Respiratory System Notes
Respiratory System Notes BIOL 2510 - 001
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This 12 page Class Notes was uploaded by Brooke Polinsky on Saturday February 27, 2016. The Class Notes belongs to BIOL 2510 - 001 at Auburn University taught by Dr. Shobnom Ferdous in Spring 2016. Since its upload, it has received 24 views. For similar materials see Human Anatomy & Physiology II in Anatomy at Auburn University.
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Date Created: 02/27/16
The Rest of the Respiratory System: 1. Thoracic Cavity Pressures A. Intrapulmonary pressure (Ppul) a. pressure in the alveoli b. decrease during inspiration, increase during expiration c. Always equalize with atmospheric pressure B. Intraplueral pressure (Pip) a. pressure in plueral cavity b. always negative relative to intrapulmonary pressure c. more negative as thoracic cavity volume increases during inspiration C. Transpulmonary Pressure a. Calculate it by: Ppul-Pip b. determines size of lungs at any given time 2. Pulmonary Ventilation and its relationship to Boyles Law A. Boyle Law: P1V1=P2V2 B. If volume decreases, pressure increases C. If volume increases, pressure decreases 3. Mechanics of Breathing A. Inspiration: a. Inspiratory muscles (external intercostals and diaphragm) contract 1. Diaphragm down 2. Rib cage up and out b. thoracic cavity volume increases 1. intraplueral pressure drops c. Lungs are stretched 1. Intrapulmonary Volume Rises d. Intrapulmonary pressure drops e. Air ﬂow to lungs: down its pressure gradient until intrapulmonary pressure= atmospheric pressure B. Expiration: a. Inspiratory muscles (external intercostals and diaphragm) relax 1. diaphragm up 2. rib cage down and in b. Thoracic cavity volume decreases 1. intrapleural pressure rises c. Elastic lungs recoil passively 1. intrapulmonary volume drops d. Intrapulmonary pressure rises e. Air ﬂow to lungs: down its pressure gradient until intrapulmonary pressure= atmospheric pressure f. Forced Expiration= contraction of abs and internal intercostals push air out 4. Pnuemothorax= presence of air in pleural cavity; abnormal amount of air in the pleural space that causes an uncoupling of the lung from the chest wall A. disease 5. Respiratory Volumes A. Tidal Volume= volume of air in and out of lungs during normal quiet breathing B. Inspiratory reserve volume (IRV)= volume of air that can be inspired forcibly beyond tidal volume C. Expiratory reserve volume (ERV)= volume of air that can be expired forcibly beyond tidal volume D. Residual Volume (RV)= volume left in lungs after forced expiration E. Be able to ﬁll out this chart 6. Respiratory Capacities= combinations of respiratory volumes A. Inspired capacity (IC)= total volume of air that can be inspired after a normal expiration a. TV+IRV= combination of tidal volume and inspiratory reserve volume B. Functional residual capacity (FRC)= volume of air left in lung after normal expiration a. ERV+RV= combination of expiratory reserve volume and residual volume C. Vital Capacity(VC)= total exchange of exchangeable air a. IC+ERV= combination of inspiratory capacity and expiatory reserve volume D. Total lung capacity (TLC)= total volume of air the lungs can hold a. IC+FRC= combination of inspiratory capacity and functional residual capacity b. Sum of all lung volumes E. Minute Ventilation= total volume of air that ﬂows in and out of respiratory system per minute a. 6 L/min during quiet breathing 7. Anatomical Dead Space= volume of air in conducting zone A. some inspired air remains in conducting zone and does't make it to alveoli for gas exchange B. alveolar ventilation rate= better measure of eﬀective ventilation than minute ventilation b/c accounts for the dead space a. Respiration rate* (TV-dead space) b. total amount of fresh air that ﬂows in and out of the the respiratory system in 1 min 8. Divisions of Respiratory System A. Respiratory zone= actual of gas exchange; bronchioles, alveoli, alveolar ducts B. Conducting zone= all respiratory passageways leading to and including terminal bronchioles 9. Three types of dead space: A. Anatomical Dead Space= does not contribute to gas exchange a. consists of air that remains in passageways b. 150 ml B. Alveolar dead space= space occupied by nonfunctional alveoli