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Published on February 12, 2008

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Pulmonary Physiology:  Pulmonary Physiology Respiratory neurons in brain stem sets basic drive of ventilation descending neural traffic to spinal cord activation of muscles of respiration Ventilation of alveoli coupled with perfusion of pulmonary capillaries Exchange of oxygen and carbon dioxide Respiratory Centers:  Respiratory Centers Located in brain stem Dorsal & Ventral Medullary group Pneumotaxic & Apneustic centers Affect rate and depth of ventilation Influenced by: higher brain centers peripheral mechanoreceptors peripheral & central chemoreceptors Muscles of Ventilation:  Muscles of Ventilation Inspiratory muscles- increase thoracic cage volume Diaphragm, External Intercostals, SCM, Ant & Post. Sup. Serratus, Scaleni, Levator Costarum Expiratory muscles- decrease thoracic cage volume Abdominals, Internal Intercostals, Post Inf. Serratus, Transverse Thoracis, Pyramidal Ventilation-Inspiration:  Ventilation-Inspiration Muscles of Inspiration-when contract  thoracic cage volume (uses 3% of TBE) diaphragm drops floor of thoracic cage external intercostals sternocleidomastoid anterior serratus scaleni serratus posterior superior levator costarum (all of the above except diaphragm lift rib cage) Ventilation-expiration:  Ventilation-expiration Muscles of expiration when contract pull rib cage down  thoracic cage volume (forced expiration rectus abdominus external and internal obliques transverse abdominis internal intercostals serratus posterior inferior transversus thoracis pyramidal Under resting conditions expiration is passive and is associated with recoil of the lungs Movement of air in/out of lungs:  Movement of air in/out of lungs Considerations Pleural pressure negative pressure between parietal and visceral pleura that keeps lung inflated against chest wall varies between -5 and -7.5 cmH2O (inspiration to expiration Alveolar pressure subatmospheric during inspiration supra-atmospheric during expiration Transpulmonary pressure difference between alveolar P & pleural P measure of the recoil tendency of the lung peaks at the end of inspiration Compliance of the lung:  Compliance of the lung V/P At the onset of inspiration the pleural pressure changes at faster rate than lung volume-”hysteresis” Air filled lung vs. saline filled lung Easier to inflate a saline filled lung than an air filled lung because surface tension forces have been eliminated in the saline filled lung Pleural relationships-lung & chestwall forces:  Pleural relationships-lung & chestwall forces Effect of Thoracic Cage on Lung :  Effect of Thoracic Cage on Lung Reduces compliance by about 1/2 around functional residual capacity (at the end of a normal expiration) Compliance greatly reduced at high or low lung volumes Work of Breathing:  Work of Breathing Compliance work (elastic work) Tissue resistance work viscosity of chest wall and lung Airway resistance work Energy required for ventilation 3-5% of total body energy Patterns of Breathing:  Patterns of Breathing Eupnea normal breathing (12-17 B/min, 500-600 ml/B) Hyperpnea  pulmonary ventilation matching  metabolic demand Hyperventilation ( CO2)  pulmonary ventilation > metabolic demand Hypoventilation ( CO2)  pulmonary ventilation < metabolic demand Patterns of breathing (cont.):  Patterns of breathing (cont.) Tachypnea  frequency of respiratory rate Apnea Absense of breathing. e.g. Sleep apnea Dyspnea Difficult or labored breathing Orthopnea Dyspnea when recumbent, relieved when upright. e.g. congestive heart failure, asthma, lung failure Pleural Pressure:  Pleural Pressure Lungs have a natural tendency to collapse surface tension forces 2/3 elastic fibers 1/3 What keeps lungs against the chest wall? Held against the chest wall by negative pleural pressure “suction” Collapse of the lungs:  Collapse of the lungs If the pleural space communicates with the atmosphere, i.e. pleural P = atmospheric P the lung will collapse Causes Puncture of the parietal pleura Sucking chest wound Erosion of visceral pleura