC, the surrounding lung tissue exerts radial traction forces on airways & stretches airways open -large lung vol, airways widen & resistance to airflow dec lower lung volumes, the airways are narrow & airflow resistance inc very low lung volumes teh small airways might close completely, especially at th ebottom of the lung...patients who have inc airways resistances often breathe at higher lung volumes to help reduce airway resistance

Answer 26

1-inc in airway resitance -asthma, bronchitis, & emphysema 2prolonged exposure to bronchial irritants that leads to obstruction and may = hypersecretion of mucous w/in airways + hyeprtrophy of airway SM 3- inc responsiveness of airway SM to various stimuli= widespread narrowing of airways 4-destruction of lung parenchyma= reduction of radial traction w/in small airways & enlargement of alveoli= greater airway resistance during expiration bc of airway collapse 5-mixture of emphysema & chronic bronchitis 6-expansion of lung is rstricted bc of alterations in lung parenchyma or bc of disease of pleura, cheast wall or neuromuscular apparatus - characterized by reduced vital capacity & small resting lung volume, but airway resistance isnt inc. - --pulm fibrosis= thickening of interstitial spaces, like w/ scar tissue w/ inc of radial traction..making it hard to expand during inspiration.

Answer 27

1-measuring lung volumes & flow rate of air Forced Vital Capacity---FVC is accomplished under max muscular effort to ensure max flow rates at all lung volumes -flow rate is determined at various times during FVC maneuver...something useful= forced expiratory volume at one second FEV1---expressed as percentage of FVC= FEV1/FVC -FEV1/FVC ratio= 0.8...in obstructive diseases such as asthma, FEV1 is reduced more than FVC= low ratio, if less than 0.6= obstructive lung disease -in pulm fibrosis FEV1 & FVC are reduced sooo ratio may be normal or inc in restrictive disease

Answer 28

1-FVC= amt of gas expelled from lungs by expiring as forcible as possible after max inspiration...\<4600 2-FEV₁=max amt of gas that can be expired in 1st second of FVC, following max inspiration...3800 3-FEF---measured over middle half of FVC maneuver which is between 25-75% of vital capacity. w/in obstructive lung disease such as asthma, FEF is dec & dec is proportional to severity of obstruction FEV1 & FEF are impaired & time required to expel the vital capacity is prolonged

Answer 29

1-max expiratory flow volume curve is constructed by plotting airflow vs lung volume -go in clockwise direction starting at TLC -airflow is at peak near beginning of forced expiration...as lung vol decreases the rate of airflow dec throughout remainder of forced expiration =max inspiration generated during rapid forceful inspiration from RV to TLC...changes in airflow w/ changes in lung volume differ during max -max inspiratory maneuver...flow reaches high level while lung volume is still low, but inspiratory flow remains constance until TLC is approached - obstructive disease the flow rate is low and lung volumes (TLC & RV) are inc -scooped out appearnce seena fter point of max flow - restrictive disease= the flow and lung volumes are reduced...arched curve may be seen after max flow

Answer 30

1-releases acetylcholine that causes contraction of SM that line the airways. produces bronchoconstriction, a reduction in bronchiolar caliber... that will inc airway resistance in humans the parasymp nervous system has greatest influence on airway SM tone 2-bronchiolar SM relaxation=bronchodilation and dec airway resistance - catecholamines epinephrine & norepinephrine react w/ B2 adrenergic receptors in airway SM - inhaled isoproterenol, nonselevtive B adrenergic receptor agonis has low affinity for A adrenergic receptors= bronchodilation, used for asthma attacks when SM tone is inc - to avoid cardiac effects of B1 adrenergic, selective B2 adrenergic agonists (albuterol or metaproterenol) are used

Answer 31

1-mast cells in CT underlying airway SM - constriction of airway SM producing bronchoconstriction - histamine constrict SM by binding to H1 receptors, histamine & leukotrienes also inc production of prostaglandins - produce bronchoconstriction (prostaglandin F-2a) while others produces bronchodilation (prostaglandin E) 2-smoke, dust, and sulfar dioxide can incite coughing & airway constriction - reactions are initiated through stimulation of irritant receptors w/in airway submucosa - produces releases of acetylcholine from efferent parasymp nerve fibers= bronchoconstriction - inc in airway resistance promotes trapping of physical irritants & expulsion via mucociliar elevator & coughing

Answer 32

``` 1-Contraction= parasym= cholinergic, acetylcholine, muscarinic receptor subtype Relaxation= symp= adrenergic, circulating epinephring/norepinephring, B3 receptor subtype ``` ``` 2-Contraction= histamine (mast cells), leukotrienes, prostaglandin Relaxation= prostaglandin E & nitric oxide ``` 3-smoke, dust, SO2

Answer 33

1-TLC= inc FRC= inc RV=inc FVC= dec FEV1= dec FEV1/FVC= dec lung compliance= normal airway resistance= inc 2-TLC= inc FRC= inc RV=inc FVC= dec FEV1= dec FEV1/FVC= dec lung compliance= inc airway resistance= inc 3-TLC= dec FRC= dec RV=dec FVC= dec FEV1= dec FEV1/FVC= inc lung compliance= dec airway resistance= dec

Answer 34

1-nasal cavities, pharynx, larynx, trachea, bronchi & bronchioles---provides passageway for air to travel to and from lungs, and to moisten & cleanse incoming air - rigid walls to keep airway open - extrapulmonary & intrapulmonary 2-respiratory brochioles, alveolar ducts & sacs & alveoli -gas exchange (O2 & CO2) between blood & air occurs in respiratory portion

Answer 35

1-lined with strat squamous in beginning and then rest w/ pseudostrat ciliated colum w/ goblet cells - mucus produced by goblet cells move towards pharynx via cilia - roof of nasal cavity is lined w/ specialized epithelium called olfactory epithelium---olfactory epithelium= reception of odors, sensory cell is a bipolar neuron - --supporting cells (sustentacular cells)= present - mucosa of nasal cavity modifies incoming air===serous secretions moistens air, mucous secretions trap incoming particles & venous sinuses warm air - paranasal sinuses are lined by mucosa but is thinner & fewer goblet cells & lamina propria is thin

Answer 36

1-lined wi/ ciliated pseudostrat colum except in areas of abrasion (oropharynx, laryngopharynx & epiglottis) -scattered lymph tissue = present and aggregates in a larger mass, forming a tonsil 2-consist of mucosa (epithelium & lamina propria), cartilage/SM & adventitia - mucosa---cililated pseudostrat columnar w/ goblet cells "resp epithelium" (no gas excahnge) - thick basement membrane - epithelium ontop of loose CT= lamina propria---has mucous & serous glands & thin wenous sinuses - lamina propia fuses w/ perichondrium of cavity= muchopericondrium - external to lamina propria= C shaped rings of hyaline= 16-20 rings, open posteriorly & connected via fibroelastic ligament and trachealis muscle(SM) - --hyaline cartilage surrounded by perichondrium & gaps between adjacent rings are filled w/ fibroelastic CT - external to cartilage/SM= CT adventitia

Answer 37

1-ciliated columnar cells= most abundant---300 cilia on surface 2-mucus secreting goblet cells 3-brush cells= columnar w/ microvilli on surface...have afferent ending on basal surface= sensory receptors 4-basal cells= cuboidal lie next to basal lamina, are stem cells that generate columnar & goblet 5-small granule cells= like enteroendocrine of gut & have smallg ranules of catecholamines, serotonin, calcitonin, & other hormones - --part of digguse neuroendocrine system DNES - --act as effectors in integration of mucous & serous processes

