RESPIRATORY SYSTEM Major function: Supply body with Oxygen and rid body of Carbon Dioxide We can live without food and water for a while, but we cannot live without oxygen for even a little while. CONTROL OF BREATHING: Involuntary: Medulla oblongata Voluntary: Cerebral Cortex-frontal lobe Respiration has 4 distinct events: 1. Pulmonary ventilation- BREATHING-INHALATION AND EXHALATION-Breathe about 12 x/ min(400-500 ml of air//breath) 2. External respiration- BLOOD and ALVEOLI gas exchange- oxygen loading and carbon dioxide unloading 3. Respiratory gas transport-CIRCULATORY-blood carries O2 and CO2 4. Internal respiration-BLOOD AND CELLS-gas exchange between Necessities: 1. Large surface area 2. Moist surface Air moves in and out for the same reason any fluid (liquid or gas) moves from 1 place to another—difference in pressure from Hi to Lo PAGE 709…WRITE THIS DOWN!!! WHAT IS ATMOSPHERIC PRESSURE? Atmospheric pressure=air at sea level exerts a pressure of 760 mm Hg-it would push up a column of mercury 760 mm Deeper in ocean, higher pres---Higher, mountains, lower pressure WHY ISN’T AIR MOVING AT THE END OF EXPIRATION AND BEFORE INSPIRATION? At the end of expiration and before the beginning of inspiration the ALVEOLI PRESSURE= 760 mm Hg SO air neither enters nor leaves Air moves when there is a difference in the pressure-brought about by change in the size of the thoracic cavity (Boyles’ Law) ---moves down the gradient-HOW ARE PRESSURE GRADIENTS ESTABLISHED? PRESSURE GRADIENTS are established by changes in the size of the THORACIC CAVITY INTRAPULMONARY PRESSURE-pressure within the alveoli of lungs always equalizes itself with the atmospheric pressure outside the body760 mm Hg (1 atmosphere of pressure=amount of pressure exerted by the gases of the atmosphere. Atmospheric pressure:At sea level this pressure would raise a column of Hg 760 mm high)-14.7 lb/square inch THINGS THAT AFFECT BREATHING= Tissue stretch of lungs Emotions Chemicals Exercise: carbon dioxide goes up-oxygen goes down-“out of breath” 1 4 IDEAL GAS LAWS----WHY “IDEAL”? Ideal-gas whose molecules are so far apart they rarely collide with each other Gas pressure-molecules collide with walls of container and exert force (pressure— FACTORS THAT AFFECT GASES???? (1) PRESSURE (2) TEMPERATURE (3) IF THE GAS IS A MIXTURE=SUM OF PRESSURE OF ALL GASES (4) SOLUBILITY OF GASES THE CHEST IS THE CONTAINER FOR THE RESPIRATORY SYSTEM 1. BOYLE’S LAW Gas’ volume is INVERSELY proportional to its pressure when held at a constant temperature P1V1=P2V2 When the volume of a container (the chest) goes up, pressure goes down, When the volume of a container (the chest) goes down, pressure goes up APPLICATION: When the volume of the thorax increases, (diaphragm-Phrenic Nerve, intercostals-Intercostal nerve), the pressure decreases and is lower than atmospheric pres= (760 mm Hg) so air from outside->into the airways (inspiration) expiration–opposite occurs 2. CHARLES’ LAW Gas volume is DIRECTLY proportional to temperature when pressure is held constant-also, pressure is directly proportional to temperature when volume is held constant SO Pressure and Volume Directly Proportional to Temp when the other is held constant APPLICATION: During INSPIRATION air expands in volume as it is warmed by respiratory mucosa 3. DALTON’S LAW (LAW OF PARTIAL PRESSURES) The total pressure exerted by a mixture of gases (such as air) is equal to the sum of the pressures of each individual gas Partial pressure=pressure each gas in a mixture exerts is directly proportional to its % in the total gas mixture— Air N2 =78.6 % O2=20.9 % CO2=.04 % H2O=.046 % X 760=P… So multiply these % X 760 mm Hg to get PO2 etc of each Partial pressure of oxygen is directly proportional to its percentage in the total gas mixture-Oxygen makes up about 21% of the atmosphere-has a PO2=0.21 x 760 = 159 mm Hg At high altitudes where atmosphere is less influenced by gravitational pull, all partial pressures decline in direct proportion to the decline in atmospheric pressure Below sea level atmospheric pressure increases by 