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330 Cards in this Set
- Front
- Back
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respiration - 'internal'
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ATP making process that occurs in the mitochondria. Requires O2 as final electron acceptor
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respiration - 'external'
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processes that enable O2 supply to the lung. Involves the processes of Ventilation, perfusion, diffusion
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ventilation
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air moves into/out of lung to remove CO2 and replenish O2. Bulk flow. Inflation and deflation
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perfusion
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blood flow around body carries O2 to the alveoli and picks up CO2 from alveoli. Bulk flow.
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diffusion
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gas exchange through cellular membrane. Depends on partial pressure differences at the interfaces.
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composition of dry air
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21% O2, 79 % N2, 0 CO2, 0 H2O
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Which processes are responisble for existence and maintenance of partial pressure differences at the blood-cell interfaces?
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perfusion and ventilation maintain large PP gradient for fast rate of transfer
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PO2 in atmosphere
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159 mmHg
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PO2 in trachea
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149 mmHg
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PO2 in alveoli
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100 mmHg
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PO2 in oxygenated blood (arteries)
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96 mmHg
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PO2 in ISF
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20 mmHG
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PO2 in cell
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4 mmHg
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PO2 in venous blood
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40 mmHg
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PCO2 in trachea
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0 mmHg
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PCO2 in alveoli
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40 mmHg (coming from the systemic circ)
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PCO2 in arteries
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40 mmHg
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PCO2 in veins
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46 mmHg
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Dalton's law
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the partial pressure of a gas in a gas mixture is the pressure the gas would exert if it occupied to the total volume of mixture alone.
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PH2O in body at 37 degrees C
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47 mmHg
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What contributes to inspired air that is not present in dry air?
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Water vapor = 47 mmHg. Must be accounted for in calculating inspired PO2 (PI O2)
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Partial pressure in a solution is
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partial pressure of a gas that is in euqilibrium with the solution
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Lungs receive what percentage of Cardiac output?
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100%
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what is the path of O2 to the blood?
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surfactant, alveolar epithelium, interstitium, capillary endothelium, plasma, RBC. All is 1 micron thick.
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which components of the lung increase the surface area?
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branching of airways, alveoli
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the lung and chest are elastic structures that ______ expansion.
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resist
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what process allows lung and chest distention?
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inspiratory muscle contraction
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what process allows expiration?
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relaxing the inspiratory muscles
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the _____ is the primary muscle of inspiration, aided by the _____.
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diaphragm, external intercostals
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abdominal muscle contraction does what to the shape of the diaphragm?
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allows it to return to its dome shape (aids in forced expiration by increasing intraabdominal pressure)
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what happens to the lungs an chest wall in pneumothorax?
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lungs collapse inward and chest wall moves outward
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the pressure of the intrapleural fluid is (+ or -)
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Negative
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spirometer measures
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flow of air into and out of lung (does NOT measure amount of air already in lungs)
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Tidal Volume (VT)
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volume of air leaving lungs during a single breath (only a fraction of air in the lungs)
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Functional Residual capacity (FRC)
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volume of air remaining in lungs at the end of a normal tidal volume. FRC = RV + ERV.
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Residual volume (RV)
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volume of air remaining in lungs at the end of a maximal expiration
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Total Lung Capacity (TLC)
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maximum volume of air at the end of a maximum inspiration (6L)
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Expiratory Reserve Volume (ERV)
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maximum volume of air expelled at the end of a normal tidal volume
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Inspiratory capacity (IC)
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maximum amount of air inhaled following a normal expiration
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Vital Capacity (VC)
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maximum volume of air that can be expired after a maximum inspiration
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Inspiratory reserve volume (IRV)
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maximum volume of air inhaled at the end of a normal inspiraiton
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pneumothorax
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when lungs and chest wall separate, chest wants to move out, lungs want to move in. Chest wall vol increases, lung volume decreases
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intrapleural pressure (increases/decreases) in inspiration
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decreases. This increases lung volume and decreases alveolar pressure, air rushes into lungs
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Inward and outward forces balance at an equilibrium position called the
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FRC - functional residual capacity
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these lung volumes cannot be measured using spirometry alone
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FRC, RV, TLC
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in Emphysema, lung compliance is (increased/decreased)
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increased
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in pulmonary fibrosis, lung compliance is (increased/decreased)
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decreased
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in alveolar edema, lung compliance is (increased/decreased)
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decreased
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surfactant (increases/decreases) lung compliance
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increases
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What effect does increased surface tension have on the alveoli?
