Respiratory System Notes
Respiratory System Notes BIOL 2510 - 001
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This 7 page Class Notes was uploaded by Ashley Barranco on Friday February 19, 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 58 views. For similar materials see Human Anatomy & Physiology II in Anatomy at Auburn University.
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Date Created: 02/19/16
Functions of Respiratory system Ch 22 Thoracic Cavity Pressures Fluid level must be kept at a minimum Excess fluid pumped out by lymphatic system If fluid accumulates, positive Pip pressure develops Lung collapse Intrapulmonary pressure (Ppul) pressure in alveoli decrease during inspiration, increase during expiration always equalize with atmospheric pressure 760 mmHG Intrapleural pressure (Pip) pressure in the pleural cavity always negative relative to intraspulmonary pressure more negative as thoracic cavity volume increases during inspiration 756 mmHg ( 4 mmHG) Transpulmonary pressure Ppul Pip determines size of lungs at a given time 760 mmHG – 756 mmHg (from diagram on slides) Atmospheric Pressure Pressure exerted by air surrounding the body 76 mmHG at sea level = 1 atmosphere Respiratory pressure described relative to P atm Negative respiratory pressure= les than P atm Positive respiratory pressure = greater than P atm Zero respiratory pressure= P atm Pulmonary Ventilation: Boyles’s Law Boyles law: P1V1 P2V2 If volume decreases, pressure increases If volume increases, pressure decreases Mechanics of Breathing: Inspiration Inspiratory muscles (external intercostals and diaphragm) contract diaphragm down rib cage and out Thoracic cavity volume increases intrapleural pressures drops Lungs are stretched intrapulmonary volumes rises Intrapulmonary pressure drops Air flow into lungs: Down its pressure gradient until intrapulmonary pressure= atmospheric pressure Mechanics of breathing: expiration Inspiratory muscles (external intercostal and diaphragm) relax diaphragm up rib cage down and in Thoracic cavity volume decreases intrapleural pressure rises Elastic lungs recoil intrapulmonary volume drops Intrapulmonary pressure rises Air flow is out of lungs down its pressure gradient until intrapulmonary pressure=atmospheric pressure Forced expiration: contraction of abs and internal intercostal push air out Pneumothorax Presence of air in pleural cavity Treatment Respiratory volumes Tidal volume(TV) : volume of air in and out of lungs during normal quiet breathing Inspiratory reserve volume (IRV) : volume of air that can be inspired forcibly beyond tidal volume Expiratory reserve volume (ERV): volume of air that can be expired forcibly beyond tidal volume Residual volume (RV) volume left in lungs after forced expiration Minute ventilation total volume of air that flows in and out of respiratory system per minute 6 liters/min during normal quiet breathing Respiratory volumes and capacities Inspiratory capacity: total volume of air that can be inspired after a normal expiration ( TV+ IRV) Functional residual capacity (FRC) volume of air left in lung after normal expiration (ERV + RV) Respiratory capacities combination of respiratory volumes Vital capacity (VC) total volume of exchangeable air (IC + ERV) Total lung capacity (TLC) total volume of air the lungs can hold (IC + FRC) TLC= sum of all lung volumes Assessing ventilation Several respiratory volumes can be used to asses status Respiratory volumes can be combined to calculate respiratory capacities, which can give info on a persons respiratory status Respiratory volumes and capacities are usually abnormal in people with pulmonary disorders Spirometer: original cumbersome clinical too; used to measure patients Anatomical dead space Anatmonical dead space: volume of air in conducting zone – 150 ml Alveolar ventilation rate (AVR) = respiration rate * (TV dead space) total amount of fresh air that flows in and out of the respiratory system in 1 min Some inspired air remains in conducting zone doesn’t make it to alveoli for gas exchange Anatomical dead