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Pulmonary Physiology

Costanzo-Respiratory Physiology

conducting zone subdivisions nose, nasopharynx, larynx, trachea, bronchi, bronchioles, terminal bronchioles
conducting zone structure & fxn bring air into and out of lungs lined with mucus-secreting ciliated cells contain smooth m. and innervated by SNS & PNS SNS activate B2 receptors and relax/dilate PNS activate muscarinic receptors and constrict/contract
albuterol B2-adrenergic agonist used to dilate airways to treat athsma
respiratory zone subdivisions respiratory bronchioles, alveolar ducts, alveolar sacs
respiratory zone structure & fxn participates in gas exchange-->thin walls & large surface area lined with alveoli walls lined with elastic fibers & epithelial cells contain type I & II pneumocytes and alveolar macrophages
type II pneumocyte synthesizes pulmonary surfactant necessary to reduce alveoli surface tension has regenerative capacity for type I and II pneumocytes
alveolar macrophages phagocytic cells fill with debri then migrate to bronchioles-->keeps alveoli free of dust & debri imp. bc respiratory zone has no cilia
gravitational effect on pulmonary blood flow blood flow not evenly distributed in lungs when standing blood flow lowest at apex and highest at base
spirometer measures static lung volume
tidal volume normal quiet breathing approx. 500 mL = air in alveoli + air in airways
inspiratory reserve volume additional volume inspired above tidal volume approx. 3000 mL
expiratory reserve volume additional volume expired below tidal volume approx. 1200 mL
residual volume volume of gas remaining in lungs after maximal forced expiration approx. 1200 mL
dead space volume of airways and lungs that don't participate in gas exchange -anatomic dead space -physiologic dead space both values should be nearly equal in normal persons-->functional dead space should be small
anatomic dead space volume of air in conducting airways 1/3 of each tidal volume fills anatomic dead space
physiologic dead space total volume of lung that doesn't participate in gas exchange = anatomic dead space + functional dead space in alveoli
type of air in alveoli at end-inspiration 1) alveolar air from previous breath 2)inspired air that participates in gas exchange
inspiratory capacity (IC) tidal volume + inspiratory volume approx. 3500 mL
functional residual capacity (FRC) expiratory reserve + residual volume approx. 2400 mL also known as equilibrium volume: volume remaining in lungs after normal tidal volume expired
vital capacity (VC) inspiratory volume + expiratory reserve volume approx. 4700 mL; value increases with body size, M gender, physical conditioning; value decreases with age volume expired after maximal inspiration
forced vital capacity total volume of air that can be forcibly expired after maximal inspiration FEV1/FVC useful in differentiating between lung disease; normally 0.8 -obstructive lung disease (athsma) ratio decreases -restrictive lung disease (fibrosis) ratio increas
muscles of inspiration *diaphragm during exercise also use external intercostal muscles and accessory muscles
muscles of expiration *normally passive process during exercise/disease use abdominal muscles and internal intercostal muscles
lung compliance describes change in lung volume for given change in pressure higher during expiration than inspiration due to surface tension between liquid-air interface inversely correlated with elastic properties ex) thick and thin rubber band
negative intrapleural pressure created by opposing forces between collapsing lung and chest wall that springs out
pneumothorax when air introduced into intrapleural space and leads to 1) collapsed lung 2) chest wall springs out
emphysema increased lung compliance due to loss of elastic fibers leading to decreased elastic recoil pt needs to breathe at higher lung volumes to increase elastic recoil class symptom: barrel-shaped chest
fibrosis decrease lung compliance due to stiffening of lung tissue AKA restrictive disease
alveolar surface tension created by attractive forces between adjacent liquid molecules lining alveoli creates high collapsing pressure in small alveoli
surfactant produced by type II alveolar cells mixture of phospholipids-->most imp. constituent dipalmitoyl phophotidylcholine reduces surface tension & collapsing press by breaking up forces between liquid molecules
neonatal respiratory distress syndrome neonates lacking surfactant-->imp. because increases lung compliance and reduces work of expanding lungs surfactant synthesis produced early as gestational WK24-almost always present by WK35 atelectasis and hypoxemia develops
transmural pressure in lungs transpulmonary press. = alveolar pressure - intrapleural pressure (+) value is expanding pressure on lungs (-) value is collapsing pressure on lungs
physiologic shunt 2% CO normally bypasses alveoli two sources: 1) bronchial blood flow and 2) coronary venous blood why Pao2<PAo2
diffusion-limited gas exchange gas exchange limited by diffusion process diffusion will continue as long as partial pressure for gas maintained