Answer 38

1-mucosa///SM & cartilage///adventitia -additional SM between epithelium & cartilage---divides the CT into a lamina propria that lies closer to epithelium & into a submucosa that lies closer to the cartilage layer ---SM is a part of the lamina propria layer= 1-mucosa= pseudostrat ciliated colum w/ goblet on thick basement membrane ---lamina propria= diffuse lymph tissue & SM, SM spirals around bronchus in R/L handed direction 2-submucosa= 2nd CT layer external to SM, mucous and mucoserous glands are present in layer 3-layer of hyaline cartilage---irregular rings or sheets, at first completely surrounds but then gets scattered w/ smaller bronchi 4-adventitia= CT -as bronchi undergo sucessive branchings= smaller in size & layers of wall get thinner...smallest branches have isolated cartilage plates, when diameter = less than 1, the cartilage disappears and = bronchiole

Answer 39

layers 1-epithelium=(bigger to smaller) epitheliums goes from pseudostrat ciliated columnar w/ goblet to simple colum or cuboidal w/ cilia and no goblet -goblet cells end before the cilia do so mucous doesnt become trapped in small resp passages -epithelium of smallest bronchioles have cell called clara cell that will secrete glycosaminoglycans to protect bronchiole epithelium 2-lamina propria has SM & elastic fibers---SM is controlled by autonomic nervous system 3-cartilage & glands arent present in wall of bronchiole

Answer 40

1-transitional structures between conducting & resp portions of resp tract -each term bronchiole divides into 2 resp bronchioles layers= 1-epi of resp bronchiole goes from simple cuboidal w/ ciliated to low simple cuboidal w/o cilia 2-underlying lamina propria has collagenous CT w/ interlacing bundles of SM & elastic fibers 3-wall of resp bronchiole= interrupted by alveoli that bud off wall -resp bronchioles divide into alveolar ducts 2-lined by numerous alveoli or clusters of alveoli opening onto its surface -lamina propria surorunding rim of alveoli, there is a knob of SM cells, SM is covered by simple cuboidal cells 3-alveolar ducts terminate in irregular spaces surrounded by alveoli===alveolar sacs 4-in interstitum of alveolar septum & alveolar lumen - derived from blood monocytes - alveolar macrophages= dust cells bc has inhaled dust - eliminated via conducting system and appear in sputum

Answer 41

1-terminal component of resp system---small sacs which open on 1 side to allow air to enter cavity - O2 & CO2 are exchange between air & blood in alveolus - alveolus is lined by epithelial cells, lining has 2 cell types that are joined by desmosomes & occluding junctions 2-attenuated squamous alveolar. 97% of alveolar surface. provides barrier of minimal thickness that is permeable to gases 3-great alveolar septal cells, interspreced w/ type 1. cuboidal & have lamellar bodies in cytoplasm... lamellar have mixture of phospholipid, neutral lipids & protein that after secretion= pulmonary surfactant -surfactant dec surface tension on alveolar surface so less inspiratory force is needed to inflate alveoli -surfactant prevents alveolar collapse during expiration fetus= no surfactant until last weeks, so if premature the infant= resp distress bc no surfactant...usually renewed w/in alveolus

Answer 42

- has central region that has type 1 capillary network surrounded by fibroblasts, SM, mast cells, elastic, & collagen fibers---central region= interstitium - interstitium surrounded on either side by epithelial lining of adjacent alveoli---epithelium has Type 1 & type 2 pneumocytes - air in alveolus is separted from bloom in capillary by alveolar septum...the barrier=blood air barrier(.5-1.5um) - --has attenuated cytoplasm of type 1 pneumocytes, fused basal laminae of type 1 pneumocyte & capillary endothelial cell, & cytoplasm of endothelial cell - small openings in alveolar septum= alveolar pores= communication/eqaulization of air pressure between adjacent alveoli

Answer 43

1-primary muscle of respiration during quiet breathing - dome shaped sheet of skeletal muscle between thoracic cavity & ab cavity - when diaphragm contracts, vertical dimension of thoracic cavity= inc and lower rib margins are lifted & moved out w/ inc transverse diameter of thorax - normal= 1 cm, forced = 10cm - phrenic nerve innervates sides---also C3-C5, if damaged may need help 2-inspiratory actions of diaphragm---connect adjacent ribs, contract the lower ribs are pulled up & forward= inc in thoracic dimensions (secondary to diaphragm) 3-inc thoracic volume, raising sternum and/or upper ribs - --**scalene** & **sternocleidomastoid** - some may reduce resistance to airlfow= flaring of nostrils, laryngeal opening. - mainly during exercise/ forced inspiration...not quiet breathing

Answer 44

1-quiet breathing, expiration= passive process bc of recoil of lungs= no muscle contraction - expiration can be active during exercise/forced/hyperventilation...during active expiration the **ab** muscles contract (**obliques, abs)** , itraab pressure= inc and diaphragm pushed up - active during coughing, vomiting, defecation, singing, valsalva maneuver - active expiration= internal intercostal muscles may contract so that will pull ribs down & in (opposite to external intercostal) = dec thoracic volume

Answer 45

1-descend downward inc vertical dimension of thoracic cavity...during active inspiration + primary muscle 2-elevate lower ribs up & out, enlarging thorax ffront to back & side to side...during active & secondary to diaphragm 3-raise sternum, elevate top 2 ribs, enlarge upper thoracic cavity...during forced inspiration, accessory inspiratory 4-patency of conducting upper airways to reduce airflow resistance...during forced inspiration= accessory inspiratory muscles

Answer 46

1-inc intra-ab pressure, exerts an upward force on diaphragm to dec vertical dimension of thoracic cavity ---only during active (forced) expiration 2-flatten thorax by pulling ribs down & in, decreasing front to back & side to side dimensions of thoracic cavity ---only during active (forced) expiration 3-lungs expand & contract during inspiration/expiration...slide back & forth w/in cavity to facilitate there is a thin layer of seroud fluid between visceral & parietal pleura. the lymph system pumps excess serous fluid from pleural cavity and by doing it= neg pressure in pleural cavity -neg intrapleural pressure keeps the lungs pulled tightly against parietal pleura of chest cavity

Answer 47

1-flow of air in/out of lungs is a function of pressure, gradients= flow - changing volume of thoracic cavity= pressure changes - volume of enclosed space increases, the pressure w/in space dec...vol decreases, pressure increases - change in intrathoracic volumes during resp cycle are produced by action of resp muscles 2-At the end of expiration the muscles are relaxed---inward elastic recoil of lung is balanced by outward elastic recoil of chest wall -intrapleural= -5 cm alveolar = 0c= cm transpulmonary= 0 cm - (-5cm) = 5c...so alveolar= atmospheric= no airflow during inspiration, contraction of muscles of inspiration= intrapleural pressure to be more negative...so the transpulm pressure gradient will increase & the alveoli distend... decrease in alveolar pressure below atmospheric pressure= air to flow into alveoli

Answer 48

