Functions of resp system
- provide O2 and eliminate CO2
- protect against microbial infection
- regulate blood pH
- phonation
- olfaction
- reservoir for blood
1/203
| Term | Definition |
|---|---|
| Functions of resp system | - provide O2 and eliminate CO2 - protect against microbial infection - regulate blood pH - phonation - olfaction - reservoir for blood |
| Components of the upper airways | - nasal/oral cavities - pharynx - larynx |
| Components of the lungs | - bronchi, bronchioles, alveoli - smooth muscle/connective tissue - pulmonary circulation |
| What are the trachea and primary bronchi made of | - C-shape cartilage (anterior) - smooth muscle (posterior) |
| What are the bronchi made of | plates of cartilage and smooth muscle |
| What are the bronchioles made of | smooth muscle |
| What zones are the larynx divided into? describe them | 1. conducting zone: leads gas to gas exchange region of lungs - "dead space" - no alveoli = no gas exchange 2. respiratory zone: where gas exchange happens - has alveoli |
| Terminal bronchioles | - smallest airway without alveoli |
| Respiratory bronchioles | - have occasional alveoli |
| Alveoli | thin-walled capillary rich sac in lungs where O2 and CO2 exchange happens |
| Type 1 alveolar cells | - lined by continuous mono-layer of flat epithelial cells - do not divide (susceptible to inhaled or aspirated toxins) |
| Type II alveolar cells | - produce surfactant: detergent-like (lipoproteins), reduces surface tension of alveolar fluid - acts as progenitor cells: injury to type 1 cells causes type II cells to multiply and divide (eventually differentiate into Type I cells) |
| What type of transport is the transfer of O2 and CO2? where does it happen | - occurs by diffusion - through the respiratory membrane (very thin) |
| What are the steps of respiration | 1. ventilation: exchange of air between atmosphere and alveoli by (bulk flow) 2. exchange of O2 and Co2 between alveolar air and blood in lung capillaries by (diffusion) 3. transport of O2 and CO2 through pulmonary and systemic circulation by (bulk flow) 4. exchange of O2 and CO2 between blood in tissue capillaries and cells in tissues by diffusion 5. cellular utilization of O2 and production of CO2 |
| How is airflow produced | 1. CNS sends rhythmic excitatory drive to resp muscles 2. resp muscles contract in pattern 3. changes in volume and pressure and chest and lungs 4. air flows in and out |
| Types of resp muscles | - pump muscles: INS - diaphragm, external intercostals, parasternal intercostals EXP - internal intercostals, abdominals - airway muscles INS - tongue protruders, alae nasi, muscles around airway EXP - muscles are airways (pharynx, larynx) - accessory muscles INS: sternocleidomastoid, scalene |
| Diaphragm | dome shaped muscle which flattens during contraction (INS), abdominal contents forced down and forward, rib cage widened - increased volume of thorax |
| External intercostal muscles | contract and pull ribs upwards increasing volume of thorax - bucket handle motion |
| Parasternal intercostal muscles | contract and pull sternum forward, increasing anterior/posterior dimension of rib cage - pump handle motion |
| Abdominals | - external/internal oblique, transversus abdominis, rectus abdominis - relaxed at rest |
| Internal intercostal muscles | - relaxed at rest - exercise: internal intercostal muscles pull rib cage down, reducing thoracic volume |
| Accessory INS muscles | - scalenes: elevate upper ribs - sternocleidomastoids: raise sternum |
| What muscles contribute to opening upper airways and reducing airway resistance | - tongue protruders - alae nasi - pharyngeal and laryngeal dilators (inspiratory) - pharyngeal and laryngeal constrictors (expiratory) |
| What is obstructive sleep apnea | - reduction in upper airway patency during sleep - reduction in muscle tone - anatomical defects |
| What kind of cell is conducting airways lined with | - epithelial cells which comprise mucus-producing and ciliated cells - entrap inhaled particulates and remove from airways |