space = 150 ml does not contribute to gas exchange consists of air that remains in passageways 150 ml out of 500 ml TV Alveolar dead space: space occupied by nonfunctional alveoli can be due to collapse or obstruction Total dead space: sum of anatomical and alevelor dead space Gas exchange Gas exchange occurs between lungs and blood as well as blood and tissues External respiration: diffusion of gases between blood and lungs Internal respiration: diffusion of gases between blood and tissues Both processes are subject to: basic properties of gases composition of alveolar gas Basic Properties of Gases Daltons law of partial pressures total pressure exerted by mixture of gases is equal to sum of pressures exerted by each gas Partial pressure: pressure exerted by each gas in mixture. Directly proportional to its percentage in mixture Total atmospheric pressure equals 760 mmHG Nitrogen makes up 78.6% of air; therefore, partial pressure of nitrogen, PN2, can be calculated by: 0.786 x 760 mmHG = 597 mmHG due to N2 Oxygen make sup 20.9% of air, so PO2 equals: 0.209 x 760 mmHG = 159 mmHG Partial Pressure Gradient Gas exchange at pulmonary and systemic capillaries is via passive diffusion of O2 and CO2 due to PPG partial pressure: individual pressure exerted by a particular gas within a mixture of gases (PO2 and PCO2) PPG occurs when the PP of a gas differs across a membrane A gas will always diffuse from a higher PP to a lower PP Basic Properties of gases Air also contains 0.04% CO2 and 0.5% water vapor, and insignificant amounts of other gases At high altitudes (under water), partial pressures increase significantly Henry’s Law for gas mixture in contact with liquids: each gas will dissolve in the liquid in proportion to its partial pressure At equilibrium, partial pressure in the 2 phases will be equal amount of each gas that will dissolve depends on: Solubility and temp Solubility: CO2 is 20X more soluble in water than O2 and little N2 will dissolve Temperature: as temp of liquid rises, solubility decreases Example of Henry’s Law: hyperbaric chambers External Respiration External respiration (pulmonary gas exchange) involves the exchange of O2 and CO2 across respiratory membranes Exchange is influenced by: Partial pressure gradients and gas solubility’s thickness and surface area of respiratory membrane Ventilationperfusion coupling: matching of alveolar ventilation with pulmonary blood perfusion Partial pressure gradients and gas solubility’s steep partial pressures gradient for O2 exists between blood and lungs venous blood PO2 = 40 mmHG alveolar PO2= 104 mmHG drives oxygen flow into blood equilibrium is reached across respiratory membrane in about 0.25 seconds, but it takes RBC about .75 seconds to travel from start to end of pulmonary capillary ensures adequate oxygenation even if blood flow increases 3X Partial pressure gradient for CO2 is less teep venous blood PCO2 = 45 mmHG alveolar PCO2 = 40 mmHg Through gradient is not as steep, CO@ still diffuses in equal amounts with oxygen reasons is that CO2 is 20 X more soluble in plasma and alveolar fluid than oxygen Properties of Gases Dalton’s Law Dalton’s Law air pressure is the sum of partial pressure of all gases present. Partial pressure= % of gas in mixture X total air pressure 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 ( on slide 31) Ventilation and Perfusion Ventilation the amount of gas reaching alveoli Perfusion the blood flow in pulmonary capillaries Local control PCO2 controals ventilation by changing diameter of bronchioles: bronchiolar diameter bronchioles leading to alveoli with high CO2 = bronchodilation Low CO2= bronchoconstriction PO2 controls perfusion by changing diameter of artery: arteriolar diameter high O2= vasodilation )increased blood flow into pulmonary capillaries) low O2=vasoconstriction )shunt blood to other areas where PO2 higher PPG and gas exchange Internal respiration: depends on metabolic activity of the tissue Partial pressure of gases in alveoli doesn’t match that of inspired air because of dead space. At any given time the air