1-contraction of muscles for inspiration inc intrathoracic vol - thorcic cavity inc= intrapleural pressure dec - during quiet breathing intrapleural dec from -4.5 cm to -8 cm - lungs are pulled out & into larger thoracic volume...the intrapulm dec - air flows into lungs down the pressure gradient - pressure gradient dissipiates as air flows into lungs & intrapulm pressure goes to 0 (atmospheric pressure) - strong inspiratory effor= reduce intrapleural pressure to -40 cm= stronger lung inflation - normal expiration, inspiratory muscles relax & intrapleural pressures inc (become less neg) - intrapulm pressure inc & creates pressure gradient for air to flow out of lungs...pressure gradient dissipates, air flow ceases & intrapulm pressure returns to atmospheric pressure

Answer 49

1-pressure exerted by weight of air in atmosphere above earths surface, 760 mm Hg 2-same as barometric pressure..atmospheric pressure is a 0 preessure pt of ref. 3-pressure w/in pleural cavity exerted outside lungs w/in thoracic cavity...less than atmospheric pressure 4-pressure w/in alveoli...bc communciate w/ atmosphere through conducting airways, air quickly flows down pressure gradient any time intrapulm pressure differs from atmospheric pressure 5-diff in pressure between inside & outside of alveoli, equal to intrapulm pressure minus intrapleural pressure

Answer 50

1-depend upon physical characteristics of lung tissues & surface tension of film lining alveolar walls 2-elasticity from elastin & collagen fibers in lung parenchyma, surrounding bronchioles & pulm capillaries - elastin can be streteched to double resting length - collagen resist stretch & act to limit further expansion of lungs, especially at large lung volumes - lungs expand during inspiration via unfolding & rearrangement of fibers w/in parenchyma - elasticity=elastic recoil, opposing compliance. if high elastic recoil= low complaince & inflates w/ difficulty...low recoil=high compliance= inflates easily - inc age=change in physical & chemical properties of elastin & collagen fibers in lungs= dec recoil= inc compliance - emphysema= degradation of elastin & collagen of lung---release of trypsin from alveolar macrophages bc of smoking= dec recoil= inc compliance = airway collapse during expiration

Answer 51

1-inc fibrous material w/in lung interstitium...lungs to stiffen which dec lung complaince. recoil= inc, smaller changes in lung volume...compliance= dec w/ edema or pulm venous pressure is inc...inhibit proper inflation of alveoli 2-recoil & radial traction are caused by effects of elastin on lung tissue...elastin surrounds single airways produces raadial traction that keeps airway open. overall elastin in lung produces inward recoil 3-lung has air, innersurface has liquid film=airliquid interface...at interface the attractive force between molecules= surface tension...attractive force= bubble that can collapse & resist expansion of alveoli during inspiration - spherical thin walled structures. smaller spheres have higher pressures - 2 alveoli of unequal sizes have same surface tension T are joined by same airwar (pores of kohn) the alveolus w/ the smaller radius will have a higher pressure P) and will empty air into larger alveolus---laplaces law

Answer 52

1-lipid protein complext by type 2 granular pneumocytes w/in alveolar wall - surfactant has both hydrophilic/phobic regions that are incorporated into air liquid interface. - interferes w/ attractive forces between H20 molecules & reduces surface tension...surfactant inc compliance of lung (reduces work for inhalation) by reducing surface tension - minimizes fluid accum in alveoli by reducing alveolar surface tension that would draw fluid to alveolar surface

Answer 53

1-air water interface is there and surface tension= very high...bc high surface tension the lung would be hard to inflate and have low complaince 2-filled w/ saline, removing air-water interface----surface tension forces would be gone, complaince is greater than air filled lung...portion of lung elastic recoil is bc of surface tension by alveolar air liquid interface 3-surfactant is added and long compliance is midway between 2 extremes

Answer 54

1-surface area of surfactant film inc the surface tension inc...the surface area of surfactant film dec the tension dec - behavior is critical in maintaining stability of diff sized alveoli and preventing collapse---smaller alveoli have smaller surface area and lower tension, collapsing pressures of smaller & larger alveoli are similar - presence fo pulm surfactant, smalla lveolus doesnt collapse & empty into a larger alveolus...surfactant helps prevent alveolar collapse (atelectasis) by reducing surface tension in small vs large 2-type 2 granular pneumocytes begin at 28-32 wk of gestation. if delayed or born premature= resp distress syndrome= less compliant lung & smaller sized alveoli= atelectasis 3-reduces surface tension in smaller vs larger--counters laplaces law, promotes stability & prevents atelectasis - reduces surface tension which increases lung compliance (reduces work requried to expand lung) - reduces surface tension which minimizes fluid accum in alveoli (otherwise it would draw fluid to surface)

Answer 55

1-elastic properties of lungs...intrapleural pressure is reduced (engative) the lung expands - at each lung volume, transpulm pressure is determined from diff between intrapulm & intrapleural pressure. - transpulm pressure constant for a little & measure lung volume w/ spirometer = PV curve - difference between inflated & deflated curves= hysteresis= changes in surface tension at alveolar air liquid interface - at 0 pressure, lung still has volume...as intrapleural pressure surrounding lung becomes less negative or positive, small airways collapse, trapping air inside alveoli = residual volume 2-compliance of lung C is change in volume of lung per change in pressure...slope of PV curve. measure of distensibility...steep curve= high compliance at lung volumes near FRC (functional residual capacity ~40%) of TLC and very compliant lung...but as get closer to TLC lung = less compliant...so at high lung volumes a greater change in pressure is required to get a chnage in volume C= delta V/ delta P

Answer 56

1-contributes to stability of alveoli in lung - surrounded by other alveoli in a honeycomb arrangement & supported by them too - 1 alveolus reduces or increases its volume is opposed by adjacent alveoli...if alveoli start to collapse the physical forced by others will prevent the collapse - 1 alveolus tries to overinflate the others will prevent it 2-when chest wall at functional residual capacity the elastic recoil of chest wall is directed outward -assist inspiration, if chest wall was unoppsed by tendency of lungs to recoil inwards, the chest wall would spring out to 705 TLC...equilibrium/resting volume of chest wall

Answer 57

-lung and chest in dyanmic equilibrium passive inward recoil of lung Pl and passive outward recoil of chest Pcw can give you recoil pressure of system Prs.... Prs= Pl + PCW -FRC functional residual capacity is where Pl and PCW are equal but opposite...all resp muscles are reaxed and lung and chest wall systems are at equilibirum at FRC -chest wall is pulled inward by lungs and lungs are pulled out by chest wall -the pleural cavity w/ subatmospheric intrapleural pressure -5, glues lungs to chest wall so lung and chest move in and out together -at volumes above FRC, net recoil pressure of resp system decreases in lung volume...volumes above FRC can only be maintained by actions of muscles of inspiration -at lung volumes below FRC, net recoil pressure of resp system favors inc in lung volume -lung volume below FRC can be mainted by expiration muscles - intrapleural pressure raised to atmospehric pressure (puncture pneumothorax), unopposed lung will recoid in, while unopposed chest will spring out...results inc ollapsed lung - --pneumothorax= intrapleural pressure becomes the same as atmospheric pressure...as a result the lung collapses in and the chest wall springs out

Answer 58