| What do ciliated cells produce | - periciliary fluid (sol layer) |
| What do macrophages in alveoli do | phagocytize foreign particles |
| Spirometry | - pulmonary function test - amount/rate of inspired and expired air |
| T/F: Residual volume cannot be measured by spirometry | True |
| Atelectasis | complete/partial collapse of lung (or lobe) - alveoli becomes deflated or collapsed |
| Tidal volume (TV) | volume of air moved in/out during each ventilatory cycle |
| Inspiratory volume (IRV) | additional volume of air that can be inspired following normal inspiration - maximum possible inspiration |
| Expiratory volume (ERV) | additional volume of air that can be expired following normal expiration - maximum voluntary expiration |
| Residual volume (RV) | volume of air remaining in lungs after maximal expiration |
| Vital capacities (VC) + formula | maximal volume of air forcibly inhaled after maximal inspiration VC = TV + IRV + ERV |
| Inspiratory capacity + formula | maximal volume of air forcibly inhaled IC = TV + IRV |
| Functional residual capacity + formula | volume of air remaining after normal expiration FRC = RV + ERV |
| Total lung capacity + formula | volume of air in lungs at the end of maximal inspiration TLC = FRC + TV + IRV = VC + RV |
| Total/minute ventilation | total amount of air moved into resp system per minute "L/min" |
| Which is usually higher? alveolar or total ventilation per minute | total |
| Alveolar ventilation formula | Va = (Vt - Vd) x frequency Vt = tidal volume Vd = dead space volume |
| T/F: Increase in breathing rate is best way to increase alveolar ventilation | False, increased depth of breathing is the best way |
| Forced expiratory volume in 1 second (FEV1) | - healthy person can blow most of their air out in 1 second |
| Forced vital capacity (FVC) | - total amount of air blown out after max inspiration as fast as possible |
| Formula of the proportion of air that is blown out in 1 second | FEV1/FVC |
| What 3 patterns could the spirometry test show | - Age, gender, weight, height (near high, just below restrictive %) - obstructive pattern (lower %) - restrictive pattern (high %) - Test will only show one |
| What does an obstructive pattern cause | - shortness of breath (difficulty exhaling all air) - damage or narrowing of airways and lungs |
| What does a restrictive pattern cause | - cannot fully fill lungs with air - stiffness in lungs - reduced vital capacity |
| Helium dilution method | - insoluble in blood but equilibrates after a few breaths - conc measured after expiring V2 = V1 x (C1 - C2) / C2 |
| What do static properties mean | - mechanical properties when no air is flowing - needed to maintain lung and chest wall at a volume |
| What are the static properties | - intrapleural pressure, transpulmonary pressure - static compliance of lung - surface tension of lung |
| What do dynamic properties mean | mechanical properties when lung is changing volume |
| What are the dynamic properties | - alveolar pressure - dynamic lung compliance - airway/tissue resistance |
| Boyles law | - Pressure and volume and inversely proportional P1V1 = P2V2 (constant T) - gas molecules always in constant motion = pressure |
| Explain the formula for bulk flow, and state it | F = Change in pressure (Palv - Patm) / Resistance - pressure difference between inside and outside lung moves air via bulk flow (F) from high pressure to low pressure |
| What happens to bulk flow (F) when Patm = Palv | F = 0 |
| Pleurae | - double layered envelope - visceral: covers external surface of lung - Parietal: convers thoracic wall and superior face of diaphragm |
| Purpose of intrapleural fluid | reduced friction of lung against thoracic wall during breathing |
| What does elastic recoil do to the lungs | tendency to collapse lungs |
| What does the chest wall do in relation to elastic recoil | pulls thoracic cage outward |