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draws fluid out of pulmonary capillaries into the alveoli
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reduced lung compliance results in (more/less) elastic recoil and renders lung (easier/harder) to inflate
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more, harder
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increased lung compliance results in (more/less) elastic recoil and makes the lung (easier/harder) to inflate
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less, easier
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emphysema is an example of (increased/decreased) lung compliance
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increased
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fibrosis and alveolar edema demonstrate (increased/decreased) lung compliance
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decreased
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what factors control lung compliance?
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1. amount elastin and collagen 2. ease of rib movment 3. surface tension of alveoli
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surface tension
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the force that attempts to decrease the surface area of the alveoli. Attractive force between the liquid molecules of the alveoli. Makes lungs more difficult to inflate.
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less elastic tissue results in
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increased compliance (emphysema)
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more elastic tissue results in
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decreased compliance (fibrosis - more elastin and collagen fibers)
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atelectasis
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alveolar collapse
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laplace's law
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surface tension generates pressure - greater pressure with a smaller sphere. P = 2T/r
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effects of surfactant
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increases compliance, increases alveolar stability (prevents actelactasis), keeps lungs dry
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compliance
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ease of inflation
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tissue resistance
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friction between the pleura and between the diaphragm and abdominal contents
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airway resistance
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80% of overall resistance to air movement, friction causes a drop in pressure of gas flowing through airways
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turbulent air flow
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creates more resistance than laminar flow
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pattern of air flow in the trachea
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turbulence (high air flow, large diameter)
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2 forces that oppose air movement
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compliance, frictional resistance (air mvmt and tissue)
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calculating airway resistance
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R = change in pressure/ air flow
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pattern of air flow in the terminal bronchiole
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laminar
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transitional
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pattern of air flow in most of lung between trachea and terminal bronchioles - air flow splits down branches
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poiseuille's law
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R = 8 nl/ pi r^ 4, thus flow of gas - V= change in P*pi*r^4/8nl
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turbulence creates (more/less) air resistance than laminar flow
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more
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probability of turbulence is increased by
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high air flow and large airway diameter
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The main site of reistance
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Medium-sized bronchi, low total CSA, high velocity.
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The lowest resistance is found in
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respiratory bronchioles, alveolar ducts, alveolar sacs. Like capillaries they're arranged in parallel, small resistance in airways.
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the difference between flow and velocity
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flow = volume/s, velocity = distance/s
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radial traction
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lung parenchyma pulls on airway, opens it more. Connective tissue stretching with inflation decreases resistance with an increase in lung volume
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obstructive disease of lung
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has higher airway resistance- compensates for it at higher volumes. Chronic bronchitis, emphysema, asthma
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during forced expiration,
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compression of peripheral airways limits air flow. Decrease in flow is the same despite volume or effort.
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what determines airway patency?
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transairway pressure (must be positive)
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transairway pressure (Pta)
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Pta= Paw-Ppl (pressure in airway (trachea) -intrapleural pressure)
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transairway pressure is positive during
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inhalation and passive exhalation
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Pta becomes negative in
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forced expiration
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alveolar pressure
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intrapleural pressure + elastic recoil pressure (PA= PPL + Pel)
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increased airway resistance causes airway pressure to decrease more quickly. Thus ____ _____ happens more quickly
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airway collapse. (Ppl becomes greater than Paw more easily)
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a spirometer measures
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airflow into and out of lungs. Cannot measure air already in lungs (RV, TLC, FRC)
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total ventilation depends on
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tidal volume and respiratory frequency.
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frictional work
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energy required to overcome friction. Increased frequency of resp, increased friction
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elastic work
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energy to expand the chest and overcome compliance. Increases at high Tidal Volume
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total work
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vary the combination of frictional and elastic work to get the same total ventilation and a decreased total work.