1-gas exchange at the pulm capillaries & tissue capillaries involve simply diffusion of O2 and CO2 down their pressure gradients...there are no active transport mechanisms 2-atmospheric air= N, O2 w/ CO2, H2...combined= barometric pressure= 750 mm. barometric= sum of individual pressures that each gas contributes 3-is directly proportional to the percentage of that gas in the total air mixture... daltons law= partial pressure of specific gas in mixture, is the pressure it would exert if it ocupied the total V in absence of others...P_x= P_B\* F_x Px= partial pressure of gas x, Pb= barometric dry gas pressure and Fx= fractional component of gas X...barometric changes w/ altitude but everything else is the same

Answer 59

1-as soon as dry atmospheric air is inspired it is warmed/mositened by conducting passages of upepr resp - water vapor exerts a partial pressure---at body temp it is 47 mmHg - humidifcation of inspired aire dilutes the partial pressure of other gases by 47 mmHg - --sum of all individual gas partial pressures must equal total barometric pressure and thennn subtract 47 to get the humidified air in lungs 2-gases dissolved in a liquid=partial pressure - amt of gas that will dissolve in fluid depends on solubility of gas in fluid & on partial pressure of gas - Henrys law===conc of gases dissolved in liquid C is equal to solubility in liquid (a) x's partial pressure of gas Px: C= a \* Px ----solubility of O2 and Co2 in blood remains constant so the amt of O2 & CO2 dissolved in pulm capillaries= directly proportional to PAO2 & PACO2

Answer 60

1-gas always diffuses from High to low partial pressure O2 diffuses from alveoli and dissolves in pulm capillary blood until PO2 becomes equal to partial pressure of O2 in alveolar gas (PAO2) CO2 diffuses from pulm capillary blood and evolves as CO2 gas in alveoli PACO2, until alveolar PCO2 is equal to PCO2 2-before inspiration, alveoli and airways are filled w/ old air (FRC)---inspiration= fresh air enters lung & occupies dead space & alveoli. 13% of alveolar air is replaced by fresh atmospheric air w/ each breath - only air in alveoli can exchange O2 & CO2 w/ blood - vol of air expire V_Eis sum of volumes coming from dead space & alveoli V_D & V_A - expired air is similar to inspired air in the beginning bc it comes from dead space...but later dead space & alveolar air are expired bc not all alveoli empty at the same time so they mix, so towards the end of expiration the air being expired= alveolar air

Answer 61

1-during inspiration, inspired air loses O2 to blood & gains CO2. if amt of O2 removed= amt of CO2 gained (CO2 production= O2 consumption) then... PIO2- PAO2 = PACO2 - PICO2 if PICO2= 0 then: PAO2= PIO2-PACO2 - basis for alveolar gas equation= alveolar O2 pressureu can be determinded by inspired O2 pressure & alveolar PCO2--- - ratio of O2 consumed to CO2 produced= resp quotient...RQ - individuals who have total carb diet have equal CO2 production & O2 consumption= 1.0 - individuals w/ mixed diet= 0.8, less CO2, more O2 - total fats= 0.7 so you have to factor diet into the PACO bc the O2 consumption is underestimated... PAO2= PIO2 - PACO2/RQ 2-0.21

Answer 62

1-rate of CO2 production, the alveolar CO2 conc (PACO2) is determined by rate of alveolar ventilation VA -**inverse** relationship between PACO2 & alveolar ventilation---ventialtion doubles then PACO2 reduced by 1/2 2-bc of humidifcation & small turnover of alveolar air w/ new inspired tiday volume, avarge PAO2= 100mmHg and atomospehric PO2=160 mmHg -O2 w/in alveoli moves down partial pressure gradient into the blood, so the new O2 arriving in lungs w/ each breath replaces that which has been diffused into capillaries...bc pulmonary blood PO2 equilibrates w/ alveolar PO2, the PO2 w/in arterial blood= 100mmHg -similarly, for CO2, body tissues try to continuously produce CO2...and is added to the blood in the systemic capillary beds & then transported to the lungs...once in the lungs, CO2 diffuses down its partial pressure gradient from blood into alveoli. CO2 is removed from lungs during expiration... because CO2 arriving from body tissues is constantly removed from the lungs, the PACO2= constant at 40 mmHg

Answer 63

1-diffusion= principal process that accounts for transfer of O2 & CO2 factors affecting= partial pressure gradients for O2, CO2 -size of surface area of alveolar membrane -solubility of O2 & CO2 -thickness of alveolar membrane -anything that significantly increases the thickness of the alveolar membrane can interfere w/ normal resp exchange of gases---pulm edema, fibrosis, pneumonia 2-excess accum of interstitial fluid between alveoli & pulm capillaries bc of pulm inflammation or left sided congestive heart failure 3-replacement of delicate lung tissue w/ thick fibrous tissue in response to chronic irritants 4-inflammatory fluid accum w/in or around alveoli

Answer 64

1-rate of transfer inc as partial pressure gradient inc---major determinant of rate of transfer 2-rate of transfer inc as surface area inc---suface area is constant under resting...surface area inc during exercise....surface area dec w/ pathological like emphysema & atelectasis 3-rate of transfer dec as thickness inc---thickness usually constant...thickness inc w/ pulm edema, pulm fibrosis, pneumonia, any pathological

Answer 65

1-w/in blood is 2 forms---dissolved O2 & chemically bound to hemoglobin. O2 is poorly soluble in fluids - amt of dissolved O2 in blood is proportional to PO2 of blood - PaO2 of 100 mmHg---only 3 ml of O2 is dissolved in 1 L of blood...resting cardiac output of 5 L/min = 15 mL/min of O2 carried in blood - resting O2 consumption of body is 250 ml of O2 per min so needs hemoglobin

Answer 66

- iron bearing protein w/in RBC...has a globin & heme group - globin= 4 highly folded polypep chain---2 identical alpha and 2 identical beta - each globin has a heme---heme is an iron containing, non protein nitrogen group & can bond w/ O2 (4 molecules of it) - 98% of it is transported w/ hemoglobin...so O2 content is blood is w/ hemoglobin - crucial role in permitting tansfer of large quant of O2 from alveoli to tissues - --hypothetical situation is presented w/ no hemoglobin in blood---alveolar PO2 and blood PO2 would equilibrate...hemoglobin added then O2 wil bind to it keeping PO2 low(storage depot for O2) O2 will move into blood until equilibrium between alveolar PO2 and blood PO2

Answer 67

- normal alveolar PO2 =100mm Hg and PvO2=40mmHg and sets the alveolar to blood PO2 at 60. = large initial O2 flux, O2 moves into capillary blood then binds to hemoflobin and equilibriates w/ PAO2 - reduces partial pressure gradient for O2 and slows down O2 flux---PO2 in blood equilibrates w/ PAO2 - high rate of O2 diffusing capacity= bc of large surface area and short diffusion distance in lung - transit time in pulm capillaries= .75 s---additional time allows for adequate O2 diffusion during exercise when time is shortened - in some athelets the output can reduce transit time in lungs= arterial hypoxemia CO2 has greater solubility, comparable volume of CO2 can be transferred so it has a smaller gradient than O2

Answer 68

1-O2 saturation of hemoglobin is ratio between actual O2 combined w/ Hb in unit vol of blood and total amt of O2---can be combined w/ Hb in same vol of blood. S_O2= amt of O2 combined w/ Hb / O2 capacity -imp factor that determines O2 saturation is PO2 of blood= conc of O2 physically dissolved in blood -PO2 inc, O2 will dissolve into blood, bind to hemoglobin & then blood PO2 will equilibrate w/ alveolar PAO₂ -PO2 dec, partial pressure gradient favors O2 unloading and O2 diffuses into tissues, disassociates w/ Hb and then blood PO2 equilibrate w/ tissue PO2... -as blood PO2 changes, O2 saturation changes in non-linear fasion 2-blood PO2 against O2-Hb saturation (SO2) figure= S shaped, sigmoidal curve