1 atmosphere for each 33 feet of descent so at 99 feet below sea level, the total pressure on the body is = to 4 atmospheres or 3040 mm Hg-so partial pressure of each gas is also multiplied 2 PO2 PCO2=partial pressure Determined by its concentration or % of the mixture—O2=21% so atmospheric PO2=.21 X 760=159.6 mm Hg APPLICATION: Used for determining direction of diffusion if know Partial Pressure of each gas Also, used for determining the pressure of oxygen in air we breathe 4. HENRY’S LAW The concentration of a gas in a solution depends on the PARTIAL PRESSURE of the gas and its SOLUBILITY as long as the temp remains constant when a mixture of gases is in contact with a liquid each gas will dissolve in the liquid in proportion to its partial pressure and its solubility in the liquid CO2 is most soluble in plasma O2 is relatively insoluble-so needs pigment to carry-Hb N2 is least soluble APPLICATION: The amount of gas dissolved in the PLASMA relates to Henry’s Law Oxygen Toxicity Although breathing oxygen at 2 atmospheres presents no problems for short periods of time, oxygen toxicity develops rapidly when the PO2 is greater than 2.5-3 atmospheres-excessive oxygen concentrations generate large amounts of harmful free radicals causing profound central nervous system disturbance resulting in coma and death Even though 80% of air is N2 it has little affect on the body because nitrogen is very insoluble in blood, HOWEVER when a deep sea diver breathes under HYPERBARIC (high pressure) conditions more nitrogen gas (80% of gases in air) dissolves in the blood and causes nitrogen narcosis->dizziness, drowsiness, giddiness, and other symptoms similar to alcohol intoxication (“RAPTURE OF THE DEEP”) If a diver ascends to surface gradually the dissolved nitrogen gas can be eliminated by the lungs without problems but if ascent is rapid, the nitrogen forms large gas bubbles in blood causing an embolus (can be moving clot or in this case a gas) If bubbles occur in the tissue, it causes excruciating pain-commonly called the BENDS–more accurate: DECOMPRESSION SICKNESS Like gas boiling out of solution in body fluids (not very soluble in body fluids so eager to get out)-and can damage the brain 3 INSPIRATION-breathe in Quiet inspiration:Diaphragm (Phrenic nerve) and external intercostal muscles (Intercostal/vagus nerve)cause thorax volume to increase Forceful inspiration: Diaphragm, external intercostals, sternocleidomastoid, pectoralis minor, and serratus anterior muscles cause thorax volume to increase As the size of the thorax increases, intrapleural /intrathoracic/intraalveolar pressure decreases and inspiration occurs Just before inspiration is beginning the intrathoracic pressure is about 4 mm Hg less than atmospheric pressure As the thorax enlarges it pulls the lungs along with it because of the COHESION between the moist pleura covering the lungs and the moist pleura lining the thorax When all of this occurs, the air pressure inside the lungs is less than atmospheric pressure and the air rushes in Then the tendency of the thorax and lungs to return to their preinspiration volume is a physical phenomenon called ELASTIC RECOIL (REPEAT:::::During inspiration COHESION occurs between moist pleura covering lungs and moist pleura lining the thorax and pulls the lungs along with it as it moves out During expiration ELASTIC RECOIL-natural tendency of lungs to contract GO TO PICTURE AT TOP OF 711 Explain inspiration and expiration using these numbers for intraalveolar pressure (Pressure=757 and 763) EXPIRATION-breathe out—passive process Inspiratory muscles relax-size of thorax decreases so intrathoracic/intrapleural pres goes up NEGATIVE PRESSURE BREATHING: NEGATIVE PRESSURE-less than atmospheric ALWAYS NEGATIVE BETWEEN PARIETAL AND VISCERAL PLEURA TO PREVENT COLLAPSE OF LUNGS: NEGATIVE PRESSURE-Super important to understand!!! The intrapleural pressure in the intrapleural space is always about 4 mm Hg less than the pressure in the alveoli and is said to be negative relative to both the intrapulmonary and atmospheric pressures