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dead space
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the volume of tidal volume that does not reach the alveoli. Stuck in conducting portion of resp system.
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alveolar volume
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the amount of air reaching the alveoli. Tv- Vd. (tidal volume - dead space volume)
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alveolar ventilation
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total flow to alveoli. = (tidal volume - dead space volume)* frequency
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how can alveolar ventilation be increased?
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increased tidal volume, increased resp. freq. Increasing tidal volume is more effective.
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what is the relationship between PCO2 and alveolar ventilation?
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they are inversely proportional.
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alveolar ventilation reflects the rate of removal of what?
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CO2
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in hyperventilation, what happens to PaCO2?
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it decreases - you're removing it faster
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physiologic dead space
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volume of airways not involved in gas exchange. Equals anatomic + alveolar dead space
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alveolar dead space
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the number of alveoli not perfused. May be indicative of a disease process that wrecks the pulmonary capillaries
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anatomic dead space
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the amount of air left in conducting portions
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in normal individuals, physiologic dead space is equal to
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anatomic dead space
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PE CO2
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mixed expired CO2. Measures CO2 diluted by O2 from the dead air space.
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the difference in CO2 between the arterial CO2 and the mixed expired CO2 calculates
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the dilution by physiologic dead space. Unperfused alveoli contain no CO2
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PE CO2 normal value
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30 mmHg
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PaCO2 normal value
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40 mmHg
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tidal volume (VT) normal volume
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500 ml
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ventilation is (higher/lower) at the base of the lung than at the apex
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higher
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intrapleural pressure is (more/less) negative at the base than at the apex
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less negative (lungs= supported by diaphragm)
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for a given change in intrapleural pressure, the (apex/base) has a greater increase in volume
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the base. Less negative - more of a pressure difference
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the diffusion constant, D
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proportional to the solubility of gas, inversely proportional to the molecular weight
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diffusion across a barrier equation
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surf area*D*(P1-P2) / thickness
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during rest, diffusion occurs across what fraction of the capillary?
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one-third
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during exercise, what happens to the amount of time an RBC spends in the capillary?
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it decreases. Need entire length of capillary for diffusion
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what simultaneous conditions allow diffusion impairment to be problematic?
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exercise or alveolar hypoxia (at high altitudes)
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which is more affected by thickening of the blood-gas barrier, CO2 or O2?
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O2. CO2 diffuses more easily
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physiologic dead space normal values
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125-175 mL
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the pulmonary circulation is (high/low) flow and (high/low) pressure
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high flow, low pressure
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little smooth muscle in pulmonary circulation
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TRUE
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pulmonary capillaries are exposed to alveolar pressure
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TRUE
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inspiration pulls open pulmonary arteris and veins by
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radial traction. NOTE - only "extra alveolar" vessels, no capillaries
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pulmonary vascular resistance is what fraction of systemic resistance
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1/10th
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what determines the caliber of alveolar vessels?
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balance between internal and alveolar pressure
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When arterial or venous pressure increases in the lung, pulmonary vascular resistance _____.
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decreases
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what allows reduced pulmonary vascular resistance at high pressures?
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recruitment and distension
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when does pulmonary vascular resistance increase?
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low and high lung volumes
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at low and ligh lung volumes, pulmonary vascular resistance
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increases
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hypoxia causes
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pulmonary vasoconstriction
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K+ channels in arteries are sensitive to
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O2. channels close in resp. to low O2, causes vasoconstriction
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what characteristic of pulmonary circulation contributes to low resistance?
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little smooth muscle
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mean pulmonary arterial pressure
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15
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pulmonary resistance is typically
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2 mmHg
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systemic resistance is usually
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19.6 mmHg
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flow rate is equal to
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cardiac output
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decreased arterial or venous pressure causes
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increased pulmonary vascular resistance
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increased cardiac output causes
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decreased pulmonary resistance
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where in the lung is the blood flow the greatest?
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the base
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why is pulmonary vascular resistance increased in low lung volume?
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alveolus, thus the capillary around it, is unstretched. Capillary smooth muscle tone causes increased resistance.
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what force draws fluid from the capillaries into the alveoli?
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surface tension and hydrostatic pressure from capillary
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what forces oppose fluid movement into the capillary?