a. can be due to collapse or obstruction C. Total Dead Space= sum of anatomical and alveolar space 10. Gas Exchange A. occurs between lungs and blood as well as blood and tissues B. External respiration= diﬀusion of gases between blood and lungs C. Internal Respiration= diﬀusion of gases between blood and tissues D. Both processes are subjected to: basic properties of gases and composition of alveolar gas 11. Basic Properties of Gases A. Dalton's law of partial pressures a. total pressure exerted by mixture of gases is equal to sum of pressures exerted by each gas b. Partial Pressure 1. pressure exerted by gas in mixture 2. directly proportional to its percentage in mixture B. Total atmospheric pressure equals 760 mmHg a. Nitrogen makes up 78.6%, therefore partial pressure of nitrogen is: 1. 0.786 x 760 mmHg= 597 mmHg due to N2 b. Oxygen makes up 20.9% of air, so partial pressure is: 1. 0.209 x 760 mmHg= 159 mmHg c. REMBER THESE CALCULATIONS!!!! C. Partial Pressure Gradient a. gas pulmonary and systemic capillaries is via passive diﬀusion of O2 and CO2 due to PPG 1. partial pressure= individual pressure exerted by a particular gas within a mixture of gases (PO2 and PCO2) 2. PPG- occurs when the PP of a gas diﬀers across a membrane 3. A GAS WILL ALWAYS DIFFUSE FROM A HIGHER PP TO A LOWER PP!!! D. At high altitudes, partial pressure declines, but at lower altitudes (under water), partial pressures increase signiﬁcantly E. Henry's Law a. For gas mixtures in contact liquids: 1. Each gas will dissolve in the liquid proportion to its partial pressure 2. At equilibrium, partial pressures in the two phases will be equal 3. Amount of each gas that will dissolve depends on: A. Solubility= CO2 is 20x soluble in water than O2, and little N2 will dissolve B. Temperature= as temp of liquid rises, solubility decreases b. Example of Henry's Law: hyperbaric chambers F. External Respiration (pulmonary gas exchange) a. involves the exchange of O2 and CO2 across respiratory membranes b. Exchange is inﬂuenced by: 1. partial pressure gradients and gas solubilities A. steep partial pressure gradient for O2 exists between blood and lungs a. MEMORIZE THESE BELOW: b. Venous blood partial pressure= 40 mmHg c. Alveolar partial pressure= 104 mmHg 1. drives oxygen ﬂow into blood 2. equilibrium is reached across respiratory membrane 3. ensures adequate oxygenation even if blood ﬂow increases 3x B. Partial Pressure gradient for CO2 is less steep: a. venous blood partial pressure= 45 mmHg b. alveolar partial pressure= 40mmHg C. Though gradient is not as steep, Co2, still diﬀuses in equal amounts with oxygen a. reason is that CO2 is 20x more soluble in plasma and alveolar ﬂuid than oxygen 2. thickness and surface area of respiratory membrane 3. Ventilation-perfusion coupling= matching of alveolar ventilation with pulmonary blood perfusion G. Dalton's Law a. air pressure is the sum of the partial pressure of all gases present b. partial pressure= % of gas in mixture x total air pressure c. as long as oxygen is more concentrated( higher PP) outside and CO2 is more concentrated (higher PP) inside, the gases will diﬀuse in the directions shown in the diagram 1. Oxygen goes into blood and carbon dioxide goes into the alveolus H. Ventilation and Perfusion a. ventilation= amount of gas reaching alveoli b. perfusion= the blood ﬂow in pulmonary capillaries c. local control 1. PCO2 controls ventilation by changing diameter of bronchioles: bronchiolar diameter A. bronchioles leading to the alveoli with high CO2--> bronchodilation B. Low CO2--> bronchoconstriction 2. PO2 controls perfusion by changing diameter of artery: arteriolar diameter A. High O2----> vasodilation (increased blood ﬂow into pulmonary capillaries) B. Low O2---> vasoconstriction (shunt blood to other areas where PO2 higher) I. Partial pressure of gases in alveoli doesn't match that of inspired air because o dead space. At any given time air in the alveoli mix of old and new air J. PO2 in pulmonary veins 100 mmHg where as in alveoli are 104 mmHg because ventilation-perfusion coupling not perfect at every alveolus 12. Transport of Respiratory Gases A. O2 Transport a. Transport blood in 2 ways: 1. 1.5% dissolved in plans 2. 