Also if a major airway is blocked the air trapped distal to the block will be absorbed by the blood and that segment of the lung will collapse Pleural Fluid:  Pleural Fluid Thin layer of mucoid fluid provides lubrication transudate (interstitial fluid + protein) total amount is only a few ml’s Excess is removed by lymphatics mediastinum superior surface of diaphragm lateral surfaces of parietal pleural helps create negative pleural pressure Pleural Effusion:  Pleural Effusion Collection of large amounts of free fluid in pleural space Edema of pleural cavity Possible causes: blockage of lymphatic drainage cardiac failure-increased capillary filtration P reduced plasma colloid osmotic pressure infection/inflammation of pleural surfaces which breaks down capillary membranes Surfactant:  Surfactant Reduces surface tension forces by forming a monomolecular layer between aqueous fluid lining alveoli and air, preventing a water-air interface Produced by type II alveolar epithelial cells complex mix-phospholipids, proteins, ions dipalmitoyl lecithin, surfactant apoproteins, Ca++ ions Stabilization of Alveolar size:  Stabilization of Alveolar size Role of surfactant Law of Laplace P=2T/r Without surfactant smaller alveolar have increased collapse p & would tend to empty into larger alveoli Big would get bigger and small would get smaller Surfactant automatically offsets this physical tendency As the alveolar size  surfactant is concentrated which  surface tension forces, off-setting the  in radius Interdependence Size of one alveoli determined in part by surrounding alveoli Static Lung Volumes:  Static Lung Volumes Tidal Volume (500ml) amount of air moved in or out each breath Inspiratory Reserve Volume (3000ml) maximum vol. one can inspire above normal inspiration Expiratory Reserve Volume (1100ml) maximum vol. one can expire below normal expiration Residual Volume (1200 ml) volume of air left in the lungs after maximum expiratory effort Static Lung Capacities:  Static Lung Capacities Functional residual capacity (RV+ERV) vol. of air left in the lungs after a normal expir., balance point of lung recoil & chest wall forces Inspiratory capacity (TV+IRV) max. vol. one can inspire during an insp effort Vital capacity (IRV+TV+ERV) max. vol. one can exchange in a resp. cycle Total lung capacity (IRV+TV+ERV+RV) the air in the lungs at full inflation Determination of RV, FRC, TLC:  Determination of RV, FRC, TLC Of the static lung volumes & capacities, the RV, FRC, & TLC cannot be determined with basic spirometry. Helium dilution method for RV, FRC, TLC FRC= ([He]i/[He]f-1)Vi [He]i=initial concentration of helium in jar [He]f=final concentration of helium in jar Vi=initial volume of air in bell jar Determination of RV, FRC, TLC:  Determination of RV, FRC, TLC After FRC is determined with the previous formula, determination of RV & TLC is as follows: RV = FRC- ERV TLC= RV + VC ERV & VC values are determined from basic spirometry Pulmonary Flow Rates:  Pulmonary Flow Rates Compromised with obstructive conditions decreased air flow minute respiratory volume RR X TV Forced Expiratory Volumes (timed) FEV/VC Peak expiratory Flow Maximum Ventilatory Volume Airways in lung:  20 generations of branching Trachea (2 cm2) Bronchi first 11 generations of branching Bronchioles (lack cartilage) Next 5 generations of branching Respiratory bronchioles Last 4 generations of branching Alveolar ducts give rise to alveolar sacs which give rise to alveoli 300 million with surface area 50-100 M2 Airways in lung Dead Space:  Dead Space Area where gas exchange cannot occur Includes most of airway volume Anatomical dead space (=150 ml) Airways Physiological dead space = anatomical + non functional alveoli Calculated using a pure O2 inspiration and measuring nitrogen in expired air (fig 37-8) % area X Ve Alveolar Volume:  Alveolar Volume Alveolar volume (2150 ml) = FRC (2300 ml)- dead space (150 ml) At the end of a normal expiration most of the FRC is at the level of the alveoli Slow turnover of alveolar air (6-7 breaths) Rate of alveolar ventilation Va = RR (Vt-Vd) Control of Airway Smooth Muscle:  Control of