NEGATIVE PRESSURE results from 2 groups of factors: those factors acting to hold the lungs to the thorax wall -Cohesion 1. those factors acting to pull the lungs away from the thorax wallRecoil/surface tension of the alveoli The negative pressure is required to overcome 2 factors that would cause collapse of lungs NEGATIVE PRESSURE MUST: (1) Overcome collapse tendency of lungs caused by surface tension of fluid lining of alveoli (bugs walk on water-mol attracted to each other) (2) Overcome tendency of elastic fibers constantly attempting to recoil 4 COMPLIANCE-ability of lungs and thorax to stretch-essential to normal respiration THE IMPORTANCE OF THE NEGATIVE PRESSURE IN THE INTRAPLEURAL SPACE AND THE TIGHT COUPLING OF THE LUNGS TO THE THORAX WALL CANNOT BE OVEREMPHASIZED...... ANY CONDITION THAT EQUALIZES THE INTRAPLEURAL PRESSURE WITH THE INTRAPULMONARY OR ATMOSPHERIC PRESSURE CAUSES IMMEDIATE LUNG COLLAPSE!!!!! PULMONARY VOLUME-very important SPIROMETER-used to measure-PICTURE SHOWN ON 714 Tidal Volume/TV=typical in and out---+500 ml x 12/min Expiratory Reserve Volume/ERV=amount you can force out after normal exp +1000 ml Inspiratory Reserve Volume/IRV= amount you can force into lungs after TV-force in— +3000 ml Residual Volume/RV=Can not force all air out of lungs-this is the amount always left in lungs —+1200 ml “Wind knocked out”=ERV and some RV knocked out and even a few alveoli collapse SO must re-inflate lungs--- requires EFFORT…still spongy and will float even after RV forced out because of the trapped air called minimal volume 40%RV PNEUMOTHORAX-RV eliminated and lung collapses Vital Capacity/VC=IRV + ERV + TV 4500-5000 ml {largest volume of air that can be moved in and out of lungs-measures largest possible EXPIRATION after largest possible INSPIRATION): Depends on: (1) Size of thoracic cavity (2) Posture (3) Volume of blood in the lungs-if more blood than normal encroaches on alveolar air space-Important in congestive heart failure (4) Excess fluid in pleural or abdom cavities decreases VC and so does Emphysema-walls stretched-lose elasticity and can’t recoil so increases the RV-Also walls break down} TLC= IRV + ERV + TV + RV 5700-6200 ml TLC=VC + RV ANATOMICAL DEAD SPACE-volume of air in nose, pharynx, larynx, trachea, and bronchi since it does not reach alveoli SO “dead air” Rule of thumb=AD Space=Same # in mls as weight in lbs (110 lbs=110 ml AD space) Volume of inspired air that actually reaches alveoli is ALVEOLAR VENTILATION=70% of TV (350 ml) PHYSIOLOGICAL DEAD SPACE =ALVEOLAR DEAD SPACE (some alveoli can’t exchange gases as in COPD) + ANATOMICAL DEAD SPACE CHRONIC OBSTRUCTIVE PULMONARY DISEASE 5 TERMS: 717 1. EUPNEA-normal breathing HYPERPNEA-increased breathing-need for O2 2. HYPERVENTILATION-increased breathing-in excess of need for O2 3. Conscious effort or hysteria 4. HYPOVENTILATION-decrease in breathing that results in CO2 build up in blood 5. DYSPNEA-labored/difficult breathing-uncomfortable or in distress-hypoventilation 6. ***ORTHOPNEA-dyspnea while lying down-so sit or stand-heart disease 7. APNEA-temporary cessation of breathing-during sleep or after swallowing-at end of a normal expiration 8. ***APNEUSIS-cessation of breathing in inspiratory position 9. RESPIRATORY ARREST-failure to resume breathing after #7 and #8 10. CHEYNE STOKES RESPIRATION-periodic type of abnormal breathing-often seen in terminally ill or in brain damaged patients-Cycles of increased TV for several breaths followed by several breaths with decreased TV 11. ***BIOT’S BREATHING-repeated sequences of deep gasps and apnea-usually from increased intracranial pressure Back to page 716 Review Dalton’s Law-the partial pressure of each gas is directly related to the concentration in the total mixture Atmospheric pressure is 760 mm Hg— Oxygen is about 21% of that so can calculate the pressure of oxygen in the atmosphere-----.21 X 760 =159.6 mm Hg The symbol used to designate partial pressure is capital P followed by the chemical symbol for the gas so PO2 TENSION means the same as partial pressure so oxygen tension