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air pressure in alveolus, osmotic pressure in capillary
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what drains fluid in the interstitium?
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lymphatics in perivascular space
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what are the 2 stages of edema?
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early - increased fluid in interstitial spaces, late - fluid in alveoli
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Pulse oximetry
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measures bound Hb - does not distinguish between oxy- and deoxy- forms
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in anemia, why is the HB saturation % misleading?
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pt. has less hgb, thus lower capacity for storing O2 in the blood. The saturation will be the same, but there will be less O2 due to fewer hgb
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in carbon monoxide poisoning, why is Hgb saturation a misleading measurement?
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hgb can be bound to CO (it has a higher affinity for it), but the CO takes the place of O2, causing a reduced blood O2 content
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P50
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the PO2 at which Hgb is 50% saturated
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left shifted O2 dissociation curves indicate
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the hb holds onto the O2 more tightly. More hgb saturation for a given O2
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right shifted O2 dissociation curve indicates
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lower Hb saturation for a given PO2. Hb gives up O2 more easily
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Bohr effect
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a right shifted O2-dissociation curve
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what factors cause a right shift O2 diss.curve?
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increased H+, Increased PCO2, increased 2,3 BPG
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what factors cause a left shift of O2 diss.curve?
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decreased H+, decreased PCO2, decreased 2,3 BPG
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P50 in a left shifted curve is ____ than normal?
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lower
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P50 in a right-shifted curve is ____ than normal?
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higher
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in venous blood, the curve is shifted (left/right) compared to arterial blood
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right
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what are the PO2 and saturation % in venous blood?
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40 mmHg, 75%
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what are the PO2 and saturation % in arterial blood?
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100 mmHg, 97.5 %
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where is carbonic anhydrase located?
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in the RBC
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what does carbonic anydrase do?
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H20 + CO2 --> H2CO3
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how is CO2 transported in the blood?
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dissolved (10%), HCO3 (60%), carbamino (30%) - CO2 bound to Hb
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how does the CO2 dissociation curve compare to the O2 dissociation curve?
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it's steeper and more linear. A smaller change in PCO2 will lead to a greater change in CO2 content.
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How does Hb that is not carrying O2 (reduced Hb) facilitate HCO3- concentration?
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reduced Hb binds H+ ions produced in RBC by H2CO3 dissociation. Thish facilitates HCO3- formation by pulling the dissociation rxn to the right.
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carbamino compound
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CO2 bound to Hb
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respiratory alkalosis/acidosis involves changes in
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PCO2 - reflecting hypo or hyperventilation
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metabolic alkalosis/acidosis involves changes in
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[HCO3-] conc. (ingestion of alkalis, loss of H+ from vomiting)
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hyperventilation causes
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low PCO2, respiratory alkalosis
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hypoventilation causes
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high PCO2, respiratory acidosis
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the body compensates for metabolic acidosis by
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hyperventilating to reduce PCO2
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the body compensates for respiratory alkalosis by
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by excreting more HCO3-
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Hering-Breuer reflex
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lung stretch receptors= stimulated with inspiration - they trigger the offswitch neurons to stop inspiration (begin expiration). This reflex only operates at tidal volumes greater than 1 L
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integrator neurons
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J-receptors
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"juxtacapillary" - in alveolar walls. Stimulated by interstitial edema or vagus. Cause rapid, shallow breathing
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C-fibers
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in bronchial walls. Sensitive to chemicals in blood (e.g. inflammation), cause broncho constriction.
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central chemoreceptors
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located in medulla. CO2 in vessels in the brain diffuses to CSF, dissociates to form H+. Lower pH (increased H+) activates chemoreceptor.
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peripheral chemoreceptors
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located in carotid bodies (@ bifurcation) and in aortic arch. Primarily respond to low PO2, also respond to high PCO2, low pH
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hypercapnia
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increased CO2
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what are the effectors in the respiratory feedback loop?
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muscles of inspiration
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pattern generators activate ____, and are regulated by the _____
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the diaphragm, integrator neurons
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the integrator receives information from
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chemoreceptors, lung receptors, and the cortex (and limbic system)
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which collections of neurons control inspiration and expiration?
