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conducting zone structure & fxn
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Pulmonary Physiology
Costanzo-Respiratory Physiology
| Question | Answer |
|---|---|
| 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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