is same as PO2 The PO2 in the atmosphere is not the same as it is when it is in the body— This compares the partial pressures of oxygen and carbon dioxide at 4 sites LOOK AT TABLE 24-2 Atm Alveolar Air Arterial Blood Venous Blood osp her e PO2 160 mm Hg 100 mm Hg 100 mm Hg 40 mm Hg PCO2 0.2mm Hg 40 mm Hg 40 mm Hg 46 mm Hg Look at Figure 24.8—Notice that alveolar oxygen and carbon dioxide remain constant This is because the alveoli are constantly ventilated-air is constantly moving in ALVEOLAR PO2 constant=100 mm PO2 BLOOD PO2 NOT constant=40mm PO2->70mm PO2->100mm PO2 6 The amount of oxygen that diffuses into blood per minute depends on several factors: 719 1. O2 pressure gradient between alveolar air and incoming pulmonary blood (Alveolar PO2-Blood PO2) Application:Alveolar air PO2 decreases as altitude increases, and therefore less oxygen enters the blood at high altitudes. At a certain high altitude Alveolar PO2= PO2 of blood entering the pulmonary capillaries and then no oxygen diffuses into the blood 2. Total functional surface area of respiratory membrane Application: In EMPHYSEMA -surface area and recoil are decreased so poor blood oxygenation ..PNEUMOTHORAX decreases functional area by collapsing alveoli 3. Respiratory minute volume=Respiratory rate/min X vol of air inspired/respiration Application: Morphine slows resp rate so decreases the respiratory minute volume and lessens the amount of oxygen entering the blood 4. Alveolar ventilation=the volume of air that actually reaches the alveoli-only part that exchanges with blood Application: Some air does not reach the alveoli-mucus in airways, etc FORM AND FUNCTION: Structural factors that facilitate oxygen diffusion into blood: 1. Walls of alveoli and capillaries are extremely thin 2. Alveolar and capillary surfaces are huge 3. Lung capillaries contain a great amount of blood 4. Every RBC comes close to alveolar air Box 24. 3 PNEUMOTHORAX PNEUMOTHORAX=presence of air in thoracic cavity causes lung/s to collapse use chest tube to draw out air and allow lungs to reinflate HOW BLOOD TRANSPORTS GASES Immediately upon entering blood, CO2 and O2 dissolve in plasma, but because liquids can hold only a small amt of gas in sol’n, CO2 and O2 combine with other molecules to form a chemical union—such as hemoglobin, a plasma protein and water, SO once bound to others, their concentration in plasma decreases and more CO2 and O2 can diffuse into blood HEMOGLOBIN-reddish protein pigment only in RBCs 4 polypeptide chains-2 alpha + 2 beta each with an iron containing HEME in the middle 1 O2 molecule combines with each Heme..1 molecule of Hb holds 4 O2 *******Also CO2 can combine with the amino acids of the alpha and beta chains So hemoglobin can be a SPONGE for both O2 and CO2 Hemoglobin also has ability to UNLOAD these 2 gases!!! 7 TRANSPORT OF OXYGEN: At PO2 of 100 mm Hg only 0.3 ml of oxygen is dissolved in 100 ml blood Many XXX more than that carried as OXYHEMOGLOBIN Normal Hb level=15 gm/100 ml blood 1.34 ml O2 per gm Hb--Then 1.34 X 15 = 20.1 ml oxygen/100 ml of blood=oxyhemoglobin Hgb deficiciency decreases amt oxygen carried-HYPOXIA To combine with hemoglobin oxygen must diffuse from plasma into the RBCs where millions of hemoglobin molecules are located Several factors affect the rate at which Hgb combines with oxygen in lung capillaries: oxygen-hemoglobin dissociation curve= Hb + O2 - Increasing PO2HbO2 And just the opposite with a decrease in PO2 HbO2- decreasing PO2 Hb + O2 Inc PO2 accelerates Hb O2 association Dec PO2 release of O2 from Hb--Dissociation Association happens so quickly that -97% of blood’s hemoglobin is saturated with O2 by time blood leaves lung capillaries to return to heart SO oxygen travels in 2 forms: (1) O2 ---dissolved in plasma..0.3 ml/100 ml (2) O2 + Hb **Majority-oxyhemoglobin 20.1 ml/100 ml Box 24. 