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Respiratory 16

Type I alveolar surface of the lung
Type II alveolar secret the surfactant, ability to differentiate into Type I
Fibroblast Collage & Elastin to create the scaffolding an attachment point
Immune Cells Macrophage & White blood cells fight off antigen formed by a pathogens
Compliance how easily it changes it shape
Elasticity tendency to return to intial size after distension
Surface Tension (ST) thin film of fluid on alveolar surface; fluid absorption osmosis driven by Na+ [phospholipid (phosphatidylcholine & phosphatidylglycerol secreted by Type II alveolar cells
Law of Laplace alveolar pressure is directly proportional to ST; inversely to radius of alveoli (small sack more readily; bigger less prone)
RDS respiratory distress syndrome
ARDS acute respiratory distress syndrome
Partial pressure pressure that a particular gas in a mixture exerts indep.
Dalton's Law total pressure of a gas mix is the sum of partial pressures of each gas in mixture
Boyle's Law implies changes in intrapulmonary pressure occur as a result of changes in lung volume - pressure of a gas is inversely proportional to volume; air moves from a higher to lower pressure GOOD AIR IN increase in lung vol decreases intra
Smooth surfaces visceral pleura -> LUNG intraplural space/pressure -> parietal pleura CHEST
Transmural Pressure difference b/t intrapulmonary and intraplural 756 mmHg Table 16.1
Efforts to overcome during respiration frictional resistance to gas flow & elastic resistance of the tissues themselves
Restrictive pink puffers overcoming elastic recoil of chest wall, parenchymal tissue, and surface tension
Obstructive blue blowers overcoming tissue resistance and airway resistance (asthma, bronchitis, emphysema)
Spirometer trace watching air move in out of lungs; tidal volume (normal in and out volume); expiratory reserve volume (what you can take on top of your tidal volume); maximal expiration (max out without collapsing lungs); residual volume, with collapse; VC=IRV+ERV+TV
Inspiratory capcity tidal volume plus inspiratory reserve volume
Functional residual capacity expiratory reserve vol plue residual vol
Vital capacity sum of IRV TV ERV
Ventilation and Perfusion Zones air in and blood to the site; higher vent lower perf PA>Pa>Pv zone 1; Pa/PA/PV zone 2; Pa>PV>PA zone 3; higher perf lower vent
Pulmonary circulation=equates to flow in systemic circulation
Ventilation-perfusion coupling=hypoxic vaso-constriction in the lung
Physical Principles of Gas Exchange membrane thickness of type 1 cells; diff coefficient of gas, surface area of membrane
Ventilation with Saturation Partial pressure O, 40 & CO2, 46 -> O, 100 & CO2, 40 Left Atrium and Ventricle Systemic arteries
Partial pressure of oxygen 50 mmHg getting oxygen onto hemoglobin of red blood cell; shift the curve to the right decrease affinity decrease in pH, increase in CO2, increase in temperature result in a decrease in the ability of hemoglobin to hold oxygen
Haldane Effect
Bohr Effect effect of hydrogen, acidic, shift affinity of hemoglobin to deliver oxygen and in the opposite carries away hydrogen
what happens at the level of the tissue pH lower CO2 higher Temperature higher, what happens at the level of the lung; pH higher, CO2 lower, Temperature lower drop-off CO2 drop-off
Allosteric effects
Carbon dioxide .7 bicarbonate, .23 blood proteins, .07 soln with plasma
Carbaminohemoglobin CO2 combined with hemoglobin CO2 + Hb-NH2 <——> H+ + Hb-NH-COO–
The chloride shift=antiport with chloride moves into RBC and bicarb out of the RBC;
Reverse chloride shift=pulling chloride out and bicarb back into the RBC
7.35 less than acidosis [ normal pH levels ] 7.45 greater than alkalosis
CO2 and Hydrogen volatile acid can be converted to a gas
Nonvolatile acids
Respiratory acidosis=caused by hypoventilation (CO2) rise in blood and thus carbonic acid
Respiratory alkalosis=caused by hyperventilation (CO2) fall in blood
Metabolic acidosis keytone bodies in diabetes loss of bicarbs (for buffering) in diarrhea
Metabolic alkalosis caused by too much bicarb or too little nonvolatile acids (from vomiting out stomach acid)
Henderson-Hasselbalch equation uses CO2 and HCO3 levels to calculate pH 6.1 + log
Fibrosis putting down too much collagen can be caused by toxicants; Type 1 necrosis, Type 2 cell proliferation, macrophage accumulation, fibroblast accumulation and smooth muscle cells, collagen increases, thickening of the air blood/
Emphysema loosing tissue, surface area and changing the compliance and elasticity (easy to get air in but difficult to get air out, less recoil)
Result in fewer, larger, alveoli smoking stimulates release of inflammatory cytokines which attract macrophages and leukocytes that secrete enzymes that destroy tissue
Destruction of alveolar cell walls, Over-inflation and distention of alveoli, gas exchange is affected, toxicant-induced version is accompanied by inflammation
Obstructive air out Restrictive air in
FEV1 decreased someone with emphysema Obstructive disorder
Dyspnea a feeling of shortness of breath; asthma results from episodes of obstruction of air flow through bronchioles (chronic mucus generation, airway constriction, chronic mucus generation)
Trigger allergens cold air
Graphics normal, emphysema, fibrotic lung disease, pulmonary edema, asthma
Abestos increase in collage in alveolar walls, presense of asbestos fibers Causes short fibers are engulfed by macrophages and leave the lung
Long fibers
Coal causes loss of tissue like an emphysema patient
Silica macrophages recruit fibroblast to the scene fibrosis collagen silicotic nodule
Abestos macrophages recruit fibroblast to scene fibrosis collagen
Oxidative burden oxidative burst prolonged accumulation of inflammatory cells quick non-specific
2nd hand smoke=more harmful temperature and unfiltered
apneustic center pons starts stimulates inspiration (inspiratories in medulla)
pneumotaxic center stopping movement antagoizes apneustic center, inhibiting inspiration
smooth muscle recruitment neuron levels and how they relate
chemoreceptors central in medulla watch PCO2 and PO2 and pH and periphery, aortic bodies & carotid bodies,carotid sinus (neurons that are sensing)
CNS control of breathing Cerebral Cortex, pons:apneu & pneu, med oblong:Chemoreceptors MO Aort and Cart, spinal cord (automatic breathing)
PCO2 the most important or crucial matrix b/c of its effects on blood pH; low CO2 hyperventilation or hypocapnia; high CO2 hypoventilation or hypercapnia
Eff of Blood PCO2 and pH on Vent periph responsive to hydrogen but it will not cross the blood brain barrier; so, in CSF CO2 will be converted to Hydrogen that is detected by central chemoreceptor
hypoxemia low blood O2 has little effect on ventilation; partial pressure of oxgen in venous blood; hemoglobin has a high affinity for oxygen;
Hypoxic steps low PO2, K channels close, cell depolarizes, Ca VG chan opens, Ca entry, exocytosis of neurotransmitters, AP signal to Medu to increase ventil
Perp positive N respiratory pressure supplying air to lungs by supplying gas
Unmyelinated C fibers are stimulated by noxious substances such as capsaicin; causes apnea followed by a rapid, shallow breathing
irritant receptors rapidly adapting, respond to smoke, smog, and particulates (causes cough)
Hering-Breuer reflex mediated by stretch receptors activated during inspiration (inhibits respiratory centers to prevent overinflation of lungs, forced exhalation)
Created by: 100001194417609



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