| How do the lungs and chest wall interact | through intrapleural space between visceral and parietal pleurae |
| Intrapleural pressure (Pip) | - pressure in pleural cavity - ALWAYS subatmospheric bc of opposing directions of lungs and thoracic cage |
| What happens if Pip = Palv | lungs collapse |
| Alveolar pressure | - pressure inside alveoli |
| What point are Palv and Patm the same | when glottic is open and no air goes in/out |
| Transpulmonary pressure (Ptp) + formula | - force responsible for keeping alveoli open Ptp = Palv - Pip |
| Which pressure should be the highest | Palv - then Pip - then Ptp (greater than 0) |
| Resistive forces | - inertia - friction |
| T/F: If flow is laminar, airway resistance is more sensitive to changes in radius | False, more sensitive when flow is NOT laminar |
| T/F: transitional airflow increases resistance | True, requires extra energy |
| T/F: the resistance is the lowest | False, resistance is the highest |
| What does Poiseuille's law state | airway resistance is proportional to viscosity of the gas and length of tube |
| In disease conditions, do airways play larger or smaller role in airflow resistance | larger |
| Lung compliance | - measure of elastic properties of lungs and how easily they expand - change in lung volume produced by a change in transpulmonary pressure |
| What is the slope of the pressure volume curve | C = Change in volume (V) / Change in pressure (Ptp) |
| Static compliance | lung compliance during periods of now gas flow - measured w/ P/V slope (end of expiratory event) |
| Dynamic compliance | pulmonary compliance during periods of gas flow (inspiration) when transpulmonary pressure continuously changes |
| T/F: dynamic compliance is less than or equal to static lung compliance | True |
| What causes dynamic compliance to fall | increase is lung stiffness or airway resistance |
| What do the first increases in VL reflect | popping open of of proximal airways |
| What do low lung volumes mean | at low lung volumes, it is difficult to pop open a collapsed airway |
| What happens when all airways are open | Pip becomes more negative and increases VL linearly |
| What happens at VL | lung compliance decreases |
| Hysteresis | difference between inflation and deflation of compliance paths - greater pressure difference required to open a previously closed airway |
| Where are the elastic components of airways | - localized in alveolar walls, around BV, and bronchi |
| Elastin | - weak spring, low tensile strength, extansible |
| Collagen | - strong twine, high tensile strength, inextensible |
| With aging, what happens with elastin and collagen | decreases, lung compliance increases (floppy lungs) |
| Floppy lungs | result of elastin and alveolar wall destruction |
| Pulmonary fibrosis | collagen deposition in alveolar walls - reduction in lung compliance (stiff lungs) - high transpulmonary Pressure changes are necessary to generate changes in lung volume |
| What is lung compliance determined by | - elastic components - surface tension at air-water interface within alveoli (ST decreases lung compliance) |
| Surface tension | measure of attracting forces acting to pull liquids surface molecules together at air-liquid interface |
| What causes alveolar collapse | inward recoil due to alveolar surface tension |
| What does the smaller bubble's radius cause | greater pressure to keep bubble inflated |
| T/F: in bubbles of different sizes, T remains constant | true |
| What is alveolar sufactant purpose | - produced by type II alveolar calls - lowers surface tension of lining fluid to breathe without effort - makes alveoli stable against collapse |
| What are the effects of hydrophobic and hydrophilic properties of surfactant cells | - decreases density of water molecules |
| What does reduced surface tension of water mean for lungs | increased lung compliance (easier to expand lungs) |