in alveoli is a mix of old and new air Po2 in pulmonary veins 100 mmHG whereas in alveoli are 104 mmHg because ventilationperfusion coupling not perfect at every alveolus Transport of respiratory gases O2 is transported in blood 2 ways 1.5% is dissolved in plasma 98.5% bound to hemoglobin oxyhemoglobin: hemoglobin + bound O2 deoxyhemoglobin: hemoglobin without bound O2 OxygenHemoglobin dissociation curve Each hemoglobin can bind 4 O2 Once the first O2 is bound, it is easier for the 2 , 3 , and 4 to bind, i.e affinity (binding strength) of hemoglobin to O@ changes with oxygen saturation OxygenHemoglobin dissociation curve: shows relationship between hemoglobin saturation and blood PO2 Key PO2 to remember 100 mmHG= PO2 of lungs 40 mmHG= PO2 of resting tissue 20 mmHG= PO2 of exercising tissues Oxygenhemoglobin is not linear relationship because affinity of hemoglobin for O2 changes with O2 binding At lower PO2, less O2 bound to hemoglobin At higher PO2, more and more O2 is bound to hemoglobin Around PO2 of 70 mmHg, hemoglobin is almost completely saturated, so greater increase in PO2 doesn’t result in much more O2 binding and O2 unloading to tissues lowest here Oxygen dissociation Steep slope in middle is due to change in hemoglobin affinity as more O2 molecules bind Plateau around PO2 of 70 mmHg so hemoglobin saturation relatively unaffected until Po2 is below 70 mmHg With tissues that are more active the arterial blood leaving lungs –PO2 = 100 mmHG: at this PO2 hemoglobin is highly saturated In tissues at rest, PO2 around 40 mmHg hemoglobin around 75% saturated meaning 25% been unloaded to tissues In exercising tissue PO2 can be around 20 mmHg only 25% hemoglobin saturated so 75% has been unloaded to tissues Factors that alter the oxygen dissociation curve are: temp blood pH PCO2 Lower temps shift curve to the left. Higher affinity of Hb for O2 Higher temps shift curve to the right. Lower affinity of Hb for O2 Bohr Effect Lower blood pH, higher PCO2 such as occurs in highly metabolically active cells. Reduce hemoglobin affinity for O2 so higher O2 unloading to tissues that need it Higher blood pH, higher CO2 levels= curve shifts to the left= decrease affinity of hemoglobin for O2 Lower blood pH, higher CO2 levels= curve shifts to left=decrease affinity of hemoglobin for O2 CO2 Transport Transported in blood in 3 ways 10% dissolved in plasma 20% bound to hemoglobin ( carbaminohemoglobin – hemoglobin + bound CO2) 70% as bicarbonate ions from CO2 reaction CO2 Transport impairments hyperventilation: breathing exceeding metabolic needs which causes low PCO2, lower H+, respiratory alkalosis (blood pH too basic) hypoventilation: breathing not meeting metabolic needs which causes high PCO@, higher H+, respiratory acidosis (blood pH too acidic) Neural Control of Respiration Respiratory centers in medulla dorsal respiratory group= integrate input from peripheral stretch and chemoreceptors= relay to VRG ventral respiratory group= control rhythm of respiration. Inspiration: impulses via phrenic nerve to diaphragm and intercostals. Expiration: stop impulses= muscles relax and lungs passively recoil Chemoreceptors central chemoreceptors: throughout brainstem peripheral chemoreceptors aortic arch and carotid sinus respond to changes in PCO2, H+ and PO2 high PCO2 and H+ stimulate chemoreceptors resulting in increase respiratory rate and depth Pulmonary disease and disorders Pneumonia inflammation of and fluid accumulation in alveoli cough acute chest pain, fever, green or yellow septum viral, bacterial, fungal or parasitic infections Asthma inflammation of airways shortness of breath, wheezing, coughing causes: genetics, exercise, cold air, allergens treatments: inhalers containing steroids reduces swelling COPD chronic obstructive pulmonary diseases difficulty breathing, hypoventilation, coughing, pulmonary infections treatment: inhalers containing steroids or bronchodilators Chronic bronchitis excessive music production, inflammation of airways emphysema destruction of alveoli
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