Warning:
JavaScript is turned OFF. None of the links on this page will work until it is reactivated.
If you need help turning JavaScript On, click here.
The Concept Map you are trying to access has information related to:
Respiratory Physiology, Elastic work(compliance)-60-66% total work Recoil Pressure due to: 50/50 in normal vent. high volumes-surface tension more imp't Lung elasticity-lung inflated by mm., then recoil -in connective fiber support system -weave of: coll-stretch 102%, elastin 115% -parenchyma stretchier than v. pleura -fibrosis/emphysema decrease stretch Surface Tension: air-liquid interface in alveoli -to shrink interface as much as possible -contributes as much pressure as CT weave (Von Neergaard expts) Alveoli Surfactant: phosphatidylglycerol, dipamityl phosphatidylcholine(lecithin) -secreted by Alveolar Type II cells -release stim'd by beta-adren. agonists, increased tidal volume -recirculated into Type IIs, then out -keeps alveoli "dry", Respiratory Physiology Histology Bilateral-2 Left lobes, 3 right lobes Most of weight for gas exchange CT support system- axial fiber system-starts at hilum periph fiber sys-starts at visc. pleura -surounds lobes/lobules -branch to septal fibers ->into interlobular septal fibers -link two fiber systems to make continuous -fiber support->coll:elastin=2:1 in parenchyma =10:1 in visc. pleura (less stretch) Alveolar interdependence-prevent collapse -help inflation w/ negative intrapleural pressure, <math xmlns="http://www.w3.org/1998/Math/MathML"> <mrow> <mtext> 20% Tissue resistance-v/p pleura, lung lobe relative mvmt, ab viscera 80% Airway resistance-Pouiseille's Law R=8ηL/πr^4, V=ΔP/R -not accurate w/ non-laminar flow -laminar only distal to term. brr. -turbulent air flow w/ high velocity V=sqrt(ΔP/R)-need higher driving P -proximal to terminal bronchioles -change w/ fibrosis, emphysema asthma </mtext> </mrow> </math> ???? 40-50% airway R b/w nose&larynx rest b/w larynx&alv. ducts -most in med. bronchi, 4-8th gen -due to v, x. area, etc smaller airways-"silent airways" -can increase R w/out changing total R, <math xmlns="http://www.w3.org/1998/Math/MathML"> <mrow> <mtext> 20% Tissue resistance-v/p pleura, lung lobe relative mvmt, ab viscera 80% Airway resistance-Pouiseille's Law R=8ηL/πr^4, V=ΔP/R -not accurate w/ non-laminar flow -laminar only distal to term. brr. -turbulent air flow w/ high velocity V=sqrt(ΔP/R)-need higher driving P -proximal to terminal bronchioles -change w/ fibrosis, emphysema asthma </mtext> </mrow> </math> ???? Reynold's Number R=ρvd/η v=linear velocity, density, dia, visc R-turbulent 1000 lower than CV system most likely in trachea/large airways, Respiratory Physiology Mechanics Applied Forces: 1. Mm. of Resp.-diaph, ext ICs, accessory mm-only for high ventilation rates -no inherent rhythm, motor nn. nn. originate in medulla -increase discharge freq, recruit motor units, recruit accessory mm. Opposing Forces: 1.Compliance of lung/chest -ease of deformation 2.Friction of tissue or air mvmt 3.Inertia of lung,chest wall,air, Factors of resistance: Physiological-1.sm. m tone (asthma) 2. secretions (mucous, inflam.) parasympas via ACh increase both -narrow lumen, increase R sympa-sm. m relax, inhibit glands -(beta2)-widen lumen, decrease R Physical-Diameter(radial traction, transmural P changes) RT-parenchyma pulls airways open TP-alv P down, enlarge airway -smoke, dust, histamine, PGs-constrict -local decreases in CO2->constrict -and dilate for CO2 increases Inertia Small Effect (5%) F=ma -chest wall-large m, low a -air-small m, high a at high vent. rates-> -chest-higher a -air-convective acceleration -resistance increases, Elastic work(compliance)-60-66% total work Recoil Pressure due to: 50/50 in normal vent. high volumes-surface tension more imp't Lung elasticity-lung inflated by mm., then recoil -in connective fiber support system -weave of: coll-stretch 102%, elastin 115% -parenchyma stretchier than v. pleura -fibrosis/emphysema decrease stretch Surface Tension: air-liquid interface in alveoli -to shrink interface as much as possible -contributes as much pressure as CT weave (Von Neergaard expts) Optimize Work 15breaths/min Vt=600mL Exercise-resp mm take 10% of air -more work in frictional than elastic vs 1% at rest -more work (66%) on elastic work, Obstructive-increased airway resistance =>reduced expiratory flow rates -always ass'd w/ airway dysfunction -FVC1.0/FVCៀ% -FEF25-75% less than 75% of predicted FVC,VC reduced in severe TLC, RV, FRC increased in severe (trap air) -emphysema, asthma, bronchospasms, chronic bronchitis -treat w/ bronchodilators (BD) -reversible if 15% improvement w/ BD Emphysema Destroys Alveolar Septa-lung like large leather bag, floppy -no radial traction to keep open -airway can be compressed Early-VC, FVC normal Advanced-FVC reduced -hypercompliant lung (less recoil) -RV, FRC increase, Applied Forces: 1. Mm. of Resp.-diaph, ext ICs, accessory mm-only for high ventilation rates -no inherent rhythm, motor nn. nn. originate in medulla -increase discharge freq, recruit motor units, recruit accessory mm. Opposing Forces: 1.Compliance of lung/chest -ease of deformation 2.Friction of tissue or air mvmt 3.Inertia of lung,chest wall,air Insp vs. Expiration Insp-diaph, ext. ICs contract ->thoracic cage expands ->lung expands, stretches -potential E stored in elastin Exp-passive when insp. mm. relax -recoil of lung apparatus, 40-50% airway R b/w nose&larynx rest b/w larynx&alv. ducts -most in med. bronchi, 4-8th gen -due to v, x. area, etc smaller airways-"silent airways" -can increase R w/out changing total R ???? Factors of resistance: Physiological-1.sm. m tone (asthma) 2. secretions (mucous, inflam.) parasympas via ACh increase both -narrow lumen, increase R sympa-sm. m relax, inhibit glands -(beta2)-widen lumen, decrease R Physical-Diameter(radial traction, transmural P changes) RT-parenchyma pulls airways open TP-alv P down, enlarge airway -smoke, dust, histamine, PGs-constrict -local decreases in CO2->constrict -and dilate for CO2 increases