Airway Smooth Muscle Neural control SNS-beta receptors causing dilatation direct effect weak indirect effect predominates Parasympathetic-muscarinic receptors causing constriction NANC nerves (non-adrenergic, non-cholinergic) Inhibitory release VIP and NO  bronchodilitation Stimulatory  bronchoconstriction, mucous secretion, vascular hyperpermeability, cough, vasodilation “neurogenic inflammation” Control of Airway Smooth Muscle (cont.):  Control of Airway Smooth Muscle (cont.) Local factors histamine binds to H1 receptors-constriction histamine binds to H2 receptors-dilation slow reactive substance of anaphylaxsis-constriction-allergic response to pollen Prostaglandins E series- dilation Prostaglandins F series- constriction Control of Airway Smooth Muscle (cont):  Control of Airway Smooth Muscle (cont) Enviornmental pollution smoke, dust, sulfur dioxide, some acidic elements in smog elicit constriction of airways mediated by: parasympathetic reflex local constrictor responses Effect of pH on ventilation:  Effect of pH on ventilation Normal level of HCO3- = 25 mEq/L Metabolic acidosis (low HCO3-) will stimulate ventilation (regardless of CO2 levels) Metabolic alkalosis (high HCO3-) will depress ventilation (regardless of CO2 levels) Pulmonary circulation:  Pulmonary circulation Pulmonary artery wall 1/3 as thick as aorta RV 1/3 as thick as LV All pulmonary arteries have larger lumen more compliant operate under a lower pressure can accommodate 2/3 of SV from RV Pulmonary veins shorter but similar compliance compared to systemic veins Total Pulmonic Blood Volume:  Total Pulmonic Blood Volume 450 ml (9% of total blood volume) reservoir function 1/2 to 2X TPBV shifts in volume can occur from pulmonic to systemic or visa versa e.g. mitral stenosis can  pulmonary volume 100% shifts have a greater effect on pulmonary circulation Systemic Bronchial Arteries:  Systemic Bronchial Arteries Branches off the thoracic aorta which supplies oxygenated blood to the supporting tissue and airways of the lung. (1-2% CO) Venous drainage is into azygous (1/2) or pulmonary veins (1/2) (short circuit) drainage into pulmonary veins causes LV output to be slightly higher (1%) than RV output & also dumps some deoxygenated blood into oxygenated pulmonary venous blood Pulmonary lymphatics:  Pulmonary lymphatics Extensive & extends from all the supportive tissue of lungs & courses to the hilum & mainly into the right lymphatic duct remove plasma filtrate, particulate matter absorbed from alveoli, and escaped protein from the vascular system helps to maintain negative interstitial pressure which pulls alveolar epithelium against capillary endothelium. “respiratory membrane” Pulmonary Pressures:  Pulmonary Pressures Pulmonary artery pressure = 25/8 mean = 15 mmHg Mean pulmonary capillary P = 7 mmHg. Major pulmonary veins and left atrium mean pressure = 2 mmHg. Control of pulmonary blood flow:  Control of pulmonary blood flow Since pulmonary blood flow = CO, any factors that affect CO (e.g. peripheral demand) affect pulmonary blood flow in a like way. However within the lung blood flow is distributed to well ventilated areas low alveolar O2 causes release of a local vasoconstrictor which automatically redistributes blood to better ventilated areas ANS influence on pulmonary vascular smooth muscle:  ANS influence on pulmonary vascular smooth muscle SNS + will cause a mild vasoconstriction 3 Hz to 30 Hz  pulmonary arterial BP about 30% Mediated by alpha receptors With alpha blockage response abolished and at 30 Hz. vasodilatation observed as beta receptors are unmasked Parasympathetic + will cause a mild vasodilatation (major constrictor effect on pulmonary vascular smooth muscle is low alveolar O2) Oxygenation of blood in Pulmonary capillary:  Oxygenation of blood in Pulmonary capillary Under resting conditions blood is fully oxygenated by the time it has passed the first 1/3 of pulmonary capillary even if velocity  3X full oxygenation occurs Normal transit time is about .8 sec Under high CO transit time is .3 sec which still allows for full oxygenation Limiting factor in exercise is SV Effect of