| Increase in SA means what for surfactant | decrease in thickness - increase in T (inside wall of alveoli) with increasing alveolar diameter |
| What does equalized pressure of diff size alveoli mean | prevents collapse of small alveoli into large |
| T/F: premature infants are born w/ surfactant | False, they lack it - decreases compliance (increased work of breathing) |
| How does the weight of the lungs effect Pip | - increases pressure (less negative) - since alveoli are more deflated, they expand more (bottom regions of lung receive more inspired air) |
| Daltons law | in a mixture of gases, each gas operates independently - total pressure = sum of individual pressures |
| What does ficks law explain | - rate of transfer of a gas through sheet of tissue is proportional to tissue area and gas partial pressure of the two sides - inversely proportional to the thickness |
| What does the diffusion constant determine | - amount of gas transferred is proportional to gas solubility |
| T/F: oxygen more soluble that CO2 | False, CO2 faster |
| Henry's law | amount of gas dissolved is proportional to partial pressure of gas in which liquid is in eq |
| T/F: partial pressures are not the same in gase and liquid | false, they are |
| Formula for conc of a gas (in a liquid) | P x solubility |
| Why is the O2 pressure in air > O2 pressure in alveoli | - warming increasing and humidifies air in resp tract = decreases pressure - loss of oxygen to blood diffusion = decrease - mixing of inspired air w/ functional residual volume = decrease |
| Determinants of oxygen pressure | oxygen pressure in atm alveolar ventilation (Va) |
| Formula for alveolar ventilation | Va = (Vt - Vd) x resp frequency |
| Determinants of alveolar CO2 pressure | CO2 pressure in atm Va metabolic rate perfusion |
| What is the effect of increasing alveolar ventilation on PO2 and PCO2 | PO2: increase PCO2: decrease |
| What is the effect of increasing metabolic rate on PO2 and PCO2 | PO2: decrease PCO2: Increase |
| Cardiac output | volume of blood pumped by heart per min (mL blood/min) |
| Does systemic circulation require high or low pressure system | high - delivers blood in peripheral tissue |
| Does pulmonary circulation require high or low pressure system | low - deliver blood to only lungs |
| Low pressure system | - only needs to pump to top of lung - avoids rupture of resp membrane and edema formation |
| Low resistance system | - R is less than 1/10 of that in systemic circulation due to short and wide vessels |
| High compliance vessels | - higher # of arterioles w/ low resting tone - thin walls and paucity of smooth muscles = can accept lots of blood - can dilate in response to modest increase in arterial pressure |
| What makes up pulmonary circulatory system | low pressure system, low resistance system, high compliance vessels |
| What is pulmonary BV | 450 mL |
| What is pulmonary capillary BV, at rest and exercise | 70mL at rest, up to 200 mL during exercise |
| Does blood move faster or slower through pulmonary capillaries when cardiac output increases | faster (0.75 -> 0.3 seconds) |
| Explain the ventilation/perfusion ration (V/Q) | - balance between ventilation (bringing in O2 and removing CO2 from alveoli) and perfusion (removing O2 and adding CO2 into alveoli) |
| What happens to PCO2 and PO2 with greater ventilation | - the more closely they approach their values in inspired air |
| High V/Q ratio | alveolar dead space |
| Alveolar Vd | regions of lung w/ high V/Q ratio - overventilated (underperfused) - portion of fresh air is reach alveoli that cannot be taken up by blood |
| Anatomical Vd | volume of conducting airways that dont participate in gas exchange |
| Low V/Q ratio | airway obstruction |
| Shunt | portion of venous blood doesnt get oxygenated and goes back to arterial blood - associated with low V/Q ratio |
| Local ventilation-perfusion ratio | (Va/Q) - local alveolar PO2 and PCO2 |
| In an upright patient, perfusion is greatest where in the lungs? | - greater near the base of the lung and falls towards apex (top of lung) |