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pneumotaxic center, apneustic area, medullary respiratory center
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pneumotaxic center
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when stimulated, turns off inspiration so you can breathe out
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apneustic area
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prolongs inspiration (gasps) when stimulated
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medullary respiratory center
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pattern generators responsible for triggering inspiration and expiration. Receive input from the integrator neurons, projects to lungs.
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which 2 groups make up the medullary respiratory center?
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dorsal respiratory group (inspiration) and the ventral respiratory group (expiration)
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dorsal respiratory center
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part of medullary respiratory center, controls inspiration. Turn these off for expiration
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ventral respiratory center
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part of medullary respiratory center, triggers expiration (exp. Is generally passive at rest)
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what activates neurons of the medullary respiratory center?
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integrator neurons
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integrator neurons activate these 2 groups of neurons:
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DRG (or VRG) in medullary respiratory center and "off-switch" neurons (self-limiting!)
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lung irritant receptors
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when stimulated, promote inspiration (cough). Triggered by cold air, cigarette smoke
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stretch receptors in lung
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when triggered, promote expiration (activate the off-switch neurons)
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which receptors are more important for regulating minute-by-minute respiration?
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central chemoreceptors
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what effect does increased PaCO2 in brain have on chemoreceptors?
|
triggers chemoreceptors in the medulla by diffusing from capillaries to CSF and increasing [H+] in CSF.
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low pH in CSF causes (increased/decreased) ventilation
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increased
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What is the most important parameter in controling respiration?
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PaCO2
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what factors decrease sensitivity to arterial PCO2?
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sleep, COPD, depressant drugs (barbituates, anesthetics)
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which receptors drive breathing in someone with COPD?
|
peripheral chemoreceptors. In COPD, CSF pH is consistently low, causes the central chemoreceptors to become insensitive.
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why is giving someone with COPD O2 a bad idea?
|
The peripheral chemoreceptors read the increased PaO2. This may inhibit the signal to breathe, since COPD patients are only relying on their peripheral chemoreceptors.
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COPD patients are (overventilated/underventilated)
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underventilated (and hypoxic)
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increased arterial PCO2 is detected by which chemoreceptors?
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central chemoreceptors (80% of response), peripheral chemoreceptors (20% of response)
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decreased areterial PO2 is detected by which chemoreceptors?
|
peripheral chemoreceptors.
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Which chemoreceptors respond more quickly to increased PaCO2?
|
Peripheral. However, Central chemoreceptors are slower but responsible for 80% of response
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which factors result in Cheyne-Stokes respiration?
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hypoxemia, J receptor stimulation, slowed circulation time
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how does ventilation vary in the lung?
|
greater at apex than at base
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how does perfusion vary in the lung?
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greater at base than at apex
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V/Q ratio in upright lung (increases/decreases) from apex to base?
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decreases
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shunt
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perfusion without ventilation. V/Q approaches 0. Adds deoxy blood to arterial system
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true or false: V/Q ratios are uniform from apex to base
|
false, V/Q is higher at apex and lower at base
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can hypoxemia resulting from shunt be reversed by administering pure O2?
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no
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The relative CO2/O2 composition at the base of the lung
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high PCO2, low O2
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the relative CO2/O2 composition at the apex
|
low PCO2, high O2
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Why does V/Q inequality depress blood PO2?
|
1. blood flows through regions of base where PO2 is low, 2. due to the shape of the O2 dissociation curve
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Why does the O2 dissociation curve respond to V/Q inequality?
|
high V/Q regions don't add as much O2 to the blood as low V/Q regions remove from the blood. (high V/Q regions = toward top of the plateau)
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true or false: V/Q inequality affects PaCO2
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false. High V/Q regions can't add much more O2 to blood (location on plateau of S curve), but low V/Q regions can still remove CO2 from blood
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V/Q inequality (can/can't) be corrected with pure O2
|
can
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acclimatization
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physiological adaptations to low availability of oxygen in the inspired air
|
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what are the effects of polycythemia?
|
increased RBC increases blood O2 for a given PO2. Also increases blood viscosity
|
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how is the dissociation curve shifted at a moderate altitude?