hydrostatic P on regional pulmonary blood flow:  Effect of hydrostatic P on regional pulmonary blood flow From apex to base capillary P  (gravity) Zone 1- no flow alveolar P > capillary P normally does not exist Zone 2- intermittent flow (toward the apex) during systole; capillary P > alveolar P during diastole; alveolar P > capillary P Zone 3- continuous flow (toward the base) capillary P > alveolar P During exercise entire lung  zone 3 Pulmonary Capillary dynamics:  Pulmonary Capillary dynamics Starling forces (ultrafiltration) Capillary hydrostatic P = 7 mmHg. Interstitial hydrostatic P = -8 mmHg. Plasma colloid osmotic P = 28 mmHg. Interstitial colloid osmotic P = 14 mm Filtration forces = 15 mmHg. Reabsorption forces = 14 mmHg. Net forces favoring filtration = 1 mmHg. Excess fluid removed by lymphatics Basic Gas Laws:  Basic Gas Laws Boyle’s Law At a constant T the V of a given quantity of gas is 1/ to the P it exerts Avogadro’s Law = V of gas at the same T & P contain the same # of molecules Charles’ Law At a constant P the V of a gas is  to its absolute T The sum of the above gas laws: PV=nRT PV = nRT:  PV = nRT P=gas pressure V=volume a gas occupies n= number of moles of a gas R= gas constant T= absolute temperature in Kelvin(C - 273) Additional Gas Laws:  Additional Gas Laws Graham’s Law the rate of diffusion of a gas is 1/ to the square root of its molecular weight Henry’s Law the quantity of gas that can dissolve in a fluid is = to the partial P of the gas X the solubility coefficient Dalton’s Law of Partial Pressures the P exerted by a mixture of gases is =  of the individual (partial) P exerted by each gas Atmospheric Air vs. Alveolar Air:  Atmospheric Air vs. Alveolar Air H2O vapor 3.7 mmHg Oxygen 159 mmHg Nitrogen 597 mmHg CO2 .3 mmHg H2O vapor 47 mmHg Oxygen 104 mmHg Nitrogen 569 mmHg CO2 40 mmHg Diffusion across the respiratory membrane:  Diffusion across the respiratory membrane Temperature  Solubility  Cross-sectional area  sq root of molecular weight 1/  concentration gradient  distance 1/  Which of the above are properties of the gas? Relative Diffusion Coefficients:  Relative Diffusion Coefficients These coefficients represent how readily a particular gass will diffuse across the respiratory membrane & is  to its solubility and 1/ to sq. rt of MW. O2 1.0 CO2 20.3 CO 0.81 N2 0.53 He 0.95 Alveolar gas concentrations:  Alveolar gas concentrations [O2] in the alveoli averages 104 mmHg [CO2] in the alveoli averages 40 mmHg The respiratory unit:  The respiratory unit Consists of about 300 million alveoli Respiratory membrane 2 cell layers alveolar epithelium capillary endothelium averages about .6 microns in thickness total surface area 50-100 sq. meters 60-140 ml of pulmonary capillary blood Diffusing capacity of Respiratory Membrane:  Diffusing capacity of Respiratory Membrane Oxygen under resting conditions 21 ml.min/mmHg mean pressure gradient of 11 mmHg. 230 ml/min increases during exercise Carbon dioxide diffuses at least 20X more readily than oxygen Expired Air:  Expired Air As one expires a normal tidal volume of 500 ml the concentrations of oxygen and carbon dioxide change O2 falls from about 159 to 104 mmHg CO2 rises from O to 40 mmHg 1st 100 ml of expired air is from dead space last 250 ml of expired air is alveolar air Middle 150 ml of expired air is a mix Alveolar air turnover:  Alveolar air turnover Each normal breath (=tidal volume) turns over only a small percentage of the total alveolar air volume. 350/2150 Approximately 6-7 breaths for complete turnover of alveolar air. Slow turnover prevents large changes in gas concentration in alveoli from breath to breath Ventilation-Perfusion ratios:  Ventilation-Perfusion ratios Normally alveolar ventilation is matched to pulmonary capillary perfusion at a rate of 4L/min of air to 5L/min of blood 4/5 = .8 is the normal V/P ratio If the ratio decreases, it is usually due to a problem with decreased ventilation If the ration increases, it is usually due to a problem with decreased perfusion of lungs Ventilation-Perfusion ratios:  Ventilation-Perfusion ratios A decreased V/P ratio as ventilation goes