Answer 69

1-high range of PO2 (60-100 mmHg) w/in pulm capillaries, a small inc in PO2 gives only small inc in SO2---bc plateau portion of ODC at high PO2 values---PO2 at 100= Hb 99% saturated...so blood leaving lungs=saturated. - PO2=60 the HB =90%saturated - plateau= safety net in loading O2 onto HB in pulm capillaries 2-ODC steepens at PO2 between 40-60 mmHg...venous PO2 of 40=75% Hb saturated w/ O2 blood in systemic at 99% saturation means that 24% of O2 bound to Hb has dissociated & diffused into tissue down the partial pressure gradient -change in PO2 of 59 leads to 24% O2 release 3-ODC= very steep at low PO2 from 10-40 - at exercise---if tissue PO2 were to fall w/in this range there would be small changes in PO2 that would lead to large changes in Hb O2 saturation= O2 unloading at the tissues - systemic capillary PO2= reduced, even larger amts of O2 are available to meet O2 demand

Answer 70

1-PCO2, pH, temp, conc of 2,3 DPG (BPG) - P50 =O2 pressure that is required for 50% Hb saturation - if Hb O2 affinity= dec then a greater pressure is required to get to 50% Hb saturation---P50=inc and ODC is shifted right - greater HbO2 affinity will shift the ODC to the left & P50 will dec - --high affinity= greater uptake in lungs but less release into the tissues...low affinity=less uptake in lungs but graeter release into tissues

Answer 71

1-rise in PCO2 or fall in pH will shift ODC to right (inc in P50)---reduces Hb-O2 affinity and matches w/ metabolically active tissue, producing more CO2 and becoming more acidic bc of production of carbonic acid or lactic acid-----facilitate in unloading of O2 to tissue ---dec in O2 affinity of Hb when pH blood falls= BOHR effect, utility of Bohr effect is w/ shifting ODC...greater amt of O2 can be release at tissues an greater amt of O2 can be taken up at lungs 2-Dec in PCO2 or rise in pH will shift ODC to left (dec p50)---lower PO2 is needed to bind given amt of O2 to Hb= inc in O2 affinity. (acid forming CO2 removed= inc in pH) so Hb has higher affinity for O2 in pulm capillaries= inc loading of O2 onto Hb 3-changes in temp alter thermodynamics of Hb-O2 binding---higher temp= dec HbO2 affinity & facilitate O2 unloading---lower temp= inc HbO2 affinity & facilitate O2 loading into blood 4-made w/in RBC during anaerobic metabolism---highly charged anion that binds deoxy Hb but not oxyhemoglobin---causes inc in 23 BPG conc = shift ODC to right= higher PO2 required to bind same amt of O2 to Hb -2,3, BPG production in RBC is inc when total Hb conc is low (anemia) or when PO2 is low (high altitude)

Answer 72

1-effect of blood PO2 on amt of O2 in blood= blood oxygen content---amt of O2 per unit volume - dissolved O2= 2%---Henrys law: C_x= alpha \* P_{x
C=conc of gas dissolved...Px=partial pressure alpha= solubity} - O2 solubility= 0.003/100mL - at arterial PO2 of 100= 0.3 O2/100 mL - at venous PO2 of 40= 0.1 O2/100 mL - when Hb is 100% saturated as in arterial blood, 1 gram of Hb will hold 1.34 mL of O2---conc of Hb in blood= 15 g Hb/100mL----can be reduced w/ anemia or inc w/ blood doping or erythropoietin - -- O2 content= (1.34 \* Hb conc \* SO2) + (0.003 \* PO2) - --O2 capacity=(1.34 \* Hb conc \* 100) + (0.003 \* PO2) ---capacity is at MAX amt of O2 carried in blood

Answer 73

1-PO2 graphed aginst Blood O2 content---since most of O2 in blood is bound to Hb there are a couple of differences---O2 content will keep increasing after 100% Hb saturation bc O2 will continue to dissolve at rate of .0003 as PO2 inc & position of curve depends upon Hb conc...PO2 & saturation, the O2 content of blood is directly proportional to Hb conc

Answer 74

1-low O2 levels in body 2-blood as low PO2 and Hb is poorly saturated---hypoventilation when gas exchange in lung is disrupted (edema or pneumonia) ---right-left shunt, ventilation/perfusion mismatch and when PIO2 is low (high altitude) ``` 3-PO2 normal, but the Hb conc is low= reduced O2 carrying capacity & O2 content Carbon Monoxide (CO) posioning---formation of carboxyhemoglobin= anemic hypoxia CO poisoning O2 carrying capacity is norm but O2 content is reduced ``` 4-circulatory, ischemic, stagnant---reduction in tissue blood flow -decrease in cardiac output during shock/congestive heart failure---obstruction to blood flow in vascular bed 5-toxic substance like cyanide intereferes w/ tissues utilization of O2---O2 conc of venous blood is high, O2 consumption by tissues is low

Answer 75

1- 3 forms: 1-physically dissolved, 2-carbamino compound, 3-as bicarbonate -as blood goes through systemic capillaries---picks up 5 mL of CO2...additional CO2 is transported to lungs where it is exhaled 2-blood through systemic capillaries---CO2 diffuses down partial pressure gradient from tissues into blood -dissolved CO2 in blood doesnt remain in dissolved form but CO2 transported in blood in 3 forms... 3-amt of CO2 physically dissolved in blood depends upon blood PCO2--CO2 is more soluble than O2 so a greater proportion is in dissolved form

Answer 76

1-CO2 binds w/ globin of Hb=carbamino Hb---reduced Hb (no O2) has higher affinity for CO2...so unloading of O2 from Hb in systemic capillaries= loading of CO2 by Hb---5% venous blood totals CO2 2-90% venous blood total CO2---chemical reaction takes place w/in RBC...CO2 combines w/ H20 to make carbonic acid---reaction occurs slowly in plasma -buuut w/in RBC---carbonic anhydrase accelerates reaction making bicarbonate, causing bicarb and H to accum w/in RBC---RBC membrane has a transported that facilitates movememnt of bicarb & Cl. but membrane is impermeable to H---so bicarb not H diffused down conc gradient out of RBC & into blood

Answer 77

1-bicarb are more soluble in blood than CO2---diffuse out of RBC and replaced by CL ions to maintain neutrality w/in RBC= chloride shift - H ions remainign w/in RBC after dissociation of H2CO3 bind w/ reduced Hb that just released its O2 molecule w/in systemic capillary - reduced Hb has a greater affinity for H than oxyhemoglobin---removal of O2 from hb inc ability of hb to bind w/ CO2 ---deoxy of Hb inc ability to carry CO2=haldane effect - uptake of CO2 into RBC inc conc of HCO3 and H w/in RBC...inc osmotic pressure of RBC which draws H20 into cells---RBC vol increaseas as RBCS go through systemic capillaries

Answer 78

1-reactions at tissue level are reversed once blood is in lungs---Co2 diffuses down partial pressure gradient & removed from body during expiration---draws HCO3 from plasma into RBC= dissolved CO2 & H20---CO2 molecules diffuse out of RBC into plasma and then into alveoli 2-relates CO2 of blood to blood PCO2 w/ all 3 forms - haldane effect= lower PO2 there will be a higher CO2 for any given PCO2 - reduced Hb has greater ability to bind H ions produced when carbonic acid dissociates and bc reduced Hb is more likely to form a carbamino compound--- - tissue capillaries the haldane effect= inc pickup of Co2 bc of O2 removal from Hb - in lungs haldane effect= inc release of CO2 bc of O2 pickup by Hb

Answer 79

MAXIMIZE O2 & CO2 TRANSPORT - haldan effect & bohr effect work together to maximize O2 & CO2 transport w/in blood - bohr= when pH of blood dec there is a dec in affinity of hemoglobin for O2= hemoglobin release an O2 molecule - haldane effect---release O2 from heme portion of hemoglobin molecule inc affinity of globin portion of hemoglobin molecule for Co2 - --bc tissue are acidic both of these happen in systemic capillaries--work together to maximize O2 relase and binding of Co2 molecules to hemoglobin -in pulm cappillaties the pH becomes less acidic= bohr & haldane to work oppositely---pH inc= inc affinity of hemoglobin for O2 = hemoglobin bing to O2 so binding of O2 to heme portion of hemoglobin decreases affinity of glbin portion of hemoglobin for CO2...so hemoglobin releases CO2---so w/in pulmonary bohr and haldane work together to maximize binding of O2 molecules + release of CO2 w/ hemoglobin