|
to the right
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how is the dissociation curve shifted at a high altitude?
|
to the left. Alkalosis causes L shift
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hypoxic vasoconstriction can lead to
|
pulmonary edema. It increases the work of the right ventricle
|
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what helps to splint the alveolus to keep it open?
|
Nitrogen (due to its low solubility)
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|
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at birth, pulmonary resistance (increases/decreases)
|
decreases
|
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acclimatization involves which mechanisms
|
polycythemia, hyperventilation, shift of O2 dissociation curve, circulatory changes
|
|
|
what effect does hyperventilation have on alveolar O2?
|
decreases PCO2, thus increasing PO2
|
|
|
does hyperventilating increase or decrease blood pH
|
increases - more alkaline
|
|
|
what is the body's initial response to hyperventilation?
|
activating the central chemoreceptors (detect high pH CSF) and slow breathing
|
|
|
what allows ventilation to increase further after the initial inhibition?
|
correction of arterial and CSF pH
|
|
|
what changes in the systemic circulation increase O2?
|
increase capillary formation (decreases distance of O2 diffusion), increase mitochondrial expression (rapidly consumes O2, keeps PP high)
|
|
|
what pulmonary circulation changes occur at high altitude?
|
generalized hypoxia causes high altitude pulmonary edema, increases the work of the right ventricle
|
|
|
absorption atelactasis
|
collapse of portions of the lung
|
|
|
what are side effects of breathing pure O2?
|
pulmonary edema (increased leakiness of capillaries), convulsions, decreased vital capacity due to absorption atelactasis (collapse of regions of lungs)
|
|
|
what causes absorption atelectasis?
|
pure O2 washes out the N2 in the blood, which reduces blood's total P. Alveolar contents get pushed into blood and the alveolus collapses.
|
|
|
what is used for carbon monoxide poisoning?
|
hyperbaric therapy - forces O2 into plasma to compensate for the carboxyhemoglobin until the blood can produce more hgb.
|
|
|
how does deposition of aerosols vary?
|
according to particle size.
|
|
|
large aerosols deposit in the
|
nasopharynx (absorbed in swallowed mucus)
|
|
|
medium particles deposit in the ____ via a process called ____
|
bronchioles, sedimentation
|
|
|
small aerosols deposit in the __
|
alveoli
|
|
|
pneumoconiosis
|
coal miner's "black lung". Deposition of coal dust in the respiratory bronchioles.
|
|
|
is the placenta in parallel or in series with other fetal organs?
|
parallel
|
|
|
which fetal adaptation allows partially oxygenated blood to access the brain more quickly?
|
foramen ovale
|
|
|
which fetal adaptation allows partially oxygenated blood to bypass the lung circulation?
|
ductus arteriosus
|
|
|
VO2 reflects
|
metabolic rate. It is determined by tissues
|
|
|
VO2 rate increases _______ up to ______
|
linearly up to VO2max
|
|
|
at VO2 max, cah work rate increase?
|
yes, using anaerobic metabolism
|
|
|
what happens to lung blood flow in exercise?
|
it becomes more uniform. Decreased V/Q inequality
|
|
|
Which way does the O2 dissociation curve shift in exercise?
|
right. Increased PCO2, [H+], temperature
|
|
|
how does CO change in response to exercise?
|
increases 4-5x
|
|
|
What increases HR initially?
|
1. decreased parasympathetic tone 2. increased sympathetic tone (heavy exercise)
|
|
|
What increases SV?
|
1. increased EDV 2. sympathetic activation
|
|
|
what increases venous return in exercise?
|
muscle contraction and breathing <-- vacuum pulls blood into heart (decreased thoracic pressure creates vacuum)
|
|
|
what happens to the a-v O2 difference in exercise?
|
it increases, increasing muscle O2 extraction
|
|
|
which area(s) receive less bloodflow in response to exercise
|
splanchnic circulation
|
|
|
which area(s) receive more bloodflow in exercise?
|
skeletal muscle, coronary
|
|
|
which organs autoregulate their bloodflow?
|
brain and kidney
|
|
|
what are some causes of local dilation?