to zero Alveolar PO2 will decrease to 40 mmHg Alveolar PCO2 will increase to 45 mmHg Results in an increase in “physiologic shunt blood”- blood that is not oxygenated as it passes the lung Ventilation-Perfusion ratios:  Ventilation-Perfusion ratios An increased V/P ratio due to a decreased perfusion of the lungs from the RV Alveolar PO2 will increase to 149 mmHg Alveolar PCO2 will decrease to O mmHg Results in an increase of physiologic dead space- area in the lungs where oxygenation is not taking place “includes non functional alveoli” Transport of O2 & CO2:  Transport of O2 & CO2 Oxygen- 5 ml/dl carried from lungs-tissue Dissolved-3% Bound to hemoglobin-97% increases carrying capacity 30-100 fold Carbon Dioxide- 4 ml/dl from tissue-lungs Dissolved-7% Bound to hemoglobin (and other proteins)-23% Bicarbinate ion-70% Oxygen:  Oxygen Carbon Dioxide:  Carbon Dioxide Blood pH:  Blood pH Arterial blood (Oxygenated) 7.41 Venous blood (Deoxygenated) 7.37 (slightly more acidic but buffered by blood buffers) In exercise venous blood can drop to 6.9 Respiratory exchange ratio:  Respiratory exchange ratio Ratio of CO2 output to O2 uptake R= 4/5=.8 What happens to Oxygen in the cells converted to carbon dioxide (80%) converted to water (20%) As fatty acid utilization for E increases the percentage of metabolic water generated from O2 increases to a maximum of 30%. If only CHO are used for energy no metabolic water is generated from O2, all O2 is converted to CO2 Oxy-Hemoglobin Dissociation:  Oxy-Hemoglobin Dissociation As Po2 , hemoglobin releases more oxygen Po2 = 95 mmHg  97% saturation (arterial) Po2 = 40 mmHg  70% saturation (venous) Sigmoid shaped curve with steep portion below a Po2 of 40 mmHg slight  in Po2  large release in O2 from Hgb Shift to the right (promote dissociation) increase temperature increase CO2 (Bohr effect) decrease pH increase 2,3 diphosphoglycerate (2,3 DPG) Carbon Dioxide:  Carbon Dioxide carried in form of bicarbinate ion (70%) CO2 + H2O  H2CO3  H+ + HCO3- carbonic anhydrase in RBC catalyses reaction of water and carbon dioxide carbonic acid dissociates into H+ & HCO3 - Chloride shift As HCO3- leaves RBC it is replaced by Cl - Bound to hemoglobin (23%) reacts with amine radicals of hemoglobin & other plasma proteins Dissolved CO2 (7%) Carbon Monoxide:  Carbon Monoxide Competes with oxygen for binding sites on Hemoglobin Has an affinity for hemoglobin (Hgb) 250 X that of oxygen Small partial pressures (Pco = .4 mmHg) of CO can decrease oxygen carrying capacity of Hgb by 50% Pco = .6 mmHg can be lethal Physiologic role of CO:  Physiologic role of CO Produced by the body in small quantities Functions Signaling molecule in nervous system Vasodilator Important role in immune, respiratory, GI, kidney, and liver systems Review paper Neural control of ventilation:  Neural control of ventilation Goals of regulation of ventilation is to keep arterial levels of O2 & CO2 constant The nervous system adjusts the level of ventilation (RR & TV) to match perfusion of the lungs (pulmonary blood flow) By matching ventilation with pulmonary blood flow (CO) we also match ventilation with overall metabolic demand Neural control of ventilation:  Neural control of ventilation Dorsal respiratory group located primarily in the nucleus tractus solitarius in medulla termination of CN IX & X receives input from peripheral chemoreceptors baroreceptors receptors in the lungs rhythmically self excitatory ramp signal excites muscles of inpiration Sets the basic drive of ventilation Neural control of ventilation:  Neural control of ventilation Pneumotaxic center dorsally in N. parabrachialis of upper pons inhibits the duration of inspiration by turning off DRG ramp signal after start of inspiration Ventral respiratory group of neurons located bilaterally in ventral aspect of medulla can + both inspiratory & expiratory respiratory muscles during increased ventilatory drive Apneustic center (lower pons) functions to prevent inhibition of DRG under some circumstances Neural Control of Ventilation:  Neural Control of Ventilation Herring-Breuer Inflation reflex stretch receptors located