| What forces does perfusion depend on | - gravity - posture |
| Compared to basal lung, is BFlow and alveolar ventilation reduced or increased in apical lung | reduced |
| What is the ideal basal VA/Q | 0.6 |
| What is the ideal apical Va/Q | 0.3 |
| Why does pulmonary hypoxic vasoconstriction occur | response to low O2 |
| O2 is carried in blood by what 2 ways | 1. dissolved (minor) 2. combined w/ hemoglobin (major) |
| What law does dissolved O2 follow | Henry's law - O2 content is proportional to pressure of O2 and solubility |
| What 4 amino acids is Hb composed of | - globins (2 alpha 2 beta) - 4 heme groups |
| What structure does each HEME ring has | poryphrin - contains an iron in ferrous (Fe2+) form, O2 binds |
| What 2 ways can Hb exists as | - deoxyhemoglobin - oxyhemoglobin |
| Explain the axis meanings of the oxygen dissociation curve | x: PO2 in blood y: % of Hb binding sites that have Hb attached |
| O2 capacity | max amount of O2 that can be combined w/ O2 |
| Hb saturation | % of available Hb binding sites that have O2 attached |
| Formula for Hb saturation | O2 combined w/ Hb / O2 capacity x 100 |
| What are the determinants of Hb saturation | - arterial PO2 (crucial) - dissociation curve: sensitive to..pH, PCO2, Temp - Cooperative binding: = sigmoidal dissociation curve |
| Cooperative binding | - O2 binds to heme group, deforms shape of heme group - changes shape of globin chain from tense to relaxed state |
| What does the change in shape of one globin chain do to the rest | - deforms the others = exposes iron in heme group = more O2 binding |
| 2 portions of the sigmoidal dissociation curve | 1. flat (plateau): between 60-100 mmHg 2. steep: 10-60 mmHg |
| What does the plateau mean for saturation | stays high over wide range of alveolar PO2 - safety factor: significant limitation of lung function still allows normal O2 saturation of Hb |
| What does the steep portion demonstrate | large amounts of O2 only lead to small decreases in PO2 |
| Why is it important that PO2 remains high in peripheral tissue | - to drive diffusion from RBC to blood cells and mitochondria |
| What do small changes in the dissociation curve cause on O2 | increase unloading |
| At rest, what is most Hb saturation leaving peripheral tissues | 75% saturated |
| What effect does steep portion demonstrate on metabolic rate | - increases it, decreases PO2 in tissue = drop in plasma PO2, diffusion of O2 from RBC, drop in PO2 in RBC |
| Anemia vs. Polycythemia | Anemia: reduced Hb Polycythemia: increased Hb or decreased BV |
| Does carbon monoxide increase or decrease O2 unloading to tissue | Decrease, CO has more affinity for Hb |
| What is the PO2 alv before diffusion vs after diffusion in resp membrane | Before: PO2 alv > PO2 blood At eq: PO2 alv = PO2 blood |
| Does O2 - Hb contribute to PO2 value | No |
| What is the PO2 alv before diffusion vs after diffusion in peripheral tissue | PO2 Blood > PO2 interstitial fluid > PO2 cell > PO2 Mitochondria |
| What does a reduction in PO2 cause | reduced affinity of O2 for Hb and more O2 released from RBC |
| What does a change to right mean for O2 dissociation curve | O2 affinity of Hb is reduced = more unloading |
| What does a change to left mean for O2 dissociation curve | O2 affinity for Hb is increased = less unloading |
| What is DPG and what are its effects on O2 dissociation curve | - end product of metabolism - shifts curve to right |
| What could high levels of DPG cause | chronic hypoxia |
| In what 3 forms in CO2 carried in blood | - dissolved - bicarbonate - carbamino compounds |
| T/F: CO2 solubility is low | false |
| Carbonate form of CO2 | Carbonic anhydrase (CA) in RBC |
| What does CA do + effect on HCO3 | Converts CO2 + H2O -> H2CO3 - this causes HCO3 to exit cells to maintain neutrality - H+ increases in venous blood (lowers pH) |
| What is a carbamino compound + rxn | - combo of CO2 w/ amino group in blood proteins (globins in Hb) - Hb + CO2 -> HbCO2 |