|
bradykinin, lactic acid, adenosine, NO, CO2
|
|
|
2 categories for pulmonary function test
|
test for hypoxemia, test for ventilatory capacity
|
|
|
forced expiration test can identify
|
obstructive or restrictive disease
|
|
|
obstructive disease involves
|
increased resistance, larger lung volumes
|
|
|
restrictive disease involves
|
low lung volumes, resistance is unchanged or lower
|
|
|
FEV
|
forced expiratory volume. Usually measured as FEV1 - volume expired after 1 sec
|
|
|
FVC
|
forced vital capacity
|
|
|
FEV/FVC ratio in obstructive disease
|
low. (less than 0.8)
|
|
|
FEV/FVC ratio in restrictive disease
|
high or normal (greater than 0.8)
|
|
|
Forced expiratory flow (FEF)
|
another measure of airway resistance. Measure time at 25% of expiration and 75% expiration (where it's linear)
|
|
|
forced expiration tests are depicted in
|
flow-volume curves. Shows rate of flow compared with change in volume
|
|
|
what method measures functional reserve capacity?
|
Helium dilution. Increased vol of lungs increased dilution
|
|
|
normal FEV/FVC ratio
|
0.8
|
|
|
what factors determine FEV1?
|
lung volume (higher lung vol, higher FEV), airway resistance (affects velocity of airflow out), airway collapse (increased pleural pressure)
|
|
|
2 categories for pulmonary function test
|
test for hypoxemia, test for ventilatory capacity
|
|
|
2 categories for pulmonary function test
|
test for hypoxemia, test for ventilatory capacity
|
|
|
why is FEV1 reduced in restrictive disease?
|
low lung volume
|
|
|
forced expiration test can identify
|
obstructive or restrictive disease
|
|
|
forced expiration test can identify
|
obstructive or restrictive disease
|
|
|
why is FEV1 reduced in obstructive disease?
|
slow flow, higher airway resistance
|
|
|
obstructive disease involves
|
increased resistance, larger lung volumes
|
|
|
obstructive disease involves
|
increased resistance, larger lung volumes
|
|
|
why is FVC decreased in obstructive disease?
|
earlier airway collapse
|
|
|
restrictive disease involves
|
low lung volumes, resistance is unchanged or lower
|
|
|
restrictive disease involves
|
low lung volumes, resistance is unchanged or lower
|
|
|
FEV
|
forced expiratory volume. Usually measured as FEV1 - volume expired after 1 sec
|
|
|
why is FVC decreased in restrictive disease?
|
low lung volume, low TLC
|
|
|
FVC
|
forced vital capacity
|
|
|
reductions in ventilation or perfusion can be measured using
|
V/Q scan. Uses radioactive gas to check absorption pattern in lung
|
|
|
FEV
|
forced expiratory volume. Usually measured as FEV1 - volume expired after 1 sec
|
|
|
FEV/FVC ratio in obstructive disease
|
low. (less than 0.8)
|
|
|
CO measures
|
diffusion capacity
|
|
|
FEV/FVC ratio in restrictive disease
|
high or normal (greater than 0.8)
|
|
|
Forced expiratory flow (FEF)
|
another measure of airway resistance. Measure time at 25% of expiration and 75% expiration (where it's linear)
|
|
|
diffusion capacity measures
|
impairment due to decreased diffusion. Uses expired CO levels to measure how much blood is taken into capillaries. Looking for DL.
|
|
|
FVC
|
forced vital capacity
|
|
|
DLCO gives information about
|
the diffusion barrier - thickness, surface area (as well as solubility and MW of the gas). Can also be reduced in cases of ventilation inequality
|
|
|
forced expiration tests are depicted in
|
flow-volume curves. Shows rate of flow compared with change in volume
|
|
|
FEV/FVC ratio in obstructive disease
|
low. (less than 0.8)
|
|
|
how can ventilation inequality be measured?
|
expired N2 conc following a single breath of pure O2. equal ventilation --> equal N2 dilution in alveoli by the O2.
|
|
|
FEV/FVC ratio in restrictive disease
|
high or normal (greater than 0.8)
|
|
|
what method measures functional reserve capacity?