in wall of airways + when stretched at tidal volumes > 1500 ml inhibits the DRG Irritant receptors-among airway epithethium +  sneezing & coughing & possibly airway constriction J receptors - in alveoli next to pulmonary caps + when pulmonary caps are engorged or pulmonary edema create a feeling of dyspnea Chemical Control of Ventilation:  Chemical Control of Ventilation Chemosensitive area of respiratory center Hydrogen ions-primary stimulus but can’t cross membranes (blood brain barrier-BBB) carbon dioxide-can cross BBB inside cell converted to H+ rises of CO2 in CSF- effect on + ventilation faster due to lack of buffers compared to plasma unresponsive to falls in oxygen-hypoxia depresses neuronal activity 70-80 % of CO2 induced increase in vent. Chemical Control of Ventilation:  Chemical Control of Ventilation Peripheral Chemoreceptors aortic and carotid bodies 20-30% of CO2 induced increase in vent. Responsive to hypoxia response to hypoxia is blunted if CO2 falls as the oxygen levels fall responsive to slight rises in CO2 (2-3 mmHg) but not similar falls in O2 sensitivity altered by CNS SNS decreasing flow-increased sensitivity to hypoxia Pathophysilogic consequences of hyperventilation:  Pathophysilogic consequences of hyperventilation SV & CO decreased Coronary blood flow decreased Repolarization of heart impaired Oxyhemoglobin affinity increased Cerebral blood flow decreased Skeletal muscle spasm & tetany Serum potassium decreased Other effect on ventilation:  Other effect on ventilation Effect of brain edema depression or inactivation of respiratory centers use of intravenous hypertonic solution (e.g. mannitol) to treat Effect of Anesthesia/Narcotics most prevalent cause of respiratory depression sodium pentobarbital morphine Stimulation of ventilation during exercise:  Stimulation of ventilation during exercise Increased corticospinal traffic which will collaterally stimulate respiratory centers in the brain stem reflex neural signals from active muscle spindles and joint proprioceptors fluctuations in O2 and CO2 levels in active muscle stimulating local chemoreceptors Respiratory adjustments at birth:  Respiratory adjustments at birth Most important adjustment is to breath normally occurs within seconds stimulated by: cooling of skin slightly asphyxiated state (elevated CO2) 40-60 mmHg of negative pleural P necessary to open alveoli on first breath Circulatory changes at birth:  Circulatory changes at birth Placenta disconnects TPR increases Pulmonic resistance decreases (elimination of hypoxia) Closure of foramen ovale (atria) Closure of ductus arteriosis (great vessels) Closure of ductus venosus (bypass liver) Effect of altitude on barometric P:  Effect of altitude on barometric P As one ascends the barometric P (bP)  PO2 = (.21) (barometric P) the fractional [O2] in air doesn’t  with altitude As bP  so does PO2 (alt  bP  PO2) 0 ft.  760 mmHg. 159 mmHg. 10,000 ft.  523 mmHg. 110 mmHg. 20,000 ft.  349 mmHg. 73 mmHg. 30,000 ft.  226 mmHg. 47 mmHg. 40,000 ft.  141 mmHg  29 mmHg. At 63,000 ft. the bP is 47 mmHg. & blood “boils” Acute effects of ascending to great heights:  Acute effects of ascending to great heights Unacclimatized person suffers deterioration of nervous system function effects due primarily to hypoxia sleepiness, false sense of well being, impaired judgement , clumsiness, blunted pain perception,  visual acuity, tremors, twitching, seizures Acute mountain sickness (onset hours - 2 d) cerebral edema hypoxia + local vasodilatation pulmonary edema  hypoxia + local vasoconst. Exposure to low PO2:  Exposure to low PO2 Hypoxic stimulation of arterial chemoreceptors (1.65 X) immediately decreased CO2 limits  After several days ventilation  5X as inhibition fades  HCO3   pH  + chemosensitive area of brainstem Chronic Mountain Sickness:  Chronic Mountain Sickness Red cell mass (Hct)   pulmonary arterial BP enlarged right ventricle  total peripheral resistance congestive heart failure death if person is not removed to lower altitude Acclimatization:  Acclimatization Great  in pulmonary ventilation  RBC (Hct)  diffusing capacity of the lungs  tissue