Answer 80

- begins at main pulmonary artery---receives mixed venous blood pumped by r. ventricle - artery branches successively---close to the branching of the airways to the level of terminal bronchioles - pulmonary arteries break up to supply pulmonary capillary bed which lies in wall of the alveoli - pulm capillaries form dense ,thin sheet in alveolar wall---covering 85-95% of alveolar surface area= efficient gas exchange - oxygenated blood is collected from capillary bed by small pulm veins---merge to form large veins that drain into l. atrium

Answer 81

1-systemic circulation---broncial arteries come from descending aorta and return to lungs - arteries have fully oxygenated blood that supply O2 and nutrients to intra pulm structures like tracheobronchial tree, pulm nerve & ganglia and SM & CT. - blood from bronchial circulation returns to r. atrium via zygos & intercostal veins 2-interconnected---join together in short circut= anastomosis - bronchial capillary bed (deoxy blood) can anastomose w/ pulm capillary bed---mixed blood becomes oxygenated in pulm capillaries & then leaves lungs via pulm vein - bronchial capillary bed (deoxy) can also drain into pulm vein ---here the deoxy bvenous blood to the oxy blood is called a **right to left shunt**---why blood leaving lungs isnt always 100% oxygenated

Answer 82

1-BP w/in pulm circulation= low compared w/ systemic circulation - pulm artery has pressures of 25/8 w/ mean pressure of 15 - aorta has pressures of 120/80, mean of 100 - left atrium, mean = 5-8 so pulmonary arteriovenous=10 - pulmoanary capillary mean= 10 mm - bc the mean pulm pressure is lower than mean aortic pressure the walls of pulm artery are thinner w/ less SM & elastin than the aorta---pulm veins= thin too - systemic arterioles= thick w/ circular SM - pulm arterioles cant vasoconstrict like systemic arteriole 2-pulm circulation is in series w/ systemic circulation gets entire cardiac output---Q P= Q\*R Bc Q is high and P (pulm circulation pressure) is low, this means Resistance is low...the pulm vascular resistance= 1/10 of systemic vascular resistance - pulm circulation is low resistance system bc of low SM tone in pulm arterioles and large cross sectional area of pulm capillaries - pulm circulation= low resistance, circulation = low resistance even when pulm pressures inc - when pulm arterial or venous inc, pulm vascular resistance dec bc of the recruitment of new pulm beds that open up & distension of already opened vessels. - distension= inc the caliber of capillary segments & predom mechanism for fall in pulm vascular resistance as pulm arterial pressure inc 3-15 & 5 4- 100 & 2

Answer 83

1-can be measured using radioactive xenon that is dissolved in saline and injected into peripheral vein - xenon reaches pulm vapillaries it is evolved into alveoli bc of low solubility - evolved xenon is counted by radiation detectors placed over chest---measured amt of radiation from eveolved xenon is proportional to pulm blood flow - results= all parts of lungs dont receive same pulm blood flow---base of lung gets more blood flow per volume than the apex of the lung---happens bc of gravity, bc of hydrostatic pressures w/in vessels & effect of starling resistors 2-pump is pumping h20 around rigid tubes---pressure in tube higher than pump will be less than pressure at level of pump -pressure in tube that is lower than pump will be greater than pressure at level of the pump---like the lungs...the pulm arterial/venous BP are lower at the lung apex and higher at the base of the lungs

Answer 84

1-pulm capillaries are surrounded by alveoli & get little support from lung parenchym---so they are liable to collapse or distend depending on pressure in/around them - blood flow through systemic capillary depends on difference between arterial & venous pressure - in lungs, alveolar pressure has to be considered - starling resistor stimulates situation in pulm capillaries, where there is arterial pressure (Pa), alveolar pressure PA, and venous pressure Pv...if PA is greater than Pa the capillar will be squeezed shut and therell be no flow 2-exposed to surrounding alveolar pressure---flow through these is determined by relationship between alveolar pressure & pressure w/in them. 3-all arteries & veins that run through lung parenchyma - pulled open by radial traction of surrounding tissue - caliber of extra alveolar vessels is greatly affected by lung volume bc this determines the pull of the parenchyma

Answer 85

1-passive factors dominate pulm vascular resistance & distribution of flow w/in pulm circulation -pulm BV are innervated by symp & parasymp nervous system---but is doubtful that autnomic nervous system has function in normal control of pulm Blood flow 2-distribution of pulm blood flow is dec when PO2 of small airway is reduced - hypoxic region of lung, SM w/in arteriole will contract---directs blood flow away from hypoxic region of lung...hypercapnia, acidosis & hypertrophy of vascular SM accentuate it - benefit===diverts mixed venous blood away from poor ventilated areas of lung that have low PAO2, by increasing vascular resistance---so mixed venous blood is sent to better ventilated areas of lung - --in states like pneumonia, hypoxic pulm vasoconstrction is limited to diseased lung - high altitude= HPV constricts pulm arteriloles throughout entire pulm circulation= inc in pulm vascular resistance - local effect, intrinsic to lungs, and = no autonomic nervous system innervation -----systemic= hypoxia causes vasodilation

Answer 86

1-dec O2= vasodilation inc O2= vasoconstriction 2-decreased O2=vasoconstricton inc O2= vasodilation 3-regional diff measured by radioactive xenon...when gas inahled, its radiation is detected by counters outside chest...base of lung= greater ventilation than does the apex of the lungs -regional effects is bc of gravity -weight of tissue above it there is distortion of lung tissue at bottom of lung---tissue at base of lung= compressed by weight of tissue above it, while apex of lung is expanded, so alveoli at base of lung are compressed and alveoli at apex are stretched open -weight of lungs compress the intrapleural space at base of lungs= vertical distribution of intrapleural pressure...intrapleural pressure= greater at base of lungs compared to apex. -gradient of intrapleural pressure and transpulm pressure from base of lungs to apex

Answer 87

1-at end of normal expiration the lung is at runctional residual capacity FRC---so the alveolus at the base of the lung has a low resting volume bc it is compressed by weight of tissue above it and there is a reduced expanding pressure bc the intrapleural pressure is less negative -at FR the alveolus at base of lung is on steep part of compliance curve...so any change in intrapleural pressure= large increase in volume of that alveolus -although an alveolus at the base of the lung has a small resting volume, it has greater expansion during inspiration -at FRC an alveolus at apex has higher resting volume than at base bc there is less lung tissue above it and there is large expanding pressure bc the intrapleural pressure is more neg, apex is also on less steep part of complaince curve,= smaller inc in the volume of that alveolus for change in intrapleural pressure ===why base is better ventilated, has more room to expand while apex is already almost fully expanded