4 CARBON MONOXIDE POISONING—Hb has 200 X the affinity for CO than it does for O2 HbCO replaces Hb O2 Hyperbaric Oxygen Chambers-(high pressure chambers) Application of Henry’s Law-Contain oxygen at higher pressure than 1 atmosphere-used to force greater than normal amounts of oxygen into a patient’s blood in cases of: Carbon monoxide poisoning Circulatory shock Asphyxiation Gas gangrene or tetanus: the anaerobic bacteria causing these infections cannot live in the presence of high levels of oxygenBox 24.5 OTHER OXYGEN BINDING PROTEINS (1) FETAL HEMOGLOBIN Dif structure (2 alpha and 2 gamma)-in the placenta fetal Hb can load up with more oxygen at a low partial pressure than adult Hb can(PO2 in maternal blood->placenta is 32mm Hg) So this is of vital importance (2) MYOGLOBIN Found in muscles-made up of only an alpha chain so 1 Heme group so it can hold only 1 O2 However!! It attracts and holds oxygen much more strongly than Hb Helps move oxygen out of blood (unloading) into muscle cells->release during increased cell respiration/exercise—reduces intracellular PO2 8 TRANSPORT OF CO2 1. Dissolved in plasma—10% 2. Carbaminohemoblobin in RBCs-20%--united with the amine groups of Hgb (and other plasma proteins-not included here) HCO2(Amount is governed by RATE LAW of chemistry—CO2 association with Hgb is accelerated by an increased PCO2 and slowed by a decrease in PCO2 3. Bicarbonate ions 70% HCO3Equations on page 724—some of the dissolved CO2 enters RBCs and combines with Hb to form carbaminohemoglobin and some combines with water to form H2CO3 --CARBONIC ANHYDRASE found in RBCs-catalyzes the reaction As this unstable compound splits, HCO3 - exits the RBC, then another negative ion moves in to take its place-CHLORIDE SHIFT H2O + CO2--->H2CO3 -->H+ + HCO3LOOK AT FIG 24.14 and 15 Carbon Dioxide and pH When carbon dioxide enters blood, most becomes carbaminohemoglobin and H+ or bicarbonate and H+ so when CO2 increases-increasing H+ makes pH go down THIS IS A VERY IMPORTANT PRINCIPLE TO UNDERSTANDING HOW AND WHY RESPIRATION IS REGULATED IN THE MANNER THAT IT IS SYSTEMIC GAS EXCHANGE Diffusion down a gas pressure gradient Alveoli Hi in O2 and low in CO2->Pul capillaries low in O2 and high in CO2 so diffusion Opposite at cells and as more activity PO2 decreases and so more O2 unloaded because pressure gradient INCREASES As dissolved oxygen diffuses out of arterial blood, blood PO2 decreases and this accelerates oxyhemoglobin dissociation to release more oxygen into the plasma for diffusion out to cells When you exercise the PCO2 goes up and the PO2 goes down in cells so the pressure gradient between cell and tissue capillaries goes up for each and CO2 moves into capillaries and pressure goes from 40->46 Increasing PCO2 and decreasing PO2 produce 2 effects: (1) Favors oxygen dissociation from oxyhemoglobin (2) Favors carbon dioxide association with hemoglobin to form carbamiohemoglobin 9 In cells PCO2 goes up as PO2 goes down SO this favors oxyhemoglobin dissociation and more carbaminohemoglobin formation=”right shift”= BOHR EFFECT BOHR EFFECT=increased PCO2 decreases affinity between Hb and O2 therefore, more O2 will be released Plasma pH becoming more acidic-normally occurs as plasma PCO2 level risehas the same effect of decreasing the affinity between Hb and O2 –more O2 will be released pH PCO2 HbO2 Hb + O2 ALSO HbO2 Hb + O2 HALDANE EFFECT-increased CO2 loading caused by a decrease in PO2 PO2 Hb + CO2--------- HbCO2 ********Page 727 Table 24.3 CONTROL CENTERS:REGULATION OF BREATHING Homeostasis of blood gases (oxygen and carbon dioxide) is maintained primarily by means of changes in VENTILATION-rate and depth of breathing Regulators found in the brain stem=RESPIRATORY CENTERS BASIC RHYTHM of respiratory cycle (inspiration/expiration) generated by the MEDULLARY RHYTHMICITY AREA—has 2 interconnected control centers:MEDULLA OBLONGATA 1. INSPIRATORY CENTER-stimulates inspiratory muscles/primary respiratory pacemaker-because normal quiet breathing involves stimulation of inspiratory muscles (mainly diaphragm) alternating with relaxation of the same muscles 2. EXPIRATORY CENTER- stimulates expiratory muscles—active only when FORCED expiration is needed CHANGE BASIC BREATHING by different inputs to Medullary Rhythmicity Area for example 1. APNEUSTIC CENTER