98.5% bound to Hemoglobin A. Oxyhemoglobin= hemoglobin + bound O2 B. Deoxyhemoglobin= hemoglobin w/o bound O2 b. Oxygen-hemoglobin dissociation curve= visual description of relationship b/t Hemoglobin saturation and blood of PO2 1. Each Hb can bind 4 O2 A. When ﬁrst O2 binds, it changes shape of Hb which increases its aﬃnity of Hb for more O2. Saturation refers to having bound O2. B. Partially saturated is bound to 1, 2, or 3, O2 molecules C. Fully saturated if bound to four O2 molecules D. Once the ﬁrst O2 is bound, it easier for the 2nd, 3rd, 4th, to bind. Aﬃnity (binding strength) of Hb to O2 changes with oxygen saturation a. same is true for unloading, after 1st O2 unloads, easier for others to follow E. Oxygen-Hb dissociation curve a. shows relationship between Hb saturation nd blood PO2 F. Key PO2 to remember a. 100 mmHg= PO2 of lungs b. 40 mmHg= PO2 of resting tissues c. 20 mmHg= PO2 of exercising tissues G. Not a linear relationship because aﬃnity of Hb for O2 changes with O2 binding H. At lower PO2, less O2 bound to Hb (high rate of dissociation) I. At higher PO2, more and more O2 bound to Hb J. Around PO2 of 70 mmHg Hb is almost completely saturated SO GREATER INCREASE IN PO2 DOESN'T RESULT IN MUCH MORE O2 BINDING (and O2 unloading to tissue is lowest here) Diagram below describes these trends A. Steep slope in the middle is due to change in Hb aﬃnity as more O2 molecules bind B. Plateau around PO2 of 70 mmHg so Hb saturation is relatively unaﬀected until Po2 is below 70 mmHg a. Another way to word this: If PO2 of inspired air is below typical- loading and unloading of O2 is still adequate C. When arterial blood is leaving lungs, PO2 is 100 mmHg. At this PO2 Hb highly saturated D. In tissues at rest PO2 is around 40 mmHg. Hb is about 75% saturated, which means that 25% has been unloaded to tissues E. In exercising tissues, PO2 can be around 20 mmHg. Only 25% of Hb is saturated, so 75% has been unloaded to tissues F. What factors alter the curve? a. Temperature, blood pH, and PCO2 b. Right shift, which is decreasing aﬃnity, is caused by low pH, high CO2 (because CO2 binds to Hb and makes carbomino Hb) and high temperature. c. If curve is shifted to the left, Hb aﬃnity increases for O2 and less is unloaded to tissues. If curve is shifted to the right, Hb aﬃnity for O2 is lower and more tissue is unloaded. d. Eﬀect of temperature 1. Lower temperature shift the curve to the left. Higher aﬃnity of Hb for O2 2. Higher temperatures shift curve to the right. Lower aﬃnity of Hb for O2. 3. Purple line is normal body temperature is the point of diﬀerence in % saturation at PO2 (of resting tissues) at diﬀerent temperatures. e. Eﬀect of PCO2 and ph: Bohr eﬀect 1. Bohr eﬀect= lower ph, higher PCO2 (occurs in highly metabolically active cells) reduce Hb aﬃnity for )2, so higher O2 unloading tissues that need it A. higher blood ph, lower Co2 than normal arterial levels, this shifts curve to the left and its an increase in aﬃnity of Hb for O2 A. CO2 Transport a. transports blood in 3 ways 1. 10% dissolved in plasma 2. 20% bound to Hb A. carbaminohemoglobin= Hb + bound CO2 3. 70% as bicarbonate ions formed from CO2 reaction b. CO2 binding/unbinding from Hb inﬂuenced by PCO2 and degree of Hb oxygenation 1. Ex: in lungs, PCO2 of blood is higher than air so CO2 dissociates from Hb 2. Ex: in Tissues, PCO2 of tissues are higher than blood, so CO2 will load onto Hb 3. As bicarbonate ions: Co2 diﬀuses into RBC, combines with H2O forming carbonic acid which dissociates into H+ and bicarbonate Ion (HCO3-) A. reaction happens faster in RBC than plasma because of carbonic anhydrase (enzyme) c. Occurs primarily in RBCs where the enzyme carbonic anhydrase reversibly and rapidly catalyzes this reaction d. In systemic capillaries, after HCO3- is created, it quickly diﬀuses from RBCs into plasma e. Outrush of HCO3- from RBCs is balanced as Cl- move into RBCs from plasma 1. this is referred to as chloride shift f. Top panel at tissues: 1. At tissues CO2 diﬀuse from tissue into systemic capillaries 2. CO2 Dissolve in plasma- transported to lungs 3. CO2 undergoes bicarbonate reaction in plasma that produces bicarbonate ions. This is slow because there are no carbonic anhydrase g. Bottom panel tissues: opposite of top panels h. Transport Impairments: 1. hyperventilation A. breathing exceeding metabolic needs B. causes low PCO2, lower H+, respiratory alkalosis (blood ph too