Answer 88

1-gas exchange is maximally efficient when both ventillation V & perfusion Q are appropriately matched in all areas of the lungs...amt of O2 extracted & CO2 delivered is proportion to the blood flow 2-perfusion of alveolus inc, venilation is unchanged, more CO2 in blood will be delviered to alveolus and more O2 will be moved from alveolus into blood in that alveolus, PACO2 will inc, and PAO2 will dec. -if ventilation stays same but perfusion dec, less CO2 brough to alveolus in blood and less O2 move from alveolus into blood---alveolus PACO2 dec and PAO2 inc 3-upright posture, ventilation/perfusion is greater at base of lungs than at apex... -ventilation to perfusion ratio (V/Q) is high at apex and low at base -V/Q=1 then ventilation is same as perfusion -V/Q \>1 there is more ventilation than perfusion -V/Q \<1 more perfusion than ventilation V/Q ratio at apex of lungs= 3.3 while at base V/Q is .63---so apex of lungs is over ventilated while base is over perfused 4-can range from 0 to infinity...alveolus well perfused w/ no ventilation V/Q= 0 - alveolus ventialted w/ no perfusion V/Q= infinity - normal lung the range of ventilation/perfusion= narrow and overall the ventilation to perfusionr atio of alveolar ventilation to pulm blood flow= 0.8

Answer 89

1-partial pressures of O2 & CO2 w/in pulm capillary will come into equilibrium w/ gas tensions in alveoli - alveolus that is well perfused & well ventilated the PO2 & PCO2 of blood entering pulm capillary will be 40 & 46 - after gas exchange & equilbration the blood leaving pulm capillaries will have equilibrated w/ alveolar PO2 & PCO2 - end capillary blood= 100 & 40 - some alveoli may have reduced ventilation bc of airway obstruction---no ventilation VQ=0, the PO2 & PCO2 of blood leaving pulm cap= same as blood entering 40 & 46---no difusion gradient or gas exchange - some alveoli may get reduced pulm blood flow bc of BV occlusion, when no perfusion VQ=infinity, therell be no blood flow through pulm cap...and no gas exchange...so alveolar PO2 & PCO2 will be same as inspired air 150 & 0

Answer 90

- for gas excahnge between alveoli & pulm cap blood there must be ventilation & perfusion - apex of lung has a high VQ ratio, but bc of relative low perfusion there is reduced gas exchange at apex - limited amt of O2 goes from alveoli into pulm cap blood and limited amt of CO2 move from pulm cap into alveoli sooo alveoli at apex of lung, PAO2 will be high and PACO2 will be low..but blood that does pass through pulm cap beds at apex of lung will become well oxygenated bc of high PAO2 -base of lung has low VQ ratio...alveoli at base get more ventilation & more perfusion so large O2 will go from alveoli into pulm capillary blood & large CO2 will go from pulm cap into alveoli...so base of lung the PAO2 will be low and PACO2 will be high---so bc of greater perfusion= more O2 uptake and more CO2 output ill occur

Answer 91

-VQ ratio is high at apex & low at base of normal upright lung VQ inewuality affects gas exchange of lung & overall amt of O2 that can be transferred from lung into blood -PO2 at apex of lung= 40 higher than at base but major share of blood leavinglung comes from base where PO2 is low -depressing Po2 of blood in pulm vein below that of mixed alveolar PO2 -mixed alveolar PO2 can be determined by using alveolar gas equation or PO2 -2 alveoli w/ low & high VQ ratio...each alveolus receives systemic venous blood that contains 14.6 bc of their differing V/Q ratios, the O2 content of blood leaving pulm caps will be different -blood leaving alveoli w/ low VQ ratio= less O2 content 19, but higher blood flow this alveoli will contribute more O2 to blood leaving lung -blood leaving alveoli w/ high VQ ratio the O2 content will be 20, but bc of low blood flow there will be less O2 to blood leaving lungs ---80% of blood goes through alveoli w/ low ratio and 20% through high ---between the 2= 19.2

Answer 92

1-matchign ventilation & blood flow w/in regions of lungs= gas ecahnge - inequality= mismatch of ventilation & perfusion= defective gas excahnge in diseases---cant transfer as much O2 or CO2 as lung that is ventilated/perfused - any situation with VQ inequality= dec in arterial PO2 Hypoxemia - VQ inequality can lead to CO2 retention

Answer 93

1-collapse of airways---emphysema - bronchoconstriction---asthma - dec lumen diameter bc of inflammation---bronchitis - obstruction by mucous---astham/bronchitis - compression of airways---edema or tumor 2-fibrosis - regional variations in surfactant production - pulm vascular congestion or edema - emphysema - diffuse or regional atelectasis - pneumothorax - compression by tumors or cysts 3-pulm emboli/thrombosis - compression of pulm vessesl (high alveolar pressure, tumors, edema, or pneumothorax) - destruction of pulm vessels - pulmonary vascular hypotension - collapse/overexpansion of alveoli

Answer 94

1-continuous cyclical pattern inspiratory muscles rhythmically contract & relax, changing volume of thoracic cavity -fills & empties lungs -resp muscles are skeletal muscles ---require nervous stimulation for contraction 2-within the brainstem, responsible for generating basic pattern of breathing - aggregations of inspiratory & expiratory neurons w/in resp centers inc neuronal firing date during inspiration/expiration - respiration is under direct neural control from brain - control of respiration doesnt reside in lungs or resp muscles - organized into sausage shaped columns w/ long axis - **dorsal resp group** **DRG**= inspiratory, descending fibers synapse on motor that supply inspiration muscl - **ventral resp group VRG**= inspiratory & expiratory, only active during forced inspiration/expiration - --**pre-botzinger complex**= rostral end of VRG, resp rhythm

Answer 95

1-pons: **apneustic & pneumotaxic** centers influence output from medullary---fine-tuning - apneustic= prolongs inspiratory effort by givign excitatory input to inspiratory neurons w/in prebotzinger - penumotaxic= impulses to apneustic & prebotzinger that switch off inspiratory effort - pneumotaxic & apneustic have antagonistic but = smooth transitions between inspiration & expiration 2-rhythmic resp activity= automatic process - cortex can modify activity of brainstem neurons bc breathing can be modified voluntarily - speaking & yaning & coughing---interrupt rhythmic breathing - hyperventilation & breath holding can alter blood gases 3-limbic system & hypothalamus= emotional ersponses, alter pattern for breathing (fear/stress) - nucleus tractus solitarus NTS- autonomic center w/in brainstem...DRG neurons located in ventrolateral portion---lots of cardioresp afferents - --lots of chemoreceptors, pulm stretch receptors (lateral), arterial baroreceptors (dorsolateral)

Answer 96

1-diaphragm & external intercostal innervated by phrenic & intercostal nerves - cell bodies are located in spinal cord - neural impulses from inspiratory neurons in medullary centers synapse on cell bodies of resp motor neurons - inspiratory neurons w/in brainstem are activated= motor neurons connected to inspiratory muscles to activate===contraction of diaphragm & external intercostal muscles= inspiratory effort - when inspiratory neurons in brainstem stop firing---diaphragm & external intercostal relax= passive expiration -expiratory neurons w/in brainstem to expiration muscles (internal intercostal & ab muscles)---forced expiration &hyperventilation, motor neurons connected to expiratory muscles become activated after they are activated by brainstem expiratory neurons

Answer 97