|
Helium dilution. Increased vol of lungs increased dilution
|
|
|
Forced expiratory flow (FEF)
|
another measure of airway resistance. Measure time at 25% of expiration and 75% expiration (where it's linear)
|
|
|
normal FEV/FVC ratio
|
0.8
|
|
|
obstructive disease and decreased DLCO indicate
|
emphysema
|
|
|
forced expiration tests are depicted in
|
flow-volume curves. Shows rate of flow compared with change in volume
|
|
|
what factors determine FEV1?
|
lung volume (higher lung vol, higher FEV), airway resistance (affects velocity of airflow out), airway collapse (increased pleural pressure)
|
|
|
restrictive disease and decreased DLCO indicate
|
fibrosis
|
|
|
what method measures functional reserve capacity?
|
Helium dilution. Increased vol of lungs increased dilution
|
|
|
why is FEV1 reduced in restrictive disease?
|
low lung volume
|
|
|
unequal ventilation will show
|
a steady increase in nitrogen conc. during exhalation to residual volume
|
|
|
normal FEV/FVC ratio
|
0.8
|
|
|
why is FEV1 reduced in obstructive disease?
|
slow flow, higher airway resistance
|
|
|
blood gas measurements use ________ to demonstrate ventilation-perfusion inequalities
|
PAO2 and PaO2
|
|
|
what factors determine FEV1?
|
lung volume (higher lung vol, higher FEV), airway resistance (affects velocity of airflow out), airway collapse (increased pleural pressure)
|
|
|
why is FVC decreased in obstructive disease?
|
earlier airway collapse
|
|
|
why is FEV1 reduced in restrictive disease?
|
low lung volume
|
|
|
why is FEV1 reduced in obstructive disease?
|
slow flow, higher airway resistance
|
|
|
why is FVC decreased in restrictive disease?
|
low lung volume, low TLC
|
|
|
why is FVC decreased in obstructive disease?
|
earlier airway collapse
|
|
|
reductions in ventilation or perfusion can be measured using
|
V/Q scan. Uses radioactive gas to check absorption pattern in lung
|
|
|
why is FVC decreased in restrictive disease?
|
low lung volume, low TLC
|
|
|
CO measures
|
diffusion capacity
|
|
|
reductions in ventilation or perfusion can be measured using
|
V/Q scan. Uses radioactive gas to check absorption pattern in lung
|
|
|
CO measures
|
diffusion capacity
|
|
|
diffusion capacity measures
|
impairment due to decreased diffusion. Uses expired CO levels to measure how much blood is taken into capillaries. Looking for DL.
|
|
|
diffusion capacity measures
|
impairment due to decreased diffusion. Uses expired CO levels to measure how much blood is taken into capillaries. Looking for DL.
|
|
|
DLCO gives information about
|
the diffusion barrier - thickness, surface area (as well as solubility and MW of the gas). Can also be reduced in cases of ventilation inequality
|
|
|
how can ventilation inequality be measured?
|
expired N2 conc following a single breath of pure O2. equal ventilation --> equal N2 dilution in alveoli by the O2.
|
|
|
DLCO gives information about
|
the diffusion barrier - thickness, surface area (as well as solubility and MW of the gas). Can also be reduced in cases of ventilation inequality
|
|
|
obstructive disease and decreased DLCO indicate
|
emphysema
|
|
|
how can ventilation inequality be measured?
|
expired N2 conc following a single breath of pure O2. equal ventilation --> equal N2 dilution in alveoli by the O2.
|
|
|
restrictive disease and decreased DLCO indicate
|
fibrosis
|
|
|
obstructive disease and decreased DLCO indicate
|
emphysema
|
|
|
unequal ventilation will show
|
a steady increase in nitrogen conc. during exhalation to residual volume
|
|
|
blood gas measurements use ________ to demonstrate ventilation-perfusion inequalities
|
PAO2 and PaO2
|
|
|
restrictive disease and decreased DLCO indicate
|
fibrosis
|
|
|
unequal ventilation will show
|
a steady increase in nitrogen conc. during exhalation to residual volume
|
|
|
blood gas measurements use ________ to demonstrate ventilation-perfusion inequalities
|
PAO2 and PaO2. Calculate PAO2 by PIO2 - (PaCO2/R).
|