basic/high) C. increase rate/depth breathing; exceeds body's needs to remove CO2 2. Hypoventilation A. breathing not meeting metabolic needs B. causes high PCO2, higher H+, respiratory acidosis (blood pH too acidic/low) C. decrease rate/depth of breathing; breathing does not meet body's metabolic needs i. Factors that inﬂuence breathing rate and depth 1. most potent and most closely controlled 2. If blood PCO2 levels rise (hypercapnia), CO2 accumulates in the brain and joins with water to become carbonic acid 3. Carbonic acid dissociates, releasing H+, causing a drop in pH (increased acidity) 4. Increased H+ stimulates central chemoreceptors of brain stem, which synapse with respiratory regulatory centers 5. respiratory centers increase depth and rate of breathing, which act to lower blood PCO2, and pH rise to normal levels j. Inﬂuence of PCO2 1. If blood PCO2 levels decrease, respiration becomes slow and shallow 2. Apena: breathing cessation that may occur when PCO2 levels drop abnormally low 3. Swimmers sometimes voluntarily hyperventilate to enable them to hold their breath for longer 4. Causes a drop in PCO2, which causes a delay in respiration, as PCO2 levels need to be built back up 5. Can cause dangerous drops in PO2 levels B. Neural Control of Respiration a. Respiratory centers in medulla 1. Dorsal Respiratory Group (DRG) A. integrate input from peripheral stretch and chemoreceptors relay to VRG B. Still a lot we don't know about DRG 2. Ventral Respiratory group (VRG) A. control rhythm of respiration B. Inspiration: impulses via phrenic nerves to diaphragm and intercostal nerves to external intercostals C. Expiration: stop impulses that cause muscles to relax and lungs passively recoil b. Respiratory Centers in the Pons 1. Pontine Respiratory Group A. transmits impulses to VRG to ﬁne tune breathing rhythms c. Chemoreceptors 1. central chemoreceptors= throughout the brainstem 2. peripheral chemoreceptors= aortic arch and carotid sinus 3. Respond to changes in PCO2, H+ and PO2 4. High PCO2 and H+ stimulate chkmrecptors resulting in increase in respiratory rate and depth 5. Only respond to very low levels of O2 C. Pulmonary Diseases and disorders a. Pneumonia- inﬂammation of ﬂuid accumulation in alveoli 1. cough, acute chest pain, fever, green or yellow septum 2. viral, bacterial, fungal, or parasitic infections 3. reduces gas exchange and may have ﬂuid build up in serous membranes b. Asthma- inﬂammation of airways 1. shortness of breath, wheezing, coughing 2. causes: genetic, exercise, cold air, allergens 3. treatment: inhalers containing steroids- reduce swelling 4. increased airway resistance and decreases airway ventilation c. COPD- Chronic Obstructive Pulmonary Diseases 1. diﬃculty breathing, hypoventilation, coughing, pulmonary infections 2. Treatment: inhalers containing steroids or bronchodilators 3. Chronic Bronchitis= excessive mucus production, inﬂammation of airways A. inhaled irritants and produce more mucus; impedes ventilation and gas exchange 4. Emphysema= destruction fo alveoli A. reduce surface area for gas exchange and lungs lose elasticity D. Internal Respiration a. involves capillary gas exchange in body tissues b. partial pressures and diﬀusion gradients are reversed compared to external respiration c. tissue PO2 is always lower then arterial blood PO2 (oxygen pressure) (40 vs. 100 mmHg), so oxygen moves from blood to tissues d. tissue PCO2 is always higher then arterial PCO@ (45 vs. 40mmHg), so Co2 moves from tissues into blood e. venous blood returning to heart has PO2 of 40 mmHg and PCO2 of 45 mmHg E. High Altitudes a. Quick travel to altitudes above 2400 meters may trigger symptoms of acute mountain sickness 1. atmospheric pressure and PO2 levels are lower at high elevations 2. symptoms: dizziness, headaches, shortness of breath, nausea 3. in severe cases, lethal cerebral and pulmonary edema may occur b. Acclimatization= respiratory and hematopoietic adjustments are made with long-term moves to high altitudes 1. chemoreceptors become more responsive to PCO2 when PO2 declines 2. substantial decline in PO2 directly stimulates peripheral chemoreceptors 3. results in an increase in minute ventilation that stabilize in few days to 2-3 L/min higher than at sea level
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