1-responds to a change in chemical comp of blood or fluid 2-peripheral arterial chemoreceptors are in the carotid bodies at the bifurcation of the common carotid & in aortic bodies above and below aortic arch - respond to changes in chemical composition of blood, especially PaO2 and send afferent impulses to lateral NTS w/in medulla - carotid body chemo affterents travel via glosso - aortic body chem afferents travel via vagus - when PaO2 falls below 60, resp centers are stimulated by signaling periph chemorec to inc ventilation---so periph chemoreceptors dont play a role in min by min control of resp only when really low - arterial chemoreceptors respond to inc in PaCO2 and dec in pHa= inc in ventilation

Answer 98

1-carotid body chemo contain glomus cells - --type 1= large vesicles w/ doapmine---close to carotid sinus nerve (glosso) - --type 2=no dapamine - PaO2 dec = inc in firing rate along carotid sinus nerve---partial pressure of O2 is the stimulus for inc discharge rate, so anemia doesnt stimulate ventilation bc O3 ontent is depressied but PO2 is normal 2-peripheral chemo= stimulates when PAO2 falls below 60 -central chemo= no direct effect, severe hypoxia depresses neuronal activity of brain (resp centers too) 3-periph chemo= weakly stimulates central chemo= strongly stimulates, primary resp signal 4-periph chemo= stimulates, acid base balance central chemo= no affect, cant penetrate blood brain barrier

Answer 99

- most important bc it is min by min control of ventilation - along ventrolateral surface of medulla---near VRG - applying H/dissolved CO2 to brain ECFbathes central chemoreceptors= breathing - inc in arterial PCO2= rise in PCO2 of CSF that surrounds brain - blood brain barrier is impermeable to HCO2 & H but permeable to CO2 - when blood PCO2 rises, CO2 diffuses into brain CSF and CO2 then dissociates & causes inc in H conc (dec pH) in CSF - H ions diffuse from CSF into ECF, dec ECF pH stimulates central chemoreceptors which will stimulate medullary resp centers to inc ventilation - hyperventilation blows off excess Co2 & arterial PCO2 so pH will go back to normal -inc in local ECF pH (dec PCO2) will inhibit ventilation...hyperventilation will temporarily reduce the urge to breathe

Answer 100

1-afferent fibers of these receptors travel to brainstem in vagus nerve to lateral NTS 2-W/in SM layer of lung airways & streating of lungs during inspiration activates the receptors - towards end of inspiration, action potentials from pulm stretch receptors travel to medullary resp center to inhibit inspiratory neurons * *Breuer Hering Reflex**- neg. feedback---cut inspiration short before lung becomes overinflated---imp when tidal volume is over 1000 (large) aka during exercise 3-lie between airway epithelial cells---noxious gas, cig smoke, inhaled dust, cold air stimulate these ones and they will bronchoconstrict & have rapid shallow breathing - this breathing w/ bronchonstriction may limit penetration of agents into gas excahnge surfaces of lungs - may play role ina sthma attacks, producing bronchoconstriction in response to released histamine - cough/sneeze 4-in lung interstitium near alveolar capillaries...J Receptors...excited by interstitial edema in lung - stimulation of pulm c activates j reflex= laryngeal closure and apnea, w/ rapid & shallow breathing - may be responsible for rapid breathing in patients w/ pulm embolus/edema or pneumonia - pulm C = dyspnea during pulm vascular congestion bc of L. ventricular failure or exercise in healthy people

Answer 101

1-mechanical or chemical stimulation of nose= explosive expiratory event===sneeze...stimulation can produce apnea & diving response 2-trachea & upper resp tract have irritant receptors...cause coughing, bronchoconstriction, apnea. laryngeal spasm can occur when larynx is stimulateed mechanically & endotracheal intubation 3-receptors in chest walls signal to brainstem resp neurons about forces exerted by resp muscles & movements of chest wall -impoulses from moving limbs are though to stimulate ventilation during early stages of exercise

Answer 102

1-ventrolateral surface of medulla, near CN 9&10 roots -stimulus= dec pH of brain ECF...inc ventilation 2-carotid bodies in bifurcation of carotid artery afferent= CN 9---stimulus= dec PO2: inc ventilation 3-aortic bodies over aorta & thoracic arteries afferent= CN 10---stimulus=dec PO2: inc ventilation 4-SM of bronchi/bronchioles afferent= CN 10---stimulus= stretch of lungs during inflation: inhibition of further inflation 5-Among airway epithelial cells afferent= CN 10---stimulus= allergens, lung inflam, histamine: bronchoconstriction & rapid shallow breathing

Answer 103

1-in lung interstitum---afferent= CN 10 stimulus= interstitial pulm edema---apnea, rapid shallow breathing 2-w/in mucosa of nosa---afferent= CN 5 stimulus= mechanical/chemical irritants---sneeze or apnea 3-w/in laryngeal mucosa---afferent= CN 10 stimulus= mechanical/chemical irritants---cough, bronchoconstriction & hypoventilation/apnea 4-w/in pharyngeal mucosa---afferent= 9 stimulus= mechanical/chemical irritants---sniff, aspiration or swallowing movements 5-skeletal joints & muscles---afferent= spinal nerves stimulus= limb movement: inc ventilation during exercise

Answer 104

1-most imp factor in control of ventilation= PCO2 of arterial blood - arterial PCO2 is tightly controlled varying w/ 3 mm - inc in PaCO2= inc in ventilation - at any PO2...raising PCO2 will inc ventilation---body is more sensitive to dec in PO2 when it is hypercapnic - dec PO2 while PaCO2 is constant = inc ventilation - at normal PCO2 of 40 the PO2 can reduce to about 60 before any inc in ventilation occurs - Po2 can be below norm level of 100 mm w/o invoking response...hypoxia min by min is small - at ane level of PaCO2 with dec PO2 = inc ventilation - w/ normal PO2 100, ventilation will increase for each 1 mm rise in PCO2 - lowering PO2 below 100= greater ventilation for any PCO2 & lower Po2= inc ventilation for ever 1 mm inc in PCo2 - body is sensitive to inc in PCO2 when it is hypoxic

Answer 105

1-inc in pulm ventilation that excees the bodys need for removal of CO2...CO2 is blown off to atmosphere and PaCO2 & PaCO2 will dec 2-below normal value for PCO2---alveolar PO2 will inc as more fresh O2 is delivered to alveoli but because hemoglobin is almost fully saturated at normal arterial Po2, little O2 is added to the blood -only small amt of extra dissolved O2 will be added to O2 content of blood during hyperventilation 3-inc ventilation that matches an inc i metabolic demand like during exercise -steady state exercise, PaO2 & PaCo2 remain constance w/ inc in gas exchange keeping pace w/ inc in O2 consumption & CO2 production---hyperventilation isnt synonmous w/ inc ventilation 4-pulm ventilation less that what is needed to meet bodys metabolic requirements for O2 delivery & CO2 removal---results in accum of CO2 in bood= hypercapnia 5-accum of Co2 in blood---alveolar Po2 will dec...during hypoventilation, CO2 accum occurs concurrently w/ O2 deficit bc both O2 & Co2 excahnge at lungs are equally affected

Answer 106

1-alveolar PO2= dec alveolar PCO2=no change 2-alveolar PO2= inc Alveolar PCO2=dec 3-alveolar PO2= dec alveolar PCO2=inc 4-alveolar PO2=dec Alveolar PCO2=inc 5-Alveolar PO2=no change alveolar PCO2= no change

Answer 107

blood entering pulm capillaries= systemic venous w/ PO2= 40 & PCO2= 46 flows through...PAO2= 100 PACO2= 40 O2 goes down partial pressure gradient from alveolar air into blood O2 equilibrates---so blood leaving pulm capillary has PO2 of 100 CO2 goes down partial pressure gradient from blood into alveolar air---blood leaving cap. has PCO2 of 40 Arterial PO2= 100 PCO2= 40 Cellular PO2= 40 PCO2= 46 PAO2= 100 PaO2= 100 Tissue=40 PvO2=40--- Presure gradient= 60 PACO2=40 PaCO2=40 Tissue= 46 PvO2=46 Pressure Gradient= 6