in PONS-stims inspiratory-longer/deeper breathing= Apneustic breathing-abnormally long and deep inspirations 2. PNEUMOTAXIC CENTER in PONS-inhibits inspiratory center and apneustic centerprevents overinflation of lungs and permits normal rhythm 10 ****DIVING REFLEX BOX 24.6 ****BOX 24.7 FACTORS THAT INFLUENCE BREATHING INVOLUNTARY: BRAIN STEM Changes in the PCO2, PO2 and pH –influence Medullary Rhythmicity Area PCO2 and pH act on chemoreceptors in medulla-sensitive to both –if PCO2 gets above 38-40 in arterial blood, it stimulates chemoreceptors to cause faster breathing with greater volume of air moving in and out per minute Chemoreceptors in medulla, carotid bodies, and aorta Large decreases in CO2 content cause the opposite (BREATHE IN SACK WHEN HYPERVENTILATING) At PCO2 35 mm=Apnea Role of PO2 not clear-hypoxic-send fewer impulses to respiraory muscles Increase breathing: (1) Rising PCO2 (2) Decreasing PO2 (Emergency only) (3) Decreasing Ph (4) Decreasing Arterial BP BP acts on baroreceptors in carotid bodies and aorta Decrease breathing: Opposite of above!!! Arterial blood pressure increase Hering-Breuer reflex—stretch receptors in lungs (prevents overinflation of lungs-inhibits Inspiratory Centerhelps control normal depth of breathing) Miscellaneous Factors that Affect Breathing: Sudden painful stimulation---reflex apnea, but if continued pain then faster and deeper breathing Sudden cold stimuli-reflex apnea Simulation of pharynx or larynx by irritating/touch->apneaChoking reflex to prevent aspiration of food or liquids VOLUNTARY: CEREBRAL CORTEX Certain limitations---hold breath->PCO2 goes up so start breathing KIDS CAN’T HOLD BREATH AND DIE!!! DISORDERS RESTRICTIVE PULMONARY DISORDERS --Decreased lung volumes and capacities Alveolar fibrosis Rheumatoid lung Obesity Metabolic disorders Pleurisy pain Injury Asbestos/toxic fumes/coal dust OBSTRUCTIVE PULMONARY DISORDERS CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD) Bronchitis Emphysema (less surface area-walls of alveoli rupture) Asthma (Inflammation of mucous membranes/spasms of bronchi) 11 OTHER PROBLEMS: Look on p 721 CARBON MONOXIDE POISONING-CO binds 200X more strongly than O2 So it knocks out O2 from HbO2 and forms HbCO-hard to remove it Because it binds so strongly—Person turns CHERRY RED rather than cyanotic so doesn’t appear to have a problem superficially –But serious---One strategy is to place a person in a HYPERBARIC OXYGEN CHAMBER CYANOSIS-respiratory distress-person turns blue HEIMLICH MANEUVER-if choking-make fist and place thumb side of fist against victim’s upper abdomen-below ribcage, above navel-press with quick upward thrustrepeat until object expelled—DON’T SLAP ON BACK!! SUDDEN INFANT DEATH SYNDROME—SIDS- crib death-usually 1 mo->1 yr--now baby’s sleep on backs—cut down number of instances—maybe if baby on stomach press on jaw and narrows airway EXTERNAL RESPIRATION (Exchange of gases in the lungs) 3 Factors influence diffusion of CO2 and O2 (1) Partial pressure gradients and gas solubilities: Steep oxygen gradient (PO2 40 mm Hg in pulmonary blood-104 mm Hg in alveoli) O2 equilibrium occurs in .25 second-1/3 of time RBC is in a pulmonary capillary (in other words, blood flow in pulmonary capillaries could be reduced by 2/3 and still provide adequate oxygenation) CO2 gradient less steep (45 mmHg comp to 40 mmHg)but carbon dioxide is 20 X more soluble in the plasma and fluids than is oxygen so equal amount of it and O2 can be exchanged (2) Thickness and Surface Area of Respiratory Membrane (1) About 0.5-1 micro meter thick-if fluid buildup HYPOXIA can result (2) SA=70-80 M2 size of racquetball court-Emphysema=alveolar walls break and bigger alveoli so less SA (3) Alveolar airflow and pulmonary capillary circulation These are always synchronized If low oxygen and high carbon dioxide levels in alveoli, pulmonary capillaries constrict and airways dilate CONVERSELY: If high oxygen and low carbon dioxide, alveolar partial pressures cause constriction of bronchioles and flushing of blood into pulmonary capillaries HOMEOSTASIS 12