vascularity ( capillary density)  ability of tissues to use O2 slight  cell mitochondria (animals) slight  cellular oxidative systems (animals) Natural Acclimatization:  Natural Acclimatization Humans living at altitudes > 13,000 ft in the Andes & Himalayas Acclimatization begins in infancy chest to body ratio  high ratio of ventilatory capacity to body mass increased size of right ventricle shift in oxy-hemoglobin dissociation curve PO2 of 40 have greater O2 in blood than lowlanders at 95 Work capacity greater than even well acclimatized lowlanders at high altitudes (17,000 ft) (87% vs. 68%) Dead Space:  Dead Space Area where gas exchange cannot occur Includes most of airway volume Anatomical dead space (=150 ml) Physiologic dead space =anatomical + non functional alveoli FRC (2300 ml) –dead space (150 ml) = 2150 ml (alveolar volume At the end of a normal expiration most of the air left in the lungs is in the alveoli The lung as an organ of metabolism:  The lung as an organ of metabolism As an organ of body metabolism the lung ranks second behind the liver One advantage the lung has over the liver is the fact that all blood passes through the lungs with every complete cycle Some examples Angiotensin I converted to Angiotensin II Prostaglandins inactivated in one pass through pulmonary circulation Defenses of the Respiratory System:  Defenses of the Respiratory System Defenses of Respiratory System:  Defenses of Respiratory System Respiratory membrane represents a major source of contact with the environment with a separation of .5 mircrons between the air & the blood over a surface area of 50-100 sq. meters The average adult inhales about 10000 L air/day Inert dust Particulate matter Plant & animal Gases Fossil fuel combustion Infectious agents Viruses & bacteria Defense Mechanisms:  Defense Mechanisms Protect tracheobronchial tree & alveoli from injury Prevent accumulation of secretions Repair Depression of Defense Mechanisms:  Depression of Defense Mechanisms Chronic alcohol is associated with an increase incidence of bacterial infections Cigarette smoke and air pollutants is associated with an increase incidence of chronic bronchitis and emphysema Occupational irritants is associated with and increased incidence of hyperactive airways or interstitial pulmonary fibrosis Upper respiratory tract:  Upper respiratory tract Nasal passages protect airways and alveolar structures from inhaled foreign materials Long hairs (vibrassae) in nose (nares) filters out larger particles Mucous coating the nasal mucous membranes traps particles (>10 microns) Moisten air – 650 ml H2O/day Nasal turbinates Highly vascularized, act as radiators to warm air Cough:  Cough Cough From trachea to alveoli sensitive to irritants Afferents utilize primarily CN X Process 2.5 L of air rapidly inspired Epiglottis closes and vocal chords close tightly muscles of expiration contract forcefully which causes pressure in lungs to rise to 100 mm Hg Epiglottis and vocal chords open widely which results in explosive outpouring of air to clear larger airways at speeds of 75 – 100 MPH Sneeze:  Sneeze Sneeze reflex Associated with nasal passages Irritation sends signal over CN V to the medulla Response similar to cough, but in addition uvula is depressed so large amounts of air pass rapidly through the nose to clear nasal passages With sneeze and cough velocity of air escaping from the mouth & nose has been clocked at speeds of 75-100 MPH Mucociliary elevator:  Mucociliary elevator Clears smaller airways Mucous produced by globlet cells in epithelium and small submucosal glands Ciliated epithelium which lines the respiratory tract all the way down to the terminal bronchioles moves the mucous to the pharynx Beat 1000 X/minute Mucous flows at about speed of 1 cm/min Swallowed or coughed out Immune reaction in the lung:  Immune reaction in the lung Alveolar macrophages Capable of phagocytosing intraluminal particles Antibodies associated with the mucosa IgG- lower respiratory tract IgA- dominate in upper respiratory tract IgE- predominantly a mucosal antibody

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