| Which has higher affinity for CO2, deoxy or oxyHb | deoxyHb - CO2 helps w/ unloading in peripheral |
| Explain CO2 movement in peripheral tissue | - CO2 exits cells dissolved in interstitial fluid and diffuses to blood - remains in plasma as dissolved CO2 (PCO2) - enters RBC and remains dissolved as CO2 - bound to deoxyHb or reacts w/ water to produce HCO3 and H (HCO3 exits RBC, H interacts w/ Hb) |
| What is PCO2 alv before diffusion | PCO2 alv < PCO2 blood - dissolved CO2 in blood diffuses to alveoli - PCO2 in plasms recalls dissolved CO2 from RBC and change eq for CO2/H2O and CO2/Hb rxn |
| Is eq the same for tissues and lungs | no, in the lungs the CO2 eq is reversed - H interacts w/ HCO3 and Hb can bind w/ O2 |
| Respiratory acidosis | - hypoventilation (CO2 production > CO2 elimination), PCO2 increases and H conc increases |
| Respiratory alkalosis | - hyperventilation (CO2 production < CO2 elimination), PCO2 decreases and H conc decreases |
| Metabolic acidosis | - increases H conc in blood |
| Metabolic alkalosis | - decrease H conc in blood |
| In what system is breathing established in | CNS - initiated in medulla by specialized neurons |
| Is breathing modified by higher or lower structures of CNS | - higher - input from central and peripheral chemoreceptors and mechanoreceptors in lung and chest wall |
| What are the respiratory neurons in the brainstem | - pontine resp group, dorsal resp group, ventral resp group |
| Prebotzinger complex | - group of neurons in ventral resp group - generates excitatory inspiratory rhythmic activity which excites inspiratory muscles |
| Which pathway do the PreBotC and pFRG take | polysynaptic pathway |
| Parafacial resp group | - group of neurons in ventral resp group - generates excitatory active expiratory rhythmic activity which excites expiratory muscles |
| Why does rhythym of breathing need to change | - metabolic demands (changes in blood) - mechanical - non-ventilatory behaviour - pulmonary/non pulmonary diseases |
| Neuro resp pathway: inspiration | preBotC: INS premotorneuron (rostral ventral group) -> phrenic/thoraic motorneurons (in cervical/thoracic spinal cord) -> diaphragm and intercostal muscles preBotC: premotorneuron (rostral VRG and parahypoglossal region) -> cranial motorneurons (in medulla) -> tongue & upper airway muscles |
| Neuro resp pathway: expiration | pFRG: premotorneurons (caudal VRG) -> thoracic & lumbar motorneurons (in spinal cord) -> intercostal & abdominal muscles |
| What are the effects of hypoxia (low PO2), hypercapnia (high PCO2), and acidosis (Low pH) on ventilation | causes increase - raises PO2, lower PCO2, increase pH |
| What do chemoreceptors do in controlling ventilation | sense changes in PO2, PCO2, pH |
| Purpose of carotid and aortic bodies | - sense hypoxia (low artial PO2) and sensitive to pH |
| Types of carotid body cells | Type I: glomus cell - chemosensitive cells Type II: sustentacular cell - act as support in carotid body |
| Glomus cells | - voltage gated ion channels - have many vesicles w/ neuroT's |
| What is the primary stimulus for peripheral chemoreceptors | - decrease in arterial PO2 |
| Glomus cells response to decrease in PO2 | - increase firing rate of AP |
| At what arterial PO2 does stimulation of chemoreceptors occur at | below 60 mmHg - flat at 60-120 mmHg |
| How do peripheral chemoreceptors control resp muscles | - activate dorsal and ventral resp groups in medulla - increase resp rate - increase tidal volume |
| Where are central chemoreceptors located | close to ventral surface of medulla (close to CSF and blood vessels) - rostral, intermediate, caudal regions |
| What receptors are responsible for hypercapnia | central chemoreceptors |
| Why does H stimulate mostly peripheral chemoreceptors | because H does not cross BBB (CO2 does) |
| What effect does strenous exercise have on ventilation | lactic acid buildup -> peripheral chemoreceptors -> hyperventilation |