perfusion-limited gas exchange gas exchange limited by blood flow partial pressure gradient not maintained-->blood flow must increase to increase gas exchange
perfusion-limited O2 transport O2 transport during normal conditions; alveolar air and capillary blood equilibrate 1/3 way down capillary
diffusion-limited O2 transport occurs during pathological conditions and strenuous exercise total O2 transfer is greatly reduced
O2 transport at high altitude Po2 in alveolar gas decreases because barometric pressure decreases; partial pressure gradient greatly reduced along with O2 diffusion equilibration is slower
dissolved O2 in blood approx. 2% of total O2 in blood-->insufficient meet demands of tissue
O2 bound to hemoglobin approx. 98% of total O2 in blood hemoglobin contains four subunits (2 alpha chains and 2 beta chains); each subunit binds one O2 molecule hemoglobin heme moiety must be in Fe2+ state to bind O2
methemoglobin heme moiety contains Fe3+ and does not bind O2 deficiency of methemoglobin reductase is a congenital variant of the disease
fetal hemoglobin beta chains are replaced by gamma chains modification results in higher O2 affinity-->facilitates O2 movement from mother to fetus
hemoglobin S abnormal variant that causes sickle cell disease beta subunits are abnormal and distorts RBC in the deoxygenated form-->can occlude small blood vessels O2 affinity is low
O2-hemoglobin dissociation curve sigmoidal shape-->affinity increases with each successive O2 molecule bound-->phenomenon called positive cooperativity
P50 on O2-hemoglobin dissociation curve point used as indicator for change in hemoglobin affinity for O2 -increase reflects decreased affinity -decrease reflects increased affinity
O2-hemoglobin dissociation curve shift to the right reflects decreased O2 affinity-->increased P50-->facilitates O2 unloading result of increased Pco2, temperature, 2,3-DPG and decreased pH
2,3-diphosphoglycerate byproduct of glycolysis in RBC binds to beta chains of deoxyhemoglobin-->reduces O2 affinity
O2-hemoglobin dissociation curve shift to the left reflects increased O2 affinity-->decreased P50-->makes O2 unloading harder result of decreased Pco2, temperature, 2,3-DPG/hemoglobin F and increased pH
carbon monoxide decreases O2 bound to hemoglobin-->has 250x higher affinity to hemoglobin than O2 shifts O2-hemoglobin dissociation curve to left-->unbound heme groups have increased affinity for O2
oxygen transport in blood 2% dissolved O2 98% O2 bound to hemoglobin
carbon dioxide transport in blood 5% dissolved CO2 3% carbaminohemoglobin-->binds to terminal amino groups on proteins 90% bicarbonate
hypoxic vasoconstriction decrease in PAO2 produces pulmonary vasoconstriction adaptive mechanism-->reduces pulmonary blood flow to poorly ventilated areas where it would be "wasted"
thromboxane A2 powerful vascoconstrictor of arterioles and veins product of arachidonic acid metabolism via cyclooxygenase pathway produced in response to lung injury in macrophages, leukocytes, and endothelial cells
prostacyclin (prostaglandin I2) potent local vasodilator product of arachidonic acid metabolism via cyclooxygenase pathway produced by lung endothelial cells
leukotrienes causes airway constriction product of arachidonic acid metabolism via lipoxygenase pathway
blood flow distribution in lung zone 1-low blood flow; PA>Pa>Pv zone 2-med blood flow; Pa>PA>Pv zone 3-high blood flow; Pa>Pv>PA
right-to-left-shunt septal defect between right and left ventricle portion of CO not oxygenated-->hypoxemia always occurs due to dilutional effect cannot be corrected by breathing high O2 gas
left-to-right shunt common and doesn't cause hypoxemia result of: 1) patent ductus arteriosus 2) traumatic injury right heart CO > left heart CO Po2 in right heart blood is elevated
V/Q distribution in lungs zone 1-highest V/Q; highest Pao2; lowest Paco2 zone 3-lowest V/Q; lowest Pao2; highest Paco2
V/Q mismatches dead space- V/Q=infinity; no perfusion; alveolar gas same comp as humidified inspired air high V/Q low V/Q- ventilation decreased shunt- V/Q=0; no ventilation; airway obstruction; right-to-left shunt; blood same comp as mixed venous blood
medullary respiratory center 1)inspiratory center: controls basic breathing rhythm; input from CNIX and X; output via phrenic n. 2)expiratory center: inactive during quiet breathing because expiration passive process; active during exercise located in reticular formation
apneustic center produces abnormal breathing pattern with prolonged inspiratory gasps due to prolonged contraction of diaphragm located in lower pons
pneumotaxic center turns off inspiration;limits tidal volume located in upper pons
hypoxemia vs hypoxia hypoxemia-->decrease in arterial Po2 hypoxia-->decrease in O2 delivery
causes of hypoxia 1)decreased CO 2)anemia 3)carbon monoxide poisoning 4)cyanide poisoning
causes of hypoxemia 1)high altitude 2)hypoventilation 3)diffusion defects-->alleviated by supplemental O2 4)V/Q defects 5)right-to-left shunts-->not alleviated by supplemental O2
Created by: kphom001



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